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Podiatry Interview Review Manual

© 2010 OZ

AJM Prism Manual – 100 pages, the best one out there

Crozer-Keystone 2nd edition – Another really good ones

Surgery Review book (OCPM/SCPM) – Simple and easy to read

Classification manual (CCPM) – Quick overview of classifications to know cold

Radiology Review notes (SCPM) – Some topics are over-detailed for the interviews

Mangold manual – Abx, Labs, Pain management, Surgery procedures, EKG (SCPM)

Sean Pimp List – Excellent list of Q and A

OZ manual

Hershey – 1 of 2 classic 1000+ notes

Presby – 1 of 2 classic 1000+ notes

Residency Review manual – Good for some classic articles, lots of pages but a quick read

Trauma manual – Didn’t read this one before interviews

ABPS questions – Good practice run Qs

NBPME 2 questions – Some what easy Qs

Scholl Misc Manual – Sample cases to work up

Classic Articles

<Additional resource you should have is the “Podiatric Medicine and Surgery Part II: Pearls of Wisdom
: that one you will have to buy ~ 50$ @ Amazon/Walmart>

PRISM And Externship Guide.

A 100-page Podiatric Residency Interview Study Manual.

This 2009 First Edition was edited by RC.

David Hockney’s Mount Fuji and Flowers

Preparing for externships and the residency interview is one of the most challenging tasks facing the podiatric
medical student. It can be a completely overwhelming exercise unless you are efficient about the way you approach the
process. If you are reading this introduction, then you are already aware that in order to be fully prepared for
residency interviews and externships, you need to study a lot more than what you got from classes and clinic in school.

You should have a strategy going into the residency interview, just as your interviewers should have a strategy about
how to evaluate you. One of the most important ways to prepare is to think about the interview process from the other
side of the table. The interviewers only have a given amount of time to spend with you; no more than 30 minutes in most
cases. This is not a lot of time. What do they really want to know about you? What information can they get from you in 30
minutes that tells them about what kind of doctor you are going to be?
Remember that the attendings of a program are essentially hiring you to help handle their patients, and at the
interview they want to know if they can trust you with this responsibility. Asking inane, esoteric questions during the
academic interview doesn’t really give them this information. On the other hand, asking basic “work-up” based questions
does. These questions allow the interviewer to see how you will be approaching their patients in the future. It gives
them information about how your mind works when dealing with patients on an everyday level. If you were an attending on
the other side of the table, would you rather know if the student can take you through the clotting cascade, or how they are
going to handle your patient in the ED with a suspected post-operative infection?

Another thing to think about is that the interviewers need to compare your answers to the other people you are going
against for the program, and they don’t have a lot of time to do this. They should have some standardized way of
quantitatively grading your performance against the performance of others. I like to think of this as “check marks”. Think
of the interviewers asking the same exact questions to each student and then having a form or a list in front of them. There
are certain “buzz words” that they want you to say and certain questions that they want you to ask during the work-up. The
more things you get correct, the more “check marks” you get on their form. And at the end of the day, they add up all the
“check marks” and see who got the most. Your goal during a 30-minute interview should be to get as many “check marks”
as possible.

This manual was put together based on the way that I studied for interviews. There is certainly no shortage of
material to study, and this manual in no way can replace or even rival some of the other study guides that are out there. The
goal of the PRISM is simply to help you be as efficient as possible with the process and to think about the interview
from the other side of the table. My goal with coming up with the following sheets was to take a given topic and fit
everything that could be asked about that topic during an interview onto a single sheet of paper. Realize that it is not all the
information on a given topic, but all the information that is likely to be asked during an interview. There’s a big
difference there.
Your goal heading into the interview process should be to have a standardized way of handling every question or
situation that you are presented with, and to get as many “check marks” as possible. Think about it. The easiest way for the
interviewers to answer the questions they have about you is to present you with a clinical scenario, and see how you work-up
that situation. Therefore, the most efficient way to study for interviews is to take a given topic, and then “work-up” a patient
in that situation. I made all of the AJM Sheets with this thought in mind (see “Gout” example on next page).

Also included in this manual are AJM Lists. Studying is by nature a passive exercise, but the interview process
involves actively answering questions and talking out loud. The Lists allow you to actively think about a topic like you will
be expected to do during the interview. It takes a broad, clinical situation/subject and asks you to come up with as many
answers as possible. I hope that they help you realize that there is not always one answer to a question, but possibly many
different answers that can all be considered correct. The more answers that you can come up with for a given List, the
more “check marks” you get during the interview.

Again, this manual is far from complete and absolutely does not contain all of the information you will be asked
during an interview. It simply hopes to change the way that you think about the interview process and highlight some
of the information that you are most likely to be asked. I limited it to 100 pages of the most commonly asked information
and the kind of stuff that I’m going to ask if I’m a residency director someday. It is not in any way meant to be

I also want this to be a “living” document. It is not intended to be commercial and should never be sold. I’m going
to take it with me when I graduate from residency, leave it with the Inova program, and distribute it electronically to anyone
who wants it. Feel free to change/update it in any way that you think would be helpful, but please keep it to exactly 100
pages. In other words, if you think something is important and should be included, you also have to decide what isn’t as
important and should be taken out. It will be interesting to see how it evolves over the years!

Good luck and please do not hesitate to contact me if there is any way that I can be of service to you.
AJM Sheet Example: Gout

CC: Pt classically complains of a “red, hot, swollen joint”. Typical patient is a male in the 6th decade (as much as a 20:1 M:F ratio).
HPI: -Nature: Intense pain out of proportion with swelling/pressure.
-Location: Single or multiple joints. Unilateral or bilateral. Most common is 1st MPJ, but can occur in any joint.
-Acute, abrupt onset; more commonly at night.
-Aggravating Factors: Pressure, WB, diet (red wine, organ meat, lard, seafood).
-History: Recurrent gouty attacks are very common
PMH: -Genetic enzyme defects, obesity, lead poisoning, tumor, psoriasis, hemolytic anemia may all be underlying causes.
-Renal disease (renal disease is 2nd most common complication of gout).
-Kidney stones
Meds: -Diuretics, low dose ASA, TB meds, warfarin may exacerbate.
SH: -Diets high in red wine, organ meat, lard and seafood may exacerbate.
All/FH: -Usually non-contributory
ROS: -May be associated with fever.

Physical Exam
-Derm: -Erythema, Calor, Edema present at affected joint
-May see tophi sticking out of skin
-Vasc: -Non-pitting edema at affected site
-Neuro: -Intense pain out of proportion
-Ortho: -Decreased PROM/AROM at affected joint with guarding.

-Plain Film Radiograph: -Increased soft tissue density with joint effusion. Tophi may be visible in soft tissue.
-Fine striated pattern of periosteal reaction along the cortex adjacent to tophi
-Lace pattern of osseous erosion
-Round osseous erosion with a sclerotic margin (“rat bite erosion” or “punched-out lesion”).
-Martel’s sign: Expansile lesion with an overhanging osseous margin.

-Joint aspirate is mandatory for diagnosis of gout:
-Needle-shaped monosodium urate crystals
-Negatively birefringent (bright yellow) when viewed under polarizing light microscope parallel to axis of lens.
-Blue when perpendicular to axis of lens.
-Serum uric acid levels > 7.5mg/dl (non-diagnostic)
-Elevated ESR
-Synovial fluid analysis: Elevated leukocytes with a predomination of neutrophils
-Generalized increased white cell count

-General Information
-Definition: Metabolic disorder secondary to the build-up of monosodium urate crystals and supersaturated hyperuricemic extracellular fluids in and around
joints and tendons causing the clinical manifestations of a red, hot, swollen joint.
-It is the most common cause of inflammatory arthritis in men over the age of 30.

-Primary: Elevated serum urate levels or urate deposition secondary to inherent disorders of uric acid metabolism.
-Uric Acid Overproduction (Metabolic Gout): 10% of patients
-Excessive amounts of uric acid excreted into the urine
-Occurs secondary to an enzyme defect, tumor, psoriasis, hemolytic anemia, etc.
-Dx: Uric Acid Level >600mg in a 24-hour urine collection
-Uric Acid Undersecretion (Renal Gout): 90% of patients
-Relative deficit in the renal excretion of uric acid.
-Secondary: A minor clinical feature secondary to some genetic or acquired process

-Symptomatic Pharmacology (relieves symptoms, but doesn’t attack underlying pathophysiology)
-Indomethacin: 50mg PO q8
-Colchicine: 0.5-1.0mg PO initially, then 0.5mg PO q1 hour until symptoms (GI) or pain relief
Then around 0.5mg PO qday as prophylaxis
-Active/Physiologic Pharmocology (attacks underlying pathophysiology and prevents recurrence)
-Allopurinol: 100-600mg PO qday as single or divided doses.
-Blocks uric acid production by inhibition of the enzyme xanthine oxidase.
-Probenecid: 250mg PO bid for one week; then 500mg PO bid
-Increases uric acid removal from urine (decreases reabsorption)
-Surgical Intervention (if you get rid of the joint, then you get rid of a potential site for gout to attack!)

-Further Reading
-Roper RB. The perioperative management of the gouty patient. J Amer Podiatry Assoc. 1984 Apr;74(4):168-72.
-Schlesinger N. Management of acute and chronic gouty arthritis: present state-of-the-art. Drugs. 2004;64(21):2399-2416.
-Keith MP. Updates in the management of gout. Am J Med. 2007 Mar;120(3):221-4.

Table of Contents:

AJM Lists [Pages 5-29] -45: Common Situational Bugs

-46: Empiric Antibiotic Choices
-5: Introduction and Proposed Schedule -47: IDSA Empiric Recommendations
-48-49: Bugs with Drug of Choice
-Surgery Lists…………………....……….6-10
-50: Antibiotic Dosing Guide
-6: HAV Procedures with Indications
-7: Risks and Complications of Surgery -Trauma…………………………………51-68
-8: Measurement of Radiographic Angles -51: Introduction and Contents
-9: Radiographic Review -52: The Trauma Work-Up
-10: Surgical Layers of Dissection -53-54: General Trauma Topics
-55: Digital Fractures
-Medicine Lists…………………….……11-15
-56: Sesamoid Trauma
-11: Post-Op Fever Etiology -57: Metatarsal Fractures
-12: Lab Infection Diagnosis -58: 5th Metatarsal Fractures
-13: Imaging Infection Diagnosis -59: Metatarsal Stress Fractures
-14: Labs and Why they are important -60: LisFranc Trauma
-15: Vascular and Neurologic Assessment -61: Navicular Trauma
-62: Talar Fractures
-Trauma Lists…………………………...16-20 -63: Calcaneal Fractures
-16: Ankle Fx DDx -64-65: Ankle Fractures
-17: Synthes Chart with Screw Anatomy -66: General Tendon Trauma
-18: Methods of Fixation -67: Achilles Tendon Work-up
-19: Hardware Insertion -68: Achilles Tendon Treatment
-20: Classifications
-Peri-Operative Medicine and Surgery….69-99
-Anatomy Lists……………………….…21-25 -69: Introduction and Contents
-Peri-Operative Medicine
-21: Ossification of Lower Extremity Bones
-70: Admission Orders
-22: 5th Metatarsal Anatomy
-71: Electrolyte Basics
-23: Dorsal Arterial Anastomosis Variations
-72: Glucose Control
-24: Lower Extremity Peripheral Nerve Blockade
-73: Fluids
-25: Dermatomes with Spinal Levels
-74: Post-Op Fever
-Social Interview Lists……………....….26-29 -75: DVT
-76: Pain Management
-General Surgery Topics
-77: AO
-78: Plates and Screws
AJM Sheets [Pages 30-100]: -79: Suture Sheet
-80: Surgical Instruments
-Diabetic Foot Infections……………….30-50 -81: Power Instrumentation
-30: Introduction and Contents -82: Biomaterials
-31: Diabetic Foot Infection History -83: External Fixation
-32: Diabetic Foot Infection Physical Exam -84: Bone/Wound Healing
-33: Wound Classification Systems -Specific Surgery Topics
-34-35: Diabetic Foot Infection Laboratory Results -85: How to “Work-Up” a Surgical Patient
-36: Common Infective Agents -86-87: Digital Deformities
-37: Diabetic Foot Infection Imaging Studies -88: Lesser Metatarsals
-38: Diabetic Foot Infection Pathogenesis -89: 5th Ray
-39: Functional Diabetic Foot Infection Anatomy -90-91: HAV
-40: Osteomyelitis -92: HAV Complications
-41: Osteomyelitis Classifications -93-94: HL/HR
-42: Charcot Neuroarthropathy -95-96: Pes Plano Valgus
-43: Charcot Classifications -97-98: Cavus
-44: Differentiating Charcot vs. Osteomyelitis -99: Equinus

-Page 100: “Can you give me some good articles to read?”

Lists Schedule:
AJM Lists were originally created to be done during an externship. Students often have a lot of
down time during the day while the residents are doing work that doesn’t need assistance. The lists give
the students something to do during this time and make it look like they’re busy instead of just standing
around doing nothing (in front of the attendings and residents). It also encourages students to collaborate,
and shows the residents/attendings that they can work well with each other and in groups.
When I was a resident, I would give the students one list and a related article each day, and then
we would try and get together once a week to go over them. It usually generated a great deal of good
discussion. If you are using these lists to study on your own, get together with a group of friends to go over
them and talk about your answers out loud. The way you know if you really understand a topic is if you
can intelligently discuss it and explain it to your peers.
Again, studying is by nature a passive exercise, but at the interview you will be expected to
actively answer questions out loud. Only about half of what the interviewers appreciate from your
answer is the actual content, the other half is how you say it. Remember that the interviewers are
probably asking the same question to every student that walks through the door, so they’ve probably heard
the same answer several times before you even sit down. What they haven’t heard is how you’ve said it!
In other words, you should also be studying “how to say it”.
See the following suggested schedule:

Mondays: Surgery
-HAV Procedures with Indications (page 6)
-Risks and Complications of Surgery (page 7)
-Measurement of Radiographic Angles (page 8)
-Radiographic Review (page 9)
-Surgical Layers of Dissection (page 10)

Tuesdays: Medicine
-Post-Op Fever Etiology (page 11)
-Lab Infection Diagnosis (page 12)
-Imaging Infection Diagnosis (page 13)
-Labs and Why they are Important (page 14)
-Vascular and Neurologic Assessment (page 15)

Wednesdays: Trauma
-Ankle Fx DDx (page 16)
-Synthes Fill-in Chart with Screw Anatomy (page 17)
-Methods of Fixation (page 18)
-Hardware Insertion (page 19)
-Classifications (page 20)

Thursdays: Anatomy
-Ossification of Lower Extremity Bones (page 21)
-5th Metatarsal Anatomy (page 22)
-Dorsal Arterial Anastomosis Variations (page 23)
-Lower Extremity Peripheral Nerve Blockade (page 24)
-Dermatomes with Spinal Levels (page 25)

Fridays: Social Questions

-Social Question Sheets: Part I (pages 26-27)
Part II (pages 28-29)
Part III (page 30)

AJM List: HAV Procedures and Indications

Clinical Scenario: You are a first year resident scheduled to be in a “bunion procedure” at a surgery center
tomorrow. You are working with the attending for the first time and want to appear as prepared as
possible. Name as many “bunion procedures” as you can.
Student Goal: Name 20 HAV procedures from distal to proximal. What are the specific clinical and
radiographic indications for each?

AJM List: Surgical Complications

Clinical Scenario: You are a first year resident at a surgery center. The attending isn’t there yet, and you
aren’t exactly sure of the specifics of the case, but you want to have all the paperwork filled out for when
the attending gets there (including the consent).
Student Goal: Name as many risks and complications of a generic foot and ankle surgery as possible.
What are some specific complications associated with some specific surgeries? How would you handle
these complications in the post-op period?

AJM List: Measurement of Radiographic Angles

Student Goal: Name as many foot and ankle radiographic measurements as possible. What are the normal
values? What clinical information is this giving you?

AJM List: Radiology Review

Clinical Scenario: There is a big difference between describing and diagnosing a radiograph. During an
interview, you need to be able to describe the findings you are seeing before you diagnose the pathology.
You also need to be able to do this out loud during the interview process.
Student Goal: Out loud, using as many terms as possible, and in a systematic manner, intelligently describe
the following radiographs before making a diagnosis.

Note: RC and I found it very helpful to practice for interviews by picking up random podiatry textbooks,
and alternating through the pictures describing the radiographs out loud.

AJM List: Surgical Layers of Dissection

Student Goal: Identify the 5 surgical planes and 3 surgical intervals of dissection. What structures will you
see in each plane/interval for a standard HAV procedure? For a standard digital procedure?

AJM List: Post-operative Fever

Clinical Scenario: On call, you are paged at 3am by a nurse to report a fever in a patient POD#2 of
Student Goal: Name as many potential causes of fever as possible. How would you diagnose and work-up
each one?

AJM List: Laboratory Infection Diagnosis

Clinical Scenario: A patient enters the Emergency Department with a suspected lower extremity infection.
Student Goal: Name as many laboratory tests that you can order to help diagnose an infection. What
clinical information is each test really telling you about the situation?

AJM List: Imaging Infection Diagnosis

Clinical Scenario: A patient enters the Emergency Department with a suspected lower extremity infection.
Student Goal: Name as many imaging tests that you can order to help diagnose an infection. Exactly what
are you looking for with each test?

AJM List: Routine Lab List

Student Goal: Identify routine labs, their normal values, and what information they are giving you about
the patient. Which labs should be drawn when an infection is suspected and why? Which should be done
in the pre-operative work-up of a patient?

AJM List: Vascular and Neurologic Assessment

Student Goal: Name as many subjective and objective vascular and neurologic assessments as possible
while performing a lower extremity examination.

AJM List: Ankle Fracture

Clinical Scenario: A patient arrives in the ED exclaiming that they “broke their ankle”. Obviously you
will take an x-ray, but what exactly are you looking for on the radiograph?
Student Goal: Name as many possible fractures that can occur following an ankle sprain.

-Bonus: What do the “Ottawa Ankle Rules” say about getting a radiograph following an ankle sprain?

AJM List: Screw Games

Thread Spheric Screwdriver: Core Drill bit Drill bit Tap

Diameter Head Hex or Diameter Thread Gliding Diameter
Diameter Cruciate? Hole Hole
Mini Frag Set



Small Frag Set


4.0mm PT

4.0mm FT

Large Frag Set


Mall Screw
6.5mm PT

6.5mm FT
Hint: pg 76 McGlam’s

-Pitch on a cortical screw?:

-Pitch on a cancellous screw?:

-Draw a screw labeled with as many anatomic landmarks identified as you can (eg. Head, major
diameter, pitch, etc):

AJM List: Methods of Fixation

Student Goal: Name as many methods as possible to fixate an osteotomy.

AJM List: Hardware Insertion Technique

Student Goal: Describe standard AO lag screw insertion technique. What is the purpose of each step?
Why are they done in that particular order? What is compromised technique? Splintage?

-Bonus: What is the quantitative measurement of “two-finger tightness?”:

-What are some strategies for hardware extraction?:

AJM List: Classifications

Student Goal: Name as many different trauma classifications as you can that cover the foot and ankle from
distal to proximal.

AJM List: Ossification Dates

Student Goal: Name every bone in the lower extremity in order of ossification date.

AJM List: 5th Metatarsal Anatomy

Student Goal: Name as many structures as you can that attach to the 5th metatarsal.

AJM List: Dorsal Arterial Anastamosis Variations

Student Goal: Draw out as many different variations as possible for the arterial supply to the dorsum of the

How does this apply to the angiosome principles? (hint: read Dr. Attinger’s work)

AJM List: Local Anesthesia and Peripheral Nerve Blockade

Student Goal: Identify as many named foot and ankle peripheral nerve blocks as possible. Which specific
nerves are being anesthetized with each block?

-Toxic Dose of Lidocaine?:

-Toxic Dose of Marcaine?:

-How and why does epinephrine influence the toxic dose of a local anesthetic?

-What are the reversing agents for local anesthetic toxicity?

AJM List: Dermatomes

Student Goal: Draw a lower extremity with all of the dermatomes illustrated with associated spinal levels
and landmarks.

-Bonus: How are dermatomes different than sclerotomes?

AJM List: Social Questions
Part I: General Questions

Strengths: Be prepared to give at least 3 personal strengths and why they will make you a good resident.
-Strength #1:
-Why it will make you a good resident:
-Strength #2:
-Strength #3:

Weaknesses: Be prepared to give at least 3 weaknesses, and more importantly, how you are remedying them.
-Weakness #1:
-Weakness #2
-Weakness #3:

Goals: Be prepared to give professional and personal goals, and how you will go about accomplishing them. Another
form this question could take is where you see yourself in a given number of years.
-Professional Goals:
-Goal #1:
-Goal #2:
-Goal #3:

-Personal Goals: -Where do you see yourself in:

-Goal #1: -5 years?:
-Goal #2: -10 years?:
-Goal #3: -25 years?:

Program Specific: For each program that you apply to, you should have a list of strengths and weaknesses for that
program. Obviously be careful with weaknesses, and always have a way that you can improve the situation. You
should be able to answer why you personally are a good fit for that program. I found it helpful to have a list of
priorities that I was looking for in the different programs, and then described how that particular program fit into my

-Program #1:
-Strength #1: -What you are able to bring to the program:
-Strength #2: -Favorite attending and why:
-Strength #3: -Least favorite attending and why:
-Weakness #1: -Favorite resident and why:
-Weakness #2: -Least favorite resident and why:
-Best case you saw at the program:
Here’s my list of priorities that I used based on what was important to me. Everyone’s list can (and really should) be
different, this is just to provide an example:
1. Surgery/Academics
-How is this program going to make you a better doctor? You’re going to learn surgery and do
some academic events at any program in the country, is there anything special about this particular
program that sets it apart? Do they really care about academics, or are they just done to meet a
requirement? (Hint: a good way to tell this is to see how often attendings are excited to show up to
and be involved in meetings). Although the quantity of surgery is important (you have be able to
get your “numbers”), also consider the quality and variety of the surgeries at a program.
2. Outside Rotations
-All programs have the same set of “core” rotations that everyone has to do. Is there anything
unique about this particular program that shows that they really care about your complete education
and want you to have outstanding quality and variety to your residency experience?
3. Location:
-This one kind of speaks for itself, but you should consider if you are going to be completely at one
hospital versus traveling to different hospitals and different surgery centers (there are pros and cons
to each). Also consider what the presence is of the program within the hospital. Is the podiatric
surgery department intricately involved in the hospital, or is it more of an afterthought?
4. Independence
-I’m an independent guy who likes to come up with and pursue my own projects and ideas. Other
people really like structure and would prefer to get an exact schedule for the next three years on day
1 of their residency. So this was something that I was really looking for, but someone else may
want exactly the opposite.
5. The Future
-How is this program going to help you accomplish your professional goals now and after you

AJM List: Social Questions
Part II: Personal Questions

Personal Questions: These questions are hard to answer and often irrelevant, but you should have answers
ready to go (even if they are made up). Answer as specifically as possible to give the interviewer
something tangible to grab onto about yourself. Always answer “Why?” before they have the chance to ask
you. “Why?” may be the most important question you get during the interview process.

-What do you like to do with your free time?

-Answer #1:
-Answer #2:
-Answer #3:
-What professional accomplishments are you most proud of?:
-What personal accomplishments are you most proud of?:
-What was your hardest/most trying experience? What did you learn from this?:
-What is your most embarrassing moment?:
-Name three things that you would bring with you to a deserted island:
-Tell me a joke:
-Favorite Movie:
-Favorite Book:
-Last movie you saw:
-Something you liked about it:
-Something you didn’t like about it:
-Last book you read:
-Favorite Band/Kind of Music:
-Last concert you went to:
-Tell me about the craziest patient you have ever had to deal with:
-What is your funniest medical story?:
-What animal would you be and why?:
-What tree would you be and why?:
-Favorite TV show:
-Favorite actor:
-Favorite actress:
-Favorite surgical instrument:
-Do you have any pets?:
-Favorite pet:
-If you could take a vacation anywhere in the world, where would it be?:
-Tell me something about yourself that few people know:
-Who’s the most important person in your life (real and/or fictional) that you have never met?:

-And of course, “Tell me a little about yourself”:

-Important Note: You should be able to spout off both a 30-second and a 5-minute answer to this
question at the drop of a hat.

-Note: These questions are very easy to answer if you think about them, but you don’t have time to think
during the interview. You don’t want to show any hesitation during this process, especially questions about
yourself. The worst answer you can give to a specific personal question is “I don’t know.” What is that
saying about you?

***Practice answering all of these questions out loud to yourself in the time leading up to interviews! You
may feel silly talking to yourself, but it is undoubtedly the best way to prepare for this line of

AJM List: Social Questions
Part III: Academic and Ethical Social Questions

Academic Social Questions: These are hidden academic questions, but ones you can’t study for in any
book. Please plan these questions out because it is very easy to get trapped in your answer if you lie.

-What journals do you read? Which is your favorite?:

-What was the last good journal article you read? (be able to cite it!):

-What was the last thing you built with your hands?:

-Favorite class in school?:

-Least favorite class in school?:

-Favorite teacher in school?:

-What types of things does the field of podiatric surgery need to do to improve in the future?:

-What is something you learned about the field of podiatric surgery since you started school/externships?:

-Have you participated in any research projects? Why or why not? What was your role in this project?:

-What would you do with your life if you couldn’t be a surgeon/physician?:

Ethical Questions: The key to answering an ethical question is to take a step back from the situation.
Pretend that someone else is in the situation and you are going to give that person advice. Don’t pretend
that you are in the situation; it actually makes it more difficult to think through the process. Remember the
concept of chain-of-command and also remember that there is a real patient involved.
Something else that really helped me out was having a clear order of my priorities. Everyone’s
can be different, but mine are:
1. Responsibility to the patient as a physician
2. Responsibility as an employee of a hospital
3. Responsibility as a resident of the residency program
4. Responsibility for my own education
5. Responsibility for the education of junior residents/students

So whatever ethical situation I was put into, I would make decisions based upon this order of
priorities. Remember that usually there is no right or wrong answer when it comes to ethical situations.
Like George Costanza said about beating a lie detector test: “It’s not a lie (wrong), if you believe it.”

The Semistructured Conversation: Many residency programs (and especially general medicine or general
surgery residency programs) have reevaluated the way that they have traditionally selected residents, and
have moved away from a structured academic interview. They have instead moved onto what’s called a
“semistructured conversation” that tries to evaluate if the applicants have the “knowledge, skills and
attitudes deemed necessary for the practice of medicine”. The questions are a kind of mix of academic and
ethical questions that can develop into more of a conversation. So while these are not purely academic
questions, they can lead into a conversation about specific academic topics. There’s actually a couple
articles about it (Neitzschman HR, Neitzchman LH, Dowling A. Key Component of Resident Selection: The
Semistructured Conversation. Acad Radio. 9: 1423-29; 2002.), and I’ve put together a long list of these
type questions on the next List.

AJM List: Social Questions
Part IV: The Semistructured Conversation Interview Questions

-Tell me about a patient care situation in which podiatric surgery altered the management of the patient.
-Describe a critical clinical situation and how you communicated with the family.
-Tell me about something you learned during one of your externships.
-How would you respond to a patient who asks, “Am I going to die?”
-Can you recall any time when you disagreed with a patient’s diagnosis or treatment?
-Tell us about the biggest argument/controversy you were involved with in podiatry school.
-Give us an example of a situation when you were pivotal in the resolution of a conflict between two other people.
-Suppose you’re in charge of the call schedule. You need to fill a slot with one of two people, one of whom has told you he
has to be out of town as best man in a wedding, and the other has to present a paper at a meeting. How would you resolve the
-Describe a time when you were in a position to give someone a bad evaluation. How did you handle it?
-What features would you add to a medical school curriculum that you think might better prepare you for a podiatric career?
-Can you recall a time when you received an evaluation with which you disagreed?
-If a referring physician insists that you perform a study on a patient and you believe that study could be harmful to the
patient, how would you handle the situation?
-Describe a patient for whom you felt very little empathy but you knew you should.
-What would you do if you saw a senior resident make a mistake that might harm a patient if not corrected promptly?
-A patient acquires your pager number and home phone number and calls several times per day. How do you handle this
patient’s needs?
-A consulting physician asks you a question, and you are not sure of the answer. How do you handle it?
-Tell me about a negative interaction you had during medical school with anyone from a transporter to an attending and how
the two of you dealt with it at the moment and afterwards.
-What do you see as the most challenging aspects of a podiatric residency?
-How would you handle a situation when you know one of your fellow residents has a problem with drugs or alcohol?
-For what reasons do you want to come this particular geographic area?
-You are on call and someone else asks you a question on a subject you know nothing about. How do you gather information
about the topic expeditiously?
-What resources did you use for researching residency programs?
-Outside of the structured lecture, what other formats did you find most helpful as learning tools?
-Describe for me how you deal with a colleague who is exhibiting evidence of substance abuse.
-Describe your response to an episode of someone cheating on the Gross Anatomy final examination.
-How would you decide (and what factors would you consider), as an HMO executive, whether to immunize 2,500 children
at $100 each or provide one liver transplant at $250,000 each?
-In what ways do you maximize your own health and well-being?
-How would you deal with a fellow resident who is not “pulling their own weight” in their work?
-What personal questions most helped you during medical school?
-Tell me about a patient from whom you learned something.
-How would you like to see podiatric surgery develop over the next 5 years?
-How do you see yourself changing between now and the end of residency?
-Tell me about your experience in using online resources, library resources, and internet resources.
-Did you ever feel as a medical student that you were not part of the clinical team? How did you address the situation in
order to optimize your learning experience?
-Can you recall an experience that made you decide to choose podiatry as a profession?
-Describe one of your most challenging cases during your externships.
-Tell me about an experience in medical school where you felt particularly competent.
-What particular skill do you feel you have that makes podiatric surgery the best specialty for you.
-As you examine different programs, what characteristics are you looking for that we might offer you?
-What diseases or topics have fascinated you in medical school and why?
-What topics interest you that you haven’t had time to explore yet?
-Tell me about an experience when you took a risk that ended up being successful.
-Can you tell me about a patient who had an impact on you?
-Can you recall a time in medical school when you had some doubt about the professional path you have chosen? What did
you do?
-A number of residents (15-20%) leave general surgery residency. What do you think influences their choice?
-How would you rate yourself in terms of your ability to establish rapport and maintain healthy relationships with other
health professionals?

AJM Sheets: Diabetic Foot Infection Work-Up
The Diabetic Foot Infection work-up is arguably the most important concept that you can study
during the interview process because it is the one topic that you are almost guaranteed of being asked at
some point. My thought process during interviews was that if I’m certain that I will be asked about it, I’m
going to spend extra time and energy knowing everything possible on the subject. Every student at
interviews is going to get something along these lines; therefore it’s important to be the most prepared and
best able to “wow” the attendings when asked. So I put together a collection of AJM Sheets (totaling about
20 pages) that goes through an in-depth work-up of a diabetic foot infection.

This topic is also a classic example of hitting as many “check marks” as possible during the
interview by having a standardized way of going through a work-up. The way this situation is often
presented at interviews is for them to simply ask you:
“There is a diabetic patient in the ED with a suspected foot infection. What do you want to know
about the patient, and what do you want to do?”
By having a standardized way of going through this work-up (or any work-up), you will seem
more prepared during the interviews, hit more check marks, and won’t stumble about thinking what to ask
next. The basics of this work-up can be applied to any clinical situation.

This work-up also highlights taking an active approach and going on the offensive during the
interview process. Take control of the interview from the interviewers. Do not simply ask if the patient
has diabetes; ask specific questions about the patient’s knowledge, management and known complications
of diabetes. This will show that you really understand the concepts and pathogenesis of the disease

This section has a lot of the same information presented in a number of different ways, giving you
a couple ways to study. While there is certainly no shortage of material to study this information from, my
favorite article on the topic is a must-read: Lipsky BA, et al. Diagnosis and Treatment of Diabetic Foot
Infections. IDSA Guidelines. CID 2004; 39: 885-910. You also certainly should read: Frykberg RG, et
al. Diabetic foot disorders. A clinical practice guideline (2006 revision). J Foot Ankle Surg. 2006 Sep-Oct;
45(5 Suppl): S1-66. And finally, the June 2006 Supplement of Plastic and Reconstructive Surgery is a
fantastic resource covering a wide variety of diabetic foot issues, mostly from the Georgetown perspective.

-Diabetic Foot Infection History (page 31)
-Diabetic Foot Infection Physical Exam (page 32)
-Wound Classification Systems (page 33)
-Diabetic Foot Infection Laboratory Results (pages 34-35)
-Common Infective Agents with Gram Stain Characteristics (page 36)
-Diabetic Foot Infection Imaging Studies (page 37)
-Diabetic Foot Infection Pathogenesis (page 38)
-Functional Diabetic Foot Infection Anatomy (page 39)
-Osteomyelitis (page 40)
-Osteomyelitis Classifications (page 41)
-Charcot Neuroarthropathy (page 42)
-Charcot Classifications (page 43)
-Differentiating Charcot vs. Osteomyelitis (page 44)
-Common Situational Bugs (page 45)
-Empiric Antibiotic Choices (page 46)
-IDSA Empiric Recommendations (page 47)
-Bugs with Drug of Choice (pages 48-49)
-Antibiotic Dosing Guide (page 50)

AJM Sheet: Diabetic Foot Infection Subjective History

CC: Pt’s can present with a wide variety of complaints ranging from the systemic signs of infection to increased ulcer
drainage to a change in mental status. Infection should always be in your differential diagnosis dealing with any situation.

HPI: Ask the patient at least the following questions:

-NLDOCAT of chief complaint
-Systemic signs of infection: Nausea, vomiting (quantity and quality), fever, chills, night sweats, ague, loss of
appetite, change in mental status, diarrhea (quantity and quality), constipation, change in sleep patterns, headache, shortness
of breath, chest pain, etc.
-Local signs of infection: Patient reported increases in pain, erythema, swelling, temperature, drainage (quantity
and quality), odor, etc.
-Ulcer specific questions if applicable: Duration of ulcer, changes in size/depth/color, dressing changes, dressing
change schedule, wound care products, last formal evaluation, primary wound care specialist, previous treatments, any
history of hospitalization for infection, etc.
-Remember: The patient probably knows their ulcer better than you!
-It is extremely important to get an antibiotic history from the patient. Are they taking any antibiotic therapy
currently (including dosage and last dose)? When was the last time they were prescribed an antibiotic?, etc. This
information can provide useful information with respect to the development of resistant organisms. Specific risk factors
include antibiotic use in the last 6 months, any fluoroquinolone use, and hospitalization in the last 6 months.
-Richard et al. Risk factors and healing impact of multidrug-resistant bacteria in diabetic foot ulcers. Diabet Metab. 2008 Sep.
-Hartemann-Heurtier et al. Diabetic foot ulcer and multidrug-resistance organisms: risk factors and impact. Diabet Med. 2004 Jul.
-Kandemir et al. Risk factors for infection of the diabetic foot with multi-antibiotic resistant microorganisms. J Infect. 2007 May.
-Tetanus Status
-NPO Status

PMH: -DM: Complete DM history including length of disease, previous complications, glucose monitoring schedule,
normal glucose readings, HbA1c values, medications, last podiatric evaluation, last internal medicine evaluation,
implemented preventative measures, evaluation of patients level of understanding of pathogenesis of disease, evaluation of
patients role in self-treatment, etc.
-Any known complications of diabetes with interventions/treatment: cardiac disease, peripheral vascular disease,
hypertension, retinopathy.
-Specifically ask about renal disease and liver disease (antibiotic implications).
-Any other immuno-compromising conditions.
-Any other PMH issues.

PSH: -Specifically any previous amputations, foot/ankle surgeries and diabetes-related surgeries.
Meds: -Detailed list of drugs, dosages, and patient compliance to schedule.
All: -True allergies and reactions to drugs, food, products, etc.

SH: -Very important and not to be overlooked.

-Work: line of work, quantity of WB and ambulation, hours, ability of the patient to take time off or take it
easy, worker’s compensation issues, etc.
-Diet and exercise.
-Home support network. Includes assessment of patient compliance and family
-Smoking, alcohol, drug use.
-House structure: stairs, bathrooms, pets.
-Other wound contamination risk factors.

FH: -Anything applicable.

ROS: -Anything applicable.

***Diabetic foot infections are one of the most challenging aspects of podiatric surgery that will take up a lot of your time,
energy, and stress if you dedicate yourself to the side of limb salvage. Taking a complete history will give you an idea of
how compliant you can expect the patient to be and how actively involved you can expect the patient to be in their care.

AJM Sheet: Diabetic Infection Objective Physical Exam
-Vital Signs: -Temperature: Hyperthermia is a non-descript sign of infection. It is important to monitor temperature on a regular
basis, and follow both current and maximum temperatures. Keep in mind however that Armstrong has documented that 82% of patients
admitted for osteomyelitis were afebrile on admission (JFAS.1996 Jul-Aug; 35(4): 280-3). It has been suggested that diabetic patients,
particularly those with ESRD, are not able to mount an effective immunologic response to the invading pathogen.
-Blood Pressure: Hypotension is a sign of sepsis and non-descript measure of infection.
-Heart Rate: Tachycardia is a sign of sepsis and non-descript measure of infection.
-Respiratory Rate: Increased respiratory rate is a sign of sepsis and non-descript measure of infection.
-Pain Level: Important to document and follow. Has been deemed the “5th vital sign” by JCAHO.
-Glucose Levels: AJM considers blood glucose level the “6th vital sign” and can be one of the most important
quantitative measurements of infection and response to therapy. Research indicates that the immune system is significantly impaired and
essentially not working at levels as high as 150-175 ml/dL. (The Portland Diabetic Project is a good place to start reading about this. Also
see Inzucchi SE. Management of Hyperglycemia in the Hospital Setting. NEJM. Nov 2006. 355;18: 1903-11). Also see the Sheet on
“Glycemic Control” on page 72.
-Ins and Outs: Important in patients with renal compromise.

-Physical Exam
-Wound Characteristics: There are several classification systems you need to know for describing wounds including:
-Wagner Classification
-University of Texas Health System Classification
-PEDIS Classification used by the Infectious Disease Society of America
-Liverpool Classification used by the Musculoskeletal Infectious Disease Society
-Acronym 3D MOBB (depth, diameter, drainage, measure, odor, base, border)
-Regardless of classification, you absolutely must document certain wound characteristics:
-Base: -Exact length, width and depth; consistency (ranging from red/granular to yellow/fibrotic to
black/necrotic. Estimate percentages for mixed bases).
-Depth—Probe to bone? [Grayson JAMA 1995. 89% positive predictive value for OM]. Also…
-Lavery LA. Probe-to-Bone Test for Diagnosing Diabetic Foot Osteomyelitis. Reliable or relic? Diabetes Care. Feb 2007; 30(2): 270-274.
-Wound Edges: -Consider hyperkeratotic, macerated, necrotic, clean, bleeding, epithelial, etc.
-Undermining? Tunneling?
-Drainage: -Consider serous, sanguinous, purulent (describe color), combination, etc.
-Mild, moderate, severe/heavy
-Describe any odor (This is probably Dr. Attinger’s most important variable in infection assessment!)
-Periwound skin: -Consider normal, erythematic (document/draw extent), streaking, stasis changes, trophic changes.
-Describe extent (anatomic level) and nature (pitting vs. non-pitting) of any edema.
-Pulses (DP, PP, PT, Pop, and Fem every time)
-Always doppler if nonpalpable at each level
-CFT, Pedal Hair
-ABI: -Values >0.9 associated with good healing potential
-Values 0.5-0.9 associated with PVD and delayed healing
-Values <0.5 associated with ischemia and problematic healing
-Be wary of elevated values secondary to vessel calcification
-TcPO2: -Values >30mmHg associated with good healing potential [Mars M. Transcutaneous oxygen tension as a predictor of success
after an amputation. JBJS-Am. 1988; 70(9): 1429-30.]
-Values <20mmHg associated with microcirculatory problems and delayed/problematic healing.
-Absolute Pressures: -Should have 40mmHg at ankle and 20mmHg at the digits for healing potential.
-Absolute/Relative skin temperature: compare B/L (normal around 94° F).
-Any other relevant vascular testing.
-Include testing for sensory, motor and autonomic neuropathy
-Sensory testing:
-Posterior column: Vibratory, Proprioception
-Anterior column: Light touch (5.07 SWMF)
-Lateral column: Pain and temperature
-Motor testing:
-Expect intrinsic weakness with advanced neuropathy
-Manual Muscle Testing
-Spinal Reflexes (Achilles, Patellar, Babinski)
-Increase in skin temperature
-Lack of sweating leading to xerosis
-Any other relevant neurologic tests (you should have an awareness of Dellon’s work and the PSSD).
-Document any/all foot deformities, especially osseous prominences.
-Expect intrinsic muscle weakness leading to digital deformities.
-Overall foot type
AJM Sheet: Specific Wound Classification Systems

-Wagner Classification: [Wagner FW: The dysvascular foot: a system of diagnosis and treatment. Foot Ankle 2: 64–122, 1981]
0: Pre-ulcerative area without open lesion
1: Superficial ulcer (partial/full thickness)
2: Ulcer deep to tendon, capsule, bone
3: Stage 2 with abscess, osteomyelitis or joint sepsis
4: Localized gangrene
5: Global foot gangrene

Modified with the following risk factors:

A: Neuropathic
B: Ischemic
C: Neuroischemic

-So an infected ulcer with localized gangrene and bone exposure on a fully sensate, ischemic foot is: Wagner 4B.

-University of Texas: [Lavery LA, Armstrong DG, Harkless LB: Classification of diabetic foot wounds. J Foot Ankle Surg 35:528–531, 1996]

0: 1: 2: 3:

A: No open lesion Superficial Wound Tendon/Capsule Bone/Joint

B: With infection With infection With infection With infection

C: Ischemic Ischemic Ischemic Ischemic

D: Infection/Ischemia Infection/Ischemia Infection/Ischemia Infection/Ischemia

-So an infected ulcer with localized gangrene and bone exposure on a fully sensate, ischemic foot is: UT-3D.

-Liverpool Classification System:

-Primary: -Neuropathic

-Modified with: -Uncomplicated

-Complicated (cellulitis, abscess, OM, etc.)

-PEDIS System: [Lipsky BA, et al. Diagnosis and Treatment of Diabetic Foot Infections. IDSA Guidelines. CID 2004; 39: 885-910].
-Recommended by the Infectious Disease Society of America.
-PEDIS is an acronym standing for perfusion (measure of vascular supply), extent/size, depth/tissue loss, infection,
and sensation.
-Each of the 5 categories is graded from 0 (minimal) to 2 (severe).
-Based on10-point scale with 10 being most serious ulcer with greatest difficulty in treatment.

AJM Sheet: Diabetic Infection Objective Laboratory Results: Basic

-Complete Blood Count (CBC) with Differential:

-Total Leukocyte Count (~4-10 x 10^3 leukocytes/ul)
-Leukocyte is a generalized term for any WBC including neutrophils/granulocytes, monocytes,
lymphocytes, eosinophils and basophils. So an increased leukocyte count can indicate a rise in any or all of these. This is the
reason why a differential is so important.
-Neutrophils/Granulocytes (Usually ~54%; increased >85%)
-Part of the humoral system.
-Phagocytic cells in the inflammatory process.
-Normally take 8-14 days to mature. Functionally last 1-2 days. Half-life 6 hours.
-Would be increased in an inflammatory state.
-PMNs: Mature neutrophils that you would expect to see in an infection.
-Band cells: Immature neutrophils. Presence indicates active, ongoing infection.
-A left shift is an increased neutrophil percentage in the presence of band cells.
-Monocytes (Usually ~6%)
-Phagocytic, bacteriocidal macrophages in the humoral system.
-Accumulate after neutrophils in acute infection.
-Presence indicates post-inflammatory state or chronic infection.
-Lymphocytes (Usually ~37%)
-Part of the cellular system.
-Produce immunoglobulins and express cellular immunity (T and B cells).
-Not normally increased in bone/soft tissue infections.
-Possibly increased in a foreign body reaction.
-Eosinophils (Usually ~2%)
-Part of the cellular system.
-Generally involved in allergic and immune responses.
-Develop in the same line as lymphocytes.
-Increased with acronym NAACP
-(Neoplasm, Allergy, Addison’s, Collagen vascular disorder, Parasites)
-Basophils (Usually ~0.5%)
-Part of cellular immunity.
-Involved with acute allergic responses and histamine release.

-Leukocytosis is an increased WBC. The absolute count tells you very little, but trending can be very
important. An increased leukocyte count indicates an increased level of inflammation, not necessarily
infection. Keep in mind that there are many other causes of leukocytosis besides infection.
-Drugs: Lithium, Corticosteroids
-Leukopenia is a decreased WBC. This could lead to a normal WBC in the presence of infection.
-Drugs: Methotrexate, Phenybutase, Dilantin, Salicylates
-[Armstrong DG. Leukocytosis is a poor indicator of acute osteomyelitis of the foot in DM. JFAS 1996 Jul-Aug; 35(4): 280-3.]

-Chem-7/Metabolic Panel
-Little information about specific infection, but insight into general health of patient.
-General increased concentrations: Dehydrated state
-Acidosis: Non-descript finding in infection
-Increased BUN: Dehydrated state
-BUN/Cr: Renal function which has antibiotic consequences
-Minerals (Ca, Mg, P)
-Abnormal in renal dysfunction with long term vascular consequences.
-Glucose, HbA1c
-Long-term effects of hyperglycemia discussed in pathogenesis section.
-HbA1C: Measure of glycosylated hemoglobin and long-term glucose control:
-1% equals approximately 20 glucose points (7% equals ~140ug/ul)
-Note that the stress of infection will probably cause a hyperglycemic state.
-H&H, Coags
-Essential to know if you are planning surgery.

AJM Sheet: Diabetic Infection Objective Laboratory Results: Advanced

-Erythrocyte Sedimentation Rate (ESR)

-Normal: <20mm/hr Moderate elevation: 20-60mm/hr Severe elevation: >60mm/hr
-Analyzed using the Westergren method, which measures the distance erythrocytes fall in one hour in a vertical
column of anti-coagulated blood under the influence of gravity.
-Sensitive, but not specific for infection as it is increased in any inflammatory state with increased fibrinogen.
-Also elevated in: Pregnancy, DM, ESRD, CAD, CVD, Malignancy, Age, etc.
-[Karr JC. The diagnosis of osteomyelitis in diabetes using ESR. JAPMA 2002 May; 95(5): 314.]
-[Lipsky BA. Bone of contention: diagnosing diabetic foot osteomyelitis. Clin Infect Dis. 2008 Aug; 47(4): 528-30.]

-C-Reactive Protein (CRP)

-Normal: 0-0.6mg/dl
-Measures a liver protein only present in acute inflammation (not normally found at all).
-Sensitive, but not specific for infection.
-Also elevated in: RA, Malignancy, MI, SLE, Pregnancy, etc.
-More expensive and technically difficult to perform.
-[Jeandrot A. Serum procalcitonin and CRP concentrations to distinguish mildly infected from non-infected diabetic foot ulcers: a pilot study.
Diabetologia. 2008 Feb; 51(2): 347-52.]

-Nutrition Analysis
-Normal Value: 3.6-5g/dl
-Value decreased with inflammation and malnutrition.
-Transport protein in liver with important functions in catabolism.
-Normal Value: 19-36 mg/dL
-Not covered well in PRISM, but check out [Arnold M. Nutrition and Wound Healing. Plast Reconstr Surg. 2006 Jun; 117(7 Suppl):

-Wound Culture and Sensitivity

-Wound cultures are still a hotly debated topic because of controversies regarding contamination, colonization and
defensive medicine. Suffice to say that swab cultures are easily contaminated by normal cutaneous flora, so should be taken
as deeply as possible without surface contamination. The ideal situation is a deep wound specimen (not just a swab)
following incision and drainage with pulse lavage before beginning antibiotic therapy.
-Gram Stain (results usually within 24 hours)
-PMNs if present: Do not overlook! Presence indicates inflammation.
-Presence of any organism: essentially irrelevant.
-Preliminary (results usually within 48 hours)
-Gram stain nature (positive/negative) and shape (cocci/bacillus) of any organism
-See chart of common organisms on next page
-Clues you into organism
-Continue Abx unless you are really off-base
-Final (results usually within 72 hours)
-Should always get sensitivities.
-Allows for conclusive Abx planning.

-Blood Cultures
-Should be drawn from 2 sites; 20 minutes apart.
-Indicates bacteremia/septicemia

-Bone Biopsy
-Gold standard for diagnosis of osteomyelitis (discussed further later)

-Consider EKG and CXR if patient is a surgical candidate.

AJM Sheet: Gram Stain Results with Common Infective Agents:

-Aerobic Gram Positive Cocci

Staph aureus Strept pyogenes (Group A)
MRSA Strept agalactiae (Group B)
Staph epi Strept bovis (Group D)
MRSE Strept Viridans

-Anaerobic Gram Positive Cocci


-Aerobic Gram Positive Rods

Bacillus anthracis
Corynebacterium diphtheriae
Listeria Monocytogenes

-Anaerobic Gram Positive Rods

Clostridium perfringens
Clostridium difficile
Clostridium tetani

-Aerobic Gram Negative Rods

Pseudomonas Shigella
E. coli Salmonella
Enterobacter Klebsiella
Proteus Serratia
Vibrio E. Corrodens
Y. pestis P. multicide

-Anaerobic Gram Negative Rods

Bacteroides fragilis

-Aerobic Gram Negative Cocci


Treponium pallidum
Borrelia burgdorferi

AJM Sheet: Imaging in Diabetic Foot Infections

-Plain Film Radiographs

-Soft Tissue: Infection characterized by radiolucent area. One should be able to see a soft tissue deficit if an ulcer is present. It is very important
to rule out emphysema (gas in the tissues) with a plain film. Can also appreciate soft tissue edema.
-Osseous Tissue:
-Early Osteomyelitis signs: No reliable ones. Possible rarefaction and periostitis.
-Subacute OM signs: Brodie’s abscess (lytic lesion surrounded by sclerotic rim).
-Chronic OM: Lysis, Malformation, Involucrum, Cloaca, Sequestra.
-Plain film radiographs are 67% specific, 60% sensitive for OM (Termaat, JBJS 2005)

-Cellulitis: T1: Diffuse and infiltrative decreased signal intensity as inflammation replaces fat.
T2 and STIR: Increased signal intensity.

-Abscess: T1/T2/STIR: Homogeneous increased signal intensity.

-Note that pus/necrotic tissue has a decreased intensity compared to inflammatory fluid.

-OM: T1: Decreased signal intensity, cortical lysis and intramedullary changes.
-Increased signal intensity in known OM indicates healing as fat infiltrates.
T2: Increased signal intensity, cortical lysis, and intramedullary changes.
-Rim sign: thin layer of active infection surrounding normal bone.
-60% Specificity, 85% sensitivity per Termaat.

-Bone Scans
-A radio-isotope is injected into the patient and imaged at specific intervals.
-Phases: -Immediate Angiogram (1-3sec): Essentially an arteriogram.
-Blood Pool (3-5min): Demonstrates blood pooling in capillaries and veins.
-Delayed (2-4 hours): Increasingly specific to activity patterns and pathology.
-4th Phase: Increasingly specific to activity patterns and pathology.

-Technetium-99 Bone Scan

-Binds to calcium hydroxyapatite and measures osteoblast/osteoclast activity.
-Half-life: 6 hours
-Excreted through kidneys which will show homogenous control signal.
-Mucomyst 600mg PO q12 day before and of surgery as renal ppx.
-Cellulitis: Focal uptake in blood pool; Negative in delayed phase.
-OM: Diffuse uptake in blood pool; Hot increased uptake in delayed phases.
-45% Specificity; 86% sensitivity per Termaat.

-WBC Scans
-Same principles and phases as bone scan, but WBCs are tagged and followed instead.

-Gallium-67 Citrate
-Uptake by siderophore complex (direct bacteria) and lactoferrin (protein-released by bacteria)
-Scan taken 48-72 hours after injection or done in triphasic manner.
-Has longer half-life
-42% Specificity; 80% Sensitivity per Termaat.

-Indium-111 Oxime
-WBCs isolated from blood sample, labeled and re-injected.
-Scan at 24 hours. Half life: 67 hours.
-Predominantly uptaken by neutrophils, so it demonstrates acute infections better than chronic infections.

-Technetium-99m HMPAO
-WBCs isolated from blood samples, tagged and re-injected. Scan at 3 hours.
-Tagged molecule is HMPAO (hexamethylpropyleneamine oxime)
-Technically easier with less radiation than indium.

-Technetium-99m Sulfur Colloid Marrow Scan

-Specific for bone marrow and neutrophil production
-Has shown promise in differentiating OM from Charcot

-Combination Sequential Technetium-Gallium Scans

-Scan at 4 hours, then at 48-72 hours. Based on half-lives.
-Increased specificity for infection if gallium has higher uptake then technetium.
-Can use any other combination.

-Computed Tomography (CT scans)

-Radiograph altered by computer to highlight specific “windows”. You can isolate soft tissue or different aspects of bone, for example.
-Soft tissue infection: Exact locations and anatomy of abnormal soft tissue density.
-OM: Increased density in the marrow.
-CT scans can be combined with contrast.

-Positron Emission Tomography (PET scans)

-A tracer is injected/inhaled into the patient which releases radioactive positrons. The positrons collide with electrons and produce gamma rays.
->90% Sensitivity and Specificity per Termaat (best in study).

AJM Sheet: Diabetic Foot Ulcer Pathogenesis

-The pathogenesis of the diabetic foot ulcer can be described via three mechanisms: neuropathy, trauma and impaired

-30-50% of diabetics have some form of sensory, motor and/or autonomic neuropathy.
-Sorbitol accumulation in Schwann cells leads to hyperosmolarity of the nerve cells leading to swelling and
cellular lysis. This leads to decreased nerve signal conduction. Microvascular damage to the nerve (described later) also
impairs healing of the damaged nerve.
-Sensory Neuropathy
-Loss of light touch/protective sensation (anterior spinothalamic tract)
-Loss of vibratory/proprioception mechanisms (posterior tract)
-Loss of pain/temperature sensation (lateral tracts)
-The patient has no warning of current, developing or impending trauma.
-Motor Neuropathy
-“Intrinsic Minus” foot-type with wasting of the intrinsic muscles and extensor substitution.
-Undetected excess plantar pressures develop.
-Autonomic Neuropathy
-Damage occurs in the sympathetic ganglion
-AV shunting occurs with global LE edema not relieved by diuretics or elevation.
-Increased skin temperature predisposes to ulceration (Armstrong)
-Decreased sweating leads to xerosis and fissuring (portal for infection)

-Trauma leading to Ulceration

-Abnormal anatomy: extrinsic and intrinsic abnormalities secondary to motor neuropathy and glycosylation.
-Decreased joint mobility: secondary to non-enzymatic glycosylation and excess collagen cross-linking of tendons,
ligaments, joint capsules (especially at the STJ and the MTPJ).
-Equinus: Increased cross-linking of collagen in the Achilles tendon (leads to increased forefoot pressures).
-Skin stiffness: secondary to glycosylation of keratin.
-Intrinsic skin weakness: trophic changes associated with PVD.
-All lead to increased plantar pressures, which is the driving force behind ulceration.

-Impaired Wound Healing

-Can be thought of as increased inflammation, decreased vasculature and decreased catabolism.
-Increased Inflammation
-The inflammatory phase of the healing process actually lasts longer than necessary.
-Inflammation initially not as effective due to decreased leukocyte adhesion and morphologic changes to
the macrophages.
-Prolongation occurs due to decreased chemotaxis of growth factors and cytokines.
-MMPs increase their activity and continue to produce an “inflammatory soup.”
-All contribute to a wound “stuck” in the inflammatory phase.
-Decreased Vasculature
-Macroangiopathy: Atherosclerotic obstructive disease of large vessels due to LDL oxidation.
-Microangiopathy: Thickened basement membrane decreases diffusion at capillary level.
-Mechanism behind neuropathy, nephropathy and retinopathy
-Think of it in terms of a decreased TcPO2
-Endothelial dysfunction:
-Decreased NO and prostaglandin to promote vasodilation
-Decreased smooth muscle cell relaxation to promote vasodilation
-AV shunting secondary to autonomic neuropathy
-Decreased vasodilation and membrane permeability in response to trauma/damage/inflammation:
-Usually regulated by substance P and vasomodulators from damaged cells and nociceptors.
-Overall leads to a “sluggish” vasculature with decreased inflow, diffusion, outflow and angiogenesis.
-Decreased Catabolism
-Decreased collagen synthesis, both in peptide production and post-translational modification
-Morphologic changes to keratinocytes
-Decreased angiogenesis
Further Reading:
-Shaw JE, Boulton AJ. The pathogenesis of diabetic foot problems: an overview. Diabetes. 1997 Sep; 46 Sep; Suppl 2:S58-61.
-Rathur HM, Boulton AJ. The diabetic foot. Clin Dermatol. 2007 Jan-Feb; 25(1): 109-20.
-Boulton AJ, et al. The global burden of diabetic foot disease. Lancet. 2005 Nov 12; 366(9498): 1719-24.

AJM Sheet: Diabetic Foot Infection Functional Anatomy
From: Essential Questions for Surgical Intervention of Diabetic Foot Infections (

Dedicating yourself to the side of limb salvage in the fight against diabetic foot disease is a demanding and
personally challenging enterprise. In the face of infection, it often seems as though all variables are against the surgeon and
the patient as together, you struggle against proximal amputation and limb loss. In fact, it often appears as though the only
constant is the unpredictability of the disease progression. But one constant always on the side of the surgeon is anatomic
knowledge. The infection can only work with the anatomy that it is given, and this is certainly something that can be used to
your advantage. Your expert knowledge in lower extremity anatomy is one of the most valuable tools that you have in your
fight. It is a constant, and it is predictable.
There are different anatomic paradigms that must be considered in terms of the evaluation of the infection source.
Certainly depth is one of these paradigms. Absolute depth measurements offer very little clinical information when
compared to a functional view of depth from the surgical layers of dissection. An infection should be evaluated in terms of
whether it extends through the dermis, superficial fascia, deep fascia, musculotendinous structures or to the level of bone
(Table 1). From this general information, specific anatomic structures can then be identified as being within the path of the
Infections tend to develop and travel along the path of least resistance. This implies that an infection will stay
within the potential space of a given surgical layer or plantar compartment before extravasation into another layer or
compartment. Often, this involves proximal extension along the relatively avascular tendon sheaths or fascial planes between
muscular layers. The studies that have been used to define the number and boundaries of plantar foot compartments have
also given information about relatively consistent fascial clefts where communication between different layers and
compartments is likely. These have involved pressurized injection imaging studies where a known compartment is infiltrated
with a contrast medium and the extravasation into other compartments can be mapped. The findings of these studies are
summarized in Table 2. These communications are obviously numerous and complex. The important concept to realize is
that an infection is likely to initially develop within the potential space of a single layer or compartment. There is a tendency
for the infection to move proximally before communicating with another layer or compartment. Note however, that patterns
of communication are present along known anatomic structures such as tendons and neurovascular structures to each of the
other compartments, as well as the dorsum of the foot and plantar superficial fascia. Intra-operative investigation of an
infection should focus on these structures to trace the extent of plantar involvement. Also note the majority of these
communications are found in the forefoot around MPJ level, so distal infections have an increased likelihood of multi-
compartment involvement.

Table 1: Surgical Layers of Dissection Used for Diabetic Ulcer Depth Measurement

Superficial Fascia
-First Dissection Interval containing superficial neurovascular structures
Deep Fascia
-Second Dissection Interval containing muscular and deep neurovascular structures
-Third Dissection Interval

Table 2: Intercompartmental Communications

Medial Compartment Central Compartment

To Central Compartment via: To Medial Compartment via:
-Adductor Hallucis tendon -Adductor Hallucis tendon
-Flexor Hallucis Longus tendon -FHL Tendon
-Peroneus Longus tendon -PL Tendon
-Neurovascular structures penetrating the medial IM septum -NV structures penetrating medial IM septum
To Distal Deep Leg via: To Lateral Compartment via:
-Flexor Hallucis Longus tendon -Long flexor tendon to 5th digit
-Short flexor tendon to 5th digit
Lateral Compartment: -Lumbrical muscle/tendon to 5th digit
To Central Compartment via: -Plantar interosseous muscle to 5th digit
-Long flexor tendon to 5th digit -PL tendon
-Short flexor tendon to 5th digit -NV structures penetrating lateral IM septum
-Lumbrical muscle to 5th digit To Distal Deep Leg via:
-Plantar interosseous muscle to 5th digit -FHL tendon
-Peroneus Longus tendon -FDL tendon
-Neurovascular structures penetrating lateral IM septum To Dorsum of Foot via:
To Dorsal Structures -Interosseous muscles
To Plantar Superficial Fascia -MPJ communications
To Plantar Superficial Fascia

AJM Sheet: Osteomyelitis General

-Osteomyelitis is a complicated issue dealing with diabetic foot infections both in diagnosis and treatment. However, there
are several definitions, classification systems, diagnostic modalities and treatment tenets that you should be aware of.

-Definitions per Resnick:

-Periostitis: Inflammation of the periosteum
-Osteitis: Inflammation of the cortex
-Osteomyelitis: Inflammation of the medullary canal
-Sequestrum: piece of dead bone floating in pus/inflammation
-Involucrum: sheath of bone surrounding pus/inflammation
-Cloaca: tract through an involucrum
-Brodie’s Abscess (1832): Chronic abscess in bone surrounded by sclerosis
-Sclerosing OM of Garre: low grade inflammatory condition

-Waldvogel and Lew [Osteomyelitis. NEJM. 1997; 336(14): 999-1007.]

-The classic Waldvogel and Lew article is NOT a classification, rather a serious of definitions. However, it can be
turned into a stratified classification based on their definitions.
-Acute Osteomyelitis: Systemic clinical signs of infection
-Chronic Osteomyelitis: Subacute clinical signs of infection
-Contiguous/Direct Extension: spread of infection to bone from exogenous source or adjacent tissue.
This can be described as an “outside-in” spread invading the cortex and proceeding to the medullary canal.
-Hematogenous Spread: Infective agent reaches medullary canal of bone from the vascular supply. This
can be described as an “inside-out” infection invading the medullary canal first and spreading to the cortex.
-Vascular Impairment: Decreases the effectiveness of the inflammatory response and Abx delivery.

-Others have done a little better job of differentiating acute vs. chronic OM:
-Weiland: Describes chronic OM as lasting > 6months.
-Schauwecker: Describes chronic OM as lasting > 6 weeks and one failed episode of tx.

-AJM has turned these definitions into a classification system that made more sense to him:
-Acute Osteomyelitis
-Contiguous/Direct Extension
-Hematogenous Spread
-Chronic Osteomyelitis
-Contiguous/Direct Extension
-Hematogenous Spread

-Cierny-Mader-Penninck Classification [A clinical staging system for adult osteomyelitis. CORR. 2003; (414): 7-24.]
-This is described as a classification, but doesn’t make much sense to AJM.

-Anatomic Stage
1: Medullary: infection of only the medullary canal (Stage 1)
2: Superficial: infection of only the superficial cortex (Stage 2)
3: Localized: infection of only the cortex (Stage 3)
4: Diffuse: infection of both the cortex and medullary canal (Stage 4)
-Physiologic Stage
A: Normal Host
Bs: Compromised Host with systemic risk factors (eg DM)
Bl: Compromised Host with local risk factors (eg smoking)
C: Treatment worse than the disease

-So a smoking DM patient with infection of only the superficial portion of the cortex is: 2Bs
-Obviously much more work needs to be done on the topic of osteomyelitis classification.

AJM Sheet: Osteomyelitis Diagnosis and Treatment

-Subjective Findings (See Diabetic Infection Work-up)

-Objective Findings (Diabetic Infection Work-up)
-Probing to bone 89% positive predictive value (Grayson JAMA 1995).
-Gold Standard: Bone biopsy. This is ideally performed when the patient has been free of antibiotics for 2 weeks.
-Imaging Studies:
-Review plain films, MRI, Bone Scans, WBC scans, CT, PET in Diabetic Infection Imaging Sheet.
-These all add evidence, but are rarely exclusively diagnostic.
-Blood Cultures: Hematogenous OM diagnosed with positive BCx and positive bone scan.

-There is much controversy regarding long-term Abx (PO vs. IV vs. PMMA) vs. Surgical Debridement.
-The Cierny-Mader Classification makes some general recommendations:
-CM Stage 1: 2 weeks IV + 2-4 weeks PO Abx
-CM Stage 2: Surgical Debridement + 2 weeks IV
-CM Stage 3&4: Surgical Debridement + 4-6 weeks IV Abx

-Antibiotic administration options

-Long-term Abx (4-8 weeks) is a conservative option because many people believe you can never cure OM and that
it can reactivate at any time for years to come.
-Doxycycline and Ciprofloxacin are reputed to have the best bone penetration.
-Most ID docs would never substitute coverage for bone penetration.
-Your Abx choices should be culture driven.
-Culture driven
-Access options: IV, PICC, Infusion pump, etc.
-PMMA beads
-PMMA: polymethylmethacrylate
-PMMA is a combination of monomer (liquid) and polymer (powder).
-Comes in 20, 40 and 60g packets.
-7% elusion in the first 24 hours with activity noted for 14 days.
-Demonstrates exponential release.
-Cierny proposes a 1:5 ratio of Abx:PMMA. Another common standard is 4-8g:40-60g.
-Increased Abx means increased elution, but decreased bead hardening.
-Smaller beads means increased surface area and increased elution.
-The Abx must be heat-labile
-Gentamycin, Tobramycin, Vancomycin, Ticarcillin, Cefazolin, Moxalactam, Cefotaxime

AJM Sheet: Charcot Neuroarthropathy

-Definition: Neuropathic osteoarthropathy first described by Musgrave in 1703 and named for JM Charcot in 1868.
-Neurovascular/French Theory/Theory of Charcot
-Trophic centers in the anterior horn of the spinal cord maintain nutrition to joints.
-Trauma to these trophic centers leads to increased blood flow and osteoclastic activity.
-Evidence for the Neurovascular Theory:
-Autonomic neuropathy in DM leads to increased AV shunting, edema and skin temperature.
-Boulton: Increased PO2 in venous system of Charcot pts (63mmHg vs. 46mmHg)
-Shows increased perfusion in neuropathic diabetics
-Edmonds: Increased blood velocity in neuropathic diabetics
-Young: Decreased bone density in patients with decreased nerve conduction velocities
-Cundy: Decreased bone density in Charcot patients
-Gough: Increased osteoclastic activity in Charcot patients
-Neurotraumatic/German Theory/Theory of Virchow and Volkmann
-Repeated trauma from biomechanical stresses during ambulation on an insensate foot.
-Evidence for the Neurotraumatic Theory:
-Eloesser and Johnson: Trauma is the necessary predisposing factor, and not underlying bone weakness, to
create Charcot changes in a neuropathic limb.
-Common sense
-Two opposing, fighting theories? Probably a little bit of both.

-Etiology: Anything that causes neuropathy!

-First described: Tabes Dorsalis (Charcot 1868)
-Most common: DM
-3 most common: DM, Syringomyelia (longitudinal cavities lined by dense tissue), and Tabes Dorsalis
-C: Myelomeningocele, Spina Bifida, CMT, MS, CP, Syringomyelia, Congenital insensitivity
M: DM, Alcoholic neuropathy, Uremia, Pernicous Anemia
I: Tabes Dorsalis, Polio, Leprosy, TB
N: Tumors in brain, spinal cord, peripheral nerve
T: Trauma to brain, spinal cord, peripheral nerve
D: Indomethacin, Intra-articular corticosteroids, phenylbutazone

-DDx: OM, AVN, inflammatory arthritis, PVS, septic arthritis, CPPD, neoplasm, etc.

-Clinical Findings: -Presents similar to infection

-Red, hot, swollen, deformed foot +/- pain
-Readily available pulses (often described as bounding)

-Radiographic Findings:
-Atrophic: -With osteopenia, pencil&cup deformities, resorption of bone ends
-Without osteophytes, sclerosis, fragmentation, soft tissue debris
-Hypertrophic: -With joint space narrowing, fractures, fragmentation, ST debris, periosteal rxn, subluxation
-Without osteoporosis
-Be aware of both types.

-Classification Systems (described in detail on next page)

-Eichenholtz Classification (1966)
-Brodsky Classification
-Schon Classification

-Acute: -Strict and immediate NWB and immobilization for 12-16 weeks.
-Edema control (Jones cast, ACE inhibitors, Diuretics, Posterior splint, Elevation, Ex Fix, etc.)
-Education and family support
-FXR every 4-6 weeks with relatively few cast changes
-Transition: -Transition to WB (CAM walker, CROW, Bracing, MAFO, Shoes, etc.)
-Permanent: -Surgical correction of underlying deformity
-Consider TAL, Arthrodesis, Wedging osteotomies, Amputation
-Adjunctive: -Bone stimulators
-Bisphosphonates: -Pamidronate (Aredia): 60-90mg over 24h. 3 doses in 2 weeks.
-Alendronate (Fosamax): 5mg PO q24h.

AJM Sheet: Charcot Classifications

-Eichenholtz Classification (1966)

-Based on plain film radiographic findings
-Originally described Stages 13, but Stage 0 added later (Yu given credit, but really Schon).
-[Yu GV, Hudson JR. Evaluation and treatment of stage 0 Charcot’s neuroarthropathy of the foot and ankle. JAPMA. 2002; 92(4): 210-20.]
-Stage 0: High risk pre-Charcot
-Radiograph: Unremarkable. Maybe increased ST density, bone flecks or change in foot architecture.
-Clinical: Sudden onset of non-pitting edema, erythema, calor, +/- pain, bounding pulses, intrinsic atrophy.
-Normal skin temp: 94°F; can increase by 12°
-Uptake in all three phases of Tc-99 bone scan
-Stage 1: Acute/Developmental
-Radiograph: Capsular distention, fragmentation, debris, subluxation
-Clinical: Red, hot, swollen foot with joint laxity
-Stage 2: Coalescence
-Radiograph: Sclerosis, resorption of debris, fusion
-Clinical: Subjectively decreased red, hot, swollen
-Stage 3: Reconstruction
-Radiograph: Decreased sclerosis (with increased vascularity) and remodeling
-Clinical: Decreased joint mobility with increased stabilization

-Brodsky Classification (1992)

-Describes location of deformity

-Type 1: Lisfranc joint (27-60% incidence)

-Type 2: Chopart’s joint and STJ (30-35% incidence)
-Type 3A: Ankle joint (9% incidence)
-Type 3B: Posterior calcaneus
-Type 4: Multiple combinations of above
-Type 5: The forefoot

-Schon Classification [Charcot neuroarthropathy of the foot and ankle. CORR. 1998; 349: 116-131.]
-Describes location and severity of condition
I: Lisfranc Pattern
-AC with increasing deformity to medial rockerbottom and ulceration.
II: Naviculocunieform Pattern
-AC with increasing deformity to lateral rockerbottom and ulceration.
III: Perinavicular Pattern
-AC with lateral rockerbottom, Talar AVN and ulceration.
IV: Transverse Tarsal Pattern
-AC with increasing deformity to central rockerbottom and ulceration.

AJM Sheet: Differentiating Osteomyelitis from Charcot

-Please keep in mind that these are not mutually exclusive and both can be present!
-These are just general guidelines and many people will vehemently argue them.

-The gold standard is a bone biopsy which would show infection in OM and not in Charcot.

-OM: Constitutional signs and symptoms of infection, infectious risk factors, history of infection.
-Charcot: Uncontrolled DM, history of Charcot, history of recent trauma.

-OM: Necrosis, pustular drainage, elevated white count, cultures, positive bone biopsy.
-Charcot: Increased joint laxity, non-pitting edema, bounding pulses, rockerbottom deformity, negative bone biopsy.

-Not enough evidence yet, but some believe that OM is positive on bone scans and WBC scans for greater than 24 hours
whereas Charcot neuroarthropathy is only positive during the first 24 hours.
-The Tc99 Sulfur Colloid scan would also theoretically be positive for infection, but not for Charcot.

-Not too much here, but check out some further reading:
-Soysal N, et al. Differential diagnosis of Charcot arthropathy and osteomyelitis. Neuro Endocrinol Lett. 2007 Oct; 28(5): 556-559.
-Shank CF, Feibel JB. Osteomyelitis in the diabetic foot: diagnosis and management. Foot Ankle Clin. 2006 Dec; 11(4): 775-89.
-Ledermann HP, Morrison WB. Differential diagnosis of pedal osteomyelitis and diabetic neuroarthropathy: MR Imaging. Semin Musculoskelet Radiol.
2005 Sep; 9(3): 272-83.
-Berendt AR, Lipsky B. Is this bone infected or not? Differentiating neuron-osteoarthropathy from osteomyelitis in the diabetic foot. Curr Diab Rep. 2004
Dec; 4(6): 424-9.
-Yu GV, Hudson JR. Evaluation and treatment of stage 0 Charcot’s neuroarthropathy of the foot and ankle. J Am Podiatr Med Assoc. 2002 Apr; 92(4): 210-
-Schon LC, et al. Charcot neuroarthropathy of the foot and ankle. Clin Orthop Relat Res. 1998 Apr;(349): 116-31.
-Berendt AT, Peters EJ, et al. Diabetic foot osteomyelitis: a progress report on diagnosis and a systemic review of treatment. Diabetes Metab Res Rev. 2008;
24(S1): S145-S161.

AJM Sheet: Common Situational Bugs

-Cellulitis with an open wound: -SA (if no streaking present)

-Strept (with streaking and palpable border)
-Usually monomicrobial

-Infected ulcer in Abx naïve pt: -SA

-Usually polymicrobial

-Chronically infected ulcer in Abx naïve pt: -SA

-Usually polymicrobial

-Macerated infected ulcer: -Pseudomonas

-Usually polymicrobial

-Chronic, non-healing ulcer with prolonged Abx therapy: -SA -MRSA

-Staph epi
-Enterococci -VRE
-Diptheroids (Corynebacterium)
-Extended GNR
-Usually polymicrobial

-Fetid Foot with necrosis and gangrene: -Resistant Gram positive cocci
-Mixed GNR

-Osteomyelitis with hemodialysis: -SA


-Osteomyelitis with IVDA: -SA


-Osteomyelitis with Decubitus Ulcer: -Gram Negatives

-Osteomyelitis with hemoglobulinopathy: -Salmonella

-Human mouth pathogens (HACEK): -Haemophilus, Actinobacillus, Cardiobacterium hominis, Eikenella corrodens, Kingella

-Water exposure: -Vibrio

-Aeromonas hydrophila

-Puncture through a shoe: -Pseudomonas

-Any dirt/soil: -Clostridium

-Cat bite: -Pasteurella multocida -Dog bite: -Strept viridans, Capnocytophaga canimorsus

-Immunocompromised pt: -Gram negatives

-Septic bursitis: -SA -Gas gangrene: -Clostridium

-Post-op infection following implant: -Staph epi

-Fruity odor/green hue: -Pseudomonas -Foul smelling discharge: -Anaerobes

-Creamy yellow discharge: -SA -White discharge: -Staph epi

AJM Sheet: Empiric Antibiotic Choices

Generalized Gram Positive Coverage:

-2nd Generation PCN -2nd Generation Quinolones -Synercid

-4th Generation PCN -Macrolides -Rifampin
-1st Generation Cephs -Bactrim
-2nd Generation Cephs -Vancomycin
-Carbapenems -Clindamycin
-Tetracyclines -Zyvox

Generalized MRSA Coverage:

-Vancomycin -Synercid
-Clindamycin -Bactrim/Rifampin
-Zyvox -Cubicin

Generalized Gram Negative Coverage:

-3rd Generation PCN -2nd Generation Quinolones

-4th Generation PCN -3rd Generation Quinolones
-Carbapenems -4th Generation Quinolones
-Tetracycline -Bactrim

Generalized Pseudomonas Coverage:

-Cephalosporins x 3 (Fortaz, Cefobid, Maxipime)

-PCN x 2 (Zosyn, Timentin)

Generalized Anaerobes:

-4th Generation PCN -Aminoglycosides

-1st Generation Cephs -Carbapenems
-2nd Generation Cephs -4th Generation Quinolones
-3rd Generation Cephs -Clindamycin
-4th Generation Cephs -Flagyl

AJM Sheet: IDSA Empiric Recommendations

-from Lipsky BA, et al. Diagnosis and Treatment of Diabetic Foot Infections. IDSA Guidelines. CID 2004; 39: 885-910.

-Uninfected Wound
-Definition: No purulence, inflammatory manifestations, or systemic manifestations
-Empiric Therapy: None

-Mildly Infected Wound

-Definition: -2+ Manifestations of Infection (purulence, induration or erythema/pain/warmth)
-<2cm of erythema
-Limited to skin and subcutaneous tissue
-No systemic complaints

-Empiric Therapy Recommendations:

-2-PCN -Bactrim
-Clinda -Augmentin
-Keflex -Levo

-Moderately Infected Wound

-Definition: -As above, in a systemically/metabolically stable patient PLUS
->2cm cellulitis OR streaking OR involvement of deep tissue

-Empiric Therapy Recommendations:

-Bactrim -Invanz
-Augmentin -Ceftin + Flagyl
-Levo -Timentin
-2-Ceph -Zosyn
-3-Ceph -Levo + Clinda
-Daptomycin + Aztreonam -Cipro + Clinda
-Zyvox + Aztreonam

-Severely Infected Wound

-Definition: -Infection as above in a patient with systemic toxicity and metabolic instability

-Empiric Therapy Recommendations:

-Primaxin -Vanco + Fortaz
-Zosyn -Vanco + Fortaz + Flagyl
-Cipro + Clinda
-Levo + Clinda

-If MRSA is likely:

-Zyvox -Vanco + Fortaz
-Zyvox + Aztreonam -Vanco + Fortaz + Flagyl
-Daptomycin + Aztreonam

-To cover all bases:

-Vanco + Aztreonam + Flagyl

AJM Sheet: Common Infective Agents with DOC:

DOC Alternatives
-Aerobic Gram Positive Cocci
Staph aureus 1-Ceph Vanco, Clinda, Azithromycin
MRSA Vanco Bactrim, Cubicin, Zyvox, Clinda
Staph epi 2-PCN 4-PCN, 1,2-Ceph, Vanco
MRSE Vanco Zyvox, Cubicin, Synercid
Enterococcus 3-PCN Vanco, Tetracyclines, Quinolones
VRE Linezolid Macrobid, Cubicin, Chloramphenicol
Strept pyogenes (Group A) 3-PCN 4-PCN, 1,2-Ceph, Vanco, Clinda
Strept agalactiae (Group B) 3-PCN 4-PCN, 1,2-Ceph, Vanco, Clinda
Strept bovis (Group D) 3-PCN 4-PCN, 1,2-Ceph, Vanco, Clinda
Strept Viridans 3-PCN 4-PCN, 1,2-Ceph, Vanco, Clinda

-Anaerobic Gram Positive Cocci

Peptostreptococcus Clinda 3-PCN, 4-PCN, Carbapenems

-Aerobic Gram Positive Rods

Bacillus anthracis Cipro 3-PCN, Vanco, Clinda
Corynebacterium diphtheriae Macrolide Clinda,
Listeria Monocytogenes 3-PCN Vanco, Bactrim, Carbapenems

-Anaerobic Gram Positive Rods

Clostridium perfringens Ertapenam Vanco, Clinda, 4-PCN, Tetracyclines
Clostridium difficile Flagyl Vanco
Clostridium tetani Clinda Flagyl

-Aerobic Gram Negative Rods

Pseudomonas Zosyn 1,2-Quin, Aztreonam, Primaxin
E. coli 3-Ceph 4-PCN, Bactrim, Quinolones
Enterobacter Bactrim Quinolone, Aztreonam, Carbapenems
Proteus 3-PCN 3-Ceph, 4-PCN, Bactrim, Quinolones
Vibrio Tetracyclines Bactrim, Cipro
Y. pestis Aminoglycosides Bactrim, Cipro
Shigella Cipro Bactrim, Amp, 4-PCN
Salmonella Cipro 3-PCN, 4-PCN, Bactrim
Klebsiella 3-Ceph 4-PCN, Bactrim, 2-Quin, Aminoglycosides
Serratia 3-Ceph Zosyn, Bactrim, Aztreonam, Quin
E. Corrodens Augmentin Tetracyclines
P. multocida Doxycycline Bactrim, 3-PCN

-Anaerobic Gram Negative Rods

Bacteroides fragilis Ertapenam Clinda, Flagyl

-Aerobic Gram Negative Cocci

Neisseria Rocephin 3-PCN, Quinolones

Treponium pallidum 1-PCN Tetracyclines, Macrolides
Borrelia burgdorferi 1-PCN Amox, Macrolides

AJM Sheet: Antibiotics/Drugs of Choice

1. Staph Aureus
-PO: Keflex -500mg PO tid or 750mg PO bid
Clindamycin -300mg PO qid
Zithromycin -500mg PO day 1, 250mg PO days 2-5
-IV: Ancef -1g IV q8
Vancomycin -1g IV q12
Clindamycin -600mg IV q8

2. Streptococcus
-PO: Keflex -500mg PO tid or 750mg PO bid
Clindamycin -300mg PO qid
-IV: Ancef -1g IV q8
Vancomycin -1g IV q12
Clindamycin -600mg IV q8

-IV: Vancomycin -1g IV q12
-PO: Bactrim -1 tablet PO bid
Rifampin 300mg + Minocycline 100mg PO bid

4. Enterococcus
-PO: Amoxicillin -250-500mg tid
Augmentin -875mg bid or 500mg tid (or bid)
Zyvox -600mg PO bid
-IV: Vancomycin -1g IV q12
Zyvox -600mg IVq12

-PO: Zyvox -600mg PO bid
-IV: Zyvox -600mg IV q12
Synercid -7.5mg/kg/hr over 1 hour q12

6. Pseudomonas
-PO: Ciprofloxacin -250-750mg PO bid
-IV: Ciprofloxacin -400mg IV q12
Fortaz -2g IV q12
Aztreonam -1g IV q8

7. E.coli, Proteus
-PO: Keflex -500mg PO tid or 750mg PO bid
Cipro -250-750mg PO bid
Levaquin -500mg PO qday
Tequin -400mg PO qday
-IV: Ancef -1g IV q8
Cipro -400mg IV q12
Levaquin -500mg IV qday
Tequin -400mg IV qday

AJM Sheet: Antibiotic Dosing Guide

1st Generation: -Pen V: 500mg q6 PO
-Pen G: 250,000 units/kg/day IV
2nd Generation: -Dicloxacillin: 250mg q6 PO
-Oxacillin: 1-2g q4 IV
-Nafcillin: 1-2g q4 IV
3rd Generation: -Amoxicillin: 500mg q8 PO
-Ampicillin: 1g q4-6 IV
4th Generation: -Augmentin: 875mg q12 PO
-Unasyn: 3g q6 IV
-Zosyn: 4.5g q6 IV
-Timentin: 3.1g q6 IV

1st Generation: -Keflex: 500mg q8 PO or 750mg PO bid
-Duricef : 2g q24 PO
-Ancef: 1g q8 IV
2nd Generation: -Ceftin: 500mg q12 PO
-Zinacef: 1.5g q8 IV
-Mefoxin: 1g q6 IV
3rd Generation: -Omnicef: 300mg q12 PO
-Vantin: 400mg q12 PO
-Rocephin: 1g q24 IV
-Fortaz: 1g q8 IV
-Cefobid: 2g q12 IV
4th Generation: -Maxipime: 2g q12 IV

2nd Generation: -Ciprofloxacin: 750mg q12 PO/400mg q12 IV
3rd Generation: -Levofloxacin: 500mg q24 PO/IV
4th Generation: -Tequin: 400 q12 PO/IV
-Avelox: 400 q24 PO

Macrolides -Biaxin: 500mg q12 PO

-Ketek: 800mg q24 PO
-Zithromax: 500 q12 IV/ 500mg PO Day 1; 250 mg PO Day2-5
-Erythromycin 500mg q6 PO

Carbapenems -Invanz: 1g q24 IV

-Primaxin: 500mg q8 IV
-Merrem 1g q8 IV

Aminoglycosides -Amikacin: 1500mg/day

-Tobramycin: 3-5mg/kg/day
-Gentamycin: 3-5mg/kg/day

Tetracyclines -Minocycline: 100mg q12 PO/IV

-Doxycycline: 100mg q24 PO
-Tetracycline: 500mg q6 PO

Misc -Bactrim DS: 160/800mg q24 PO

-Aztreonam: 1g q8 IV
-Vancomycin: 1g q12 IV
-Clindamycin: 600mg q8 IV; 300mg q6 PO
-Zyvox: 600mg q12 PO/IV
-Cubicin: 4mg/kg q12 IV
-Synercid: 7.5mg/kg q8 IV
-Flagyl: 500mg q8 PO
-Rifampin: 300mg q12 PO/IV
-Tygacil: 100mg loading dose; then 50mg q12 IV

AJM Sheets: Trauma
Trauma is another area that is often highlighted during the interview process. This section first details a
trauma-specific work-up, and then goes through some specific traumatic conditions.

In terms of the interview, you generally will be expected to work-up, diagnose and classify based on
radiographs, CTs and MRIs. While you should certainly have an understanding of treatment interventions and
protocols, this will probably be less emphasized than diagnosis and classification.
A lot of these classifications are very visual (and I don’t have room for that in 100 pages), so I’ve tried to
include a lot of specific references with pictures of the classifications (mostly to McGlamry’s and Gumann’s texts).
I’ve also tried to include a lot of references to “classic” articles and review articles. Textbooks with good
trauma information for additional reading include specific ones (Gumann’s, Scurran’s, Rang’s, etc), but also general
ones (McGlamry’s, Myerson’s, Hansen’s, etc).

I said that while I was studying for the Diabetic Foot Infection work-up, I tried to learn as much as possible
on the topic and really tried to “wow” the attendings at the interview. However, my strategy was different when
dealing with trauma and the specific surgical work-ups. Here I tried to demonstrate “competence” as opposed to
“mastery” of the material. With specific surgeries, you’re really not supposed to have strong, pre-formed opinions
as a student or as an intern. That’s what your residency is for; developing surgical opinions. If you already know
what to do in every surgical situation, then what’s the point of doing a residency? So while on externships and at the
interview, you should really try to walk a fine line between:
1. Displaying competence in knowledge of the baseline material
2. Displaying that you still have a lot to learn, and that you are eager to learn it

-The Trauma Work-Up (page 52)
-General Trauma Topics (pages 53-54)
-Digital Fractures (page 55)
-Sesamoid Trauma (page 56)
-Metatarsal Fractures (page 57)
-5th Metatarsal Fractures (page 58)
-Metatarsal Stress Fractures (page 59)
-LisFranc Trauma (page 60)
-Navicular Trauma (page 61)
-Talar Fractures (page 62)
-Calcaneal Fractures (page 63)
-Ankle Fractures (pages 64-65)
-General Tendon Trauma (page 66)
-Achilles Tendon Work-up (page 67)
-Achilles Tendon Treatment (page 68)

AJM Sheet: Trauma Work-up

-The Trauma Work-up is very similar to the regular patient work-up, but with a few things added. You still need to go
through the HPI, PMH, PSH, Meds, Allergies, SH, FH, ROS and complete physical exam in that order. In addition, there
are three other topics that you need to address on every trauma patient for every work-up:

1. ABCDE’s of the Primary Survey

-Airway: Three common forms of airway obstruction are cervical spine injury, swollen tongue and facial fracture.
-Breathing: Note how this is different than an established airway. Someone can have an airway, but still not be
-Circulation: Assess vascular status in all four extremities. Two large-bore (18-gauge) IV’s should be started
immediately if fluid replacement is considered necessary.
-Deficits (Neurological): There are two ways to assess this.
-Alert, responds to Verbal stimuli, responds to Painful stimuli, or Unresponsive
-Glasgow Coma Scale
-Based upon three criteria: eye opening, verbal response, motor response.
-Based on scale of 0-15 with a higher score indicating a better prognosis.
-13+ associated with a good prognosis; 7- associated with a poor prognosis.
-Exposure: Complete exposure of the patient to evaluate further, unknown damage.

-Secondary Survey: This is when you go through a normal history including HPI, PMH, etc. and a
comprehensive physical exam.

2. Tetanus Status
-Clostridium tetani is a racquet-shaped gram-positive bacillus. It releases an exotoxin causing a pre-sympathetic
-Triad of tetanus symptoms: Trismus, Risus Sardonicus, and Aphagia.
-Characteristics of a tetanus-prone wound: greater than 6 hours old, clinical signs of infection, deep, devitalized
tissue, contamination, traumatic mechanism of injury, etc.

-Basic Tetanus Algorithm:

-Unknown tetanus status: -Clean wound: Give the toxoid; Hold the TIG
-Tetanus-prone wound: Give the toxoid; Give the TIG

-Incomplete tetanus status: -Clean wound: Give the toxoid; Hold the TIG
(No booster within 5 years) -Tetanus-prone wound: Give the toxoid; Give the TIG

-Complete tetanus status: -Clean wound: Hold the toxoid; Hold the TIG
(Booster within 5 years) -Tetanus-prone wound: Hold the toxoid; Hold the TIG

-Dosages: -Toxoid: 0.5ml

-TIG (tetanus immunoglobulin): 250-300 units

3. NPO status
-All trauma patients are potential surgical candidates, so get this information for the weenie anesthesiologists.
-Traditional guidelines recommend:
-Nothing by mouth after midnight the night before elective surgery
-Nothing by mouth within 6-8 hours of any type of surgery

-These strict guidelines are in the process of changing however, particularly with regard to allowing the ingestion
of small amounts of clear liquids up to the time of surgery. If interested, please read:
-[Brady M, Kinn S, Stuart P. Preoperative fasting for adults to prevent perioperative complications. Cochrane
Database Syst Rev. 2003; (4): CD004423.]
-[Murphy GS, et al. The effect of a new NPO policy on operating room utilization. J Clin Anesth. 2000 Feb; 12(1):

AJM Sheet: General Trauma Topics

-In addition to having a good trauma work-up, there are a few other things that are helpful to know regarding foot and ankle

1. Podiatric Surgical Emergencies

-Infection with emphysema (gas gangrene)
-Open fracture/dislocation
-Compartment syndrome
-Necrotizing Fasciitis
-General Neurovascular compromises

2. Mangled Extremity Severity Score (MESS)

-[Helfet DL, et al. Limb salvage versus amputation. Preliminary results of the Mangled Extremity Severity Score. CORR 1990; 256: 80-6.]
-[Bosse MJ, et al. A prospective evaluation of the clinical utility of the lower-extremity injury-severity scores. JBJS-Am 2001; 83(1): 3-14.]
-Based on 4 criteria: Skeletal/Soft Tissue Injury, Limb Ischemia, Age, and Shock
-Based on a scale from 1-11 with a higher score leading to an increased incidence of amputation.
-A score of 7+ has an increased likelihood of amputation.

3. Open Fractures
-Note that 30% of lower extremity open fractures are associated with polytrauma.
-Mainstays of treatment: Aggressive incision and drainage with copious lavage.
-It is generally recommended to never primarily close an open fracture until devitalized soft tissue has demarcated,
but this certainly isn’t always the case in practice. In fact, the Ortho Trauma service at INOVA routinely primarily closes
open fractures following I&D with ORIF.

-Gustilo-Anderson Classification of Open Fractures [Gustilo RB, Anderson JT. Prevention of infection in the treatment of one
thousand and twenty-five open fractures of long bones: retrospective and prospective analyses. JBJS-Am. 1976; 58(4): 453-8.]
I. Clean Wound <1cm in diameter
-Abx choice: 1st generation cephalosporin (Ancef)
II. Wound 1.0-5.0cm in diameter with minimal soft tissue damage
-Abx choice: Ancef, Clindamycin
III. Wound >5cm in diameter with extensive soft tissue damage
-Abx choice: Ancef (or high dose PCN), Clindamycin and Aminoglycoside
-IIIA: Adequate soft tissue coverage
-IIIB: Extensive soft tissue damage with periosteal stripping and massive contamination
-IIIC: Arterial damage requiring primary repair

4. Fracture Blisters
-Location: Subepidermal
-Note that the fluid is sterile. Fracture blisters are histologically similar to 2nd degree burns.
-Most common LE etiology? Secondary to high-energy trauma such as ankle fx, calcaneus fx or Lisfranc injury.
-2 Common Types of Fracture Blisters
-Clear fluid: Most common (75%). Very tense in appearance.
-Hemorrhagic: Most severe. Roof is flaccid. Takes longer to re-epithelialize.
-Treatment is controversial, but the conservative approach is to never incise through a fracture blister and to delay
surgery until re-epithelialization.
-[Strauss EJ, et al. Blisters associated with lower-extremity fracture: results of a prospective treatment protocol. J Orthop Trauma. 2006 Oct;
20(9): 618-22.]

5. Shock
-Signs/Symptoms of Shock: Tachycardia, Tachypnea, delayed capillary refill, decreased pulse pressure, change in
mental status, decreased systolic pressure, decreased urinary output and decreased H&H.
-Types of Shock:
-Hypovolemic: most common; defined as the acute loss of circulating blood. Treatment is aggressive fluid
-Cardiogenic: induced by myocardial dysfunction.
-Neurogenic: secondary to decreased sympathetic tone from head and spinal cord injuries.
-Septic: shock secondary to infection.
-Goal of Treatment: restore organ perfusion.

AJM Sheet: General Trauma Topics
-Foreign Bodies/Puncture Wounds
-When should a foreign body be removed?
-Clinical signs of infection, known contaminated object, pain, object close to NV elements, intra-articular
-Recommended imaging studies for a foreign body?
-Plain film radiography (no oblique views!), fluoroscopy, CT, MRI, US
-How will wooden objects appear on US?
-hyperechoic with a hypoechoic dark shadow
-How large must a glass foreign body be to be visible on plain film radiography? Does leaden matter?
-A piece of glass, regardless of whether it is leaden, must be >5mm to be visible.
-Classification for foreign bodies?
-Resnick Classification [Resnick CD. Puncture wounds: therapeutic considerations and a new classification. J Foot Surg. 1990
Mar-Apr; 29(2): 147-53.]
-I. Superficial/cutaneous: usually visible without signs of infection.
-II. Subcutaneous or articular without signs of infection.
-IIIA. Subcutaneous or articular with signs of infection.
-IIIB. Bone penetration without signs of infection.
-IV. Bone penetration with known osteomyelitis.
-Patzakis Classification [Patzakis MJ. Wound site as a predictor of complications following deep nail punctures of the foot. West
J Med. 1989 May; 150(5): 545-7.]
-Zone 1: Toe to met head (50% incidence of osteomyelitis in this limited study.)
-Zone 2: Midfoot (17% incidence of osteomyelitis in this limited study.)
-Zone 3: Calcaneus (33% incidence of osteomyelitis in this limited study.)
-Puncture wound common bugs
-Most common? Staph Aureus
-2nd most common? Beta-hemolytic strept
-Puncture through shoe gear? Pseudomonas
-Puncture involving soil or a farm? Clostridia
-Human bites? Eikenella corrodens
-Cat bites? Pasteurella multocida
-Dog bites? Enterobacter, Pseudomonas, Staph, Bacillus
-Mainstays of foreign body/puncture wound treatment?
-Tetanus status, antibiotics, aggressive I&D with copious lavage

-Gun Shot Wounds

-High velocity GSWs are characterized by speeds >2500 ft/s. This is significant because high velocity GSWs have a tendency
to yaw and tumble leading to increased cavitation.
-Cavitation: Large wound is created under a situation of negative pressure. This negative pressure “sucks” outside
contaminants into the wound.
-[Holmes GB. Gunshot wounds of the foot. CORR. 2003 Mar; (408): 86-91.]

-Compartment Syndrome
-First described by Volkmann. Myerson has good articles/chapters on this topic.
-[Perry MD, Manoli A. Foot compartment syndrome. Orthop Clin North Am. 2001 Jan; 32(1): 103-11.]
-[Myerson M, Manoli A. Compartment syndromes of the foot after calcaneal fractures. Clin Orthop Relat Res. 1993 May: 142-50.]
-Results when interstitial pressure exceeds capillary hydrostatic pressure, so the microcirculation shuts down.
-The foot has anywhere from 3-11 compartments depending on who you read:
-Intermetatarsal Compartments X 4: contains the interossei muscles
-Medial Compartment: Abductor Hallucis
-Lateral Compartment: Abductor digiti minimi
-Superficial Central Compartment: FDB
-Deep Central Compartment: Adductor Hallucis
-Calcaneal Compartment: Quadratus Plantae and lateral plantar artery
-Dorsal Compartment: EHB and EDB
-P’s of Compartment Syndrome (These are very generalized.)
-Pain out of proportion and not controlled by analgesics -Paralysis
-Pain with passive dorsiflexion of the toes -Pulselessness
-Paresthesia -Pressure
-Normal compartment pressure? 0-5mm Hg
-When do you start getting worried? 20-30mm Hg
-When do you consider surgical intervention? >30-40mm Hg
-How is diagnosis made? Wick or slit catheter to measure compartment pressures
-Decompression via fasciotomy, debridement of necrotic tissue, copious lavage and delayed closure
-Incision approaches: Consider dorsal vs. medial approaches
-Complications: permanent loss of function with structural deformity (Volkmann contractures), myoneural necrosis, sensory
loss, chronic pain

AJM Sheet: Digital Fractures

-Even suspected digital fractures should be worked up according to a standard, full trauma work-up during the interview if
the case is presented as a trauma. The following describes unique subjective findings, objective findings, diagnostic
classifications and treatment.

-History of trauma. “Bedpost” fracture describes stubbing your toe while walking at night. Also common are injuries from
dropping objects on the foot.

-Edema, erythema, ecchymosis, open lesions, subungual hematoma, and onycholysis should all be expected.
-Any rotational/angulation deformities should be identified on plain film radiograph.

Diagnostic Classifications
-Rosenthal Classification [Rosenthal EA. Treatment of fingertip and nail bed injuries. Orthop Clin North Am. 1983; 14: 675-697.]
-Zone I: Injury occurs with damaged tissue completely distal to the distal aspect of the phalanx.
-Zone II: Injury occurs with damaged tissue completely distal to the lunula.
-Zone III: Injury occurs with damaged tissue completely distal to the most distal joint (IPJ in hallux; DIPJ in

-Zone I Injuries
-If injury involves no exposed bone and a total tissue loss less than 1cm squared, then:
-Allow to heal in by secondary intention.
-If injury involves a total tissue loss greater than 1cm squared, then:
-A STSG or FTSG should be used depending on weight-bearing position.
-Zone II Injuries
-Flaps and Skin Grafts generally employed:
-Atasoy flap: plantar V Y advancement
-[Atasoy E. Reconstruction of the amputated fingertip with a triangular volar flap. JBJS-Am 1970; 52: 921-926.]
-Kutler flap: biaxial V  Y advancement
-[Kutler W. A new method for fingertip amputation. JAMA 1947; 133: 29-30.]
-Zone III Injuries
-Usually requires distal amputation (Distal Symes amputation)

Miscellaneous Notes
-Hallux fracture is regarded as the most common forefoot fracture.
-Digital fractures without nail involvement and displacement/angulation/rotation can be treated conservatively with

-If a subungual hematoma is present, then there is a 25% incidence of underlying phalanx fracture.
-If a subungual hematoma covers >25% of the nail, then the nail should be removed.
-Only 1mm squared of free space from onycholysis is necessary for hematoma development.

-For proper nail function and adherence, there should be no onycholysis within 5mm of the lunula.
-A Beau’s line is a transverse groove often associated with nail trauma.

AJM Sheet: Sesamoid Trauma

-The following describes unique subjective findings, objective findings, diagnostic classifications and treatments.

-History of trauma is very important in this case. You want to differentiate between acute and chronic conditions involving
the sesamoids. Be careful to elicit any neurologic complaints that could be present.

-Expect edema, erythema, ecchymosis and open lesions. Take the time for proper palpation.
-Joplin’s neuroma is irritation of the medial plantar proper digital nerve.
-Associated with rigidly plantarflexed first metatarsals, anterior cavus, etc.
-One of the most difficult things to differentiate is an acute sesamoid fracture from a bipartite sesamoid. There are
several generic plain film radiographic characteristics found in acute fractures:
-Jagged, irregular and uneven spacing
-Large space between fragments
-Abnormal anatomy
-Bone callus formation
-Comparison to a contra-lateral view

-Also useful are:

-HISTORY of acute incident
-Bone scan (would show increased osteoblastic/osteoclastic activity with acute fracture).

Diagnostic Classifications
-Jahss Classification [Jahss MH. Traumatic dislocations of the first metatarsophalangeal joint. Foot Ankle. 1980 Jul; 1(1): 15-21.]
-Type I
-Mechanism: Dorsal dislocation of the hallux
-Intersesamoid ligament: Intact
-Fracture?: No sesamoid fracture
-Treatment: Requires open reduction
-Type IIA
-Mechanism: Dorsal dislocation of the hallux
-Intersesamoid ligament: Ruptured
-Fracture?: No sesamoid fracture
-Treatment: Closed reduction/Conservative Care
-Type IIB
-Mechanism: Dorsal dislocation of the hallux
-Intersesamoid ligament: Ruptured
-Fracture?: Fracture of at least one sesamoid
-Treatment: Closed reduction/Conservative Care
-Type II Variant
-Mechanism: Dorsal dislocation of the hallux
-Intersesamoid ligament: Ruptured
-Fracture?: Separation of a bipartite sesamoid
-Treatment: Closed reduction/Conservative Care

-Immobilization (NWB SLC, PWB SLC, Surgical Shoe, CAM Walker, etc.)
-Dancer’s Pad
-Excision of the fractured fragment or entire sesamoid

Miscellaneous Notes
-Ilfeld’s Disease: Agenesis of the fibular sesamoid
-[Ilfeld FW, Rosen V. Osteochondritis of the first metatarsal sesamoid. CORR 1972; 85: 38-41.]
-Incidence of Bipartite Sesamoid in Population:
-As much as Kewenter: 35.5%
-As few as Inge: 10.7% with 75% of cases being unilateral

AJM Sheet: Metatarsal Fractures
-The following describes unique subjective findings, objective findings, diagnostic classifications and treatments.

-Subjective and Objective

-All will point to some form of traumatic injury. Common injuries leading to metatarsal fracture include direct trauma, blunt trauma, shearing, ankle sprains,
-Most important in your work-up will be how you read the plain film radiographs. Remember that at least two views are necessary to accurately describe
displacement/angular/rotational abnormalities.

-Metatarsal Head/Impaction Fractures

-MOI: Direct or indirect trauma
-Radiographic findings: -Examine for evidence of displacement/angulation/rotation
-Expect a shortening mechanism
-Examine for intra-articular nature of fracture
-Treatment: -Conservative
-Closed reduction generally unsuccessful
-ORIF with fixation of K-wire, screws or absorbable pins
- immobilization for 4-6 weeks and NWB
-Early PROM suggested
-Subsequent arthrosis is a common complication

-Metatarsal Neck Fractures

-MOI: Shearing forces or direct trauma
-Radiographic findings: -Expect elements of shortening, plantarflexion and lateral displacement of the distal segment.
-Treatment: -Conservative
-Closed reduction generally unsuccessful
-ORIF effective in restoring and maintaining alignment with K-wires, IM pinning and plates.
-NWB in SLC for 4-6 weeks
-General Information:
-Metatarsal neck fractures often involve multiple metatarsals due to the mechanism of injury. Multiple fractures are very unstable due to loss of
function of the deep transverse metatarsal ligament, which usually prevents displacement.
-Vassal Principle: Adjacent fractures generally improve alignment after reduction of the initial fracture because soft tissue structures are
returned to their normal position through traction.

-Midshaft Metatarsal Fractures

-MOI: Result of direct, blunt or torsional injuries
-Radiographic findings: -Expect oblique fracture line, but transverse, spiral and comminuted are all possible.
-Expect elements of shortening, plantarflexion and lateral displacement of the distal segment.
-Treatment: -Based on displacement and fracture type:
-Non-displaced fractures: NWB SLC 4-6 weeks
-Fractures with >2-3mm of displacement and >10 degrees of angulation: ORIF

-Transverse displaced fractures

-Consider buttress plate, compression plate, IM percutaneous pinning, crossed K-wires
-Long oblique or spiral fractures
-Consider screws, plates, IM pinning, cerclage wiring
-Consider screws, plates, cerclage wiring, K-wires and external fixation

-Metatarsal Base Fractures

-MOI: Direct trauma (MVA, fall from height, etc.) Usually associated with Lisfranc’s trauma.
-Radiographic findings: -Generally remain in good alignment/angulation because of surrounding stable structures.
-Treatment: -Conservative
-NWB SLC 4-6 weeks with good alignment
-ORIF with displacement/alignment/angulation

-First Metatarsal Fractures

-MOI: Direct trauma (MVA, fall from height, crush, etc.) and indirect trauma (torsional, twisting, avulsions, etc.)
-Radiographic findings: -Variable
-Examine for distal intra-articular fractures
-Examine for avulsion-type fractures
-Treatment: -Conservative
-SLC 4-6 weeks with non-displaced fractures
-Be wary of closed reduction because extrinsic muscles may displace after apposition.
-Various ORIF techniques detailed above
-Percutaneous pinning and cannulated screws are option in first metatarsal
-ORIF should be utilized if intra-articular fracture involves >20% of articular surface

AJM Sheet: 5th Metatarsal Base Fractures

-The following describes unique subjective findings, objective findings, diagnostic classifications and treatments.

Subjective and Objective

-All will point to some form of traumatic injury. Common injuries leading to metatarsal fracture include direct trauma, blunt
trauma, shearing, ankle sprains, etc.
-Most important in your work-up will be how you read the plain film radiographs. Remember that at least two views are
necessary to accurately describe displacement/angular/rotational abnormalities.

Diagnostic Classifications
Stewart Classification
-[Stewart IM. Jones fracture: Fracture of the base of the fifth metatarsal bone. Clin Orthop. 1960; 16: 190-8.]
-Type I: Extra-articular fx at metaphyseal-diaphyseal junction (True Jones Fracture)
-MOI: Internal rotation of the forefoot while the base of 5th met remains fixed
-Radiographic findings: -Usually oblique or transverse fx at metaphyseal-diaphyseal junction
-Treatment: -NWB SLC 4-6 weeks for non-displaced fractures
-ORIF with displacement >5mm
-Misc: -Fracture first described by Sir Robert Jones in 1902 from injuring himself while ballroom
dancing. [Jones R. Fracture of the base of the fifth metatarsal bone by indirect violence. Ann Surg. 1902; 35(6): 776-82.]
-Very unstable fracture with high incidence of non-union/delayed union secondary to variable
blood supply. Remember that the diaphysis and metaphysis are generally supplied by two different arterial sources.
-[Smith JW. The intraosseous blood supply of the fifth metatarsal: implications for proximal fracture healing. Foot Ankle.
1992 Mar-Apr; 13(3): 143-52.]

-Type II: Intra-articular avulsion fracture

-MOI: Shearing force caused by internal twisting with contracture of peroneus brevis tendon
-Radiographic findings: -1 or 2 fracture lines
-Intra-articular in nature
-Treatment: -NWB SLC 4-6 weeks for non-displaced fractures
-ORIF with displacement >5mm
-Type III: Extra-articular avulsion fracture
-MOI: Reflex contracture of peroneus brevis with ankle in plantarflexed position
-Radiographic findings: -Extra-articular; Involvement of styloid process
-Treatment: -NWB SLC 4-6 weeks for non-displaced fractures
-ORIF (pins, screws, tension-band wiring) for displacement >5mm
-Consider excision of fragment and reattachment of peroneus brevis tendon
-Type IV: Intra-articular, Comminuted fracture
-MOI: Crush injuries with base of 5th met stuck between cuboid and the external agent
-Radiographic findings: -Multiple fragments; joint involvement
-Treatment: -NWB SLC 4-6 weeks for non-displaced fractures
-ORIF with displacement
-Consider bone grafting and fragment excision with severe comminution
-Misc: -High rate of non-union/delayed union
-Type V: Extra-articular avulsion fractures of the epiphysis
-MOI and treatment similar to Type II and III fractures
-Note that this can only occur in children (similar to a Salter-Harris Type I fracture)

Torg Classification
[Torg JS, et al. Fractures of the base of the fifth metatarsal distal to the tuberosity. JBJS-Am. 1984; 66(2): 209-14.]
-Radiographic classification of Jones fractures describing potential for non-union development.
-Type I: Acute injuries
-Radiographic findings: Narrow fracture line without intra-medullary sclerosis
-Type II: Delayed Union
-Radiographic findings: Widened fracture intersurface with evidence of IM sclerosis
-Type III: Non-Union
-Radiographic findings: Complete sclerotic obliteration of the IM canal

AJM Sheet: Stress Fracture Work-up
Also called: March fx, Hairline fx, Fatigue fx, Insufficiency fx, Deutschlander’s dz, Bone exhaustion, etc.

-CC: Patient presents complaining of a diffuse foot and ankle pain. Classic patient is a military recruit or athlete.
-HPI: -Nature: Pain described as “sharp with WB” or “sore/aching.” May have element of “shooting” pain.
-Location: Described as diffuse, but can be localized with palpation. Common areas include dorsal metatarsal or
distal tib/fib.
-Course: Subacute onset. Usually related to an increase in patient’s physical activity.
-Aggravating factors: Activity
-Alleviating factors: PRICE
-PMH: -Look for things that would weaken bone (eg. Osteoporosis)
-SH: -Look for recent increases in physical activity or a generally active patient
-PSH/Meds/All/FH/ROS: Usually non-contributory


Physical Exam
-Derm: -Generalized or localized edema
-Ecchymosis is rare
-Vasc/Neuro: Usually non-contributory
-Ortho: -Painful on localized palpation (positive pinpoint tenderness)
-Possible pain with tuning fork

-Plain Film Radiograph: -Localized loss of bone density and bone callus formation are hallmark signs
-Note that there must be a 30-50% loss of bone mineralization before radiographic presentation
of decreased bone density. This generally takes 10-21 days in a stress fracture.
-Bone Scan: -Increased uptake in all phases regardless of time of presentation

-General Stress Fracture Information

-Somewhere between 80-95% of all stress fractures occur in the LE with the most common sites being the metatarsals (20%
with 2nd metatarsal most commonly involved [11%]) and the distal tibia/fibula.
-Stress fractures can occur via two mechanisms:
-Chronic strain upon a normal bone
-A chronic, normally benign strain upon a weakened bone

-Conservative treatment is mainstay:
-Immobilization and NWB for 4-6 weeks (SLC, Unna boot, surgical shoe, etc.)
-Be certain of anatomic position with no angulation/rotation/displacement (very uncommon)

AJM Sheet: Lisfranc Trauma

-Dr. Jacques Lisfranc was a French gynecologist who was called into the service of Napoleon’s army where he served as a trauma surgeon in the 1820’s and
30’s. He also served under Dr. Dupuytren during this time.
-Del Sel first described Lisfranc dislocations following equine injuries (JBJS 1955).

-Tarsometatarsal joint: 9 bones, ~13 joints, 7 weak dorsal ligaments, 7 strong plantar ligaments, the Lisfranc ligament
-Myerson described three functional columns of the Lisfranc joint. Ouzounian and Shereff described the sagittal plane motion of each of these columns.
-Medial Column: 1st met and medial cuneiform: 4mm of motion in the sagittal plane.
-Central Column: 2nd/3rd mets and central/lateral cuneiforms. 1mm of motion in sagittal plane.
-Lateral Column: 4th/5th mets and cuboid. 10mm of motion in the sagittal plane.

-Mechanism of Injury
-Accounts for 0.2% of all traumatic injuries. Most common in MVA and sports injuries.
-Occurs either by direct crushing (i.e. dropping something on the foot) or indirectly (usually a plantarflexed and abducted foot).

-Midfoot pain and tenderness. Possibly exacerbated with pronation, abduction or plantarflexion.
-Plantar ecchymosis
-Be wary of compartment syndrome! Always check neurovascular status.
-Plain Film Radiography
-Pathognomonic “fleck sign” representing an avulsion fx in the 1st IM space.
-Look for deviations from normal in the AP, MO and Lat views. Normal is:
-AP: Medial border of the 2nd met continuous with the medial border of the central cuneiform. Lateral border of the
medial cuneiform continuous with the medial border of the central cuneiform.
-MO: Medial border of the 4th met continuous with the medial border of the cuboid. Lateral border of the 3rd met
continuous with the lateral border of the lateral cuneiform.
-Lat: No sagittal displacement. Look for lateral column shortening with a “nutcracker fracture” of the cuboid.
-“Lisfranc variant” is fracture damage extending proximally into the cuboid-navicular region.
-Consider stress radiographs with the foot in plantarflexion or abduction.
-CT, Bone Scan, MRI could all be utilized.

-Classification originally described by Quenu and Kuss, then modified by Hardcastle, then modified by Myerson. The Myerson Classification is
listed with the Quenu and Kuss equivalent in parentheses.
-Type A: Total incongruity in any plane (QK: Homolateral)
-Type B: Partial incongruity (QK: Isolateral)
-B1: 1st met goes medial
-B2: Lesser mets go lateral
-Type C: Divergent (QK: Divergent)
-C1: Partial (only 1st and 2nd mets involved)
-C2: Total (all mets involved)

-Literature strongly favors ORIF with any displacement (>2mm between the 1st and 2nd mets). Exact anatomic reduction is the key to prognosis.
-If plain film and stress radiographs show no displacement, then NWB SLC for 6 weeks with films q2 weeks looking specifically for
-Goal: Reduction and stabilization of the medial and central columns. You must reduce the lateral column, but it is usually left unfixed because
of the pronating mobile adapter mechanism. The medial and central columns do not have as much sagittal plane motion, but you still don’t want excess
compression with associated chondrolysis to develop.
-1st met to medial cuneiform, 2nd met to central cuneiform, and 3rd met to lateral cuneiform with crossed 0.062” K-wires (removed at 8
weeks), cannulated cancellous screws (removed at ~12 weeks) or 3.5mm corticals. Consider putting a notch 1.5cm distal to the joint for screw to prevent
stress risers. Drill the hole for the screw in the superior aspect of the notch and not the base to prevent splitting the base.

-Consider 4th met to cuboid and 5th met to cuboid with a single 0.062” K-wire
-Lisfranc Screw: Medial cuneiform to 2nd met base, screw in a lag fashion
-Length of the lateral column must be restored following a “nutcracker fracture.” Consider using an H-plate or external fixation.
-Longitudinal over the 1st IM space (provides access to 1,2,3) and longitudinal over the 4th IM space (provides access to 3,4,5).
-Longitudinal in the 1st IM space, 3rd IM space and lateral to the 5th met.

-NWB SLC for 8 weeks transitioned to PWB SLC for 4 weeks transitioned to rehab. High impact activity can usually be resumed at 6 months.

-ARTHRITIS! Essentially everyone develops post-traumatic arthritis to some extent.

Additional Reading:
-[Myerson M. The diagnosis and treatment of injuries to the Lisfranc joint complex. Orthop Clin North Am. 1989; 20(4): 655-64.]
-[Hardcastle PH, et al. Injuries to the tarsometatarsal joint. Incidence, classification, and treatment. JBJS-Br. 1982; 64(3): 349-56.]
-[Desmond EA, Chou LB. Current concepts review: Lisfranc injuries. Foot Ankle Int. 2006; 27(8): 653-60.]

AJM Sheet: Navicular Trauma

-Suspected navicular trauma should be worked up with a primary and secondary survey. The following describes unique
subjective findings, objective findings, diagnostic classifications and treatments.

-History of trauma ranges from contusions to ankle sprains to forced abduction/plantarflexion of the forefoot.

-MMT of the posterior tibialis tendon is important in these cases.
-Multiple view plain film radiographs are extremely important because of the possible obliquity of some fractures. CT scans
and MR images may also be necessary for complete visualization and analysis of stress fractures.

Relevant Anatomy
-The navicular is surrounded by a number of joints of varying stability. The TNJ proximally is very mobile, while the distal
NCJ and lateral NCJ are very stable. The navicular is also very stable medially because of the insertion of the PT tendon.
-Vascular anatomy to the navicular can be extremely important as described by Sarrafian:
-It has been demonstrated that the central 1/3 of the navicular is relatively avascular.
-The dorsalis pedis artery adequately supplies the dorsal and medial aspects.
-The medial plantar artery adequately supplies the plantar and lateral aspects.
-The central 1/3 has variable, radially-projecting branches from anastomosis of these arteries.

Diagnostic Classification
-Watson-Jones Classification
-Type I: Navicular Tuberosity Fractures
-Occur secondary to eversion and posterior tibialis contracture
-Watch for associated “nutcracker fracture” of cuboid and anterior calcaneal process fractures
-Must be differentiated from accessory navicular
-Treatment: -Displacement <5mm:
-Conservative immobilization
-Displacement >5mm consider:
-Excision of fragment with reattachment of tendon
-ORIF with a cancellous screw
-Type II: Dorsal Lip Avulsion Fractures
-Occur secondary to plantarflexion/frontal plane mechanisms.
-Must differentiate from os supranaviculare and os supratalare accessory ossicles.
-Generally intra-articular
-Generally treated with conservative immobilization
-Type III: Navicular Body Fractures. Described by Sangeorzan.
-[Sangeorzan BJ, et al. Displaced intra-articular fractures of the tarsal navicular. JBJS-Am. 1989; 71(10): 1504-10.]
-IIIA: Coronal Plane Fracture with no angulation
-~100% successful reduction usually achieved
-IIIB: Dorso-lateral to Plantar-medial fracture with adduction of the forefoot
-67% successful reduction usually achieved
-IIIC: Comminution with abduction of the forefoot
-50% successful reduction usually achieved

-Principles of ORIF for Type III fractures:

-Must achieve 60% reapproximation of proximal joint space
-Incision placed dorsal-medial, between the TA and TP
-Complications involve post-traumatic arthritis and/or AVN
-Fixation Options using 3.5mm Cortical Screws:
-Two screws directed lateral to medial
-Two crossed screws directed proximal to distal
-One screw directed proximal-medial to distal-lateral into the middle cuneiform
-Consider FDL transfer in the presence of a weakened PT tendon
-Type IV: Stress Fracture of the Navicular
-Generally occurs secondary to running
-Torg describes typical stress fracture occurring in central 1/3 of body in the sagittal plane.
-DDx: Tibialis anterior tendonitis
-Usually plain films, CT and bone scans are necessary to diagnose

AJM Sheet: Talar Fractures

-Talar fractures are generally associated with high energy trauma, and a standard evaluation with primary and secondary surveys
should precede any specific talar evaluation. The following describes unique subjective findings, objective findings, diagnostic
classifications and treatment considerations.

-History of trauma with a high incidence of MVC. The classic description of a talar neck fracture comes from a forced dorsiflexion
of the foot on the ankle (“aviator’s astragulus”). Talar fractures account for approximately 1% of all foot and ankle fractures.

-Important to verify neurovascular status, and rule out dislocations and compartment syndromes.
-Imaging: -Canale View: Plain film radiograph taken with the foot in a plantarflexed position. The foot is also pronated
15 degrees with the tube head orientated 75 degrees cephalad. This view allows for evaluation of angular
deformities of the talar neck.
-CT scan is essential for complete evaluation and surgical planning.

Relevant Anatomy
-An intimate knowledge of the vascular supply to the talus is essential with regard to avascular necrosis (AVN):
-Dorsalis Pedis: Supply the superior aspect of the head and neck (artery of the superior neck)
-Anastomoses with the peroneal and perforating peroneal arteries
-Artery to the sinus tarsi: supplies the lateral aspect of the talar body
-Forms an anastomotic sling with the artery of the tarsal canal
-Posterior Tibial Artery:
-Deltoid branch: medial aspect of the talar body
-Artery of the canalis tarsi: majority of the talar body
-Forms an anastomotic sling with the artery of the tarsal sinus
-Also sends branches to the posterior process
-Peroneal/Perforating Peroneal Artery: supplies posterior and lateral aspects of the talar body
-Anastomoses with the dorsalis pedis artery branches

Classifications/Named Fractures:

Hawkins Classification: Talar neck fractures Berndt and Harty: Talar dome fractures
Type I: Non-displaced (~13% incidence of AVN) Type 1: Chondral Depression
Type II: Displaced fracture with STJ dislocation (~50% incidence) Type 2: Partial chondral fracture, seen on MRI
Type III: Displaced fracture with STJ and ankle dislocation (~95%) Type 3: Nondisplaced complete osteochondral fracture
Type IV: Displaced fracture with STJ/ankle/TN dislocation (>95%) Type 4: Displaced complete osteochondral fracture
-(Type IV added by Canale and Kelly)

Sneppen: Talar body fractures Modified Hawkins: Lateral process fractures

Type 1: Osteochondral fracture Type I: Simple bipartite fracture
Type 2: Sagittal, Coronal, Transverse body fracture Type II: Comminuted fracture
Type 3: Lateral process fracture Type III: Chip fracture of anteroinferior lateral process
Type 4: Posterior tubercle fracture
Type 5: Crush fracture

Others: -Shepherd’s fracture: Acute fracture of posterolateral talar process

-Cedell’s fracture: Acute fracture of the posteromedial talar process
-Snowboarder’s fracture: lateral process fractures

-NWB in SLC 6-8 weeks versus ORIF depending on nature of fracture and degree of displacement.
-Titanium hardware may be used so that MRI evaluation may be used in post-operative period to evaluate for AVN!
-Hawkins sign: radiolucency of the talar body noted at 6-8 weeks after fracture. This sign is indicative of intact vascularity.
However, the absence of this sign does not indicate that osteonecrosis and talar collapse are eminent.

Additional Readings:
-Talar fractures are relatively uncommon in the medical literature. Most studies are case reports or small retrospective
reviews leading only to Level IV or V evidence.
-[Ahmad J, Raikin SM. Current concepts review: talar fractures. Foot Ankle Int. 2006 Jun; 27(6): 475-82.]
-[Golano P, et al. The anatomy of the navicular and periarticular structures. Foot Ankle Clin. 2004 Mar; 9(1): 1-23.]
-[Berndt A, Harty M. Transchondral fractures of the talus. JBJS-Am. 1959; 41: 988-1020.]
-[Canale ST, Kelly FB. Fractures of the neck of the talus. Long-term evaluation of seventy-one cases. JBJS-Am. 1978 Mar; 60(2): 143-56.]

AJM Sheet: Calcaneal Fractures
-The standard trauma work-up again applies with primary and secondary surveys. The following describes unique subjective
findings, objective findings, diagnostic classifications and treatment considerations.

-Demographics: Men>Women; Age range generally 30-60; account for ~2% of all fractures; 2-10% are bilateral; 10% associated
with vertebral fracture (most commonly L1); 1% associated with pelvic fracture and urethral trauma.
-Common mechanisms of injury: Direct axial load, vertical shear force, MVC, gastroc contraction, stress fracture, ballistics,
iatrogenic surgical fracture

-Physical Exam: -Pain with palpation to heel -Mondor’s Sign: characteristic ecchymosis extending into plantar medial foot
-Short, wide heel -Hoffa’s sign: less taut Achilles tendon on involved side
-Inability to bear weight -Must rule out compartment syndrome
-Imaging: -Plain film Imaging: -Bohler’s Angle: normally 25-40 degrees (decreased with fracture)
-Critical Angle of Gissane: normally 125-140 degrees (increased with fracture)
-Both demonstrate loss of calcaneal height
-Broden’s View: 2 oblique views to view the middle and posterior facets
-Isherwood Views: 3 oblique views to highlight all facets
-Calcaneal Axial View: demonstrates lateral widening and varus orientation
-CT Scan: -Gold standard for evaluation and surgical planning
-The coronal view forms the basis of the Sanders Classification
Sanders Classification: Uses widest view of posterior facet on semicoronal CT cut
-Type I: Non-displaced articular fx -A, B and C further describe the fx (lateralmedial)
-Type II: Two-part posterior facet fx -A/B: divide posterior facet into equal 1/3’s
-Type III: Three-part posterior facet fx -C: divides posterior facet from sus tali
-Type IV: Four-part/comminuted fx

-See page 1845 of McGlam’s, or 224 of Gumann’s for actual pictures.

-[Koval KJ, Sanders R. The radiographic evaluation of calcaneal fractures. CORR. 1993 May; 290: 41-6.]
-[Sanders R. Displaced intra-articular fractures of the calcaneus. JBJS-Am. 2000 Feb; 82(2): 225-50.]
Rowe Classification:
-Type I: -Type IA: Plantar tuberosity fractures (medial more common than lateral)
-Type IB: Sus tali fracture (remember FHL: pt will have pain with hallux PROM)
-Type IC: Anterior process fractures (remember your anatomy: bifurcate ligament)
-further divided into three parts by Degan Classification
-Type II: -Type IIA: Extra-articular “beak” fracture of posterior-superior calcaneal body
-Type IIB: Intra-articular “tongue-type” Achilles avulsion fracture
-Type III: Extra-articular calcaneal body fracture
-Type IV: Intra-articular joint depression fracture
-Type V: Intra-articular comminuted fracture

-See page 1830 of McGlam’s or page 223 of Gumann’s for pictures.

-[Rowe CR, et al. Fractures of os calcis: a long term follow-up study of one hundred forty-six patients. JAMA 1963; 184: 920-3.]
-[O’Connell F, Mital MA, Rowe CR. Evaluation of modern management of fractures of the os calcis. CORR 1972; 83: 214-23.]
Essex-Lopresti [Essex-Lopresti P. The mechanism, reduction technique, and results in fractures of the os calcis. Br J Surg 1952; 39: 395-419.]
-Differentiated between extra-articular (~25%) and intra-articular (~75%) fractures and further sub-divided intra-articular fractures
into tongue-type and joint depression fractures (both with the same primary force, but different secondary exit points).
Zwipp [Rammelt S, Zwipp H. Calcaneus fractures: facts, controversies and recent developments. Injury 2004; 35(5): 443-61.]
-Assigns 2-12 points based on: -Number of fragments -Number of involved joints
-Open fracture or high soft tissue injury
-Highly comminuted nature, or associated talar, cuboid, navicular fractures

-Appreciate the debate in the literature between cast immobilization vs. percutaneous reduction vs. ORIF vs. primary arthrodesis.
[Barei DP, et al. Fractures of the calcaneus. Orthop Clin North Am. 2002 Jan; 33(1): 263-85.]
-Goals of therapy are to restore calcaneal height, decrease calcaneal body widening (reduce lateral wall blow-out), take it out of
varus, and articular reduction.
-Review the lateral extensile surgical approach [Benirschke SK, Sangeorzan BJ. Extensive intraarticular fractures of the foot. Surgical management
of calcaneal fractures. CORR. 1993 Jul; 292: 128-134.]
-Complications: Wound healing, arthritis, lateral ankle impingement, malunion, nonunion, etc.
-[Benirschke SK, Kramer PA. Wound healing complication in closed and open calc fractures. J Orthop Trauma. 2004; 18(1): 1-6.]
-[Cavadas PC, Landin L. Management of soft-tissue complications of the lateral approach for calcaneal fractures. Plast Reconstr Surg. 2007;
120(2): 459-466.]

AJM Sheet: Ankle Fracture Evaluation

-The standard trauma work-up again applies with primary and secondary surveys. The following describes unique subjective
findings, objective findings, diagnostic classifications and treatment considerations.
-Residents and attendings love to ask questions about ankle fractures for whatever reason, so this is certainly a subject where
you should know the classification systems cold, and do a lot of the additional readings. We’ll keep it brief here.

-Relevant Anatomy to Review (not just for this topic; think lateral ankle instability, peroneal tendonopathy, sprains, etc.):
-Ankle Ligaments: -Lateral: ATFL, CFL, PTFL
-Medial: Superficial Deltoid: superficial talotibial, naviculotibial, tibiocalcaneal
Deep Deltoid: anterior talotibial and deep posterior ligaments
-Syndesmotic Ligaments: -AITFL, PITFL (and inferior transverse tibiofibular ligament), Interosseous ligament

-Ottawa Ankle Rules
[Stiell IG, et al. A study to develop clinical decision rules for the use of radiology in acute ankle injuries. Ann Emerg Med. 1992; 21(4): 384-90.]
-Developed by ED docs to minimize unnecessary radiographs following ankle sprains. X-ray only required if:
-Bone tenderness along distal 6cm of posterior edge of fibula or tibia
-Bone tenderness at tip of fibula or tibia
-Bone tenderness at the base of the 5th met
-Bone tenderness on the navicular
-Inability to bear weight/walk 4 steps in the ED

-Lauge-Hansen Classification
-First submitted as a doctoral thesis [Lauge-Hansen N, Anklebrud I. 1942]. Co-authored with a guy named “Ankle”-brud!
-[Lauge-Hansen N. Fractures of the ankle: analytic, historic survey as the basis of new experimental roentgenologic and clinical investigations.
Arch Surg 1948; 56: 259.]
Stage I Stage II Stage III Stage IV
Supination Lateral collateral Near vertical medial NA NA
ligament tear/ avulsion malleolar fx (Muller D)
Adduction fibular fx (Weber A)
Pronation Transverse avulsion fx AITFL syndesmotic Short, oblique lateral NA
medial rupture or avulsion of malleolus fracture
Abduction malleolus/deltoid its insertion (Weber B)
rupture (Muller B) Transverse on lateral
Supination AITFL syndesmotic Spiral lateral malleolus PITFL syndesmotic Transverse avulsion fx
rupture or avulsion of fracture (Weber B) rupture or avulsion of medial
External its insertion Long, posterior spike its insertion malleolus/deltoid
Rotation on lateral radiograph rupture (Muller B)

Pronation Transverse avulsion fx AITFL syndesmotic Oblique or spiral fibular PITFL syndesmotic
medial rupture or avulsion of fracture rupture or avulsion of
External malleolus/deltoid its insertion suprasyndesmotic its insertion
Rotation rupture (Muller B) (Weber C)

-The problem with the Lauge-Hansen classification: This was an experimental/laboratory study looking at the
result of forced talar movement on a fixed tibia-fibula. But most ankle fractures in real-life occur when a moving
tibia-fibular acts on a fixed foot.

-Danis-Weber/AO Classification for lateral malleolar fractures (From AO Group)

AO Type A: Type B: Type C:
Infrasyndesmotic Transyndesmotic Suprasyndesmotic
1 Isolated Isolated Simple diaphyseal fibular fx

2 With medial malleolar fx With medial malleolar fx or Complex diaphyseal fibular fx

deltoid rupture
3 With posterior-medial fx With medial lesion and posterior- Proximal fibular fx
lateral tibial fx

-Mueller Classification for medial malleolar fractures (From AO group)

Avulsion Transverse at level Oblique Near vertical
of mortise

AJM Sheet: Ankle Fracture Treatment

-Additional named fractures associated with the ankle:

-Tillaux-Chaput fx: AITFL avulsion from the anterolateral tibia
-Wagstaff fx: AITFL avulsion from the anteromedial fibula
-Volkmann fx: PITFL avulsion from the posterior-lateral tibia
-Bosworth fx: PITFL avulsion from the posterior-medial fibula
-Maisonneuve fx: Weber C-type proximal fibular fracture that occurs within 10cm of the fibular neck
-Pott’s fx: Generic term for a bimalleolar ankle fracture
-Destot fx: Generic term of a trimalleolar ankle fracture
-Dupuytren fx: At least a bimalleolar fracture when the talus gets lodged up between the tibia and fibula
-Posterior Malleolar Fractures: Different than an avulsion fracture of the PITFL; this is a true fx involving a portion of the
tibial plafond cartilage. CT is usually done to estimate a percentage of the involved joint space. The rule of thumb (although
certainly not proven) is that fractures involving >25-30% of the joint space require ORIF.

-Principles of Fixation:
-This is one area where there is a lot of controversy in the medical literature. There are certainly some things you want to
accomplish besides the generic concept of “anatomic reduction”. I can’t get too much into it in this limited space, but I will try
and give you a couple sides of the argument and some reading to do. The question you are really trying to answer is: “How
reduced is reduced enough?” Then we’ll briefly cover some specific aspects of the surgeries themselves. One thing to
appreciate is that most of these arguments are made about SER fractures (because they are the most common):
-Restore fibular length
-Most people agree that the fibular fracture is the dominant fracture. In other words, if you adequately reduce
the fibula, then the other fractures and dislocations more or less fall into line because of the soft tissues (poor
man’s definition of the Vassal Principle). It doesn’t mean that the other fractures don’t require fixation, but
it means there’s no real sense in fixating the other fractures unless you have the dominate fracture fixated (or
at least reduced).
-The other concept is that a fixed fibula is essentially acting as a buttress, keeping the talus within the ankle
-The fibula is generally shortened in ankle fractures, so you want to get the full length back with your
reduction (generally visibly seen by reduction of the posterior spike on a lateral view).
-[Yablon IG, et al. The key role of the lateral malleolus in displaced fractures of the ankle. JBJS-Am. 1977; 59(2): 169-173.]
-Restore the ankle mortise (medial clear space and the syndesmotic gap)
-This goes back to the fibula keeping the talus in the ankle mortise. The classic article you need to know is
Ramsey and Hamilton that showed a 42% decrease in the tibiotalar contact area when the talus was displaced
1mm laterally. From this, people inferred that if the talus isn’t perfectly reduced back into the mortise, then
gross instability occurs.
-This is assessed by:
-Medial clear space (from the talar shoulder): Should be ~4mm or less after reduction
-Tib-Fib Overlap: Approximately >10mm on AP view at 1cm superior to the joint line
-Talar Tilt: <10 degrees absolute, or <5 degrees compared to other side
-[Ramsey PL, Hamilton W. Changes in tibiotalar area of contact caused by lateral talar shift. JBJS-Am. 1976; 58(3): 356-7.]
-[Park SS, et al. Stress radiographs after ankle fracture: the effect of ankle position and deltoid status on medial
clear space measurements. J Orthop Trauma. 2006; 20(1): 11-18.]
-Fix the syndesmosis?
-Another area of controversy where there is no clear answer is when and how to fixate the syndesmosis with
internal fixation. One point is clear: the purpose of placing internal fixation across the syndesmosis is to
stabilize the fibula against the tibia to prevent lateral migration of the talus and instability. If the fibula is
stable against the tibia with all of your other fixation, then you don’t really need any additional fixation.
How can you tell? Radiographic findings and the Cotton hook test for instability intra-operatively.
-Other questions where people have opinions, but no clear answers are: What type of screws? How many
screws? How many cortices? How far above the ankle? Temporary vs. permanent fixation? Weight-
bearing? etc.

-Lateral Malleolus:
-Fracture is primarily reduced and fixated with a single 2.7mm cortical screw with interfrag compression.
-Then a generic 1/3 tubular plate or a specialized contoured plate is used for buttress stabilization.
-Attempt for 6 cortices proximal to fracture with 3.5 bicortical screws
-Get as many distal screws as you can. 3.5 bicortical if above the ankle joint. 4.0 unicortical if not.
-Proximal fibular fractures still amendable to 1/3 tubular plating, but may need to double-stack the plates.
-Should appreciate the concept of lateral vs. posterior anti-glide plating.
-Medial Malleolus:
-Several options including 4.0 cancellous, K-wires, plating, cerclage, etc.
-Additional Reading:
-[Mandi DM, et al. Ankle fractures. Clin Podiatr Med Surg. 2006 Apr; 23(2): 375-422.]
-[Mandracchia DM, et al. Malleolar fractures of the ankle. A comprehensive review. Clin Podiatr Med Surg. 1999 Oct; 16(4): 679-723.]
-[Kay RM, Matthys GA. Pediatric ankle fractures: evaluation and treatment. J Am Acad Orthop Surg. 2001; 9(4): 269-78.]
-[Jones KB, et al. Ankle fractures in patients with diabetes mellitus. JBJS-Br. 2005; 87(4): 489-95.]
-[Espinosa N, et al. Acute and chronic syndesmosis injuries: pathomechanics, diagnosis and management. Foot Ankle Clin. 2006 Sep; 11(3): 639-57.]
AJM Sheet: General Tendon Trauma

-Mechanism of Injury
-Tendon is actually the strongest part of the muscle-tendon-insertion system. It is much more likely for the complex
to fail at the myotendinous junction or at the tendinous insertion, but acute tendon injuries do occur. They are usually the
result of direct trauma, or overload on an intrinsically weakened tendon.
-Tension overload on a passive muscle
-Eccentric overload on an actively contracting muscle
-Blunt Trauma

-Factors which can intrinsically weaken tendons

-Increased age: -increased cross-linking of collagen fibrils decreases tendon elasticity
-decreased reaction time and muscular contraction speed
-decreased vascularity
-Sex: -M>F
-Systemic inflammatory process: -RA, SLE, Gout, etc.
-Underlying endocrine dysfunction: -Xanthoma (hyperbetalipoproteinemia), DM, Hyperparathyroidism
secondary to renal failure, hyperthyroidism, infection, intratendinous calcifications, etc.
-Medications: -Fluoroquinolones, Corticosteroids

-Tendon Healing
-As with most tissue, there is a generalized inflammation, reparative and remodeling phase.
-Week 1: Severed ends fill in with granulation tissue
-Weeks 2-3: Increased paratenon vascularity; collagen fibril alignment
-Week 4: Return to full activity without immobilization

-Imaging in Diagnosis of Acute Tendon Injury

-Plain Film Radiograph: -May see avulsions, soft tissue swelling, accessory bones/calcifications

-Tenograph: -Radiopaque dye injected into tendon sheath and viewed on plain film radiograph
-Technically difficult with many false positives and negatives

-Ultrasound: -Tendon normally appears hyperechoic to muscle on US.

-Look for discontinuity of fibers, possible alternating hyperechoic/hypoechoic bands, and an area
of intensely hyperechoic hematoma.
-It is very important that the US head is held perpendicular to the long axis of the tendon.

-CT: -Tendon normally appears as a homogenous, well-circumscribed oval surrounded by fat on CT. It
normally has a higher attenuation than muscle.
-Will be able to appreciate discontinuity on CT with injury.

-MRI: -T1: Tendons normally have a uniform low-intensity (very black). Will be uniform with variable
high-intensity signal with injury.
-T2: Tendons are normally relatively low-intensity. Will light up with high-intensity signal with
-Remember the magic angle phenomenon. Any MRI signal shot at 55 degrees to the course of
the tendon will show a false-positive damage signal. Very common in the peroneals.
-[Mengiardi B, et al. Magic angle effect in MR imaging of ankle tendons: influence of foot positioning on prevalence and
site in asymptomatic patients and cadaver tendons. Eur Radiol. 2006 Oct; 16(10): 2197-2206.]

-Principles of Repair
-It is possible, but rare to get acute tendon injury to any of the long tendons of the leg. An Achilles tendon work-up
will be featured in another AJM sheet, but realize there are some basic principles that apply to any tendon.
-One is generally able to primarily repair the tendon. Non-absorbable suture is preferred.
-Special attention should be paid to vascular supply. Remember that the majority of a tendon’s vascularity comes
from the mesotenon, and therefore should be preserved as much as possible.
-If primary repair is not possible, consider using lengthening tendon slides, tendon grafts, tendon transfers and
biomaterials such as Graft-Jacket (allograft dermal tissue matrix) or Pegasus (equine pericardium) to restore the
integrity of the tendon.
-The goal of treatment should be to allow early PROM without gapping of the tendon.

AJM Sheet: Achilles Tendon Rupture Work-Up

CC: Typical complaint is pain, weakness and swelling in the back of the leg following an acute injury. The typical patient is
the “weekend warrior” type. This is a 30-50 y/o male participating in a strenuous athletic activity after a generally inactive
HPI: Nature: Pain, weakness and swelling. Pain is surprisingly non-intense allowing the patient to ambulate. The patient
may relate an audible “pop” or “snap”. They may also relate feeling like they were “kicked or shot” in the back of the leg.
Location: Distal posterior leg. The left leg is more affected. Some people theorize that this has to do with the
majority of people having right-handedness and a greater strength and proprioception of the RLE.
Duration, Onset, Course: Acute onset with gradually progressive increase in swelling and edema.
Mechanism of Action: -Three classic MOA are described:
-Unexpected dorsiflexion with triceps contraction
-Pushing off during WB with the leg extended (tennis lunge)
-Violent dorsiflexion on a plantarflexed ankle
-Also consider lacerations and blunt trauma
Previous History: obviously more likely to re-rupture
PMH: -Inflammatory conditions: RA, SLE, Gout
-Endocrine dysfunction: DM, Renal failure with hyperparathyroidism, hyperthyroidism, Xanthoma
-Infection: Syphilis
Meds: -Corticosteroid injection
-Fluoroquinolone use
SH: -Smoking
-Sedentary lifestyle with weekend activity

Derm: -Posterior, Medial and Lateral Ecchymosis
-Open lesion associated with laceration
Vasc: -Posterior, Medial and Lateral edema
Neuro: -Sural Neuritis
Ortho: -Palpable gap (“hatchet strike defect”)
-Positive Thompson test
-Negative Jack’s test
-Pain in the area
-Increased PROM ankle dorsiflexion
-Decreased AROM ankle plantarflexion
-Retraction of proximal gastroc belly
-Apropulsive gait
Other specific tests: -Mattles test: Foot should be in plantarflexed position with patient prone and knee at 90°
-Simmonds’ test: Foot should be in plantarflexed position with patient prone
-Various needle tests (O’Brian, Cetti)
-Toygar’s skin angle: Normally 110-125 degrees. Increases to 130-150 degrees with rupture.

-Plain film: -r/o Rowe Type IIB avulsion fracture
-Radiodense gap
-Obliteration of Kager’s triangle
-Soft tissue edema
-US: -Alternating hyperechoic and hypoechoic bands
-Hyperechoic hematoma
-MRI: -TI: -Ill-defined low-intensity with mixed high-intensity signal
-T2: -High-intensity signal from hematoma

AJM Sheet: Achilles Tendon Rupture Treatment

-Anatomy Review
-Muscles of the Triceps Surae (origins, insertions, NV supply, action)
-Plantaris (origins, insertions, NV supply, action)
-Segmental Blood Supply of Tendon
-“Twisting” of tendon

-Specific Information regarding the Watershed Area

-Lagergren and Lindholm
-Used microangiographic technique on human cadavers
-Found decreased vascularity 2-6cm proximal to insertion
-Theorized this was secondary to atrophy from inactivity
-Conflicting information from laser Doppler flowmetry studies
-Found uniform vascularity throughout tendon
-Found decreased vascularity with age and in men
-Found decreased vascularity with physical loading/stress of tendon, specifically at insertion
-Found increased stress/strain at the watershed area regardless of vascularity

-Kuwada Classification of Achilles Tendon Ruptures

[Kuwada GT. Classification of tendo Achilles repair with consideration of surgical repair techniques. J Foot Surg. 1990; 29(4): 361-5.]
-Type I: Partial tear involving <50% of tendon. Note that in a partial Achilles tear, the posterior fibers are torn first. So the direction of the
tear/rupture is from posterior to anterior.
-Type II: Complete tear with <3cm deficit
-Type III: Complete tear with a 3-6cm deficit
-Type IV: Complete tear with a >6cm deficit

-Puddu Classification of Chronic Achilles Pathology

-Peritendonitis: Inflammation of the surrounding tissues, not the tendon itself. This pain will remain stationary as the tendon is taken through a
range of motion.
-Tendonosis: Intra-tendinous degeneration. This pain will move proximally and distally as the tendon is taken through a range of motion.
-Peritendonitis with tendonosis: combination of the two pathologies.

-The podiatric surgeon is faced with three options: do nothing, cast immobilization and surgical repair. There’s a lot of information out about this in the
medical literature now, particularly with open repair vs. immobilization and when to start weight-bearing/PT.

-Do nothing
-Gap will eventually fill in with fibrotic scar tissue
-Usually requires later surgical intervention

-Cast Immobilization
-AK cast versus SLC
-Schuberth is proponent of AK casting
-Knee should be in a 20 degree flexed position
-General recommendations:
-Gravity equinus cast x 4 weeks
-Reduction of 5 degrees every 2 weeks to a neutral ankle position (~4-6 weeks)
-Heel lift and PT until normal ankle PROM
-Return to full activity at approximately 6 months

-Surgical Repair
-Surgical approach
-Midline to medial incision to avoid superficial neurovascular structures
-Pt in a prone or supine frog-legged position
-Use full-thickness flaps with emphasis on atraumatic technique
-Primary Open Repair
-Keith needles with non-absorbable suture (or fiberwire) with absorbable sutures to reinforce
-There are three common stitches used:
-Bunnell: Figure of 8 or weave stitch
-Krakow: Interlocking stitch
-Kessler: Box stitch
-Augmented Open Primary Repair
-Lynn: Plantaris is fanned out to reinforce
-Silverskoild: 1 strip of gastroc aponeurosis brought down and twisted 180 degrees
-Lindholm: Utilizes multiple strips of gastroc aponeurosis
-Bug and Boyd: Strips of fascia lata are used to reinforce
-V Y lengthening of the proximal segment with primary repair
-Reinforcement with FHL
-Graft Jacket, Pegasus, etc.
-Percutaneous Primary Repair
-Ma and Griffith described a percutaneous Bunnell-type approach
-May be associated with high re-rupture rates

-Post-Op Treatment
-SLC in gravity equinus with gradual reduction over 6-10 weeks
AJM Sheets: Peri-Operative Medicine and Surgery

Peri-Operative Medicine
-Admission Orders (page 70)
-Electrolyte Basics (page 71)
-Glucose Control (page 72)
-Fluids (page 73)
-Post-Op Fever (page 74)
-DVT (page 75)
-Pain Management (page 76)

General Surgery Topics

-AO (page 77)
-Plates and Screws (page 78)
-Suture Sheet (page 79)
-Surgical Instruments (page 80)
-Power Instrumentation (page 81)
-Biomaterials (page 82)
-External Fixation (page 83)
-Bone, Bone Healing and Wound Healing (page 84)

Specific Surgery Topics

-How to “Work-Up” a Surgical Patient (page 85)
-Digital Deformities (pages 86-87)
-Lesser Metatarsals (page 88)
-5th Ray (page 89)
-HAV (page 90-91)
-HAV Complications (page 92)
-HL/HR (pages 93-94)
-Pes Plano Valgus (pages 95-96)
-Cavus (pages 97-98)
-Equinus (page 99)

This particular section is intended to be more general, as opposed to a specific surgical study
guide. It is ridiculous to think that you could learn foot and ankle surgery in 100 pages, especially with
only 15 pages dedicated to specific deformities. In other words, you should absolutely not be doing all of
your specific surgical preparation for externships and interviews from the PRISM. Many of the Sheets
from the Specific Surgery Topics section are simply summarizations of the 3rd edition of McGlamry’s
chapters for example. This may be an area where you feel the PRISM could be updated in the future.

Again, I said that while I was studying for the Diabetic Foot Infection work-up, I tried to learn as
much as possible on the topic and really tried to “wow” the attendings at the interview. However, my
strategy was different when dealing with trauma and the specific surgical work-ups. Here I tried to
demonstrate “competence,” as opposed to “mastery” of the material. With specific surgeries, you’re really
not supposed to have strong, pre-formed opinions as a student or as an intern. That’s what your residency
is for, developing surgical opinions. If you already know what to do in every surgical situation, then what’s
the point of doing a residency? So while on externships and at the interview, you should really try to walk
a fine line between:
1. Displaying competence in knowledge of the baseline material
2. Displaying that you still have a lot to learn, and that you are eager to learn it.

Page 85’s “How to Work-Up a Surgical Patient” gets into this concept a little deeper.

AJM Sheet: Admission Orders/ADC VANDILMAX
(Note: If I wanted to be mean during an interview, I would have you write out a set of admission or post-op orders as I was asking you other questions.)

Admission: Pt is admitted to the general medical floor on the Podiatric Surgery Service under Dr. Attending.
Most patients on the podiatric surgery service are admitted to the general medical floor or a surgical floor. Any pts
admitted to a critical care unit or telemetry unit will probably be on a medicine service with a podiatric surgical consult.

Diagnosis: Infection of bone of right 2nd toe

Always use terminology that everyone in the hospital can understand, but also be as specific as possible.

Condition: Consider: -Stable -Fair -Guarded -Critical

Podiatric surgery pts will generally always be in stable or fair condition.

Vitals: Vitals recorded q8 hours per nursing.

Always designate how often you want them recorded. Also common is “q-shift.”
Consider neurovascular checks to the affected limb if indicated.

Ambulatory Status: Consider: -CBR (Complete bed rest) -As tolerated

-NWB -OOB to chair
Always designate which leg the order is for. Be specific with PWB status (“toe-touch” or “heel-touch”). If order is for
CBR, consider DVT ppx and a bed pan order. If the order is OOB, specify # of times and length per day.
Also consider Physical Therapy and/or Occupational Therapy orders here.

Nursing Instructions: Consider: -Accuchecks (how often and when?) -Ice and elevation
-Bedside Commode -Dispense Post-op shoe/Crutches
-Wound Care -Dressing Instructions
-Drain management -Off-loading instructions

Diet: Consider: -Regular diet -ADA 1800-2200 calorie -Mechanically soft

-Renal diet -Cardiac diet -NPO
-Decreased Na -Decreased K+

Ins/Outs/IVs: Consider: -Measurement and recording of Ins and Outs (especially dialysis pts)
-IV Fluids

Labs: Consider: -CBC with diff -Chem-7/Met Panel -Coags

-Type and Screen -Wound cultures -Blood cultures
-D-Dimer -HbA1c -CRP
Always detail when the labs should be done. For example, initial CBC and Chem-7 should be taken “upon arrival to the
floor.” Additionally, 2 sets of blood cultures should be taken from 2 different sites.

Medications: Consider: -Write out all at-home medications in full -Pain medication
-Antibiotics -Insomnia
-Anti-emetics -DVT ppx
-Constipation -Diarrhea
-SSI -Fever
-Throat lozenges -Anti-pruritic
Be as specific as possible. SSI needs to be written out in full. Many medications require hold parameters. For example,
fever medications should not be given unless the temperature reaches 101.5° F. Anti-HTN agents should be held if the blood
pressure or heart rate drops too low.

Ancillary Consults: Consider: -General Medicine -Infectious Disease

-Vascular Surgery -Cardiology
-Pulmonary -GI
-Renal -Social Work
-Home Care -Case Manager

X-rays/Imaging: Consider: -Plain film radiographs -CT scans -US Doppler

-MRI -CXR -Bone Scans
-Vascular Studies -EKG
AJM Sheet: Electrolyte Basics

-Manifestations: Primarily neurologic, lethargy, headache, confusion, obtundation
-Treatment: -Restrict water intake and promote water loss -Correct underlying disorder
-Replace Na+ deficits
-Manifestations: Change in mental status, weakness, neuromuscular irritability, focal neurologic deficits, coma,
-Treatment: -Replace water loss and promote sodium excretion
-Water deficit = ([Na+]-140)/140 x Total Body Water in liters
-Rapid correction of either of these disorders is dangerous due to rapid shifts of water in and out of brain cells. It should
therefore be corrected slowly over 48-72 hours. Aim correction at 0.5 mEq/L/hr with no more than a 12 mEq/L correction over the first 24

-An abnormal potassium level is a major reason a surgery will be cancelled and/or delayed. You should have a specific
understanding how to raise and lower potassium levels in the peri-operative setting.
-Manifestations: Fatigue, myalgia, muscular weakness, cramps, arrhythmia’s, hypoventilation, paralysis, tetany
-Treatment: -Minimize outgoing losses -Treat underlying cause
-Correct K+ deficit via oral or IV means (K+ riders added to fluid, oral KCL, etc.)
-Manifestations: Cardiac toxicity (peaked T waves, prolonged PR, torsades de pointes), muscle weakness, paralysis,
-Treatment: -Increase cellular uptake of K+
-Insulin (10-20 units) with 50 g IV glucose
-IV NaHCO3 (3 ampules in 1L of 5% dextrose)
-Albuterol (5-10mg nebulized over 30-60 minutes)
-Increase K+ excretion
-Loop diuretic, Thiazide diuretic
-Kayexalate (cation exchange resin) (25-50mg mixed with 100ml 20% sorbitol to prevent constipation)
-Calcium Gluconate (10ml of 10% solution over 2-3 minutes emergently to reduce membrane excitability)

-Chloride and Carbon Dioxide:

-Not going to talk much about this, but you should have a basic understanding of Acid-Base Regulation.
-Equation for determining Anion Gap:
Anion gap (all units mmol/L) = (Na + K) - (Cl + [HCO3-])
-Normal gap (~8-20mmol/L)
-Negative/lowered gap (<8mmol/L): Alkalotic state
-Positive/elevated gap (>20mmol/L): Acidotic state
-MUDPILES algorithm: methanol/metformin, uremia, diabetic ketoacidosis, propylene glycol,
infection, lactate, ethanol, salicylate/starvation
-BUN and Creatinine:
-Measures of kidney function and hydration status
-BUN (Blood Urea Nitrogen): Protein metabolism waste product eliminated by the kidneys. This can be increased if your
kidneys aren’t eliminating it properly, or in a dehydrated state where it’s a relatively high concentration.
-Creatinine: A more direct measure of kidney function from elimination of this skeletal muscle waste product.
-Creatinine clearance and estimated glomerular filtration rate (GFR) with the Cockcroft-Gault Equation:
[(140-Age in years) x Weight in kg] / [72 x Serum creatinine] x 0.85 if female
-GFR < 60 ml/min indicates chronic kidney disease; < 15 indicates kidney failure
-Antibiotics and other drugs should be dosed appropriately in these situations
-Renal protective agents are utilized prior to procedures that are known to affect the kidneys in patients with kidney
disease. A common example of this is an angiogram with dye to evaluate the vascular status of a patient with diabetic foot disease.
-Pre-procedural hydration -Mucomyst (N-acetylcysteine) (also used for acetaminophen OD)
-Sodium Bicarb Protocols
-[Lawlor DK. Prevention of contrast-induced nephropathy in vascular pts. Ann Vasc Surg. 2007 Sep: 593-7.]

-Glucose covered in another AJM sheet

AJM Sheet: Blood Glucose and Glycemic Control

-The importance of in-patient management of blood glucose cannot be overstated. This is an area however
where medicine tends to be very passive with regard to intervention. Rigid control of blood glucose in the in-patient
setting has been definitively shown to:
-Reduce mortality -Reduce in-patient complications
-Reduce infection rates -Decrease length of stay
-Reduce hospital costs
-Specifically with regards to diabetic foot disease, a single blood glucose level higher than 150-175mg/dl
significantly limits the function of the immune system for a period of days, particularly cytokine activation and
-My favorite article of the 2006-7 academic year was Inzucchi SE. Management of Hyperglycemia in the Hospital Setting. NEJM.
Sep 2006; 355: 1903. It is a must-read on this topic. I also strongly recommend obtaining a FREE copy of the Yale Diabetes
Center Diabetes Facts and Guidelines 2006. They will mail it to you (FOR FREE!) by calling 203 737-1932 or emailing An online version is also available at
You are a complete sucker if you don’t take advantage of this resource. And if you are really interested in this topic, research
the work of the Portland Diabetic Project.

Oral Agents
-Sulfonylureas: Bind to β-cell receptors stimulating insulin release
-Glyburide (Micronase) -Glipizide (Glucotrol) -Glimepiride (Amaryl)
-Biguanides: Decrease production of glucose in the liver
-Metformin (Glucophage)
-Thiazolidinediones: Increase peripheral cellular response to insulin
-Rosiglitazone (Avandia) -Pioglitazone (Actos)
-α-glucosidase inhibitors: Reduce intestinal carbohydrate absorption
-Acarbose (Precose) -Miglitol (Glyset)

Type Onset Peak Duration
Rapid Acting
Lispro (Humalog) 10-15 minutes 1-2 hours 3-5 hours
Aspart (Novolog) 10-15 minutes 1-2 hours 3-5 hours
Short Acting
Regular 0.5-1hr 2-4 hours 4-8 hours
Intermediate Acting
NPH 1-3 hours 4-10 hours 10-18 hours
Lente 2-4 hours 4-12 hours 12-20 hours
Long Acting
Glargine (Lantus) 2-3 hours None 24+ hours
Detemir (Levemir) 1 hour None 24 hours
70/30 0.5-1 hour 2-10 hours 10-18 hours
(70% NPH/30% Regular)

In-patient Recommendations
-There is increasing data that sliding scales are completely inefficient at in-patient glucose management.
Sliding scales are passive, reactionary scales that compensate after a hyperglycemic incident occurs. Inzucchi
recommends the following, instead of a sliding scale:
-Basal Rate: Lantus or other long acting
-Start 0.2-0.3 Units/kg/day; then increase 10-20% q1-2 days prn
-Prandial Coverage: Novolog or other rapid acting
-Start 0.05-0.1 Units/kg/day; then adjust 1-2 Units/dose q1-2 days prn

Diabetic NPO Recommendations

-Type 2 DM: -1/2 the normal dose of long acting if they get any
-BG checks q6 hours with short acting agent available for coverage
-D5W or D5-1/2NS at 50-75cc/hr while NPO
-Type 1 DM: - Strongly consider an insulin drip
-1/2 – 2/3 normal dose of long acting agent
- BG checks q6 hours with short acting agent available for coverage
- D5W or D5-1/2NS at 75-100cc/hr while NPO

AJM Sheet: Fluids

-Fluid management is a difficult topic to cover because it can be used for a variety of different problems/purposes. It can be
used to maintain fluid balance in a patient who is NPO, correct electrolyte disturbances, and/or provide glucose to name just a
few examples. This sheet will cover the basics of short-term maintenance therapy and show differences in electrolyte
concentrations between the most common fluids.

-Maintenance therapy for the NPO patient

-An NPO patient is still losing water that needs to be replaced to ensure homeostasis. Sources of water loss include:
-Urine output: At least 500ml/day
-Insensible water losses (Skin and Respiration): At least 500ml/day
-This can increase by 150ml/day for each degree of body temperature of 37°C.
-Gastrointestinal losses: Extremely variable
-Direct blood volume loss from the surgery itself
-Electrolytes are also lost to varying degrees. In the short term, it is usually only necessary to replace Na+, K+ and
glucose. The other electrolytes usually do not need replacement until around 1 week of parenteral therapy.

-Pediatric Considerations
-Pediatric patients should be aggressively rehydrated after a surgical procedure for two reasons:
-They will lose a higher percentage of their total fluid volume during a procedure.
-They have a tendency to “third space” and shift fluid balances in the perioperative period.
-To determine the total intravascular volume of a pediatric patient:
-The first 10kg of body weight account for about 80ml/kg.
-So a 7kg kid would be (7x80) = 560ml
-The next kg’s account for about 70ml/kg
-So a 25kg kid would be (10x80 + 15x70) = 1850ml

-General Recommendations:
-At the very least you should replace fluid to account for water loss. This is at least 1L/day, but you can
certainly increase this and lose the excess through the urine.
-It is also recommended to provide some electrolyte supplementation:
-Na+: 50-150 mEq/day
-K+: 20-60 mEq/day
-Glucose: 100-150g/day to minimize protein catabolism and ketoacidosis

-Common parenteral solutions:

IV Solution Osmolality (mOsm/kg) Glucose (g/L) Na+ (mEq/L) Cl- (mEq/L)

D5W 278 50 0 0
D10W 556 100 0 0
D50W 2778 500 0 0
0.45% NaCl 154 (5% available) 77 77
0.9% NaCl 308 (5% available) 154 154
3% NaCl 1026 0 513 513
Lactated Ringer’s 274 (5% available) 130 109
-LR also contains 4 mEq/L K+, 1.5 mEq/L Ca2+, and 28 mEq/L lactate

-Common administrations:
-Normal adult: NS or 1/2 NS or LR at 75-120ml/hr +/- 20mEq KCl
-Diabetic patients: D5-1/2NS at 50-100ml/hr +/- 20mEq KCl while NPO
There usually isn’t a need to deliver extra glucose (D5) to diabetic patients while they are PO.

-The key to fluid management is an understanding and knowledge of exactly why you are giving fluids in the first place, what
you hope to accomplish, what substances you are giving in the fluid and how much you are giving.

-Obvious care needs to be taken with diabetic patients, those with renal pathology, and those with CHF.

Additional Reading:
-[Grocott MP, et al. Perioperative Fluid Management and Clinical Outcomes in Adults. Anesth Anal. 2005 Apr; 100(4):1093-106.]
-[Paut O. Recent developments in the perioperative fluid management for the paediatric patient. Curr Opin Anaesthesiol. 2006 Jun;19(3):268-77.]

AJM Sheet: Post-Op Fever

-General Information
-When dealing with a fever work-up, always note what the baseline temperature of the patient is and the method of
-Fever in most institutions is defined as greater than 101.5° F.
-Temperatures between 98.6-101.5° are low-grade fevers.

-Intra-operative causes of fever

-Inflammatory process of the surgical procedure itself
-Transfusion Reaction
-Malignant Hyperthermia
-Pre-existing Sepsis

-The 5 “W’s” of Post-Operative Fever

-Wind: Atelectasis, aspiration pneumonia, PE
-Wound: Surgical site infection, thrombophlebitis (IV site), pain
-Water: UTI, dehydration, constipation
-Walk: DVT
-Wonder Drugs: Virtually any drug can cause fever, but the most common are antimicrobials and heparin.

-Timeline General Guide

-0-6 hours post-op: Pain, anesthesia rxn, rebound from cold OR, endocrine causes (thyroid crisis, adrenal
-24-48 hours post-op: atelectasis, aspiration pneumonia, dehydration, constipation
-72+ hours: infection (3-7 days), DVT, UTI, drug allergy, thrombophlebitis

-Temperature General Guide (in degrees F)

-107: Anesthetic Hyperthermia
-106: -
-105: Blood transfusion reaction
-104: Closed abscess
-103: Atelectasis; pneumonia; drug reaction; liver disease
-102: Wound infection
-101: Draining abscess
-100: Benign post-op fever; post-anesthesia overshoot

-General Knowledge
-Usually only two infectious agents can cause a fever within a few hours of surgery:
-Group A Strep (GAS)
-Clostridium perfringens
-Dialysis patients typically run approximately 1 degree F cooler than the normal population, so a fever for HD
patients wound be defined as 100.5° F. This is hypothesized to be due to a resetting of the hypothalamic set point.
-The majority of causes of fever are non-infectious. AJM always carries with him a copy of the DDX of fever
copied from Harrison’s text (it’s 2 pages long!). Common non-infectious causes of post-op fever include:
-Surgical site inflammation
-The purpose of any fever work-up is to find the source!
-If you are thinking infection, then infection from where: Surgical site? Pulmonary? Urine? Blood? Does
the patient have any peripheral vascular access lines?

AJM Sheet: Deep Vein Thrombosis (DVT)

-Signs and Symptoms

-Homan’s Sign: Pain in calf with dorsiflexion of the ankle
-Pratt’s Sign: Pain with compression of the calf
-Edema -Fever -SOB
-Calor -Palpation of clot

-Risk Factors
-Virchow’s Triad: -History of DVT -Collagen Vascular Dz
-Hypercoagulable state -Family History of DVT -Trauma
-Immobilization -Pregnancy -Infection
-Vessel Wall Injury -Oral Contraceptives -Post-partum
-Age > 75 -Hormone Replacement Therapy
-Malignancy -Obesity -HIV/AIDS
-There is also the acronym I AM CLOTTED: Immobilization, Afib/CHF, Malignancy/MI, Coagulopathy, Longevity (age),
Obesity, Trauma, Tobacco, Estrogen/BCP/HRT, DVT/PE history.
-Compression Ultrasound: can actually visualize the clot
-D-Dimer > 500ng/ml: Not sufficient as a stand alone test
-Consider full coagulation work-up for hypercoagulable states
-Contrast venography
-Impedance plethysmography

-Goals of Treatment: 1. Prevent pulmonary embolism
2. Prevent clot extension
3. Prevent recurrence
-Immediate Anti-Coagulation
-IV Unfractionated Heparin
-Law of 8018
-Initial Dose 80mg/kg IV bolus and then 18mg/kg/hour
-PTT should be checked q6 until it stabilizes at 1.5-2.5X normal (46-70s)
-Goal is to get PTT in this range
-LMWH may also be used
-Enoxaparin (Lovenox): 1mg/kg subcutaneous q12

-Heparin Dosing Guide

-Initial Dose: Law of 8018 with PTT checks q6
-If PTT <35s: 80 units/kg IV bolus, then increase infusion rate by 4 units/kg/hr
-If PTT 35-45s: 40 units/kg IV bolus, then increase infusion rate by 2 units/kg/hr
-If PTT 46-70s: No change to dosing. Continue with 18mg/kg/hour infusion rate
-If PTT 71-90s: Decrease infusion rate by 2 units/kg/hr
-If PTT >90s: Hold infusion for 1 hour, then decrease infusion rate by 3 units/kg/hr
-Continued Anti-Coagulation
-Warfarin (Coumadin)
-Load at 10mg or 7.5mg PO qdaily for 2 days
-Decrease/adjust dose to a target INR=2.5
-DO NOT stop heparin infusion until INR reaches 2.5
-INR should be maintained at 2.5 for 3-12 months
-Consider placement of IVC filter (inferior vena cava)

-Pulmonary Embolism (PE)

-PE occurs when a clot from a peripheral location embolizes to the pulmonary vasculature
- <25% of deep vein thromboses distal to the iliac veins go on to develop PE.
-The more proximal the clot, the more likely it is to develop into a PE.
-“Classic Triad” of signs and symptoms of a PE: Dyspnea/SOB, Chest Pain, Hemoptysis
-Please note that less than 14% of patients experience the classic triad
-Diagnosis of a PE
-Gold standard: Pulmonary Angiography, spiral CT
-V/Q study
-Treatment of PE
-Thrombolytic Therapy: -Urokinase: 4400units/kg IV over 10 min, then 4400units/kg/hr for 12 hours
-Streptokinase: 1.5 million units IV over 60 minutes
-Pulmonary Embolectomy
-Various filters

AJM Sheet: Pain Management
-Pain Management is a subject that you will be dealing with a lot during residency, but something that you
won’t receive much formal education on. Honestly, you probably won’t get many interview questions about it
either, but it’s something that I think is important. This is a shameful plug, but Clinics in Podiatric Med and Surg
had a whole edition to the subject (July 2008) that is worth reading. Specifically for the residency interview, read
Articles 1, 5 and 8. I also wrote the “Perioperative Pain Management” chapter in the 4th edition of McGlam’s.
-The “attack points” are a concept that AJM made up to promote an active approach to multimodal pain

-Acute Operative Pain Physiology “Attack Points” (In Clinics: The Physiology of the Acute Pain Pathway)
Attack Point Physiology Intervention
Stimulus Stimulus: Noxious stimuli resulting in Resolution/Limitation of Stimulus
tissue damage to superficial and deep -Prevention of secondary aggravation
somatic structures.
Anti-Inflammatory Pharmacologics
Transduction: Nociceptor activation by -NSAIDs
chemical, mechanical or thermal means. Carboxylic Acid Derivatives
Proprionic Acid Derivatives
Post-Injury Inflammatory Response: Acetic Acid Derivatives
Normal response to cellular damage with Fenamates
the chance to develop into the Enolic Acid Derivatives
pathophysiologic mechanism of peripheral Naphthylkanones
sensitization. COXII Selectives
-Topical Agents
-Local Anesthetics

Anti-Inflammatory physiotherapeutics

Transmission Peripheral sensory afferents carrying the Local Anesthetics

action potential of the noxious stimulus
from the periphery to the CNS. Sodium Channel Blockers
-Normally controlled by myelinated A-
delta and unmyelinated C fibers.
-Allodynia is a pathophysiologic state of
sensitization when A-beta fibers transmit
light touch as painful.
Modulation Spinal Cord Dorsal Horn Opioids
-Peripheral Excitatory Signals
-Peripheral Inhibitory Signals Calcium Channel Blockers
-Central Excitatory Signals
-Central Inhibitory Signals NMDA Receptor Antagonists



Perception Ascending Central Processes Anxiolytics

Descending Central Processes
Patient Emotional Response Anti-Depressants

Patient Education

-Multimodal Approach to Active Pain Management

A passive unimodal therapy like Percocet has very little total effect on the physiology of pain. Opioids and
acetaminophen influence small portions of the modulation attack point, but essentially do not influence any of the other attack
points. A multimodal approach actively intervenes at several attack points with several therapies to interrupt the known
physiologic and pathophysiologic mechanisms.
-Pre-emptive Analgesia (In Clinics: Perioperative Pain Management)
-The concept of pre-dosing pain medications before surgery to interrupt pain pathways before they start
AJM Sheet: AO

-AO: Arbeitsgemeinschaft fur Osteosynthese fragen

-Plates and screws for fx fixation first described by Alain Lambotte in 1907.
-Robert Danis (Belgium surgeon) published “The Theory and Practice of Osteosynthesis” in 1949.
-Described use of compression plate called a coapteur.
-Maurice Mueller, a pupil of Danis, founded AO with other Swiss surgeons in 1959.

-Principles of AO
1. Accurate and precise anatomic reduction of fracture fragments (especially in joints).
2. Atraumatic surgical technique with emphasis on preservation of blood supply.
3. Rigid/Stable fixation
4. Early mobilization

-The “Guide to Internal Fixation” by the AO group is a great book that reads fairly quickly. You should also read the text
“Internal Fixation of Small Fractures” and “AO Principles of Fracture Management” from the AO group. General notes
from these books are included throughout the following sheets dealing with specific traumatic fractures.

-General Principles of the Lag Technique

-Why? Generates compression. So? Compression leads to lack of motion and therefore primary bone healing.
Motion disrupts angiogenesis, decreases oxygen tension levels and inhibits osteogenesis. So, it is the lack of motion and
NOT the compression that is osteogenic.

-Orientation of the screw 90° to the fracture line obtains optimal compression.
->20° displacement from perpendicular is significant
-Weakest in translation from axial loading
-Orientation of the screw 90° to the long axis optimally prevents displacement with axial loading.
-Weak in compression
-Ideal screw placement for a long, oblique fracture:
-One central anchor screw 90° to the long axis
-One proximal and one distal compression screw 90° to the fracture line

-Principles of Insertion
-AO Recommendations: Overdrill, Underdrill, Countersink, Measure, Tap, Screw
-Some underdrill before overdrill
-Some don’t overdrill until after tapping
-Two finger tightness = 440-770lbs.
-To prevent thermal necrosis: -Sharp tip
-Fast advancement (2-3mm/sec)
-Slow drill speed (300-400rpm)
-Firm force (20-25lbs)
-Screw Pull-out
-Directly proportional to screw diameter, screw length and bone strength (cortical nature).
-Indirectly related to pilot hole diameter.
-To increase screw pull-out, maximize bone-screw contact.

-Fairly Irrelevant Definitions

-Stress: pressure on a material
-Strain: measurable deformation following a given stress
-Stress-Strain Curve/Load Deformation Curve
-Elastic Range: -Non-permanent strain/deformation with a given stress
-Proportional stress and strain (Hook’s Law)
-Slope of the line is the stiffness (Young’s Modulus of Elasticity)
-Yield Point: -Past the yield point, a given stress causes a non-proportional increase in strain.
-Plastic Range: -Permanent deformation past the yield point
-Ultimate Failure Point
-Fatigue Failure: failure from repetitive cyclic loading
-Creep: temperature dependant permanent deformation of a metal
-Stress Shielding: Internal fixation absorbs physiologic stress from bone and results in bone resorption per Wolff’s

AJM Sheet: Screws and Plates
-Screw Anatomy/Definitions
-Head: more efficient hexagonal vs. cruciate
-Land: underside of the head which contacts the near cortex. Want as much land-bone contact as possible to reduce
stress at any one location. This is the same principle as washers and countersinking.
-Shank: unthreaded portion of the screw
-Run-out: junction between the shank and the threads. Represents the weakest portion of the screw.
-Thread diameter: diameter of threads + core (major diameter)
-Core diameter: diameter without the threads (minor diameter)
-Pitch: distance between threads
-Tip: can be round, trocar or fluted
-Axis: central line of the screw
-Rake Angle: thread to axis angle
-Thread Angle: angle between the threads

-Cortical and Cancellous Screws

-Please memorize Table 1, page 76 in McGlamry (Also AJM List: page 17)
-Cortical: tighter pitch designed for hard cortical bone
-Cancellous: higher pitch designed for metaphyseal and epiphyseal bone

-Self-Tapping Screws
-Fluted tip that clears debris as it is advanced
-Require larger pilot holes, have decreased thread-bone contact and have the ability to cut its own path different
from the underdrill

-Cannulated Screws
-Classically 3.0, 4.0, and 7.3mm, but really have just about any size available now
-Advantages: self-drilling, self-tapping, good for hard to visualize fractures, avoids skiving of cortical bone on
insertion and has definite co-axial nature with K-wire.
-Disadvantages: hollow core, decreased thread-core ratio, decreased pull-out strength

-Herbert Screws
-Proximal and distal threads separated by a smooth shaft. Headless.
-Leading threads have increased pitch, so it draws the trailing threads.
-Does generate interfragmental compression, but not a lot.

-Interference Screws
-FT, headless screw
-prevents axial displacement. Does not generate compression.

-Malleolar Screws
-Essentially a self-cutting, PT cortical screw.

-Quarter Tubular Plate: For use with screws from the mini fragment set
-One-Third Tubular Plate: For use with screws from the small fragment set
-Many other shapes and sizes of plates are available that specifically fit just about any bone/situation.

-General Plate Characteristics:

-Dynamic Compression (DCP): Wider/Deeper holes that allow for eccentric drilling and axial compression
-Limited Contact (LC): Essentially grooves on the underside of the plate that limit periosteal contact
-Locking: see -Miranda MA. Locking plate technology and its role in osteoporotic fractures. Injury. 2007 Sep; 38 Suppl 3:S35-9.
-Egol KA, et al. Biomechanics of locked plates and screws. J Orthop Trauma. 2004 Sep; 18(8): 488-93.

-General Plate Functions:

-Neutralization -Interfragmentary Compression
-Buttressing -Tension Band

-AO Basic Stabilization Rule: Ideally you want 3 or 4 cortical threads in each main fragment distally, and 5 or 6 proximally.

AJM Sheet: Suture Sheet

-Suture materials are best classified as to whether they are absorbable vs. non-absorbable, synthetic vs. natural, and
monofilament vs. multifilament.
1. Absorbable (usually used for deep closure)
A. Natural
-Pig collagen, sheep intestine, cow intestine or cat gut
-May be chromic (treated with chromic salts to increase strength and decrease hydrolysis)
-Digested by lysosomal enzymes in 20 days
B. Synthetic
1. Vicryl (Polyglactin 910)
-Braided. May be coated (polyglactin 370 or calcium stearate)
-65% tensile strength at 14 days
-Hydrolyzed (to CO2 and H20) in 80-120 days
-Vicryl Rapid: Hydrolyzed in 42 days; loses strength in 7-10 days
-Vicryl Plus: Coated with broad spectrum antibiotic Triclosan (also found in toothpaste)
2. Dexon (Polyglycolic acid)
-Braided. May be coated (polycaprolate 188)
-Hydrolyzed in 100-200 days
3. PDS (Polydiaxonone)
-70% tensile strength at 14 days
-Hydrolyzed in 90 days
4. Maxon (Polyglyconate)
-Hydrolyzed in 180 days; Longest lasting absorbable (“Max”-imum)
5. Monocril (Poliglecaprone)
-20-30% tensile strength at 14 days
-Hydrolyzed in 90-120 days

2. Non-absorbable (usually used for superficial closure/skin sutures)

-It can be argued that all sutures are eventually absorbable!
A. Natural
1. Silk
-Made from silk worm
-Actually very slowly absorbed (hydrolyzed in 1 year)
-Very low tensile strength
2. Cotton/Linen
-Weakest suture
B. Synthetic
1. Nylon (Ethilon, Surgilon)
-Both monofilament and braided available
-Highest “knot slippage” rate: monofilaments are at a higher risk of knot slippage
2. Polypropylene (Prolene, Surgilene)
-Can be used in contaminated/infected wounds (Nonabsorbable, synthetic, monofilaments best
in this situation). This is the least reactive suture.
3. Polyester (Ethibond, Dacron)
-Strong suture. May be used for tendon repair.
-Braided. May be coated with silicone.
4. Fiberwire (polyethylene multifilament core with a braided polyester jacket)
5. Stainless Steel
-Monofilament or braided (braided is called Flexon)
-Strongest suture with longest absorption rate
-Used for bone fixation and tendon repair, but may corrode bone at stress points

Other Notes:
-Sutures are also classified according to size. They can range from 0-0 (very thick) to 9-0 (extremely thin).
-Surgeon’s choice is extremely variable and you usually just work with what you are used to, but here are some safe bets:
-Capsule closure: 2-0 or 3-0 Vicryl
-Subcutaneous tissue closure: 3-0 or 4-0 Vicryl
-Skin: 4-0 Nylon or Prolene
-Skin sutures are removed at 10-14 days because at this point the tensile strength of the wound equals the tensile strength of the
-This was the very first AJM sheet!

AJM Sheet: Podiatric Surgery Instrumentation
This sheet is simply a summary of the first chapter of McGlamry’s text by Dr. Malay.

-General Information
-Surgical Instruments are composed of stainless steel which itself is composed of several different metals:
-Carbon: gives instrument “hardness”
-Chromium: chromium oxide layer prevents corrosion of instrument
-Tungsten Carbide: extreme “hardness” for grasping surfaces (teeth of needle drivers)
-There are two different series of stainless steel depending on how it is manufactured:
-300 series Austenitic: Implants and internal fixation. Resists corrosion with resilience.
-400 series Martenitic: Cutting instruments. Hardness maintains sharp edges and jaw alignments.

-Categories of Instruments
***Know how to appropriately handle each instrument if handed it during an interview.
***Be able to identify each instrument if handed it or shown a picture during an interview.
1. Surgical Blades
-Most common: 10, 15, 11, 62 on a minihandle
-Purpose: Sharp (blade) and blunt (handle) dissection
-Cutting edge width: 0.015”
2. Scissors
-Most common: Tissue: Metzenbaum, Mayo, Iris, Crown&Collar (Sistrunk)
Non Tissue: Suture, Utility, Bandage
-Purpose: Dissection
3. Hemostats
-Most common: Mosquito (Halsted), Kelly, Crile
-Purpose: Grasping and holding
4. Pick-ups
-Most common: 1-2 (Rat tooth), Adson-Brown, Atraumatic (Potts-Smith)
-Purpose: Grasping and Holding
5. Retractors
-Most Common: Hand Held: Skin Hooks, Senn, Ragnell, Malleable, Army-Navy, Volkmann Rake,
Self-retaining: Weitlaner, Holzheimer, Heiss
-Purpose: Retraction and exposure
6. Elevators
-Most Common: Freer, Sayre, Key, Crego, McGlamry, Langenbeck
-Purpose: Dissection
7. Rasps
-Most Common: Joseph, Maltz, Bell, Parkes
-Purpose: Cutting
8. Miscellaneous
-Bone-Cutting Forceps
-Bone Handling Clamps
-Reduction Forceps (Lewin, Lane, Lowman, Verbrugge)
-Needle Holders (Mayo-Heger, Sarot, Ryder, Halsey, Webster)
-Suction-Tip (Frazier)

AJM Sheet: Power Instrumentation General Information
This sheet is simply a review of McGlamry’s Chapter 2 by Dr. Alfred Phillips.
-General Information
-Hardest material in the human body? Teeth Enamel
-Power instrumentation developed by which medical field? Dentistry

-Power Sources (3)

1. Pneumatic
-Advantages: Delivers high power and torque, does not overheat, cheap
-Disadvantages: Does not operate at slow speeds, bulky, burdensome, cords prone to contamination
-General: -Most commonly driven by compressed nitrogen
-Tank pressure > 500 psi
-Dynamic instrument pressure: 90-110 psi
2. Electric
-Advantages: Light, quiet, small, good for office use
-Disadvantages: Prone to overheating, expensive
-General: -Utilizes an alternating current drive
3. Battery
-Advantages: No cords
-Disadvantages: Loses power quickly, bulky handling
-General: -Utilizes direct current

-Brands: Stryker, Hall-Zimmer, Microaire

-Torque: Measurement of power and force. Units: Newtons/cm^2
-Cortical bone requires more torque to cut through than cancellous bone.
-Speed: Distance per time
-Pod procedures usually require 20,000 rpm.
-Decrease risk of thermal necrosis by decreasing torque and increasing speed.
-Collet: Distal end of a saw where the saw blade attaches
-Stroke: One arc of excursion for a saw blade
-Oscillation: One back and forth motion of a saw blade. (Two strokes equal one oscillation).

-Power Saws
-Sagittal Saw: Cuts in the same plane as the instrument
-Better for longer and deeper cuts
-4° arc of excursion
-Blade may be positioned anywhere within a 160-180° arc.
-Oscillating Saw: Cuts in plane perpendicular to instrument
-7° arc of excursion
-Blade may be positioned anywhere within a 360° circle.
-Vary by cutting depth, width, thickness, shape and number of teeth
-Shapes: straight (most commonly used), inward flair, outward flair
-The angulation of the teeth and NOT the thickness of the blade determine the thickness of a cut.
-Blades may contain holes which collect debris, thereby decreasing heat and friction.

-Wire Drivers
-K-Wires (Kirshner wire)
-Sizes: 0.028”, 0.035”, 0.045”, 0.062”
-Threaded vs. Non-threaded. Note that the direction of the driver only matters with threaded wires.
-K-Wires provide splintage (stability, but no compression)
-Steinman Pins
-Sizes: 5/64”-3/16”
-Rotary Cutting
-Power Drill Bit Sizes: 1.1, 1.5, 2.0mm
-Shapes: Round, Barrel, Straight, Straight-tapered
-Definitions: -shank vs. shaft vs. head
-flute vs. blade
-edge angle vs. clearance angle vs. rake angle
-Surgical Skills Section
-Surgical skills are something best learned by practice, practice, practice. A few hints are listed below:
-The surgeon’s hands provide 3 functions when operating power instrumentation:
-Control of power of the instrument
-Control of direction of the instrument
-Stability between the instrument and the surgical site
-Review concepts of: -Axis guide
-Reciprocal planing
-With a saw or K-wire, always divot perpendicular to the cortex, and then redirect.
-The spin of a burr should be parallel to the grain of the cortex or parallel the ridge of bone to be removed.
-Poor man’s ways to practice handling and control of surgical instruments:
-K-wire through a Nerf ball
-Sagittal saw through a wine cork or wood blocks

AJM Sheet: Biomaterials
Summary of McGlamry’s Chapter 3 by Dr. Cicchinelli.

-Properties of the ideal implant material: clinically inert, no inflammatory or foreign body response, noncarcinogenic,
nonallergenic, structurally stable, capable of sterilization, capable of fabrication in desired forms, serve as a scaffold for new
bone growth and gradual biodegradation.

-Host Response to Implant

-Cellular Response (Acute)
-Immediately after implantation, implants are covered with a coat of proteins that denature and elicit an
inflammatory response. Denatured fibrinogen accumulates neutrophils and macrophages.
-Detritic Synovitis: Foreign body reaction to shards of silicone materials in the lymphatic system.
-Environmental Stress Cracking: Surface defects on polyetherurethane implants secondary to chronic
inflammation. Chronic inflammation results from fragmentation and leads to intracortical lysis and cyst formation.
-Tissue Remodeling Response: Normal for implants to have fibrous capsule formation.
-Infection Potential
-Susceptible to S. Aureus and S. Epidermidis infections
-Malignancy and Type III hypersensitivity reactions extremely rare

-PLLA (Polylactic-L-Acid: L is enantiomer)
-Degrades to lactic acid via hydrolysis
-Retains strength 36 weeks and degrades in 2-3 years
-Available in FT 2.0, 2.7, 3.5 and 4.5mm screws
-PGA (Polyglycolic Acid)
-Degrades to glycolic acid and glycine
-Elliptical. Provides compression secondary to shape.
-Brittle and rigid
-Highest likelihood of FB rxn or complication (<4%)
-PDS (Poly-para-dioxanone)
-Tapered form swaged on metallic wire. Provides compression secondary to shape.
-Flexible and malleable

-Increased degradation times are good because it decreases the load the body has to clear.
-These screws don’t “bite” like metal screws, but swell 2-4% in the first 48 hours.
-Advantages: decreased stress shielding, no second operation for removal.
-Disadvantages: more expensive than metallic screws, but are cheaper in the long run if you remove >31% of
metallic screws in your practice.

-Metallic Implants
-Surgical Stainless Steel
-316LVM (low carbon vacuum remelting)
-Iron, 17-25% chrome, 10-14% nickel, 2-4% molybdenium, 1% carbon
-Nickel most commonly causes reaction: allergic eczematous dermatitis.
-Very inert, integrates into surrounding bone, resists corrosion, decreased capsule formation
-Addition of 6% aluminum and 4% vanadium increases the strength similar to steel
-Nitrogen implantation forms a stable oxide layer
-Black metallic wear debris is often seen. No toxicity or malignancy associated with this.
-Cobalt Chrome and Alloys
-30% cobalt, 7% chromium, <0.034% moly/carbon
-Used in joint replacement prostheses

-Corrosion: breakdown of metallic alloys because of electrochemical interactions within the environment

AJM Sheet: General External Fixation

-Selected History
-377BC: Hippocrates with wood from a cornel tree
-1904: Codvilla (Italy) used unilateral fixator for limb lengthening
-1951-1991: Ilizarov (Siberia, Russia). Father of modern ex-fix and developer of external ring fixator for WWII vets from old bus parts.

-General Principles
-Tension-Stress Effect (Ilizarov)
-Distraction performed at proper rate and in the proper area leads to tissue growth similar to hormone-mediated growth at adolescent
growth plates.
-Too fast: Stretching and traction injuries
-Too slow: Bone callus consolidation preventing future distraction
-An important principle is that all tissues (bone, skin, muscle, NV structures, etc.) become mitogenically active and grow. They proliferate as
opposed to “stretching”. Much of this has to do with the distraction serving as a mechanical stimulus for growth factor release (such as osteoblastic growth
factor) and dramatic increases in vascularity.
-Tension-Stress Effect Influences:
-Stability: increased stability leads to increased osteoblastic activity
-Rate: Ideal is 1mm/day in 4 increments
-Bone Cut: Best to keep medullary canal and as much periosteum intact as possible. Best technique is a percutaneous subperiosteal
corticotomy with a Gigli saw or osteotome/mallet.
-Location of Bone Cut: Metaphysis found to be superior to other areas

-Behrens Principles of External Fixation

-Avoid and respect neurovascular structures
-Allow access to injured area for future fixation
-Meet mechanical demands of the patient and the injury
-Tajana’s Stages of Callus Development
-Colloidal (0-2 weeks): formation of microreticular network
-Fibrillar (2 weeks-1 month): collagen organization
-Lamellar (1 month-years): formation of compact lamellar tissue and calcification

-Advantages of Ex-Fix -Complications of Ex-Fix

-Decreased soft tissue dissection -Pin tract infection vs. irritation
-Immobilization of multiple regions -Pain
-Allows for post-operative adjustment -Cage rage
-Skin grafting and wound debridement available -Non-unions
-Early ROM and WB -Fracture
-NV injury
-Knowledge of cross-sectional anatomy is essential for the application of external fixation. There are numerous manuals and tests available
demonstrating proper pin and wire placement in a given location.
-The key is to have solid bone with avoidance of neurovascular structures.
-As a general rule, the medial and anterior aspects of the tibia are safe locations.

-Types of External Fixators

-Unilateral Fixators
-EBI Dynafix and Orthofix
-Can be straight (uniplanar) or articulated (multiplanar)
-Allow for compression/distraction in a single plane only
-Attached to bone via half-pins
-Rigidity and stiffness determined by half-pins/bone interface. Want pins spread over a large area.
-Weak in the sagittal plane
-Circular Fixators (Multi-lateral)
-Generate compression/distraction in multiple planes
-Tensioned wires generate stability; half-pins generate rigidity.
-Best if these are located 90° to each other for optimal stability
-Can be formulated to allow for immediate WB
-Hybrid Fixators
-Orthofix, Dynafix, Smith&Nephew, Rancho
-Combination of unilateral and circular fixators
-Taylor Spatial Frames
-Allows for reduction of triplanar complex deformities

-Brief Indications
-Limb Lengthening/Distraction
-Percutaneous metaphyseal subperiosteal corticotomy with Gigli saw or osteotome/mallet
-Apply fixation before corticotomy
-Distraction begins 7-14 days after corticotomy at 1mm/day
-Angular Deformities
-CORA principle (center of rotational angulation)
-Double Taylor spatial frame
-Dynamization: release of tension from wires and loosening of half-pins to allow bone a period of introductory WB
-Ligamentotaxis: pulling of fracture fragments into alignment with distraction
AJM Sheet: Bone, Bone Healing and Wound Healing
-Bone Properties/Variables
-Bone is a two component system consisting of minerals (increases the yield and ultimate strength of bone) and collagen (mostly
Type II).
-Porosity. Increased porosity leads to increased compressive strength of bone. Cortical bone has <15% porosity and
cancellous bone has ~70% porosity.
-Strength. Strength is defined as the amount of force a material can handle before failure. Bone can handle a 2%
increase in length before failure. Bone is has the greatest strength in compression, followed by tension and is weakest in shear. Strength is
affected by collagen fiber orientation, trabecular orientation, age, presence of defects and osteoporosis.
-Stiffness. Cortical bone has 5-10 times the stiffness of cancellous bone.

-Vascular Supply to Bone

-Blood supply to bone comes from two sources. A nutrient artery feeds the endosteal and medullary vessels and supplies the
inner 2/3-3/4 of bone. The periosteal vessels supply the outer 1/3 of bone from muscle and tendon attachments.
-The amount of vascular disruption following a fracture depends on the force/displacement of the fracture and which vascular
systems are disrupted.

-Phases of Bone Healing

-Inflammation (10%)
-Hematoma fills the area with fibrin, RBCs, neutrophils, platelets, macrophages, fibroblasts (from PMNs).
-Mesenchymal cells from the cambium layer differentiate into osteoblasts and chondrocytes.
-Chemotaxis by growth factors (transforming growth factor beta, platelet derived, and macrophage derived)
-Reparative/Regenerative (40%)
-Soft callus forms and is replaced by bone.
-Cartilage, fibrocartilage, collagen and hydroxyapatite deposition
-Cartilage replaced by bone like endochondral ossification
-Remodeling (70%)
-Callus completely replaced by bone
-Vascular network is normalized
-Remodels according to Wolff’s Law
-Piezoelectric Effect: appearance of electrical potentials within bone in response to the application of an external force
-Compression side: electronegative leading to bone production
-Tension side: electropositive leading to bone resorption
-Types of Bone Healing
-Direct Osseous Repair (Primary Intention, Direct Healing)
-No callus formation; no motion
-Cutting cone: Osteoclasts in the front, osteoblasts in the back. Travels across the fx line (Schenk and Willinegger).
-Gap Healing: Bone deposition at 90° to the orientation of bone fragments
-Indirect Osseous Repair
-Callus formation

-The literature has demonstrated that cyclic loading and dynamization have resulted in decreased healing times, decreased
stiffness, increased torque and increased energy absorption in rabbit and dog bones. A practical means to accomplish this in human
subjects hasn’t been perfected yet.

Wound Healing
Additional Readings:
-[Broughton G, Janis JE, Attinger CE. Wound healing: an overview. Plast Reconstr Surg. 2006 Jun; 117(7 Suppl): 1S-32S.]
-[Broughton G, Janis JE, Attinger CE. The basic science of wound healing. Plast Reconstr Surg. 2006 Jun; 117(7 Suppl): 12S-34S.]
-[Hunt TK, Hopf H, Hussain Z. Physiology of wound healing. Adv Skin Wound Care. 2000 May-Jun; 13(2 Suppl): 6-11.]
-[Lawrence WT. Physiology of the acute wound. Clin Plast Surg. 1998 Jul: 25(3): 321-40.]
-[Falanga V. Wound healing and its impairment in the diabetic foot. Lancet 2005; 366: 1736-43.]

Phases of Wound Healing:

1. Substrate/Lag/Inflammatory Stage (Days 1-4)
-Inflammation characterized by edema/erythema/calor/dolor
-PMNs start out dominating, but are eventually taken over by macrophages
2. Proliferative/Repair Phase (Days 3-21)
-Collagen proliferation and macrophages
-Myofibroblasts also begin working
3. Remodeling/Maturation Phase (Day 21+)

AJM Sheet: How to “Work-Up” a Surgical Patient

With regard to specific surgery and the interviews, it’s always important to “know your program”. In other words, programs tend
to have favorite procedures that they routinely do. For a given bunion deformity, one program may primarily do Austin-Akins, whereas
other programs may never do an Akin, and still others may always do a Lapidus in the exact same situation. Some people may feel very
strongly in favor of the lateral release, while others may never do it for any situation. This could even happen between two attendings at
the same program in the same room during your interview! If you give a hard, definitive answer for a procedure choice, one attending may
completely agree with you while another may think it’s completely the wrong choice. So if you are asked what type of procedure you
would do for a given situation, be as general as possible, but always give the reason/specific indications why you are choosing that
procedure or group of procedures. Name a couple different similar procedures instead of sticking by your guns with one procedure.
Additionally, your interviewers may not expect you to know for sure what procedure to choose, but they will definitely expect you to be
able to completely work-up the patient and know which procedures are acceptable for which indications.

The two work-ups that you should have down cold are the HAV and flatfoot work-ups. Practice, practice, practice working
through these situations out loud, and practice, practice, practice going through the radiographic analyses of these deformities out loud.
Again, RC and I found it helpful while studying for interviews to pick up random podiatry textbooks and just flip through the pages,
alternating our description of the radiographs out loud.

There are of course many, many radiographic angles that you can use to describe during either of these work-ups, so focus the
majority of your energy on those that will have the most impact on your treatment choice. Here’s the way that I think about these
deformities. This certainly isn’t the “right” way; it’s just the way that helped me as I first started doing this out loud:

I simply use the radiographic angles to define two aspects of the deformity:
-Where is the deformity?
-In which bone or bones, and/or which joint or joints is there deformity?
-Is the deformity mild, moderate or severe?

Once you have successfully answered these questions in your mind, then the remainder of the radiographic work-up
falls into place. For example, if you identify a deformity at the first metatarsal-phalangeal joint, then you can use your
radiographic angles to define it:
“In the area of the patient’s presenting complaint I see a (mild, moderate, or severe) hallux abductovalgus deformity at
the level of the metatarsal-phalangeal joint as defined by a (mildly, moderately, or severely) increased intermetatarsal angle,
(mildly, moderately, or severely) increased hallux abductus angle, and approximate tibial sesamoid position of (1-7). The PASA
and DASA of this joint appear (within normal limits or deviated). There (does or does not) appear to be a hallux interphalangeus
deformity as defined by the (increased or normal) hallux interphalangeus angle. The overall length of the first metatarsal appears
(normal, shortened, or long) compared to the remainder of the lesser metatarsal parabola on the AP view. On the lateral view the
first metatarsal appears (dorsiflexed, plantarflexed, or normal) compared to the second metatarsal using Seiberg’s index. There
(is or is not) an underlying metatarsus adductus as defined by the metatarsus adductus and Engle’s angles. Generally, the
rearfoot appears (rectus, pronated, or supinated) as defined by…”
Now that you have defined the location and severity of the deformity with your angles, suggest procedures based on
these specific abnormal findings. For every abnormality that you described, suggest a procedure (or group of procedures) to
correct it. “I would consider doing a distal metatarsal osteotomy in this case to laterally translate and plantarflex the capital
fragment of the first metatarsal to decrease the intermetatarsal and hallux abductus angles in addition to reducing the sesamoids.”
If you described the DASA and interphalangeus angles as normal, then don’t suggest an Akin procedure! If you described a mild
deformity, then don’t suggest procedures that are indicated for moderate to severe deformities!
I also use the above questions to classify each and every surgical procedure. For each surgical procedure I think: This
procedure will correct for a (mild, moderate, or severe) deformity of this bone or at that joint.

Here I use a similar approach, but think of it in terms of planal dominance:
-In which plane does the deformity present?

“Consistent with the patient’s presenting complaint we see a (mild, moderate, or severe) pes planovalgus deformity. In
the sagittal plane I see a (decreased or increased) calcaneal inclination angle, talar declination angle, talar-calcaneal angle, first
metatarsal inclination angle, Meary’s angle, and medial column fault on the lateral view. I would also evaluate the patient for
equinus using the Silfverskiold test to determine a sagittal plane deformity. In the transverse plane I see a (decreased or
increased) talar-calcaneal angle, cuboid abduction angle, talar head coverage, talar-first metatarsal angle, metatarsus adductus
angle on the AP view. In the frontal plane we can see the Cyma Line is (anteriorly displaced, posteriorly displaced or normal) on
the lateral view, and that the subtalar joint alignment, ankle joint alignment and calcaneal position are (normal or abnormal) on
the long leg calcaneal axial views.”
Now that you have defined the deformity on your own terms, you can now suggest how to fix it using the same tools.
“I would consider performing a (Gastroc recession, TAL, Cotton osteotomy, medial column arthrodesis, etc.) to correct for the
sagittal plane deformity, a (Evans osteotomy, CC joint distraction arthrodesis, etc.) to correct for the transverse plane deformity,
and a (medial calcaneal slide, STJ implant, etc.) to correct for the frontal plane deformity.

This is a little philosophic, but radiographic angles aren’t real. They only come into reality if you use them, so only
use them as tools to your advantage. You can use them to first define the deformity on your own terms, and then to show
that your intervention was successful.
AJM Sheet: Digital Deformity Work-Up

-CC: Pt can complain of generalized “corns, calluses and hammertoes.”
-HPI: -Nature: “Sharp, aching and/or sore” type pain. May have a “tired feeling” in the feet.
-Location: Usually dorsal PIPJ/DIPJ of the toes or submetatarsal
-Course: Progressive onset and course.
-Aggravating factors: WB, shoe gear (especially tight shoes)
-Alleviating factors: NWB, wide shoebox, sandals
-PMH/PSH/Meds/Allergies/SH/FH/ROS: Usually non-contributory

Physical Exam
-Derm: -Hyperkeratotic lesions can be seen submetatarsal, dorsal PIPJ or DIPJ of the lesser digits, distal tuft of the lesser digits, or
interdigitally. All can have erythema, calor and associated bursitis.
-5th digit is usually dorsolateral at the PIPJ, DIPJ or lateral nail fold (Lister’s corn). Hyperkeratotic lesion of the adjuvant 4th
interspace may also be present (heloma molle).
-Vasc/Neuro: Usually non-contributory
-Ortho: -See discussion on pathomechanics
-Positive Coughlin test: Vertical shift of >50% of the proximal phalanx base on the met head. Also called the “draw sign” or
Lachman’s test.
-Kelikian push-up test: Differentiate between a soft-tissue and osseous deformity
-Specific to the 5th digit:
-Toe usually has a unique triplanar deformity (dorsiflexion, adduction and varus).
-Bunionette, splay foot and equinus may be present
-The 5th digit is in the most susceptible position in terms of a muscular imbalance deformity because the FDL has such
an oblique pull on the 5th digit as opposed to the relatively axial pull of the other digits.

-Plain film radiograph: “Gun barrel” sign

Specific Deformities
-Hammertoe: Extension at MPJ level; flexion at PIPJ level, neutral/extended DIPJ
-Mallet toe: Neutral at MPJ and PIPJ level; flexion at DIPJ level
-Claw toe: Extension at MPJ level; flexion at PIPJ and DIPJ level
-Curly toe: Claw/hammertoe deformity with an additional frontal plane component
-Digitus Adductus: Digital deformity with adduction in the transverse plane
-Digitus Abductus: Digital deformity with abduction in the transverse plane
-Heloma Molle: Generally occurs in the 4th interspace with a curly toe deformity of the 5th digit. Using this example, the head of the
proximal phalanx of the 5th digit abuts the base of the proximal phalanx of the 4th digit causing a hyperkeratotic lesion in the proximal 4th

-Digital deformities are thought to occur via one of three potential mechanisms. Each involves a muscular imbalance at the digital level.
-The way AJM thinks of digits is from distal to proximal. During weight-bearing, the toes cannot function in propulsive gait to aid in load
transfer if the most distal segment is not stabilized. The distal phalanx is stabilized by the long flexor tendons holding it solidly against the
weight-bearing surface. With the distal phalanx stabilized, the short flexor tendon can hold the middle phalanx against the weight-bearing
surface. With the middle phalanx stabilized, the lumbrical muscles hold the proximal phalanx against the ground. The lumbrical muscles
must work against the extensor tendon complex, but this complex is usually not actively firing to extend the MPJ during propulsion. The
interosseous muscles also stabilize the proximal phalanx in the transverse plane. When the proximal phalanx has been effectively
stabilized against the weight-bearing surface, the head of the metatarsal can effectively move through its range of motion and transfer load
across the metatarsal parabola. Any disruption in the stabilization process will lead to abnormal biomechanics and deformity.
-Flexor Stabilization: -Most common origin of hammertoe deformity
-Occurs when the PT muscle is unable to effectively resupinate the midtarsal and subtalar joints at
the beginning of propulsion. To compensate, the FHL and FDL fire earlier, longer and with
greater force to resupinate the foot. This puts too much force on the distal and middle phalanges
causing the toe to “buckle” in a dorsiflexed position at the MPJ. This retrograde buckling puts the
PIPJ in a vulnerable dorsal position and also pushes the metatarsal head plantarly.
-Flexor Substitution: -Occurs when the triceps surae muscle group is unable to effectively plantarflex the foot during
propulsion for whatever reason. To compensate, the muscles of the deep posterior compartment
(PT, FHL, and FDL) again fire earlier, longer and with greater force leading to the same type of
-Extensor Substitution: -Can occur in two ways
-One way is when the TA is unable to dorsiflex the foot through the swing phase. In this case the
EDL and EHL fire earlier, longer and with greater force than normal and are actually actively
extending the MPJ. This easily overpowers the lumbricals and leads to retrograde buckling.
-The other way is in a situation with anterior cavus where the EDL is actually at a mechanical
advantage over the lumbricals. Passive stretch of the EDL, rather than active contraction,
overpowers the lumbricals and leads to deformity.

AJM Sheet: Digital Deformity Treatment

-Do nothing: Digital deformities are not a life-threatening condition and can be ignored if the patient is willing to put up
with it.
-Palliative care: Periodic sharp debridement of hyperkeratotic lesions
-Splints/Supports: -Metatarsal sling pads
-Silicone devices
-Toe crests
-Orthotics: -Cut-outs of high pressure areas
-Metatarsal pads to elevate the metatarsal heads
-Correction of the underlying deformity

Surgical Options
-Two approaches to remembering digital surgical options are the acronym HEECAT, and an anatomic approach thinking of
procedures moving from superficial to deep.
-Head arthroplasty: Post procedure (1882)
-Extensor hood and PIPJ capsule release
-Extensor tendon lengthening
-Capsulotomy (MPJ)
-Arthrodesis (PIPJ)
-Tendon transfer (flexor longus tendon transfer to function in MPJ plantarflexion)

-Anatomic Approach
-Percutaneous tenotomy
-Both the extensor and flexor tendons can be transected through a percutaneous approach
-Extensor Tendon lengthening
-Done proximal to MPJ level with a Z-lengthening
-Of the PIPJ and MPJ
-Remember the “J” maneuver for release of the collateral ligaments
-Extensor hood release is also usually performed
-Some use the McGlamry elevator in this step to free plantar attachments
-PIPJ Arthroplasty
-Post procedure 1882
-Resection of the head of the proximal phalanx at the surgical neck
-PIPJ Arthrodesis
-Fusion of the PIPJ using a variety of techniques: table-top, V, peg-in-hole, etc.
-Fusion maintained with K-wire crossing the MPJ extending into the distal 1/3 of the metatarsal
-Flexor Tendon Transfer
-Transfer of the FHL tendon dorsally to act as a more effective plantarflexor of the proximal
-Girdlestone-Taylor technique: Tendon is bisected, crossed and sutured on the dorsal aspect.
-Kuwada/Dockery technique: Tendon is re-routed through a distal drill hole
-Schuberth technique: Tendon is transferred through a proximal drill hole
-Soft tissue fusion of one digit to a normal adjacent digit to help “bring it down”
-Interposing skin is removed and the digits are sutured together

-You should be able to go through the steps of a Post procedure for an interview.
-Please also review the neurovascular elements for each digit and be able to recite which cutaneous nerves supply which
corner of each digit.

5th digit skin incisions

-It is possible to alter your skin incision to incorporate a derotational element to your skin closure. While the
osseous work can be accomplished using a longitudinal or lazy “s” incision (proximal medial to distal lateral), those are
really best for uniplanar deformities. 5th digit HT is usually a triplanar deformity.
-Two semi-elliptical incisions directed proximal lateral to distal medial.
-The more oblique the incision is, the greater transverse plane correction.
-The more longitudinal the incision is, the greater the frontal plane correction.

AJM Sheet: Lesser Metatarsal Deformity Work-up

-CC: Pt presents complaining of “pain in the ball of my foot.”
-HPI: -Nature: Generalized pain (aching, sharp, sore, etc.)
-Location: Submetatarsal. Can usually be localized to an exact metatarsal.
-Course: Gradual and progressive onset. “Has bothered me for years.”
-Aggravating factors: WB for long periods, shoe gear, etc.
-PMH/PSH/Meds/All/SH/FH/ROS: Usually non-contributory

Objective: Physical Exam

Derm: -Diffuse or focal hyperkeratotic lesions submetatarsal
Vasc/Neuro: Usually non-contributory
Ortho: -Many of the same signs/symptoms as HT digital deformity. HT often present.
-Anterior displacement of the fat pad -Hypermobility of the first ray
-Anterior Cavus foot type -Hypermobility of the fifth ray

Objective: Imaging
-Plain film radiograph: -Look for irregularities of the metatarsal parabola
-Look for excessively plantarflexed or dorsiflexed position on lateral/sesamoid axial views

General Information
-Lesser metatarsalgia has several possible etiologies:
-Retrograde force from hammertoes. Please see AJM Sheet: Digital Deformities.
-An excessively long and/or plantarflexed metatarsal leads to increased load bearing under that particular metatarsal.
-An excessively short and/or dorsiflexed metatarsal can lead to increased load bearing on the adjacent metatarsals.
-Hypermobility of the first ray leads to increased load bearing under at least the second metatarsal.
-Hypermobility of the fifth ray leads to increased load bearing under at least the fourth metatarsal.
-Anterior cavus and equinus deformities lead to increased pressures across the forefoot.
-Before a surgical option is considered, it is extremely important to understand where the increased load is coming from. The goal of
treatment should be to restore a normal parabola and weight-bearing function to the foot. Failure to correct the underlying deformity will
dramatically increase the rate of recurrence and transfer lesions.

Treatment: Conservative
-Do nothing: Lesser metatarsal deformities are not a life-threatening condition.
-Palliative care: Periodic sharp debridement of hyperkeratotic lesions
-Splints/Supports: -Metatarsal sling pads -Toe crests
-Silicone devices
-Orthotics: -Cut-outs of high pressure areas
-Metatarsal pads to elevate the metatarsal heads
-Correction of the underlying deformity

Treatment: Surgical
-Structural correction of lesser metatarsals
-Distal metatarsal procedures
-Duvries: plantar condylectomy on both sides of the MPJ
-Jacoby: “V” shaped cut in the metatarsal neck to allow for dorsiflexion of the head
-Chevron: “V” shaped cut similar to a Jacoby, but with removal of a wedge of bone to obtain metatarsal shortening as
-Dorsiflexory wedge osteotomy: similar to a Watermann of the first metatarsal
-Weil: Distal dorsal to proximal plantar oblique cut to allow for distal metatarsal dorsiflexion and shortening. Can be
made in several planes to obtain desired dorsiflexory/shortening effects.
-Osteoclasis: Through and through cut through the metatarsal neck allowing the distal head to find its own plane.

-Metatarsal shaft procedures

-Cylindrical shortening
-Giannestras step-down procedure: Z-shaped cut which can allow for shortening and distal dorsiflexion.

-Metatarsal base procedures

-Dorsiflexory wedge: (1mm of proximal dorsal shortening equivalent to ~10 degrees of dorsiflexion)
-Buckholtz: Oblique dorsiflexory wedge which allows for insertion of a 2.7mm cortical screw
-By far, the most common complications are floating toe, recurrence and transfer lesions caused by undercorrection and overcorrection.
While you can evaluate the parabola and transverse plane in the OR with a C-arm, you really can’t appreciate the sagittal plane.
-Studies have demonstrated that osteoclastic procedures allowing the distal segment to find their own plane without internal fixation have
the least occurrence of recurrence and transfer lesions, but they also have a higher rate of malunion, delayed union and non-union.
-[Derner and Meyr. Complications and Salvage of Elective Central Metatarsal Osteotomies. Clinics Pod Med Surg. Jan 2009.]
AJM Sheet: 5th Metatarsal Deformity Work-up
Also called: Tailor’s Bunion or Bunionette Deformity

-Very similar to work-ups for lesser metatarsal deformities and digital deformities. Pts may complain of pain related to the
lateral column in general, 5th digit, plantar 5th met head, lateral 5th met head or 4th interspace heloma molle.

-Plain Film Radiograph: -4-5 Intermetatarsal Angle > 9 degrees (Normal is 6.47 degrees per Fallat and Buckholtz)
-Lateral Deviation Angle > 8 degrees (Normal is 2.64 degrees per Fallat and Buckholtz)
-[Fallat LM, Buckholtz J. J Am Podiatry Assoc. 1980 Dec; 70(12): 597-603.]
-Splay Foot Deformity
-Plantarflexed 5th metatarsal position
-Structural changes to 5th metatarsal head

General Information
-Numerous authors have chimed in on the etiology of the 5th Metatarsal Deformity:
-Davies: incomplete development of deep transverse metatarsal ligament
-Gray: malinsertion of adductor hallucis muscle
-Lelievre: forefoot splay
-Yancey: congenital bowing of metatarsal shaft
-Root: abnormal STJ pronation
-CMINT, etc, etc, etc.

-Do nothing: 5th metatarsal deformities are not a life-threatening condition.
-Palliative care: Periodic sharp debridement of hyperkeratotic lesions
-Splints/Supports: -Shoe gear modification with large toe box
-Derotational tapings
-Orthotics: -Cut-outs of high pressure areas
-Metatarsal pads to elevate the metatarsal heads
-Correction of the underlying deformity

-Exostectomy: Removal of prominent lateral eminence from 5th met head
-Arthroplasty: Removal of part/whole of 5th met head
-Distal Metatarsal Osteotomies:
-Reverse Hohmann
-Reverse Wilson
-Reverse Austin
-Crawford: “L” shaped osteotomy allows for insertion of cortical screws
-LODO (Long Oblique Distal Osteotomy): similar to Crawford but simply oblique
-Read [London BP, Stern SF, et al. Long oblique distal osteotomy of the fifth metatarsal for correction of tailor's bunion: a
retrospective review. J Foot Ankle Surg. 2003 Jan-Feb;42(1):36-42.] Especially if externing at Inova!
-Medially-based wedge
-Proximal Osteotomies:
-Transverse cuts
-Oblique cuts
-Medially based wedges

AJM Sheet: HAV Work-up

CC: “Bump pain,” “Big toe is moving over,” Typical patient is female although it is unclear whether there is a higher
incidence among females, or if there is a higher complaint incidence among females.
HPI: -Nature: Throbbing, aching-type pain
-Location: Dorsomedial 1st MPJ is most typical presentation. Pain could also be more medial (suggesting
underlying transverse plane deformity such as met adductus) or dorsal (suggesting OA of 1st MPJ).
-Course: Gradual and progressive
-Aggravating Factors: Shoe wear, WB
PMH: -Inflammatory conditions (SLE, RA, Gout, etc.)
-Ligamentous Laxity (Ehlers-Danlos, Marfan’s, Downs syndrome)
-Spastic conditions (40% incidence of HAV among those with CP)
PSH: -Previous F&A surgery
FH: -Hereditary component (63-68% family incidence among general population, 94% with juvenile HAV)
-Johnston reports an autosomal dominant component with incomplete penetrance
Meds/All: Usually non-contributory
ROS: Usually non-contributory

Objective: Physical Exam

Derm: -Dorsomedial erythema +/- bursa Ortho: -Dorsomedial eminence -Pes plano valgus
-Submet 2 lesion -Varus compensation -Equinus
-Nail bed rotational changes -Underlying met adductus -Hypermobile 1st ray
-Pinch callus -PROM 1st MPJ -LLD
Vasc/Neuro: Usually non-contributory -Tracking vs. Track-bound 1st MPJ

Objective: Radiographic Evaluation

Plain Film Radiographs: -Increased soft tissue density
-In first met head: subchondral bone cysts, osteophytes, hypertrophy of medial eminence
-Overall metatarsal parabola
-1st MPJ joint space: ~2mm of clear space; Congruent vs. Deviated vs. Subluxed
Angular deformities:
-Met Adductus (<15 degrees) -Meary’s Angle
-Engle’s Angle (<24 degrees) -Seiberg’s Angle
-IMA (<8 degrees) -TDA
-HAA (<15 degrees) -CIA
-HIA (<10 degrees) -Cyma Line
-Tibial sesamoid position (1-7) -Calcaneal-Cuboid Angle
-PASA (<8 degrees) -Talar Head Uncovering
-DASA (<8 degrees) -Talar Axis
-Met protrusion distance (<2mm) -Kite’s Angle

HAV Dissection and Capsule Procedures

-Anatomic Dissection
-1st incision is through epidermis and dermis
-Incision is planned along the dorsomedial aspect of the 1st MPJ, just medial to EHL and lateral to the medial dorsal
cutaneous nerve.
-From midshaft of 1st metatarsal to just proximal to the hallux IPJ
-Subcutaneous tissue is dissected to deep fascia/capsular layer
-NV structures: Superficial venous network, medial dorsal cutaneous nerve
-Be wary of the anterior resident’s nerve (Extensor capsularis)!
-Lateral Release
-Sequence of events:
-Release of adductor hallucis tendon from base of proximal phalanx and fibular sesamoid
-Release of fibular metatarsal-fibular sesamoid ligament and lateral capsule
-Tenotomy of the lateral head of the FHB between the fibular sesamoid and the proximal phalanx
-Optional excision of the fibular sesamoid
-Medial Capsulotomies
-Washington Monument: Strongest medial capsulotomy allowing for both transverse and frontal plane correction
-Lenticular (Elliptical): Allows for transverse and frontal plane correction with removal of redundant capsule
-Inverted L: Transverse plane correction with removal of redundant capsule
-Medial T: Transverse plane correction with removal of redundant capsule
-Medial H: Transverse plane correction with removal of redundant capsule

AJM List: HAV Procedures and Indications
Distal Phalanx
1. Medial Nail Bed Rotation: Corrects soft tissue mal-alignment

Hallux IPJ
2. Amputation of the distal phalanx: Permanent correction of abnormal Hallux Interphalangeus Angle (HIA)
3. IPJ Fusion: Corrects abnormal HAI

Proximal Phalanx
4. Distal Akin: Corrects abnormal HAI with a medially-based wedge osteotomy at distal proximal phalanx
5. Central Akin: Corrects for long proximal phalanx seen with concurrent HL/HR
6. Oblique Akin: Corrects for distal articular set angle (DASA) midshaft proximal phalanx
7. Proximal Akin: Corrects for DASA of the proximal phalanx
8. Keller Arthroplasty: Corrects for abnormal Hallux Abductus Angle (HAA) and with concurrent HL/HR
9. Keller-Brandis Arthroplasty: Same as the Keller, but with removal of 2/3 of the proximal phalanx
10. Bonney-Kessel: Dorsiflexory osteotomy with concurrent HL/HR with modified forms correcting for abnormal DASA
11. Distal Hemi-Implant: Corrects for abnormal HAA or DASA with concurrent HL/HR
12. Regnauld: Allows for correction of DASA and abnormal proximal phalanx length in presence of HL/HR
13. Sagittal Z: Corrects for DASA and abnormal proximal phalanx length in presence of HL/HR

14. Total Implant: Correction of HAA in presence of HL/HR
15. McKeever arthrodesis: Allows for permanent correction of DASA, PASA and HAA
16. McBride: Soft tissue reconstruction for correction of HAA
17. Modified McBride: Bone and soft tissue reconstruction for correction of HAA and medial eminence
18. Silver: Correction of medial eminence
19. Hiss: Modified McBride with Abductor hallucis advancement
20. External Fixation: Double Taylor frame for gradual soft tissue realignment
21. Hallux Amputation: Permanent correction of abnormal HAA

Distal 1st Met

22. Proximal Hemi-Implant: Correction of PASA and HAA with concurrent HL/HR
23. Mayo: First met head resection for correction of HAA with HL/HR
24. Stone: Mayo with sesamoid articulation left intact
25. Reverdin: Correction of PASA. Incomplete osteotomy.
26. Reverdin-Green: Correction of PASA with incomplete osteotomy and plantar shelf
27. Reverdin-Laird: Correction of PASA and IMA with complete osteotomy and plantar shelf
28. Reverdin-Todd: Correction of PASA, IMA and sagittal plane deformity (elevatus)
29. Youngswick: Correction of IMA and elevatus
30. Austin: Correction of IMA
31. Bicorrectional Austin: Correction of IMA and PASA
32. Tricorrectional Austin: Correction of IMA, PASA and elevatus
33. Mitchell: Rectangular osteotomy with lateral spicule to correct for IMA, elevatus and metatarsal length. Perpendicular to first met axis.
34. Roux: Wedged Mitchell to also correct for PASA
35. Miller: Mitchell with osteotomy oblique to first met axis for further correction of IM and length
36. Hohmann: Transverse through and through cut to correct for IMA and sagittal plane
37. Wilson: Oblique through and through osteotomy to correct for IMA and metatarsal length
38. Distal L: Similar to a Reverdin-Green without correction of PASA
39. Kalish: Austin with a long dorsal arm to allow for screw internal fixation
40. Mygind: Mexican hat procedure of distal first metatarsal for correction of IM and length
41. Off-set V/Vogler: Proximal Kalish
42. Peabody: Proximal Reverdin
43. Short-arm Scarf: Correction of IMA
44. Percutaneous DMO: Percutaneous Hohmann
45. DRATO (Derotational Abductory Transpositional Osteotomy): Can be used to correct frontal plane, IMA, sagittal plane and wedged for PASA
46. Distal Crescentic: Correction of IMA
47. Distal Crescentic with a shelf: Correction of IMA with greater stability

Central 1st Met

48. Scarf: Correction of IMA
49. Ludloff: Correction of IMA. Dorsal-proximal to distal-plantar cut.
50. Mau: Correction of IMA. Distal-dorsal to proximal-plantar cut.

Proximal 1st Met

51. Cresentic: Correction of IMA
52. Cresentic Shelf: Correction of IMA with greater stability
53. OBWO: Correction of IMA
54. Trethowan: OBWO using medial eminence for graft
55. CBWO (Loison-Balacescu): Closing base wedge proximal osteotomy. Corrects IMA.
56. Logroscino: CBWO with Reverdin. Corrects IMA and PASA.
57. Juvara: Oblique CBWO
58. Proximal Austin: Correction of IMA
59. Lambrinudi: Plantar CBWO to correct for sagittal plane

1st Met-Cunieform
60. Lapidus with internal fixation
61. Lapidus with external fixation
62. Cotton: OBWO of the cuneiform to correct for transverse plane
63. Westman: OBWO of the cuneiform to correct for sagittal plane
64. Cotton-Westman: OBWO of the cuneiform to correct for transverse and frontal plane

65. 2nd digit amputation
66. EHL lengthening

AJM Sheet: HAV Complications

-Early (<1 year)
-Usually due to wrong procedure choice, surgical error, or a post-operative complication.
-As little as 1% and as much as 14% rate reported (Kitaoka on 49 feet).
-Late (>1 year)
-Usually due to an unrecognized underlying deformity (such as met adductus, Ehlers-Danlos, equinus, 1st
met hypermobility, etc.)
-Symptoms usually worse than initial presentation
-Treatment: Distal soft tissue procedures or a proximal osteotomy usually indicated

-Hallux Varus
-Defined as a purely transverse plane adduction
-Hallux Malleus: extension at MPJ with flexion at IPJ

-Underlying causes: -Long 1st metatarsal
-Round 1st metatarsal head
-1st MPJ hypermobility

-Iatrogenic causes: -Staking of the 1st metatarsal head

-Overcorrection of the IM angle
-Overzealous medial capsulorraphy
-Fibular sesamoidectomy
-Over extensive lateral release
-Overcorrection of the PASA
-Overzealous bandaging

-Treatment: -Soft tissue rebalancing (medial releases and lateral tightenings)

-EHB tendon transfer
-Reverse distal osteotomies
-Resection arthroplasty, implant, arthrodesis

-MalUnion/Delayed Union/Non-Union
-Consolidated osteotomy with an angular or rotational deformity
-Most common is sagittal plane abnormality (“dorsal tilting”)
-Must be corrected with an osteotomy


AJM Sheet: HL/HR Work-up

CC: Pt will generally complain of a “painful big toe.”
HPI: -Nature: Aching, Dull, Throbbing
-Location: Dorsal 1st MTPJ and within the joint
-Course: Usually gradual and progressive. May follow an acute traumatic event.
-Aggravating Factors: Shoe gear, WB
-Alleviating Factors: Ice, NSAIDs, Rest
PMH: -Inflammatory Condition: RA, SLE, Gout
PSH: -Past 1st MTPJ surgery
Meds/Allergies/SH/FH: Non-contributory
ROS: Non-contributory

Objective: Physical Exam

Derm: -Hyperkeratotic lesions: Plantar hallux IPJ, Medial pinch callus hallux IPJ, Submet 2
-Erythema, Calor, Dorsal 1st MTPJ bursa
Vasc/Neuro: Non-contributory
Ortho: -Decreased PROM 1st MTPJ -Varus Deformity Gait: -Early Heel-off
-Dorsal eminence 1st MTPJ -Plantar Contracture -Apropulsive Gait
-Dorsal eminence 1st Met-Cun -Equinus -Abductory Twist
-Hypermobile 1st ray

Objective: Imaging
Plain Film Radiographs: -Osteophytes at 1st MTPJ -Long 1st met
-Irregular Joint Space Narrowing -Long hallux proximal phalanx
-Lateral view: dorsal flag sign, dorsal lipping -Elevated 1st met
-Loose bodies (joint mice) -Osteophytes at hallux IPJ, 1st met-cun
-Square-shaped 1st met head

General HL/HR Information

-Hallux Limitus vs. Hallux Rigidus
-This is a progressive deformity, so what defines rigidus from limitus? Bony ankylosis and sesamoid immobilization.
-Functional HL is defined as a decreased PROM with the foot loading and in a neutral position, and normal PROM when the foot is unloaded.
Dannanberg first defined functional HL.
-Flexor Stabilization of the hallux: Essentially a hammertoe of the hallux with extension at the MTPJ and plantarflexion at the IPJ.
-Axis of rotation of the 1st MTPJ: Normally found in the center of the metatarsal head allowing for a gliding motion of the hallux up and over
the first metatarsal head. In a HL/HR deformity the axis of rotation moves distally and plantarly leading to dorsal jamming of the joint.
-Met Primus Elevatus: Dorsiflexed position of the 1st metatarsal.
-Primary: Structural. Distal segment is dorsiflexed compared to proximal segment.
-Secondary: Global. Due to some extrinsic variable. This can be measured by Meary’s Angle on a lateral plain film radiograph or
using the Seiberg technique comparing the 1st and 2nd metatarsal positions.
-What stimulates osteophyte production in and around the joint?: Loss of functional cartilage.


-Normal PROM of the 1st MTPJ is classically described as 65-75 degrees of dorsiflexion of the hallux referenced to the weight-bearing surface
(same as 85-95 degrees of dorsiflexion referenced to the 1st met shaft). Plantarflexion is 30 degrees to the weight-bearing surface.
-Hetherington contradicts this somewhat by finding an average ROM of 31degrees of dorsiflexion during pain-free gait in asymptomatic patients.

-Compensation Patterns for Lack of Motion

-Distal: Hallux IPJ leading to OA and plantar hyperkeratotic lesions
-Lateral: Lesser metatarsalgia
-Proximal: 1st met-medial cuneiform joint increased motion and OA
-Gait patterns: Abductory twist with roll-off; early heel-off; apropulsive gait

-HL/HR Etiology
-Many people have reported potential causes of HL/HR including Root, Lapidus and Nilsonne:
-Acute Trauma -Chronic degenerative trauma
-Pes planus with 1st met hypermobility -Long first metatarsal
-Short first metatarsal with hallux gripping -Long hallux proximal phalanx
-Iatrogenic -Compensated varus deformity
-Neuromuscular imbalance -Plantar contracture
-Spastic conditions -Square first metatarsal head shape
-Met primus elevatus
-No single characteristic has been shown to reliably lead to HL/HR except acute trauma
-Coughlin (FAI 2003) performed a retrospective analysis and seemed to demonstrate that there are no reliable underlying indicators for
development of HL/HR.

-Classification Systems
-Numerous exist; usually in the mild, moderate, severe format:
-Mild: Mild pain; Normal PROM; Radiographic evidence of osteophytes
-Moderate: Increasing pain; Decreasing PROM; Osteophytes and irregular joint space narrowing on radiograph
-Severe: Increasing pain; Decreasing PROM; Osteophytes, irregular joint space narrowing, subchondral sclerosis on radiograph.
-Rigidus: Increasing pain; Absent PROM; Sesamoid immobility
-Examples of classifications include the Regnauld, Hanft and KLL.

AJM Sheet: HL/HR Treatment

-Do nothing
-Activity modification
-Orthotics: First ray cut-out, Morton’s extension, rocker-bottom sole
-Meds: PO NSAIDs, Intra-articular corticosteroid injections

-Surgical options are always divided into joint-sparing and joint-destructive procedures, and further divided into
whether the correction occurs at the proximal phalanx, at the MTPJ, or at the first metatarsal.

-Joint Sparing
-Proximal Phalanx
-Sagittal “Z”
-Central Akin
-1st MTPJ
-1st Metatarsal
-Dorsal OBWO

-Joint Destructive
-Proximal Phalanx
-Distal Hemi-Implant
-1st MTPJ
-Total Implant
-McKeever arthrodesis
-1st Metatarsal

AJM Sheet: Flatfoot Work-up
-This is a lot of information to cover in 2 pages, so these sheets will focus on clinical and radiographic signs, as well as
indications for specific surgeries. Also, will try and include a good amount of additional readings.

-Wide range of presenting ages and complaints.
-Always think about posterior tibialis tendon dysfunction when someone complains of “medial ankle pain.”

-Underlying Orthopedic Etiologies: -Compensated forefoot varus -Forefoot valgus
-Rearfoot valgus -Equinus
-Compensated and uncompensated ab/adduction deformities
-Muscle imbalances (PTTD) -Ligamentous laxity
-Tarsal coalitions
-Planal dominance
-Normal STJ axis: 42° from transverse/16° from sagittal
-Normal MTJ-O: 52° from transverse/57°from sagittal
-Normal MTJ-L: 15° from transverse/9° from sagittal

-Clinical findings: -“Too many toes” sign (forefoot abduction) -Hubscher maneuver
-Evaluation for flexible versus rigid deformity -RCSP
-Single and double heel raise -Subjective gait analysis

-Radiographic evaluation:
-Lateral: -Decreased calcaneal inclination angle -Anterior break in Cyma line
-Increased talar declination angle -Meary’s Angle
-Increased first metatarsal declination angle -Midfoot “breaks” or “incongruity”
-Calcaneal-cuboid “break”

-AP: -Increased talo-calcaneal angle -Talar-first metatarsal axis

-Cuboid-abduction angle -Intermetatarsal angle
-Talar head coverage -Forefoot adduction angle or Engle’s Angle
-Look for “skew foot” deformity

-Harris-Beath: Evaluation of tarsal coalitions

-Long-Leg Calcaneal Axial Views: Evaluation of structural rearfoot deformities

-Johnson and Strom [Johnson KA, Strom DE. Tibialis posterior tendon dysfunction. CORR. 1989; 239: 196-206.]
-Later modified by Myerson who added Stage IV (he does that a lot):
-[Myerson MS. Adult acquired flatfoot deformity: treatment of dysfunction of the posterior tibial tendon. JBJS-Am. 1996;
78: 780-92.]
-[Bluman EM, et al. Posterior tibial tendon rupture: a refined classification system. Foot Ankle Clin. 2007 Jun; 12(2):
-Stage I: Tenosynovitis with mild tendon degeneration; flexible rearfoot; Mild weakness of single heel raise and
negative “too many toes” sign
-Stage II: Elongated tendon with tendon degeneration; flexible rearfoot; Marked weakness of single heel raise and
positive “too many toes” sign
-Stage III: Elongated and ruptured tendon; Rigid valgus rearfoot; Marked weakness of single heel raise and positive
“too many toes” sign
-Stage IV: Same as Stage III with a rigid ankle valgus
-Funk: Classification based on gross intra-operative appearance
-[Funk DA, et al. Acquired adult flatfoot secondary to posterior tibial tendon pathology. JBJS-Am. 1986; 68: 95-102.]
-Type I: Tendon Avulsions -Type III: In-continuity tears
-Type II: Complete midsubstance rupture -Type IV: Tenosynovitis
-Jahss or Janis Classifications: There are several MRI classifications generally along the lines of:
-[Conti S, Michelson J, Jahss M. Clinical significance of MRI in preoperative planning for reconstruction of posterior tibial tendon ruptures.
Foot Ankle. 1192; 13(4): 208-214.]
-[Janis LR, et al. Posterior tibial tendon rupture: classification, modified surgical repair, and retrospective study. JFAS. 1993; 31(1): 2-13.]

-Type I: Tenosynovitis, increased tendon width, mild longitudinal splits

-Type II: Long longitudinal splits with attenuated tendon
-Type III: Complete rupture

Additional Reading:
-[Mendicino RW, et al. A systemic approach to evaluation of the rearfoot, ankle and leg in reconstructive surgery. JAPMA. 2005; 95: 2-12.]
-[Lamm BM, Paley D. Deformity correction planning for hindfoot, ankle and lower limb. Clin Podiatr Med Surg. 2004 Jul; 21(3): 305-26.]
-[Greisberg J, Hansen, Sangeorzan. Deformity and degeneration in the hindfoot and midfoot joints of the adult acquired flatfoot. Foot Ankle Int.
2003 Jul; 24(7): 530-4.]
-[Weinraub GM, Saraiya MJ. Adult flatfoot/posterior tibial tendon dysfunction: classification and treatment. Clin Podiatr Med Surg. 2002 Jul;
19(3): 345-70.]

AJM Sheet: Flatfoot Treatment
-Again, this is a lot of information to cover, so we’ll just focus on organizing general procedures and indications, but supplement
it with some additional reading.

-Conservative Treatments
-Not going to be discussed here, but try reading:
-[Elftman NW. Nonsurgical treatment of adult acquired flatfoot deformity. Foot Ankle Clin. 2002 Mar; 7(1): 95-106.]
-[Marzano R. Functional bracing of the adult acquired flatfoot. Clin Podiatr Med Surg. 2007 Oct; 24(4): 645-56.]

-Johnson and Strom/Myerson Classification:

-In addition to describing the deformity, this classification system (discussed on a previous sheet) also makes general
treatment recommendations:
-Stage I: Conservative treatment; Tenosynovectomy; Tendon Debridement
-Stage II: Tendon transfer; Rearfoot arthrodesis
-Stage III: Isolated rearfoot arthrodesis; Triple arthrodesis
-Stage IV: TTC arthrodesis; Pantalar arthrodesis

-General Surgical Procedures/Indications:

-Keep in mind that it is very common to do combinations of these procedures.

Soft Tissue Procedures:

-FDL Tendon Transfer: FDL is sectioned as distal as possible (consider anastomosis of stump to FHL) and either
attach proximal FDL to the PT, within the PT sheath or into the navicular under tension.
-Cobb: Split TA tendon, transfer to the PT or into the navicular
-Young’s Tenosuspension: TA rerouted through navicular
-Anastomosis of PB and PL: Removes PB as deforming force
-STJ implant (arthroeresis)
-TAL -Gastroc recession

Rearfoot Osseous Procedures:

-Evans Osteotomy (1975): opening wedge calcaneal osteotomy
-Silver (1967) is a more proximal (and less common) Evans-type opening wedge
-[Sangeorzan BJ, et al. Effect of calcaneal lengthening on relationships among the hindfoot, midfoot and forefoot. Foot Ankle. 1993;
14(3): 136-41.]
-[Raines RA, et al. Evans osteotomy in the adult foot: an anatomic study of structures at risk. Foot Ankle Int. 1998 Nov; 19(11): 743-7.]
-[Weinraub GM. The Evans osteotomy: technique and fixation with cortical bone pin. JFAS. 2001; 40(1): 54-7.]
-[DeYoe BE, Wood J. The Evans calcaneal osteotomy. Clin Podiatr Med Surg. 2005 Apr; 22(2): 265-76.]
-Medial Calcaneal Slide (Koutsogiannis - 1971): medial translation of posterior calcaneus
-[Weinfeld SB. Medial slide calcaneal osteotomy. Technique, patient selection and results. Foot Ankle Clin. 2001 Mar; 6(1): 89-94.]
-[Catanzariti AR, et al. Posterior calcaneal displacement osteotomy for adult acquired flatfoot. JFAS. 2000; 39(1): 2-14.]
-Double Calcaneal Osteotomy: Evans with a medial calcaneal slide
-[Catanzariti AR, et al. Double calcaneal osteotomy: realignment considerations in eight patients. JAPMA. 2005; 95(1): 53-9.]
-[Nyska M, et al. The contribution of the medial calcaneal osteotomy to the correction of flatfoot deformities. Foot Ankle Int. 2001
Apr; 22(4): 278-82.]
-STJ arthrodesis -Triple arthrodesis
-Tibiotalocalcaneal arthrodesis -Pantalar arthrodesis
-Closing wedge of the medial calcaneus: Essentially the opposite of an Evans but with more NV structures
-Dwyer (1960)
-Slakovich: opening wedge behind the sus tali
-Baker-Hill: opening wedge osteotomy with graft horizontally under the posterior calcaneal facet

Midfoot/Forefoot Osseous Procedures:

-Cotton: opening wedge osteotomy with graft in medial cuneiform
-Kidner: advancement and reattachment of PT tendon (+/- resection of portion of navicular)
-TN arthrodesis: called a Lowman when wedged and combined with TAL
-Medial column arthrodeses
-Miller: NC and 1st met-cun arthrodesis
-Lapidus (1931/1960): 1st met-cun arthrodesis
-Hoke: arthrodesis of navicular with 1st/2nd cuneiforms
-Any other combinations
-[Greisberg J, et al. Isolated medial column stabilization improves alignment in adult-acquired flatfoot. CORR. 2005 Jun;
435: 197-202.]

-Additional Reading:
-[Hix J, et al. Calcaneal osteotomies for the treatment of adult-acquired flatfoot. Clin Podiatr Med Surg. 2007 Oct; 24(4): 699-719.]
-[Mosier-LaClair S, et al. Operative treatment of the difficult stage 2 adult acquired flatfoot deformity. Foot Ankle Clin. 2001 Mar; 6(1): 95-
-[Roye DP, Raimondo RA. Surgical treatment of the child’s and adolescent’s flexible flatfoot. Clin Podiatr Med Surg. 2000 Jul; 17(3): 515-30.]
-[Toolan BC, Sangeorzan, Hansen. Complex reconstruction for the treatment of dorsolateral peritalar subluxation of the foot. JBJS-Am. 1999
Nov; 81(11): 1545-60.]
-[Weinraub GM, Heilala MA. Adult flatfoot/posterior tibial tendon dysfunction: outcomes analysis of surgical treatment utilizing an algorithmic
approach. J Foot Ankle Surg. 2001 Jan-Feb; 40(1): 54-7.]
AJM Sheet: Cavus Foot Work-up

-The cavus foot work-up is one of the most feared in the residency interview process because of its complex nature. The most important
technique during this work-up is to use a standardized system to identify several specific variables which will let you best identify the
deformity and decide on a treatment course:
-Underlying Etiology of the Deformity (Spastic vs. Progressive vs. Stable)
-Forefoot vs. Rearfoot driven deformity (Anterior Cavus vs. Posterior Cavus)
-Plane of the Deformity (Sagittal vs. Frontal vs. Transverse vs. Combination)
-Rigid vs. Flexible

-Underlying Etiology of the Deformity (Spastic vs. Progressive vs. Stable)

-Obtained through a good PMH and physical exam
-Brewerton of the Royal Hospital in London identified 75% of 77 patients seen at his pes cavus clinic to have an underlying
neuromuscular disorder.
-Common Congenital Conditions leading to neuromuscular dysfunction:
-Spina bifida -Charcot-Marie-Tooth
-Myelodysplasia -Friedreich’s Ataxia
-Cerebral Palsy -Roussy-Levy syndrome
-Muscular Dystrophy -Dejerine-Sottas
-Poliomyelitis -Etc, etc, etc.
-Also consider MMT, clonus, deep tendon reflexes, EMG studies and nerve conduction studies during your physical exam.

-Forefoot vs. Rearfoot Driven Deformity

-Anterior Cavus: plantar declination of the forefoot in relation to the rearfoot. Subdivided based on apex of deformity:
-Metatarsus Cavus: Apex at Lisfranc’s joint. Generally more rigid.
-Lesser Tarsus Cavus: Apex in the lesser tarsus area
-Forefoot Cavus: Apex at Chopart’s joint
-Combined Cavus: Combination of any of the above

-The apex of the deformity can be found several different ways:

-Intersection of Meary’s lines (longitudinal axes of talus and first met)
-Intersection of Hibb’s Angle (longitudinal axes of calcaneus and first met)
-Dorsal boney prominences
-Joint space gapping
-Posterior Cavus: Dorsiflexion of the rearfoot in relation to the forefoot
-Generally defined as an increased calcaneal inclination angle (>30 degrees) and a varus positioning.
-Usually the result of an anterior cavus; rarely presents as separate entity.

-An anterior cavus and a posterior cavus can be defined based on radiographic evidence and a physical exam measure called the
Coleman Block Test. In this test the forefoot, or the medial and lateral portions of the forefoot, are suspended off of a block. If the
calcaneus returns from a varus to a normal position, the deformity is forefoot driven. A deformity is rearfoot driven only if the varus
positioning of the calcaneus remains after all forefoot elements are removed.

-Biomechanical compensation for a sagittal plane cavus deformity:

-Digital retraction: HT deformity where EDL gains mechanical advantage and uses a passive pull.
-MPJ Retrograde buckling: As per above
-Lesser Tarsal Sagittal Plane Flexibility: The lesser tarsus “absorbs” some of the dorsiflexion. They can be clearly
seen when comparing NWB and WB lateral views of an anterior cavus foot.
-Pseudoequinus: Occurs when the ankle joint must dorsiflex because the lesser tarsus cannot “absorb” all of the
dorsiflexion. Limits the amount of “free” dorsiflexion available during gait.

-Plane of the Deformity:

-Sagittal Plane: -Anterior Cavus (Global, Medial Column, or Lateral Column)
-Posterior Cavus
-Muscular Cavus (Gastroc Equinus, Gastroc-Soleus Equinus)
-Osseous Equinus (Tibiotalar exostosis)
-Transverse Plane: -Met adductus (measured via met adductus angle or Engle’s angle)
-Met abductus (measured via met adductus angle)
-Frontal Plane: -Forefoot Varus
-Forefoot Valgus
-Rearfoot Varus
-Rearfoot Valgus

-Rigid vs. Flexible Deformity

-Flexible deformities can be manipulated out during the physical exam and are obvious comparing NWB and WB lateral
-Rigid deformities show no compensation with manipulation of weight-bearing.
-Defining each of these variables during your work-up will give you a clear enough understanding of the deformity to recommend a
treatment option.

AJM Sheet: Cavus Foot Treatment

-Basic principles of treatment based on definition of deformity:

-Underlying Etiology:
-Progressive/Spastic conditions are generally treated with osteotomies and arthrodeses.
-Stable conditions are generally treated with soft tissue procedures and osteotomies.
-Forefoot vs. Rearfoot Driven:
-Forefoot driven conditions are treated with manipulation of the bones and soft tissue of the forefoot.
-Rearfoot driven conditions require rearfoot osteotomies and arthrodeses.
-Plane of the Deformity:
-Procedures are chosen by which plane you want correction in.
-Rigid vs. Flexible:
-Rigid deformities are generally treated with osteotomies and arthrodeses.
-Flexible deformities can usually be managed with soft tissue procedures and tendon transfers.

-Soft Tissue Releases: Reduces contracture of the plantar fascia seen with long standing disease.
-Subcutaneous Fasciotomy: Cuts the plantar fascia at its insertion.
-Steindler Stripping: Removes all soft tissue from the plantar surface of the calcaneus.
-Plantar Medial Release: Releases plantar musculature and ligaments from the plantar-medial foot.

-Tendon Transfers: Used to treat flexible conditions based upon plane of the deformity.
-Jones Suspension: Transfer of EHL through the first metatarsal head.
-Heyman Procedure: Transfer of EHL and EDL tendons through each of the respective metatarsal heads.
-Hibbs Procedure: Transfer of EDL into lateral cuneiform; EHL into first metatarsal; EDB into sectioned tendons.
-STATT: Tibialis anterior is split and sutured into peroneus tertius.
-Peroneus Longus Transfer: Peroneus longus is split and anastomosed to the TA and peroneus tertius tendons.
-Peroneal Anastomosis: Increases the eversion power of the foot.
-PL/PT transfer to calcaneus: Tendons are attached into the calcaneus via bone anchors to aid weak Achilles

-Osseous Procedures: Reduction of rigid deformities. Can be used to correct multi-planar deformities.
-Cole Procedure: Dorsiflexory wedge is removed from Chopart’s joint.
-Japas Procedure: “V” shaped osteotomy through the midfoot (apex proximal) to dorsiflex forefoot.
-Jahss Procedure: Essentially a Cole procedure performed at Lisfranc’s joint.
-Dorsiflexory Metatarsal Osteotomies
-Dwyer Osteotomy: Closing wedge osteotomy out of lateral calcaneus to reduce rigid rearfoot varus.
-Dorsiflexory Calcaneal Osteotomy: Must be used with caution

-Arthrodesis Procedures: Used as last resort to correct rigid deformities in the face of progressive disease.
-Hoke: STJ and TNJ arthrodesis
-Ryerson (1923): Triple arthrodesis

-Additional Reading:
-[Younger AS, Hansen. Adult cavovarus foot. J Am Acad Orthop Surg. 2005 Sep; 13(5): 302-25.]
-[Statler TK, Tullis BL. Pes Cavus. JAPMA. 2005; 95: 34-41.]

AJM Sheet: Ankle Equinus

-This sheet is not a work-up because equinus rarely presents as a chief concern, but rather as a concomitant and underlying deformity. It
may be seen and deemed correctable in the following deformities:
-Charcot arthropathy -Digital deformities
-Pes plano valgus -Met primus elevatus
-HAV -Plantar fasciitis
-Medial column hypermobility -Diabetic foot ulcerations -Etc.

-First TAL: Paris on Achilles in the “Iliad”
-First medically documented procedure: Stromeyer on Dr. Charles Little. Dr. Little was a prominent physician suffering from
cerebral palsy (CP) who then became an advocate for surgical correction of equinus.

-Review the origins/insertions/course/action/NV supply of the gastroc and soleus.
-Review the concept of the “twisting” fibers within the Achilles tendon.
-[White JW. Torsion of the Achilles tendon: its surgical significance. Arch Surg 1943; 46: 784-7.]

-Muscular Equinus
-Spastic vs. Non-Spastic
-Gastroc Equinus
-Gastroc-Soleal Equinus
-Osseous Equinus
-Tibio-talar exostosis
-Combination equinus

-Biomechanic Compensation for Equinus (proximal to distal)

-Lumbar lordosis -STJ pronation
-Hip flexion -MTJ pronation
-Genu recurvatum -Forefoot abduction
-No compensation (toe walking) -Medial column hypermobility

-Testing for Equinus

-Silfverskiold test
-Stress dorsiflexion plain film radiographs
-WB wall test

-Conservative Treatment
-Stretching -Heel Lifts (?) -Casting
-Physical Therapy -Neuromuscular blockage injections (Botox)
-Surgical Correction
-Gastroc Equinus
-Neurectomy of motor branches of tibial nerve
-Proximal recession (Silfverskiold procedure)
-Release of muscular heads of gastroc +/- reattachment to tibia +/- neurectomy
-Distal aponeurotic recession
-Vulpius&Stoffel (1913): Inverted “V” shaped incision without suture reapproximation
-Strayer (1950): Transverse incision with proximal dissection and suturing (absorbable)
-Baker (1956): Tongue and groove with suturing (two incisions distal)
-Fulp&McGlamry: Inverted tongue and groove with suturing (two incisions proximal)
-Endoscopic recession
-Gastroc-Soleal Equinus
-Sagittal plane “Z” lengthening: equal medial and lateral portions
-Frontal plane “Z” lengthening: equal anterior and posterior portions
-Hoke Triple Hemisection (1931): 2 medial cuts/1 lateral cut
-White slide technique
-Similar to the Hoke procedure
-1cm  3cm  3 cm

Additional Reading:
-[Pinney SJ, Hansen, Sangeorzan. The effect on ankle dorsiflexion of gastrocnemius recession. Foot Ankle Int. 2002 Jan; 23(1): 26-9.]
-[Pinney SJ, Hansen, Sangeorzan. Surgical anatomy of the gastrocnemius recession. Foot Ankle Int. 2004 Apr; 25(4): 247-50.]
-[Lamm BM, Paley, Herzenberg. Gastrocnemius soleus recession: a simpler, more limited approach. JAPMA. 2005; 95: 18-25.]
-[Graham HK, Fixsen JA. Lengthening of the calcaneal tendon in spastic hemiplegia by the White slide technique. A long term review. JBJB-Br. 1988 May;
70(3): 472-75.]
AJM Sheet: Page 100

One of the most frequent questions asked by students and externs is “Can you give me some good articles to read?”

-I tried to do this by incorporating current and historical articles throughout this edition. All referenced articles (as well as
other suggested readings) can be found on the Inova Pubmed page:
-My NCBI link on the left

-User Name: INOVA

-Password: resident
-Although this was specifically designed for the use of externs and residents at the Inova program, the collection of
articles on this page can be used by anyone. Additionally, anyone is welcome and encouraged to update these collections
with articles they feel are valuable.


In conclusion, this PRISM was not designed to help you pass the boards or even to directly
make you a better physician; it simply hopes to make you better prepared and more efficient as
you approach externships and the residency interview. Use, change, and pass this guide along as
you see fit, keeping in mind the general goal of selfless education of the next generation. Good
luck, and please don’t hesitate to contact me if there is any way that I can be of service to you.

Original Author
Brett Chicko, DPM

Second Edition
Sandi Pollard, DPM
Hubert Lee, DPM
Table of Contents
Introduction William Urbas, DPM ................................................................................. i
Brett Chicko, DPM ................................................................................... ii

Chapter 1 Anatomy ......................................................................................................1

Chapter 2 Antibiotics ...................................................................................................7

Chapter 3 Bugs and Drugs ........................................................................................19

Chapter 4 Labs ...........................................................................................................25

Chapter 5 Medicine ....................................................................................................29

Chapter 6 Clinical Podiatry ......................................................................................51

Chapter 7 Biomechanics ............................................................................................59

Chapter 8 Surgery ......................................................................................................67

Chapter 9 Trauma......................................................................................................85

Chapter 10 Bone Tumors ............................................................................................91

Chapter 11 Wound Care .............................................................................................97

Chapter 12 Classifications
Forefoot ..........................................................................................99
Other Classifications ....................................................................121

Chapter 13 Special Studies ........................................................................................127

Chapter 14 Name That Surgery! ..............................................................................131

Chapter 15 Special Surgical Section

Introduction ..................................................................................149
Achilles Tendon
Achilles Tendon Repair ...................................................150
Delayed Repair of the Achilles Tendon ...........................152
Excision of Calcification of Achilles Tendon ..................154
Murphy Procedure ...........................................................155
Ankle Arthrodesis ............................................................156
Tibio-Calcaneal Arthrodesis ............................................158
Subtalar Arthrodesis.........................................................160
Talo-Navicular Arthrodesis .............................................161
Triple Arthrodesis ............................................................163
Calcaneal Osteotomy
Calcaneal Slide Osteotomy ..............................................164
Evans ................................................................................165
Peroneal Brevis Tendon Repair and Reconstruction .......166
Posterior Tibial Tendon Repair-Substitution ...................167
Posterior Tibial Tendon Transfer .....................................169
Split TA Tendon Transfer (STATT) and
Tibialis Anterior Tendon Transfer (TATT) .....................170
Ankle Fracture Weber A ..................................................171
Ankle Fracture Weber B ..................................................173
Medial Malleolar Fractures ..............................................177
Posterior Malleolar Fracture ............................................180
Syndesmotic Repair .........................................................181
ORIF Calcaneus ...............................................................183
ORIF Talus Neck .............................................................185
Tibial Periarticular Fracture Reduction & Fixation .........188
Other Surgeries
Ankle Arthroscopy ...........................................................190
Arthrosurface 1st Metatarsal Implant ...............................193
Brostrom-Gould ...............................................................195
Fibular Derotational and Lengthening Osteotomy ..........196
Ilizarov Method................................................................197
Osteochondral Lesions of the Talus .................................198
Tarsal Tunnel Release ......................................................199

Chapter 16 Case Studies

Case 1 ..........................................................................................201
Case 2 ..........................................................................................203

Chapter 17 The Interviews ........................................................................................205


Dear Student:

In the pages that follow is useful information that will help make your externships, interviews
and transition from student to resident a little bit easier. This information contained within is not
the end all on the subject, but the tidbits that need to be on your “Mind’s Fingertips”.

This booklet is a useful guide on the need-to-know, need-to-keep information. Please use it as it
was intended--a guide on the ever-changing world of medical information. My thanks go out to
the Podiatric Surgical Residents at Crozer-Keystone Health System for the formation of this


William M. Urbas, DPM

Crozer-Keystone Residency Director

Author’s Introduction
This manual is NOT meant to replace “McGlamry’s”, the “Presbyterian Manual”, the “Podiatry
Institute Manual” or any other reference source. Those manuals are excellent resources and
should be used to continue to learn the information. To this day, I still use those texts for
information and reference.

This manual is based on questions I came across as an extern or a resident, either from my own
questions or questions from a superior. I would write these questions down and after I looked up
the answers, I would keep the questions with their answers in a log.

Later, as a resident, I was quizzing a student in order to get her ready for her interviews. The
student asked me, “Why can’t there be a book of these questions?” After that I started to put
together the manual. I also added some additional items to complete the manual.

In no way, shape or form do I claim that the answers written here are the only answers possible,
nor do I even claim that they are all 100% correct. These answers are the ones that I came up
with when I researched the questions. It is up to you to go to the true references--not only to
make sure that the answers are correct, but also to make sure that you understand why.

Therefore, the purpose of this manual is so that the reader can have some questions and answers
so that he or she can go to the sources and really learn podiatry.

I am not able to provide all of my sources because when I started writing down the answers, I
had no idea of turning it into a manual. However, my major sources are, “The Comprehensive
Textbook of Foot Surgery”, “The Presbyterian Manual” and “The Podiatry Institute Manual”. A
special thank you to my attendings and co-residents at the Crozer-Keystone Health Systems in
Springfield, PA, especially Dr. Urbas our residency director, mentor and friend.

Good Luck and Happy Studying,

Brett Chicko, DPM

How many bones are in the foot?
26 (not including sesamoids)

How many joints are in the foot?


Name the accessory ossicles

Os Intermetatarsium Between 1st cuneiform and 1st and 2nd metatarsal bases
Os Vesalianum Proximal 5th metatarsal base
Os Tibiale Externum Accessory navicular
Os Supranaviculare Dorsal aspect of navicular
Os Peroneum Sesamoid bone in PB tendon
Os Calcaneus Secondarius Dorsal, anterior process of calc
Os Sustentaculi Posterior aspect of sustentaculum tali
Os Trigonum Posterior aspect of talus (Steida process)
Os Subtibiale Distal to medial malleolus
Os Subfibulare Distal to lateral malleolus

Name the avascular necroses

Renandier Tibial sesamoid
Trevor Fibular sesamoid
Theiman Phalanges
Freiberg Metatarsal heads
Iselen 5th metatarsal base
Buschke Cuneiforms
Kohler Navicular
Lance Cuboid
Diaz Talus
Severe Calcaneus
Blount Proximal, medial tibial epiphysis
Osgood-Schlatter Tibial tuberosity
Legg-Calve-Perthes Femoral epiphysis

What attaches periosteum to bone?

Sharpey fibers

What are the different types of coalitions?

Syndesmosis – fibrous
Synchondrosis – cartilaginous
Synostosis – osseous


What is the difference between a coalition and a bar?
Coalition – intra-articular fusion of two bones
Bar – extra-articular fusion

What is the most common coalition in the foot?

Distal and middle phalanx of 5th digit

What is the most common coalition in the rearfoot?


What is a Steida process?

Enlarged Os Trigonum

What is the only bone in the foot without any muscle origin or tendon insertion?

What are the plantar muscle layers of the foot from superficial to deep?
1. Abductor hallucis, flexor digitorum brevis, abductor digiti minimi
2. Quadratus plantae, 4 lumbricals
3. Flexor hallucis brevis, adductor hallucis, flexor digiti minimi
4. 3 plantar interossei, 4 dorsal interossei

What layer of the foot does FDL run?

2nd layer – it is the origin of the lumbricals and the insertion of QP

What deformity will result from cutting QP?

Digits 4 and 5 will become adductovarus

How is EDL attached to the proximal phalanxes?

Sling wraps around capsule which attaches to plantar plate, DTML, and flexor tendon sheath
thus attaching to plantar proximal phalanx. No direct insertion to proximal phalanx.

What is the origin and insertion of the capsularis tendon?

Origin – extensor hallucis longus muscle or tendon
Insertion – first metatarsophalangeal joint capsule

What is the Master Knot of Henry?

Fibrous connection between FHL and FDL tendons

What structures attach to the fibular sesamoid?

Plantar metatarsal-phalangeal ligament
Lateral metatarsal-sesamoidal ligament
Intersesamoidal ligament
Phalangeal-sesamoidal ligament
FHB tendon
ADH tendon


Are the sesamoids capsular or extra-capsular?

What is the Lisfranc ligament?

Attaches lateral aspect of medial cuneiform to medial base of 2nd metatarsal

What structures in the Lisfranc joint are not connected by ligaments?

1st and 2nd metatarsals

What is the spring ligament?

Plantar calcaneonavicular ligament

What ligaments compose the bifurcate ligament?

Dorsal calcaneonavicular and calcaneocuboid ligaments

Which is stronger – the lateral ankle ligaments or the deltoid ligament?

Deltoid ligament

What are the components of the deltoid ligament?

Superficial – tibionavicular, tibiocalcaneal, posterior tibiotalar
Deep – anterior tibiotalar

What tendons pass over the deltoid ligament?

Tibialis posterior and FDL

What are the lateral ankle ligaments?

Anterior talofibular, calcaneofibular, posterior talofibular

What angle do the ATFL and CFL create?


What is the strongest lateral ankle ligament?

Posterior talofibular

Which ankle ligaments are extra-capsular? Which are capsular?

Calcaneofibular ligament is extra-capsular, all others are capsular

What tendons pass over the lateral ankle ligaments?

Peroneus brevis and longus

What ligaments support the ankle syndesmosis?

Anterior-inferior tibiofibular ligament
Posterior-inferior tibiofibular ligament
Interosseous tibiofibular ligament


What is the Bassett ligament?
Anterior-inferior tibiofibular ligament

What is another name for the flexor retinaculum?

Laciniate ligament

What is another name for the superior extensor retinaculum?

Transverse crural ligament

What is another name for the inferior extensor retinaculum?

Cruciate crural ligament

Where does plantaris insert?

Medial aspect of tendo-Achilles into the calcaneus

What is the incidence of peroneus quartus?


What is the Hoke tonsil?

Fibrous, fatty plug within the sinus tarsi

What is pes anserinus?

Insertion of sartorius, gracilis, and semitendinosus (anteromedial aspect of proximal tibia) where
bursa may cause knee pain (pes anserinus bursitis)

What is a Bakers cyst?

Swelling of the bursa between the tendons of the medial head of the gastrocnemius and the
semimembranosus muscles

What is a fabella?
Sesamoid bone occasionally found in tendon of lateral head of gastrocnemius

What nerves form the sural nerve?

Medial sural cutaneous nerve – branch of the tibial nerve
Sural communicating branch – branch of the lateral sural cutaneous nerve, which originates from
the common peroneal nerve

Does a neuroma lie dorsal or plantar to the deep transverse intermetatarsal ligament?

Where do these muscles run in relation to the deep transverse intermetatarsal ligament?
Interossei – dorsal
Lumbricals – plantar


What layers of the foot do the plantar nerves run?
Medial plantar nerve – in the 1st layer (between FDB and abductor hallucis)
Lateral plantar nerve – between the 1st and 2nd

What is the innervation to the plantar muscles of the foot? Blood supply?
(Never LAFF at A FAD)
N – medial plantar Nerve
L – 1st Lumbrical
F – FDB (innervated by both medial and lateral plantar nerves)
A – medial plantar Artery
D – 1st Dorsal interossei

What are the branches of the femoral nerve?

Nerve to femoral artery
Small muscular branch to pectineus
Anterior division (cutaneous)
 Anterior femoral cutaneous
 Nerve to sartorious
 Intermediate femoral cutaneous nerve
 Medial femoral cutaneous nerve
Posterior division (muscular)
 Saphenous nerve
 Infrapatellar branch
 Medial crural cutaneous nerve
 Nerve to rectus femorus
 Nerve to vastus medialus
 Nerve to vastus intermedialus
 Nerve to vastus lateralus

What are the branches of the femoral artery?

Superficial epigastric artery
Superficial circumflex iliac artery
Superficial external pudendal artery
Deep femoral (profunda femoris) artery
Medial femoral circumflex artery
Lateral femoral circumflex artery
Descending genicular artery
Femoral artery continues as the popliteal artery


Trace the path of a drop of blood from left ventricle to the hallux
Ascending aorta → aortic arch → descending aorta → thoracic aorta → abdominal aorta →
common iliac artery → external iliac artery → femoral artery → deep femoral artery →
popliteal artery → anterior tibial artery → dorsalis pedis → 1st dorsal metatarsal artery →
1st dorsal common digital artery → 1st dorsal proper digital artery

What are the sources of blood supply to the talus?

Essentially the 3 major blood supplies to the foot
 Superior surface of head and neck – artery of sinus tarsi and branch from anterior tibial
artery or dorsalis pedis
 Medial side of body – artery of tarsal canal and posterior tibial artery
 Lateral turbercle – anastamosis of branch of peroneal artery with medial calcaneal branch

What are the sources of blood supply to tendons?

Myotendinous junction, paratenon, and at the insertion to bone


What should you always consider before starting an antibiotic?
 What is the most likely infecting organism?
 Have a gram stain and C&S been done? What are the results?
 Allergies?
 Kidney function (check BUN and Cr)? Many antibiotics are renally metabolized so it is
imperative to make sure the kidneys are functioning properly.
 What medications is the patient currently taking? Be concerned of possible drug
 Any other reason you may or may not want to give the antibiotic?

Name That Drug

Augmentin amoxacillin/clavulonic acid
Zosyn piperacillin/tazobactam
Unasyn ampicillin/sulbactam
Timentin ticarcillin/clavulonic acid
Zyvox linezolid
Invanz ertapenem
Cubicin daptomycin
Tygacil tigecycline
Bactrim trimethoprim/sulfamethoxazole (TMP/SMX)
Rocephin ceftriaxone
Avelox moxifloxacin
Zithromax azithromycin
Primaxim imipenem/cilastatin
Synercid dalfopristin-quinupristin
Cleocin clindamycin
Flagyl metronidazole

What is the dose?
500 or 875 mg PO BID

How much clavulonic acid is in Augmentin 500 mg? Augmentin 875 mg?
Both have 125 mg

What is the indication?

PO antibiotic for outpatient therapy of polymicrobial infections

What is the spectrum of activity?

Staph (not MRSA), Strep, Enterococci, Gram negatives, anaerobes


Does it cover Pseudomonas?

What is the dose?
3.375 g IV q6h
Renal dose – 2.25 g IV q6h
Alternate dose – 4.5 g IV q6h

What is the indication?

Approved for use in adults for the treatment of moderate to severe diabetic foot infections

What is the spectrum of coverage?

Staph (not MRSA), Strep, Enterococci, Gram negatives, anaerobes

Does it cover Pseudomonas?


What is the dose?
3.0 IV q6h
Renal dose – 1.5 g IV q6h

What is the indication?

Empiric therapy for polymicrobial diabetic foot infections

What is the spectrum of activity?

Staph (not MRSA), Strep, Enterococci, Gram negatives, anaerobes

Does it cover Pseudomonas?


What is an alternative for a patient with a PCN allergy?

(there are others)

What is the dose?
3.1 g IV q4-6h

What is the indication?

Broad spectrum antibiotic for polymicrobial infections


What is the spectrum of activity?
Staph (not MRSA), Strep, Gram negatives, anaerobes

Does it cover Pseudomonas?


What should you watch for?

Increased Na+ load (5.2 meq/gram)

Which cover Pseudomonas?
(4th and 5th generations)
piperacillin, Zosyn
ticarcillin, Timentin
carbenicillin, mezlocillin, azlocillin

What are IV alternatives for PCN allergic patients?

clindamycin, vancomycin, Levaquin, Bactrim

How are PNC’s excreted?

All are renally excreted except mezlocillin, azlocillin, piperacillin (the ureidopenicillins are 20-
30% renal)

What concern is there of a patient on both PCN and probenecid?

Probenecid will increase duration of serum levels of PCN and most cephalosporins

What is the cross-reactivity of cephalosporins and PCN?
1-10% (depending on whom you talk to)

Are cephalosporins contraindicated for a patient with a PCN allergy?

Many people will say yes, and according to Dr. Warren Joseph, ―Cephalosporins should be
avoided entirely in patients with a history of anaphylaxis to penicillin.‖ However, he states that
if there is a questionable allergy history (rash or upset stomach), ―Cephalosporins can be used
with little worry.‖ Personally, I will give a cephalosporin to a patient with a PCN allergy if all
he or she had was an upset stomach and I document this.

How to treat serious hospital acquired Gram negative infections?

3rd generation cephalosporins, aminoglycoside (i.e. Rocephin, gentamycin)

What is the coverage of cephalosporins for each class?

1st Generation
Gram positive – Staph (not MRSA) and Strep
Gram negative – Proteus, E. coli, Klebsiella, Salmonella, Shigella (PECKSS)
Anaerobes – not Bacteroides


2nd Generation
Gram positive – similar to 1st gen
Gram negative – more coverage, H. influenza, Neisseria, Proteus, E. coli, Klebsiella,
Salmonella, Shigella (HEN PECKSS)
3rd Generation
Gram positive – less than 1st and 2nd gen
Gram negative – expanded coverage, ceftazadime covers Pseudomonas
4th Generation
Gram positive – similar to 1st gen
Gram negative – similar to 3rd gen, including Pseudomonas
No anaerobic coverage

Name a couple cephalosporins for each generation

1st Generation – cefazolin (Ancef), cephalexin (Keflex)
2nd Generation – cefaclor (Ceclor), cefuroxime (Ceftin)
3rd Generation – ceftriaxone (Rocephin), ceftazidime (Fortaz), cefdinir (Omnicef)
4th Generation – cefepime (Maxipime)

How are they excreted?

Renally except for ceftriaxone (renal/hepatic) and cefoperazone (hepatic)

What is the main indication?

What is its spectrum of activity?

All Gram positives, including MRSA and MRSE

What is the dose?

1 g IV q12h with slow infusion

When are levels drawn?

Peak taken 30 min after the 3rd dose
Trough taken 30 min before the 4th dose

What should the peaks and troughs be?

Peak 15-30 mg/mL
Trough <10 mg/mL

How do you adjust the dose?

If the peak is too high, decrease the dose
If the peak is too low, increase the dose
If the trough is too high, increase the interval between doses
If the trough is too low, decrease the interval between doses


What happens when you infuse too quickly?
Red Man syndrome – erythema and pruritis to the head, neck, and upper torso. It is caused by an
anaphylactoid reaction where histamine is released by mast cells. (A different Red Man
syndrome is associated with excessive Rifampin that causes a bright reddish-orange
pigmentation of the skin.)

How can you decrease the risks of Red Man syndrome?

Slow infusion over one hour

How do you treat Red Man syndrome?

Antihistamines (Benadryl 25-50 mg IV q2-4h) until symptoms resolve
Symptoms are self-limiting

What are other side effects?

Ototoxicity and nephrotoxicity

Does the duration a patient has been on vancomycin increase the risks of side effects?
Yes. Vancomycin has a reservoir effect: the more often a patient receives vancomycin, the
higher the chance of getting either ototoxicity or nephrotoxicity. Therefore, use vancomycin
carefully; it is a powerful drug with severe side effects.

When should PO vancomycin be used?

Treatment of Pseudomembranous colitis (125 mg PO q6h)

What is the dose?
One tab PO BID

How much is in the single strength tablet? Double strength?

Single strength – TMP 80 mg / SMX 400 mg
Double strength (DS) – TMP 160 mg / SMX 800 mg

How does it work?

Trimethoprim and sulfamethoxazole inhibit folate synthesis in bacteria which prevents DNA

What is the spectrum of activity?

Broad spectrum covering Gram positives (MRSA) and Gram negatives

Does it cover Pseudomonas?


What allergy should be avoided?



What are the side effects?
Hemolytic anemia, hypersensitivity

What are the contraindications?

Patient on oral hypoglycemic or with G6PD deficiencies

What is the dose?
250 mg PO, two tabs on the first day then one tab for the next four days

What is the spectrum of activity?

Staph, Strep, and some anaerobes (but not bacteroides)

Can you give it to a patient with a PCN allergy?


What is the half-life?

68 hours

What is the dose?
500 mg IV q6-8h (most common) or 1 gm IV q6-8h

What is the spectrum of activity?

Very broad spectrum including most Gram positive, Gram negative, and most anaerobes

Does it cover MRSA? Pseudomonas?

No and no

What is a side effect?

Seizure in patients with history of seizures
1% risk with 500 mg dose, 10% risk with 1 g dose

How does it work?

imipenem – antibiotic
cilastatin – renal dehydropeptidase inhibitor, which prevents imipenem from being metabolized
by the kidneys

Which antibiotic is nicknamed ―Gorillamycin‖?

imipenem (because of its very broad of spectrum activity)

What is the dose?
1 g IV q24h


What is the indication?
Approved for use in adults for the treatment of moderate to severe diabetic foot infections

What is the spectrum of activity?

Gram positive, Gram negative, and anaerobes

Does it cover Pseudomonas?


What class is Invanz?

It is a structurally unique 1-β-methyl-carbapenem related to β-lactams

What is the dose?
400-600 mg PO/IV q12h

What is an indication?
Oral Zyvox may be used for outpatient treatment of MRSA infections

What is the spectrum of activity?

All Gram positives, including MRSA and VRE

What is a major side effect?

Thrombocytopenia (check CBC)

Why isn’t it used more often?

It is expensive

What are some common quinolones?
ciprofloxacin (Cipro), levofloxacin (Levaquin), moxifloxacin (Avelox)

What is the dose of Cipro?

250-750 mg PO q12h
200-400 mg IV q12h

What is the dose of Levaquin?

250-500 mg PO/IV q24h

What is the dose of Avelox?

400 mg PO/IV q24h

What is the spectrum of activity?

Gram negative, including Pseudomonas
Cipro – limited Gram positive
Levaquin and Avelox – better Gram positive


What are side effects?
Tendonitis and tendon ruptures

Who should not be given quinolones?

It is contraindicated in children with open growth plates. Risk of cartilage degeneration.

What is the dose?
1-2 g IV q8h

What is the spectrum of activity?

Gram negative aerobes and pseudomonas (its main indication)

What are the major side effects?


Why isn’t it used more often?

It is expensive

What are some major aminoglycosides?
Gentamycin, Tobramycin, Amikacin

What is the spectrum of activity?

Gram negative aerobes

What are the side effects?

Ototoxicity – irreversible
Nephrotoxicity – reversible
Neuromuscular blockade – prevented by slow infusion

What are the doses, peaks, and troughs?

Dose Peak (µg/mL) Trough (µg/mL)
Gent and Tobramycin 3-5 mg/kg q8h 6-10 2
Amikacin 15 mg/kg q8h 20-30 <10

How to dose gentamycin?

1. Loading dose is 2 mg/kg for Gent and Tobra (7.5 mg/kg for Amikacin)
2. Determine creatinine clearance (CC)
CC = (140 - Age) x Weight (in kg)
72 x Serum Creatinine
For females, multiply the CC by 0.85
3. Maintenance dose is adjusted for CC (e.g. If the CC is 0.75, then the patient has 75%
kidney function. Give 75% of a normal dose.)


What is the dose?
600-900 mg IV q8h or 150-300 mg PO BID

What is the spectrum of activity?

Most Gram positive and most anaerobes

What is a side effect?

Pseudomembranous colitis

How is clindamycin metabolized?


What is the dose?
500 mg PO TID

What is the spectrum of activity?

Some Gram positive anaerobes and most Gram negative anaerobes

What antibiotics cover MRSA?
PO – linezolid, Minocycline, Cipro/rifampin, Bactrim/rifampin
IV – vancomycin, linezolid, minocycline, Cipro/rifampin, Bactrim/rifampin, Synercid,
tigecyclin, telavancin
Topical – Bactroban

What are the only FDA-approved drugs for treating MRSA?

telavancin (Vibativ)

How do you treat VRE?
linezolid or dalfopristin-quinupristin

What is the only PO therapy for VRE?



What drugs cover Pseudomonas?
Aminoglycosides – gentamycin, tobramycin, amikacin
Ceftazidime, cefepime

Polymicrobial Infections
What are some empiric therapies for polymicrobial foot infections?
Vanco/Zosyn, Clinda/Cipro, Vanco/Invanz

What are the only FDA-approved drugs for treating diabetic foot infections?
(The 3 Z’s)

Antibiotic-Associated Diarrhea
What are two main causes of antibiotic-associated diarrhea?
Pseudomembranous colitis – Clostridium difficile
Non-specific colitis – Staph aureus

How to you test for Clostridium difficile?

Order ―check stool for C diff‖

What is the most common cause of Clostridium difficile colitis?

clindamycin (though any antibiotic can cause it)

How do you treat Clostridium difficile colitis?

Vanco 125 mg PO q6h
Flagyl 500 mg PO TID

What antibiotics are metabolized by the liver?
(3 C’s and 1 E)

Can antibiotics affect PT/INR?

Yes. Antibiotics can affect normal flora, which alters Vitamin K. Therefore, the PT/INR can


What can β-lactams cause?

What is the MOA of aminoglycosides? Macrolides?

Aminoglycosides bind to bacterial 30s ribosomes inhibiting protein synthesis
Macrolides bind to bacterial 50s ribosomes inhibiting protein synthesis
(A boy at 30 does not become a Man until 50)

What antibiotics can be safely used with PMMA beads?

Vancomycin, gentamycin, tobramycin, cefazolin
The curing of PMMA is exothermic, therefore the antibiotic must be not be heat-labile

What open fractures should be treated with antibiotics?

Grades 2 and 3


Bugs and Drugs
Gram Positives
What are Gram positive, catalase positive cocci in clusters?
Staphylococcus aureus

DOC for Staph?

Keflex or Ancef

Alternative for Staph?

clindamycin, Levaquin, Vancomycin, Azithromycin, dicloxacillin, nafcillin

Alternative for Staph if PCN allergy?

clindamycin, Levaquin, Vancomycin, Azithromycin

What if the organism is resistant to methicillin?

MRSA (methacillin-resistant Staph aureus)


Vanco IV, Bactrim PO (if sensitive)

Alternative for MRSA?

Synercid or linezolid

Topical DOC for MRSA?


DOC for Strep?

Keflex or Ancef

What are Gram positive, catalase negative cocci that are in pairs or chains?

DOC for Strep?

Keflex or Ancef

Alternative for Strep?

clindamycin, Levaquin, vancomycin

Alternative for Strep in PCN allergy?

clindamycin, Levaquin, vancomycin

DOC for Enterococcus?

amoxicillin or vancomycin


Alternative for Enterococcus?
Augmentin, linezolid

What if the organism is resistant to vancomycin?

VRE (vancomycin-resistant Enterococcus)

DOC for VRE?

linezolid or Synercid

DOC for Diptheroids?


Gram Negatives
What is a short, Gram negative rod?
Escherichia coli

DOC for E. coli?

Keflex or Ancef

Alternative for E. coli if PCN allergy?

Cipro or Levaquin

DOC for Proteus?

Keflex or ampicillin

Alternatives for Proteus if PCN allergy?

Cipro or Levaquin

DOC for E/C/S/M group?

Quinolone (Cipro or Levaquin)

Alternatives for E/C/S/M group?

3rd generation cephalosporin, Aztreonam, Bactrim

What is a small Gram negative rod with pili and polar flagella?
Pseudomonas aeruginosa

DOC for Pseudomonas?


Alternative for Pseudomonas?

3rd gen cephalosporins, Aztreonam, Zosyn, Timentin

How does Pseudomonas typically present?

blue-green purulence with grape-like odor


What Gram negative spirochete causes Lyme disease?
Borrelia burgdorferi

DOC for Lyme disease?

doxycyline or Rocephin

Alternative for Lyme disease?


DOC for Bacteroides?
Augmentin, Zosyn, Unasyn, Timentin

Alternatives for Bacteroides if PCN allergy?

clindamycin/Cipro, Primaxin, Flagyl

What is a large, Gram positive, anaerobic, ―racquet-shaped‖ rod that forms spores?
Clostridium perfringens

DOC for Clostridium?

Penicillin, imipenem, clindamycin, tetracycline

What are two soft tissue clinical manifestations caused by Clostridium?

Anaerobic cellulitis and gas gangrene

Why is gas gangrene a surgical emergency?

It rapidly progresses to shock and renal failure and is fatal in 30% of cases

Less Common Organisms

DOC for Aeromonas?
Cipro PO/IV

Alternative for Aeromonas?


DOC for Pseudomonas cepacia?


Alternative for Pseudomonas cepacia?


DOC for Necrotizing Fasciitis?


DOC for superficial thrombophlebitis?



DOC for Gonorrhea?
Ceftriaxone or PCN if sensitive

DOC of Cutaneous Larva Migrans?

Promethia under occlusion

What organisms may form gas in soft tissue?
Gram positive – Clostridium perfringens, Staphylococcus, Streptococcus, Peptostreptococcus
Gram negative – Bacteroides, E. coli, Klebsiella, Serratia

What are some anaerobes?

Gram positive – Actinomyces, Clostridium, Peptostreptococcus
Gram negative – Bacteroides, Fusobacterium

What is the drug of choice (DOC) for a patient with diabetes and a PCN allergy?

DOC for severe limb-threatening infection?


What are most common organisms of bite wounds?

Human – Eikenella corrodens
Cat and dog – Pasteurella multocida

What is Gram negative rod is associated with dog bites?


DOC for cat and dog bites?


What are the most common organisms causing cellulitis?

Staph and Strep

Which type of Strep can cause impetigo, cellulitis, and erysipelas?

Group A Strep

What is the difference between cellulitis and erysipelas?

Cellulitis – confined superficial infection
Erysipelas – superficial infection that extends into the lymphatics

What is the most common organism that causes acute hematogenous osteomyelitis?
Staphylococcus aureus (adults), Gram negative rods (elderly)

What is the most common organism that causes osteomyelitis following a puncture wound?
Pseudomonas aeruginosa


What is an anaerobic Gram positive filamentous bacteria?

What organism may be found following a puncture wound in the ocean?

Vibrio vulnificus

What type of bacteria is gonorrhea?

Gram negative diplococci

What is gonorrhea cultured on?

Chocolate agar

What is the treatment for gonorrhea?


If a patient is currently on an antibiotic, how long should it be stopped before taking a

wound culture?
At least 48 hours (if possible)


What is in a CBC?
WBC, hemoglobin, hematocrit, platelets

What are normal lab values for CBC?

Note: normal values vary between labs
WBC 4.8-10.8 k/µL
Hemoglobin ♂ 14.0-18.0 g/dL, ♀ 12-16 g/dL
Hematocrit ♂ 42-52%, ♀ 37-47%
Platelets 145-400 k/µL

With an infection, what is expected to happen to the WBC count after surgery?
Eventually it should go down, but in post-op days 1-2, the WBC may actually increase a bit.
This is may occur because surgery activates the body's reaction to the infection.

What should be done if the patient’s WBC is over 10?

First, decide if the patient has an infection
 If there is an infection, then antibiotics and possible incision and drainage (I&D) should
decrease the WBC count
 If there is not an infection, then the cause must be determined. Is the increase acute or
chronic? Is there another source of infection (other than the foot)? Is the patient on
corticosteroids? Is there a combination of medical conditions causing this?

What to do if platelets are low (under 150-350 k/mL)?

Can transfuse platelets, but this is not commonly done

What are the minimum levels for hemoglobin and hematocrit for elective surgery?
Hemoglobin 10 gm/dL and Hct 30%

What should be done if the Hemoglobin/Hematocrit (H/H) is below 10/30?

If necessary, transfuse 1-2 units of packed red blood cells (PRBC)

What is the condition called?


What are causes of microcytic, hypochromic anemia?

Iron deficiency, thalassemias, lead poisoning

What are causes of macrocytic, megaloblastic anemia?

Vitamin B12/folate deficiency


Following a transfusion of PRBC, when will changes in the H/H be seen?
Approximately 3 hours. Therefore, order new labs to be drawn 4 hours after last unit given.

What is in a BMP?
Sodium, potassium, chloride, carbon dioxide, BUN, creatinine, glucose

What is in a CMP?
BMP with ALP (alkaline phosphatase), ALT (alanine amino transferase, also called SGPT),
AST (aspartate amino transferase, also called SGOT), bilirubin, albumin, total protein, calcium

What are normal values for BMP?

Note: normal values vary between labs
Sodium 135-146 mmol/L
Potassium 3.5-5.1 mmol/L
Chloride 96-106 mmol/L
CO2 24-32 mmol/L
BUN 10-20 mg/dL
Creatinine 0.7-1.3 mg/dL
Glucose 70-110 mg/dL

What do Na+, K+, Cl and CO2 tell you?

These electrolytes indicate nutritional status

What should be done if Na+ is low?

Give NSS or regular salt

What should be done if K+ is too low?

Hypokalemia may cause cardiac arrhythmias, muscle weakness, paresthesias, cramps
Manage hypokalemia
 Give K-Dur (potassium chloride supplement)
 Give potassium-rich foods (i.e. banana)

What should be done if the K+ is too high?

Hyperkalemia may cause cardiac arrhythmias, lethargy, respiratory depression, coma
Order EKG
Manage hyperkalemia
 Calcium gluconate
 Sodium bicarbonate
 Dextrose with insulin
 Kayexalate

What do BUN and creatinine indicate?

Renal function


What should be done if the creatinine is too high?
Consult renal if creat is over 1.5 for a couple of results
Note: creat may be increased after muscle breakdown or loss

Which is a more important indicator – BUN or creatinine?

Creat is more important, because BUN is influenced by hydration state. If the BUN is high but
creat is normal, then the patient is most likely dehydrated and rehydration should correct the
BUN. However, if both BUN and creat are high, then the patient most likely has renal damage.

What do PT/PTT/INR tell you?
The coagulable state of the patient. If the levels are high, it will take longer for the patient to
develop a clot and stop bleeding. It requires blockage of only one pathway to anticoagulate the

What are normal values for PT/PTT/INR?

Note: normal values vary between labs
PT 11.7-14.5 sec
INR 0.9-1.1
PTT 23-36 sec

What can cause an elevated PT/INR?

Vitamin K disorders

What does INR stand for? Why was it developed?

International Normalized Ratio
There are different methods to determine PT, and thus each lab has a different normal value for
PT. INR was devised to standardize all the results.

If the patient is on Coumadin for anticoagulation, what should the INR be?
Intense anticoagulation 2-3

What causes the PTT to be high?


Which pathway does PTT check?

Intrinsic (―PITT‖)

Which pathway does PT check?

Extrinsic (―PET‖)


What are reasons for post-op fever?
Wind (12-24 h)
 Atelectasis (from muscle relaxers)
 Post-op hyperthermia
Water (~24 h)
Walk (~48 h)
 PE
Wound (~72 h)
 Post-op infection
Wonder drug (anytime)
 Drug fever

What are treatments of post-op fever?

 Encourage incentive spirometer
 Chest x-ray
 Straight catheter
 Urine analysis (UA) with Gram stain, culture and sensitivity
 Treat with antibiotics if necessary
 Heparin or Lovenox protocol
 Use SCDs, TEDs, or get patient out of bed
 X-ray, Gram stain, culture and sensitivity, blood cultures
 Begin antibiotic
Wonder drug
 D/C drug
 Give reversal drug if necessary

When do fever peaks occur?

Between 4-8 pm

What part of the brain regulates the body's temperature?


What is malignant hyperthermia?

A side effect of general anesthesia – tachycardia, hypertension, acid-base and electrolyte
abnormalities, muscle rigidity, hyperthermia


What is the treatment for malignant hyperthermia?
Dantrolene (for muscle relaxation) 2.5mg/kg IV x l, then 1 mg/kg IV rapid push q6h until
symptoms subside or until max dose of l0 mg/kg

If a risk of malignant hyperthermia is suspected, what pre-operative test may be

CPK – elevated in 79% of patients with malignant hyperthermia

What is the mechanism of action for local anesthetics?
Block Na+ channels and conduction of action potentials along sensory nerves

What is the toxic dose of lidocaine (Xylocaine)?

300 mg plain (4.5 mg/kg)
500 mg with epi (7.0 mg/kg)

What is the toxic dose of bupivacaine (Marcaine)?

175 mg plain (2.5 mg/kg)
225 mg with epi (3.2 mg/kg)

How to convert percentage of solution to mg/mL?

Move decimal point of percentage one place to right
(e.g. 1% solution has 10 mg/mL)

What are the side effects of lidocaine and bupivacaine associated with systemic exposure?
CNS effects – initial excitation (dizziness, blurred vision, tremor, seizures) followed by
depression (respiratory depression, loss of consciousness)
Cardiovascular effects – hypotension, bradycardia, arrhythmias, cardiac arrest

What can be given to help reverse local anesthetic-induced cardiovascular collapse?

Intravenous fat emulsion (Intralipid)

Is there a risk with intra-articular injections of bupivacaine?

Studies have shown chondrocyte death following prolonged exposure to bupivacaine

In what age group should bupivicaine be avoided?

Children <12 year of age

How are amides (lidocaine and bupivacaine) metabolized?


How are esters (Novocain) metabolized?

Plasma pseudocholinesterase

What is the only local anesthetic with vasoconstriction?



How is cocaine metabolized?
Plasma pseudocholinesterase (just like other esters)

Can local anesthetics cross the placental barrier?


What does MAC (as in MAC with local) stand for?

Monitored anesthesia care

For anesthesia, what cannot be given to a patient with an egg shell injury?
propofol (Diprivan)

Pain Medications
Pain management with a codeine allergy?
S – Stadol
T – Toradol
T – Talwin
U – Ultram
D – Darvon
D – Darvocet
D – Demerol
N – Nubain

First choice for oral?

Darvocet N-100 one tab PO q4-6h prn pain

First choice for non-narcotic oral?

tramadol (Ultram) 50 mg one to two tabs PO q4-6h prn pain, max daily dose of 400 mg per day

First choice for non-narcotic IV?

Toradol 30-60 mg IV

Choice narcotic IV pain med?

Note: many hospitals, including our own, do not use Demerol due to its side effects

Name two non-narcotic analgesics

ketoralac (Toradol), tramadol (Ultram)


Drugs and Usual Doses
What schedule are these drugs?
Percocet II high potential for abuse – requires narcotic script
Vicodin III moderate potential for abuse
Tylenol #3 III moderate potential for abuse
Darvocet IV low potential for abuse

Percocet 5/325?
oxycodone/acetaminophen (5 mg/325 mg)
1-2 tabs PO q4-6h prn pain

oxycodone/acetaminophen (5 mg/325 mg/5 mL)
Essentially a liquid form of Percocet that is good for pediatric patients

What is the difference between Percocet and Percodan?

Percocet has 325 mg of acetaminophen and Percodan has 325 mg of ASA

Vicodin 5/500?
hydrocodone/acetaminophen (5 mg/500 mg)
1-2 tabs PO q4-6h prn pain

Tylenol #3?
codeine/acetaminophen (30 mg/300 mg)
1-2 tabs PO q4-6h

Darvocet-N 100?
propoxyphene/acetaminophen (100 mg/650 mg)
1 tab PO q4h prn pain

tramadol 50 mg
1-2 tabs PO q4-6° prn pain

ketorolac 10 mg
30 mg IV q6h
1 tab PO q4-6h prn pain
An NSAID not to be used more than 5 days due to possible significant side effects

1 tab PO q4h prn pain

oxycodone extended release


Morphine sulphate?
2-4 mg IV q2-6h prn mod-severe pain
For very painful dressing change or bedside debridement – 2 mg IV x one dose

MS Contin?
morphine sulfate extended release (15-30 mg)
1 tab PO q8-12h prn pain

2-8 mg PO q3-4h prn severe pain
1-4 mg IV q4-6h prn severe pain
This drug is very strong

Our hospitals do not use this due to its side effects

What therapeutic effects are seen with acetaminophen?
Analgesic and anti-pyretic

What is the maximum daily dose?


What therapeutic effects are seen with most NSAIDs?
Analgesic, anti-pyretic, and anti-inflammatory

What pathway do NSAIDs work on?

Cyclooxygenase (COX)
NSAIDs nonselectively inhibit both COX-1 and COX-2 pathways

What is the most common side effect of NSAIDs?

GI disturbance (except with COX-2 inhibitors, because COX-1 protects the stomach lining)

What is the only FDA-approved COX-2 inhibitor?

celecoxib (Celebrex)
Others were withdrawn due to increased risk of heart attack and stroke

Which NSAIDs only have anti-inflammatory effects?

indomethacin, tolmetin

Do NSAIDs decrease joint destruction?

No, they only decrease inflammation


Do NSAIDs affect bone healing?
NSAIDs and COX-2 inhibitors may inhibit bone healing via their anti-inflammatory effects

What NSAID causes irreversible inhibition of platelet aggregation?


What NSAID does not inhibit platelet aggregation?

The COX-2 inhibitor, Celebrex

What is the only IV NSAID?

ketorolac (Toradol)

Which NSAID is often given during surgery or immediately post-op to decrease pain and
Toradol 30 mg IV

What are the NSAIDs with the least nephrotoxicity?

Celebrex, Relafen, Lodine

What is the effect of NSAIDs on asthma?

Can increase symptoms of asthma

What are the safest NSAIDs for a patient with asthma?

Diclofenac, ketoprofen

Which NSAIDs treat collagen vascular disease?

Ibuprofen, sulindac, tolmetin

Which NSAIDs are not renally cleared?

Indomethacin, sulindac

What are the cardiovascular effects of NSAIDs?

Can cause vasoconstriction and increase blood pressure

Which NSAIDs have the least cardiovascular effects?

Diclofenac, ketoprofen

Which NSAIDs are the most hepatotoxic?

Ibuprofen, naproxen, diclofenac

What should be given for an indomethacin overdose?

Benadryl – decreases serotonin and histamine release

What is Arthrotec?
diclofenac/misoprostol – an NSAID with protection for the stomach


What is the anti-inflammatory dose of ibuprofen?
1200-3200 mg/day in divided doses

What NSAIDS work on both the lipooxygenase and cyclooxygenase pathways?

Ketoprofen and diclofenac

What is the difference between Cataflam and Voltaren?

Cataflam is diclofenac potassium and has an immediate release
Voltaren is diclofenac sodium and has a delayed release

What are the only pro-drugs for NSAIDs?

nabumetone and sulindac

What is the only nonacidic NSAID?


Which NSAIDs have fewer pulmonary problems?

ketoprofen and diclofenac

What are some once a day NSAIDs?

celecoxib (Celebrex), piroxicam (Feldene), oxaprozin (Daypro), nabumetone (Relafen), others

What drugs do NSAIDs interact with and what are the effects?
Coumadin – increases action of Coumadin
Sulfonylureas – increases action of sulfonylureas
Corticosteroids – increases GI risk
Anti-epileptics – increases anti-epileptic toxicity
Antihypertensives – antagonizes antihypertensive meds
Digoxin – increases digoxin’s effect
Methotrexate – decreases methotrexate’s clearance
Lithium – decreases lithium’s clearance
Probenecid – increases concentration of NSADs

What are causes of acute arterial occlusion?
Embolism – detached thrombus, air, fat, or tumor
Thrombus – occlusion of vessel by plaque or thickened wall
Extrinsic occlusion – traumatic, blunt, penetrating

What is the triad of pulmonary embolism?

Chest pain
Hemoptysis (although tachycardia is more common)


What tests can be ordered to diagnose a PE?
Chest X-ray
Ventilation perfusion scan
Pulmonary angiography

What is Virchows triad?

Venous stasis – tourniquet, immobilization
Endothelial wall damage/abnormality – surgical manipulation, trauma, smoking
Hypercoagulability – birth control, coagulopathy, history of DVT

What does the Virchow triad predict?

Risk of DVT
Previous DVT is #1 risk factor for having another DVT

What are risks factors for DVT?

I – immobilization
A – arrhythmia
M – MI (past history)
C – coagulable states
L – longevity (old age)
O – obesity
T – tumor
T – trauma
T – tobacco
E – estrogen
D – DVT (past history)

How is a DVT diagnosed clinically?

Pain, heat, swelling, erythema of unilateral limb
Positive Pratt sign – squeezing of posterior calf causes pain
Positive Homan sign – abrupt dorsiflexion of foot causes calf pain
Pulmonary embolism

What tests can be ordered to diagnose a DVT?

Doppler ultrasound

For long term DVT prophylaxis, what drugs can be ordered? Why?
Heparin – works right away
Coumadin – takes 3-5 days and causes an initial transient hypercoagulable state

What are treatments for a DVT?

Thrombolytic agents
Heparin 5000 Units IV bolus, then 1000 Units IV q1h and monitor PTT


How to dose Heparin for perioperative DVT prophylaxis?
5000 units SC 2h prior to surgery
5000 units SC q12h until patient ambulates

What is the half-life of heparin?

1.5 hour

How does heparin work?

Intrinsic pathway
Potentiates antithrombin III 100-fold, which inhibits the serine protease in the clotting cascade

How is heparin reversed?

Protamine sulfate 1 mg per 100 units of heparin

What is enoxaparin (Lovenox)?

Low molecular weight heparin

How to dose Lovenox for perioperative DVT prophylaxis?

30 mg SC q12h for 7-10 days (adjust dose to q24h for renal patients)

What is the half-life of Lovenox?

4.5 hours

What are the advantages of using Lovenox vs. regular Heparin? Disadvantages?
Advantages – Lovenox has longer plasma half-life with significant anticoagulation in trough
Disadvantages – increased post-op complications when used with spinal/epidural anesthesia

How do you check Lovenox?

There is no test for the effects of Lovenox

How is Lovenox reversed?

Recombinant Factor VII

How to dose Coumadin?

5-10 mg PO daily for 3-4 days then adjust for INR

What is the half-life of Coumadin?

20-60 hours

How long before Coumadin is therapeutic?

3-5 days

How does Coumadin work?

Extrinsic pathway
Interferes with clotting factors II, VII, IX, X


How is Coumadin reversed?
Vitamin K
Fresh frozen plasma

What are the INR values?

Normal l
Intense anticoagulation 2-3

What are levels of heparin and Coumadin for DVT/anticoagulation prophylaxis?

Heparin – maintain 2-3 times normal PTT
Coumadin – maintain 2 times normal INR

What nonpharmacologic measures are used for perioperative DVT prophylaxis?

Early ambulation – most important
TEDs – thromboembolic deterrent stockings
SCDs – sequential compression devices

What is a surgical treatment for a patient with prior DVTs or recurrent PEs?
Greenfield filter

What level of the body is a Greenfield filter inserted?

Inferior vena cava below the renal veins

What is Pletal?

What is Trental?

What is an indication for Pletal or Trental?

Intermittent claudication

What is CRPS?
Complex regional pain syndrome (previously known as RSD – reflex sympathetic dystrophy) is
a progressive disease of the autonomic nervous system causing constant, extreme pain that is out
of proportion to the original injury

What are the different types and causes of CRPS?

CRPS Type I (reflex sympathetic dystrophy)
 Nerve injury cannot be immediately identified
 Spontaneous pain not limited to single nerve distribution
 Abnormal response in sympathetic nervous system
 Abnormal reflex leading to vasomotor instability and pain


CRPS Type II (causalgia)
 Distinct, "major" nerve injury has occurred
o Trauma
o Peripheral nerve injury
o Drugs – anti-TB, barbiturates, cyclosporine
 Continued pain not necessarily limited to injured nerve distribution

What are the stages of CRPS?

1. Acute – early (0 to 8-20 weeks)
 Constant pain out of proportion (intense burning)
 Possible edema, muscle wasting
 Hyperhidrosis
 Pain increased by light touch, movement, emotion
2. Dystrophic – mid (2-6 months, possibly up to 1 year)
 Increased edema that is indurated (brawny edema)
 Constant pain by any stimulus
 Skin is cool pale and discolored
 X-ray shows diffuse osteoporosis
3. Atrophic – late (over 6-12 months)
 Intractable pain spreads proximally to involve entire limb
 Decreased dermal blood flow causing cool, thin shiny skin
 Fat pat atrophy
 Joint stiffen, may proceed to ankylosis

What are radiographic findings of CRPS?

Periarticular, mottled, irregular bony demineralization (30-60% of cases) and cortical thinning

What are bone scan findings of CRPS?

The 3-phase bone scan has sensitivity of 96% and specificity of 98%. A normal scan does not
exclude the diagnosis. The findings of the bone scan are based on the phase.
1. Acute
 Increased flow and blood pool activity in the affected extremity
 Increased activity particularly in a periarticular distribution on delayed images
2. Dystrophic
 Flow and blood pool abnormalities begin to normalize
 Increased activity on delayed images persists
3. Atrophic
 Flow and blood pool activity can be normal or decreased (in about 1/3 of patients)
 Normal or decreased activity is commonly seen on delayed images, however,
persistent increased delayed activity has been reported (up to 40%)
 Decreased flow in advanced stages may be related to disuse, which is a common
feature of post-hemiplegic CRPS


What are treatments of CRPS?
Anti-inflammatory drugs
Antidepressant drugs
Local peripheral nerve blocks
Paravertebral sympathetic ganglion blocks
Physical therapy

For diabetic patients, who gets diabetic ketoacidosis and who gets diabetic coma?
Type I (IDDM) – DKA
Type II (NIDDM) – coma

What are signs of hypoglycemia?

Nervousness, tachycardia, diaphoresis, nausea, headache, confusion, tremor, seizures, coma

What are signs of hyperglycemia?

Polyuria, polydipsia, weight loss

What is the function of a biguanide?

Antihyperglycemic (not hypoglycemic)

What is a typical supplemental insulin scale?

BG (mg/dL) Low Medium
<120 0 0
121-150 1 2
151-180 2 4
181-210 3 6
211-240 4 8
241-270 6 10
271-300 8 12
301-350 10 14
351-400 12 16
>400 call physician

What are the only FDA-approved drugs for treating diabetic neuropathy?
duloxetine (Cymbalta)
pregabalin (Lyrica)

What are clinical findings of OA?
 Pain relieved with rest
 Stiffness aggravated with activity
 Crepitus with motion
 Asymmetric joint swelling


What are radiographic findings of OA?
 Asymmetric joint space narrowing
 Broadening and flattening of articular surfaces
 Osteophytes at joint margins
 Subchondral sclerosis

What is the most common inflammatory arthritis in men over 30?

What are the stages of Gout?

1. Asymptomatic hyperuricemia
2. Acute gouty arthritis
3. Intercritical gout
4. Chronic tophaceous gout

What are clinical findings of gout?

 Asymmetrical, monoarticular arthritis
 Sudden onset of red, hot, and swollen joint
 Excruciating pain with acute attack
 Tophaceous deposits
 Most commonly affects 1st MPJ

What are radiographic findings of gout?

 Radiographic findings appear late in the disease after multiple attacks
 Bone lysis in acute stages
 Periarticular swelling with preserved joint space
 Tophi at joint margins
 Rat bite – punched-out, periarticular erosions
 Cloud sign – tophaceous material
 Martel sign – periarticular overhanging shelves of bone

What are laboratory tests for gout?

 Uric acid – males >7 mg/dL, females >6 mg/dL, though may be normal during attack
 Synovial fluid analysis provides a more accurate diagnosis

What would a joint aspirate of gout show?

Needle-shaped monosodium urate crystals that are negatively birefringent under polarized light
(CPPD are rhomboid-shaped and positively birefringent)

What is a martini sign?

Histology showing a PMNC engulfing a crystal

If gout is suspected, what should a specimen be sent in?

One in formaldehyde (dissolves gouty tophi) and one in alcohol (does not dissolve gouty tophi)


How to treat acute and chronic gout?
 Colchicine
 NSAIDS – indomethacin
 Corticosteroids
 Colchicine (prophylactically)
 Allopurinol
 Uricosurics – probenecid, sulfinpyrazone

What is the dose colchicine?

0.6 mg PO q1h until symptoms resolve, GI side effects occur, or max dose of 6 mg reached

What is the max daily dose of colchicine?

6 mg

Can allopurinol, probenecid or sulfinpyrazone be used for acute gout?

No, because they may cause an initial hyperuremia

How to determine if patient is an overproducer or underexcretor?

Take a 24 hour uninalysis

Which is more common – to be an overproducer or an underexcretor?

Underexcretors make up approx 90%

What medication should be given if the patient is an overproducer? Underexcretor?

(Over-Achieving, Under-Paid)
Overproducer → Allopurinol
Underexcretor → Probenecid

Rheumatoid Arthritis
What are clinical findings of RA?
 Symmetric, progressive, polyarticular, and degenerative inflammatory arthritis
 Age of onset between 3-4th decades
 Females > males
 Pain first thing in morning
 Stiffness after rest and reduced with activity
 Rheumatoid nodules (25%)
 Nail fold infarcts, splinter hemorrhages
 Swan neck deformities – flexed DIPJ and extended PIPJ
 Boutonniere deformities – extended DIPJ and flexed PIPJ
 Other – bullous dermatosis, Raynaud phenomenon, vasculitis


What are laboratory findings of RA?
 Rheumatoid factor – positive
 RBC – slight to moderate anemia
 WBC – elevated in acute cases and normal to decreased in chronic
 ESR & CRP – moderate to marked elevation
 Synovial fluid analysis – elevated WBCs with cloudy fluid

What are radiographic findings of RA?

 Clinical symptoms may present several years prior to radiographic findings
 Peri-articular edema
 Periosteal elevation and ossification
 Marginal erosions
 Subluxation and contractures (Swan neck deformities)
 Fibular deviation of digits
 Osteoporosis
 Symmetric joint space narrowing and destruction (late stage finding)

What causes the fibular deviation of digits?

Erosive changes of medial plantar metatarsal heads compromises the integrity of medial
collateral ligaments leading to lateral deviation of digits

What is pannus?
Granulation tissue that secretes chondrolytic enzymes which break down articular cartilage

Psoriatic Arthritis
What are clinical findings of PA?
 Polyarthritis including DIPJ involvement
 Sausage digits
 Psoriatic skin changes
 Nail lesions

What are laboratory findings for PA?

 HLA-27 – positive
 Rheumatoid factor – negative

What are radiographic findings of PA?

 Erosions with bony proliferation
 Symmetric narrowing of joint space
 Increased periosteal activity
 Pencil-in-cup appearance
 Osteopenic changes


Reiter Syndrome
What are clinical findings of RS?
 Polyarticular, asymmetric arthritis of lower extremity (mostly affects small bones of feet,
ankle, knee, SI joint)
 Most affects males
 Capsulitis with digital edema
 Bony erosions
 Reiter Syndrome Triad (can't see, can't pee, can't climb a tree)
o Conjunctivitis
o Urethritis
o Arthritis
o Also keratoderma blenorrhagicum

What are laboratory findings for RS?

 HLA-27 – positive
 Rheumatoid factor – negative
 ESR – elevated
 Synovial fluid analysis – Pekin cells

What are radiographic findings of RS?

 Fluffy periosteal reactions
 Large, bilateral heel spur formation
 Inflammation and widening of Achilles tendon insertion
 Deossifications

Ankylosing Spondylitis
What are clinical findings of AS?
 Mostly males affected
 Bilateral sacroiliitis – low back pain and stiffness
 Heel pain
 Peripheral joint pain

What are laboratory findings for AS?

 HLA-27 – positive
 Rheumatoid factor – negative

What are radiographic findings of AS?

 Irregular joint widening with erosions
 Reactive sclerosis
 Bony ankylosis
 Sacroiliac joint fusion
 Bamboo spine


Septic Arthritis
What are clinical findings of SA?
 Painful, hot, swollen joint
 Systemic signs of fever, N/V, tachycardia, confusion

What are laboratory findings for SA?

 WBC – elevated with left shift
 ESR – elevated
 CRP – elevated
 Blood cultures – positive
 Synovial fluid analysis – elevated WBC with cloudy white or gray color

What are radiographic findings of SA?

 Normal in early stages
 Joint effusion
 Juxta-articular osteopenia

What are etiologies of SA?

Contiguous, hematogenous, direct implantation, surgical contamination

What is the most common offending organism of SA?

All ages – Staphylococcus aureus
Neonates – Streptococcus and Gram negatives
Children – H. influenza
Teenagers – Neisseria gonorrhea
Puncture wounds – Pseudomonas aeruginosa
Adults with sickle-cell – Salmonella

What is the treatment for SA?

Needle drainage of joint
Open arthrotomy if osteomyelitis, joint implant, or chronic infection
Initial joint immobilization followed by passive ROM
Appropriate IV antibiotics for 2 weeks followed by 2-4 weeks of oral antibiotics

Other Diseases
What is brachymetatarsia?
Premature closure of epiphyseal plate of metatarsal resulting in a short metatarsal
Usually the 4th metatarsal is affected

What are some conditions associated with brachymetatarsia?

Downs syndrome
Turners syndrome
Cri du chat
Pseudo- or pseudopseudohypoparathyroidism
May be idiopathic


What is the maximum length that a metatarsal may be acutely lengthened for correction of
1 cm graft allows acceptable stretching of neurovascular structures

If more than 1 cm of lengthening is required, what procedure may be performed?

Callus distraction with Mini-Rail fixation

How much lengthening is typically achieved with callus distraction?

1 mm per day (0.25 mm q6h)

What is achondroplasia?
Dwarfism – all bones short with tibia undergrowth and fibular overgrowth causing genu varum

What is fibular hemimelia?

Aplasia or hypoplasia of the fibula

What is DISH?
Diffuse Ideopathic Skeletal Hyperostosis – characterized by multiple ossifications at tendinous
or ligamentous insertions

What is Apert syndrome?

Multiple bony coalitions

What is Paget disease?

Osteitis deformans – abnormal bony architecture caused by increased osteoblastic and
osteoclastic activity. More common in elderly.

What malignant bone degeneration may be seen with Paget disease?


What are the stages of Paget?

1. Destructive – osteolytic
2. Mixed – osteolytic and osteoblastic
3. Sclerotic – osteoblastic

What are the stages of Charcot?

1. Acute or destructive
2. Coalescence
3. Remodeling

What conditions are associated with positive HLA-B27?

Ankylosing spondylitis, Reiter disease, psoriatic arthritis, reactive arthritis, enteropathic


What are components of CREST syndrome?
Raynauds phenomenon
Esophageal dysmotility

What is the treatment of cutaneous larva migrans?

Promethia under occlusion

What is the treatment for Lyme disease?

Doxycycline 100 mg PO daily or Rocephin l g IV daily

DOC for necrotizing fasciitis?

Primaxin 250-1000 IV q6-8h (most commonly 500 mg IV q8h)

What is Felty syndrome?

Rheumatoid arthritis, splenomegaly, leukopenia

What is mycosis fungoides?

Cutaneous T-cell lymphoma that can resemble eczematoid or psoriasis

What is erythrasma?
Chronic, superficial infection of intertriginous skin caused by Corynebacterium minutissimum.
Interdigital lesions appear as maceration.

What is ecthyma?
Ulcerative pyoderma of the skin often caused by Streptococci. Infection extends into dermis and
is characterized by ulcers with overlying crusts.

What is cellulitis?
Acute spreading infection of dermal and subcutaneous tissue commonly caused by group A Strep
or Staph aureus. Affected area is erythematous, warm, edematous, and tender.

What is erysipelas?
Superficial infection that extends into the lymphatics. Lesions are erythematous, indurated with
sharply-demarcated margins, and have erythematous, ascending streaks.

What is lymphangitis?
Inflammation of the lymphatics as a result of a distal infection

What is psoriasis?
Hereditary disorder with chronic scaling papules and plaques in areas of body related to repeated
minor trauma. Positive Koebner phenomenon and Auspitz sign. Also present are joint pain and
nail changes including pitting, beau lines, oil spot, subungual hyperkeratosis, and discoloration.


What is lichen planus?
Inflammatory dermatosis involving skin or mucous membranes with pruritic, violaceous papules
clustered into large, flat-topped lesions with distinct borders. Lesions possibly covered with
Wickham striae (white streaks). Ridges, onycholysis, subungual hyperkeratosis, and

What is another name for menopausal lipoma?

Juxtamalleolar lipoma

What is the main screening test if AIDS is suspected?

ELISA (Enzyme Linked Immunosorbent Assay)

What test should be performed to confirm the diagnosis of AIDS?

Western blot

Miscellaneous Drugs
What are some effects of steroids?
 Decreases production of prostaglandins, cytokines, and interleukins
 Decreases proliferation and migration of lymphocytes and macrophages
 Decreases osteoblast activity

What are differences between phosphate and acetate-based steroids?

Phosphate-based – soluble with shorter half-life
 Minimize inflammatory reaction and edema
Acetate-based – insoluble with longer half-life
 May delay inflammatory process or healing and can mask infection

What is a common complication following steroid injection?

Steroid flare – hypersensitivity reaction. Apply ice.

How are glucocorticoids metabolized?

Metabolized in the liver and secreted in urine

What is diazepam?
Valium, a benzodiazepine, is an anxiolytic/anticonvulsant/muscle relaxant

How to reverse diazepam?

Flumazenil (Romazicon) for benzodiazepine reversal
0.2 mg IV over 15 seconds, then 0.2 mg IV prn over 1 minute up to 1 gram total


What are drugs for insomnia?
B – Benadryl
E – estazolam
H – Halcion
A – Ambien
R – Restoril
D – Dalmane
Most commonly used are Benadryl 25 mg PO qhs or Ambien 5 mg PO qhs

What drugs leave a metallic taste in the mouth?

Flagyl, Lamisil

What is given for a Tylenol overdose?

acetylcysteine (Mucomyst)

What can cause Gray Baby Syndrome?


What is chloramphenicol?
An antimicrobial


Clinical Podiatry
What are the clinical patterns of tinea pedis? What are common infecting organisms?
Chronic (moccasin or papulosquamous)
 Trichophyton rubrum
Acute (interdigital or vesicular)
 Trichophyton mentagrophytes
 Trichophyton mentagrophytes with Pseudomonas or Proteus

What are the clinical patterns of onychomycosis? What are common infecting organisms?
Distal subungual onychomycosis (DSO) ~ 90%
 Most common
 Trichophyton rubrum
Proximal subungual onychomycosis (PSO) ~ 1%
 Seen in immunocompromised patients
 Trichophyton rubrum
Superficial white onychomycosis (SWO) ~ 10%
 Trichophyton mentagrophytes
Candidal onychomycosis
 Candida albicans

What test confirms tinea pedis or onychomycosis?

Potassium hydroxide (KOH) preparation of skin or nail specimen
Septate hyphae confirms diagnosis

Who does Lamisil work?

Inhibits ergosterol synthesis

What is phenol?
Carbolic acid

During a P&A procedure, why is alcohol used after phenol?

Phenol is soluble in alcohol, and the alcohol will irrigate excess phenol from the nail groove

For a nail avulsion, what can be done for anesthesia if the patient is allergic to all local
Saline block (pressure induced block)
Pressure cuff
Benadryl block (blocks histamine release)


In evaluating a bunion, what does the position of the tibial sesamoid indicate? Why isn’t
the fibular sesamoid evaluated?
The tibial sesamoid indicates the abnormal affects of the adductor and flexor brevis tendons.
Once the fibular sesamoid reaches the intermetatarsal space, it travels in the frontal plane (as
opposed to transverse), therefore the tibial sesamoid is a more reliable indicator of deformity.

What are some causes of hallux varus?

 Clubfoot
 Metatarsus adductus
 MPJ dislocation
 Fracture
 Overcorrection of intermetatarsal angle
 Excessive resection of medial eminence or staking the head
 Fibular sesamoidectomy
 Overaggressive capsulorrhaphy
 Bandaging too far into varus

What is staking the head?

Excessive resection of the 1st metatarsal head with cutting into the sagittal groove may lead to
hallux varus

Describe the types of hammertoes

Flexor stabilization
 Most common
 Stance phase
 Flexors overpower interossei
 Pronated foot
Extensor substitution
 Swing phase
 Extensors overpower lumbricals
 Anterior cavus, ankle equinus, anterior compartment muscle weakness
Flexor substitution
 Least common
 Stance phase
 Deep compartment muscles overpower interossei
 Supinated, high arch foot or weakened Achilles

What is the result of accidentally severing the quadratus plantae?

Adductovarus deformity of digits 4 and 5 as the pull of FDL is unopposed


What are differences between flexible, semi-rigid, and rigid deformities?
Flexible – reducible when NWB and WB
Semi-rigid – reducible when NWB only
Rigid – non-reducible

What is a Haglund deformity?

Pump bump

What x-ray measurements evaluate a Haglund deformity?

Parallel pitch lines
Fowler & Philip
Total angle

What is the Silfverskiöld test?

Determines gastroc vs. gastroc-soleus
Positive test
 Dorsiflexion of the foot to neutral or beyond with the knee in flexion
 Gastroc equinus
Negative test
 Lack of dorsiflexion of the foot to neutral with knee in flexion and in extension
 Gastroc-soleus equinus

What is the Lachman test?

Determines if there is a plantar plate tear or rupture. While stabilizing the metatarsal, a dorsal
translocation of the proximal phalanx greater than 2 mm is suggestive of rupture.

What is the Mulder sign?

Identifies a Morton neuroma by a palpable click when compressing metatarsal heads and
palpating the interspace

What is the Sullivan sign?

Separation of digits caused by a mass within the interspace

What is Q angle?
Angle between the axis of the femur and the line between the patella and tibial tuberosity

What to do if patient has edema with a cast?

If edema goes down in AM → gravity edema → normal
If edema does not go down in AM → abnormal

What is Raynaud phenomenon?

Recurrent vasospasm of digits usually in response to stress or cold


What are the stages of Raynauds Phenomenon?
White → blue → red
 Pallor – spasm of digital arteries
 Cyanosis – deoxygenation of blood pools
 Rubor – hyperemia

What is an ABI?
Ankle Brachial Index – compares ankle to arm pressures
Normal 1
Intermittent claudication 0.6-0.8
Rest pain 0.4-0.6
Ischemic ulcerations <0.4

What may falsely elevate the ABI?

Vessel calcifications/non-compressible vessels

What other tests are typically performed with an ABI?

Segment pressures
 Measured at high thigh, above the knee, below the knee, ankle, midfoot, and toe
 Normal 70-120 mm Hg
 Drop between segments >30 mm Hg indicate disease in vessel above
Pulse volume recordings (PVRs)
 Normal waveforms are triphasic
 Waveforms are widened and blunted with severe disease

What is the most common type of skin cancer?

Basal cell carcinoma – found on sun-exposed parts of the body

What skin cancer may appear cauliflower-like?

Squamous cell carcinoma – found on sun-exposed parts of the body

What is the most common type of melanoma?

Superficial spreading melanoma – found on any part of the body

Most malignant?
Nodular melanoma – may be misdiagnosed as pyogenic granuloma

Most benign?
Lentigo melanoma – typically found on back, arms, neck, and scalp

Typically found on the palms, soles, and nail beds?

Acral lentiginous melanoma

What is a Hutchinson sign?

Pigment changes in the eponychium seen with subungual melanoma


What is the most common vascular proliferation?

What vascular malignancy appears as red-blue plaques or nodules and has a high
incidence in AIDS?
Kaposi sarcoma

What conditions may be associated with plantar fibromatosis?

Ledderhose disease
Dupuytren contracture
Peyronie disease

What is another name for congenital convex pes valgus?

Vertical talus

What are radiographic findings of CCPV?

Calcaneus in equinus, plantarflexed talus, dorsally dislocated navicular, increased talo-calc angle

What additional radiographic study should be obtained for neonates with CCPV?
Lumbosacral films

What are three coalitions of the rearfoot?
Talocalcaneal, calcaneonavicular, and talonavicular

What percentage of tarsal coalitions are bilateral?


Which is most symptomatic?



Which is most common?

T-C > C-N > T-N

Which T-C facet is most commonly fused?

Medial > anterior > posterior

What are the ages of fusion?

T-N (3-5 years)
C-N (8-12 years)
T-C (12-16 years)


What are clinical symptoms of tarsal coalitions?
Limited ROM of STJ and possibly MTJ
Peroneal spastic flatfoot

What are radiographic findings of tarsal coalitions?

 Rounding of lateral talar process
 Talar beaking due to increased stress on talonavicular ligament
 Asymmetry of anterior subtalar facet
 Narrowing or absence of middle and posterior subtalar facets
 Halo sign – circular ring of increased trabecular pattern due to altered compressive forces
 Anteater sign – C-N coalition in which calcaneus has elongated process on lateral view
 Putter sign – T-N coalition in which neck of talus unites with broad expansion of

The anterior facet is best seen by which radiographic views?

Medial oblique, Ischerwood

The middle and posterior facets are best seen by which radiographic view?
Harris Beath

What are treatments for symptomatic tarsal coalitions?

 Orthotics or supportive therapy
 Immobilization
 Badgley – surgical resection of coalition or bar with interposition of muscle belly
 Isolated fusion or triple arthrodesis

What are the 3 components of clubfoot?
FF adductus, RF varus, ankle equinus

What ligaments/capsules are contracted?

 Posterior tib-fib
 Posterior talo-fib
 Lateral calcaneofibular
 Syndesmosis
 Superficial deltoid
 Tibionavicular
 Calcaneonavicular
 Talo-Navic, Navic-Cunei, and Cunei-1st MT joints
 Spring ligament


What muscles/tendons are contracted?
 Achilles tendon
 Plantaris tendon
 PT, FDL, and FHL
 Abductor hallucis
 Tibialis anterior

What is the technique for correction of clubfoot called?

Ponseti technique
 Serial casting
 First correct the FF and RF deformities, and then correct ankle equinus
 During manipulation, pressure is applied to the head of the talus (not the calcaneus)
 4-8 casts, percutaneous Achilles tenotomy (last cast for 3 weeks), occasional TA transfer,
and D-B bar brace until age 3 y/o to prevent relapse

What is the most accepted theory about clubfoot?

Germ plasma defect-malposition of head and neck of talus

What is the Simon rule of 15?

For clubfoot, children <3 years → talo-navicular subluxation
T-C angle is <15° and talo-1st metatarsal angle is >15°


1st Ray/Bunion Evaluation
Hallux interphalangeal angle
Normal 0-10°

DASA (distal articular set angle)

Normal 7.5°

PASA (proximal articular set angle)

Normal 7.5°

Types of joint deformities

Congruent – joint lines are parallel
Deviated – joint lines intersect outside joint
Subluxed – joint lines intersect inside joint

Types of bunion deformities

 Bony deformity
 Abnormal PASA and DASA
 Soft tissue deformity with subluxed or deviated joint
 Normal PASA and DASA
 Elements of both structural and positional with subluxed or deviated joint
 Abnormal PASA and DASA

Hallux abductus angle

Normal 10-15°

IM angle (intermetatarsal angle)

Normal 8-12°
Head procedure if mild 10-13°
Shaft procedure if moderate 14-17°
Base procedure if severe 18-21°
Lapidus procedure if hypermobile 1st ray

Metatarsus adductus angle

Normal <20°


True IM angle
True IM angle = (metatarsus adductus angle - 15) + IM angle

1st Metatarsal protrusion distance

Normal +/- 2 mm compared to the 2nd metatarsal

Tibial sesamoid position

Normal 1-3


Normal 65-75° dorsiflexion and 40° plantarflexion

1st Metatarsal-medial cuneiform angle

Normal 22°

1st ray ROM

Normal 5 mm dorsiflexion + 5 mm plantarflexion = 1 cm total ROM

5th Ray/Tailor Bunion Evaluation

Fallat & Buckholz 4th IM angle
Angle between bisection of 4th metatarsal and proximal-medial cortical border of 5th metatarsal
Normal 6°
Pathologic 8.7°

Fallat & Buckholz Lateral Deviation angle (lateral bowing)

Angle of line bisecting head and neck of 5th met and line adjacent to proximal-medial cortex
Normal 2.64°
Pathologic >8°

Metatarsal length
Longest 2 > 3 > 5 > 4 > 1 shortest

Metatarsal protrusion
Longest 2 > 3 > 1 > 4 > 5 shortest

Lesser MPJ dorsiflexion/plantarflexion

30-40° Dorsiflexion and 50-60° plantarflexion

Metatarsal declination angle

Normal 21°

Metatarsal abductus angle

Normal 0-15°


IM angle of 2nd and 5th metatarsals
Normal 14-18°

IM angle of 1st and 2nd metatarsals
Pathologic >12°

IM angle 4th and 5th metatarsals

Normal 4-5°
Pathologic >9°
(Schoenhause says normal 4th IMA is 8°)

1st IM angle >12° and 4th IM angle >8°
With metatarsus primus adductus, there is a high predilection of splayfoot

Talar neck angle
Long axis of head and neck with long axis of the body
Birth 130-140°
Adult 150-165°

Talar head and neck

Plantarflexed 25-30°
Medially aligned 15° to body

Talar torsion angle

Head is laterally rotated on the body
Fetus 18-20°
Childhood 30°
Adult 40°
Note: this motion brings the supinated foot in utero to a more pronated adult position

Talar declination angle

Normal 21°
Pronation – increases
Supination – decreases

Meary angle – Lateral view

Intersection of longitudinal axis of talus and 1st metatarsal
Normal 0°
Increases with either pronation or supination
Pronation – moves axis of the talus plantar to 1st metatarsal
Supination – moves axis of the talus dorsal to 1st metatarsal


Cyma line
S-shaped line formed by the articulation of T-N and C-C joints
Pronation – moves line anteriorly
Supination – moves line posteriorly

Talo-navicular joint
Normal 75° coverage
Pronation – decreases coverage
Supination – increases coverage

Forefoot abductus
Normal 8° (0-15°)

Calcaneal inclination angle
Normal 21°
Pronation – decreases
Supination – increases

Hibb angle – Lateral view

Intersection of longitudinal axis of calcaneus and 1st metatarsal

Fowler & Philip angle

Angle formed from the intersection of a line along the anterior tubercle and the plantar tuberosity
and another line along the posterosuperior prominence at the Achilles tendon insertion
Normal <70°
Haglunds deformity >75°

Total angle of Ruch

Fowler & Philip angle + calcaneal inclination angle
Normal 90°
Haglunds deformity >90°

Calcaneal-cuboid abduction
Normal 0-5°
Increases with pronation

Kite angle (Talocalcaneal) – AP view

Infant 30-50°
Adult 20-40°
Pronation – increases
Supination – decreases

Talocalcaneal angle – Lateral view

Normal 25-50° (does not change with age)


Rearfoot Angles
Subtalar joint axis direction
STJ goes through 1st ray in neutral, 2nd ray in supination, and is medial to 1st ray in pronation

STJ axis of motion

Lateral, posterior, plantar → medial, anterior, dorsal
48° from frontal plane
42° from transverse plane
16° from sagittal plane

From neutral, 2/3 motion in inversion (20°) and 1/3 in eversion (10°)

Longitudinal midtarsal joint

75° from frontal plane
15° from transverse plane
9° from sagittal plane

Oblique midtarsal joint

38° from frontal plane
52° from transverse plane
57° from sagittal plane

Bohler angle
Angle formed by the intersection of a line from the superior aspect of the anterior process to
superior aspect of the posterior facet and another line from the superior aspect of the posterior
facet to superior point of the calcaneal process
Normal 25-40°
Decreases with intra-articular calcaneal fracture

Gissane angle
Angle formed by the intersection of a line along the posterior facet and another line along the
middle and anterior facets
Normal is 125-140°
Increases with intra-articular calcaneal fracture

Toyger angle
Line drawn down posterior aspect
Normal should be a straight line (180°)
Decreases with Achilles rupture


Normal 10-20° dorsiflexion and 20-40° plantarflexion

Lateral, posterior, plantar → medial, anterior, dorsal

Tibial torsion
Birth 0°
6 years 13-18°
Adult 18-23°

Tibial varum/valgum
Compare distal 1/3 of tibia to ground
Birth 5-10° varum
>2 years 2-3° valgum

Angle of inclination
1 year 146°
4 years 137°
Adult 120-136° (avg 127°)

Angle of declination (antetorsion angle)

1 year 39°
10 years 24°
Adult 6°

Angle of anteversion
Birth 60°
Adult 10-12°

Lower Extremity Joint ROM

Hip flexion/extension with knee extended
Normal flexion 90-100°
Normal extension 10-20°

Hip flexion with knee flexed

Normal flexion 120-130°

Rotation of hip
Adults Children
Internal rotation 35-40° 20-25°
External rotation 35-40° 45-50°


Hip abduction/adduction
Abduction 24-60° (avg 36°)
Adduction <30°

Knee flexion/extension
Flexion 130-150°
Extension 5-10°

Knee rotation with knee flexed

Medial rotation 40°
Lateral rotation 40°

Knee valgum/varus (bow leg, knock knee)

Birth 15-20° (genu varum)
2-4 yrs 0° (straight)
4-6 years 5-15° (genu valgum)
6-12 years 0° (straight)
12-14 years 5-10° (genu valgum)
> 14 years 0° (straight)

Clinical Tests
What is the Ortolani test?
Test for congenital hip dislocation in newborns. With newborn supine and hip and knees flexed,
the hips are adducted while pressing downward and abducted while lifting upward. An unstable
hip will dislocate when adducted and reduce when abducted.

Barlow test?
Test for a hip that is dislocatable but not dislocated in infants. With infant supine and hip and
knees flexed, push posteriorly in line with the shaft of femur. An unstable femoral head will
dislocate posteriorly from acetabulum.

Galeazzi (or Allis) sign?

Sign of unilateral congenital hip dislocation in infants. With infant supine and hip and knees
flexed, the knees should be level. If a knee is lower, that hip is dislocated.

Trendelenberg test?
Test for weak hip abductors. As patient stands on affected limb, pelvis drops to opposite side.


Surgical Prophylaxis
What are indications for the use of antibiotics?
 Implants (joint or internal fixation)
 Prolonged surgery (>2 h)
 Trauma surgery
 Revisional surgery
 Immunocompromised patient
 Extensive dissection required
 Intra-operative contamination
 Endocarditis (SBE)

What antibiotics are most commonly used?

Clindamycin if PCN allergy
Vancomycin if concerned about MRSA

Peri-operative Management
What pre-op orders are needed for an in-house patient?
 NPO after midnight, except AM meds with sips of water
 Hold all AM hypoglycemics and cover with SSI (if patient with DM)
 Accu-Check on call to OR (if patient with DM)
 Begin ½NSS @ 60 mL/h at 0600 (D5W½NSS if patient with DM)
 Labs – CBC with diff, PT/PTT/INR, BMP
 Chest X-ray, EKG (if necessary)
 Consult medicine for medical clearance (if not already done)
 Anesthesia to see patient (if necessary)

What are indications for ordering a chest X-ray?

>40 years of age, smoker, any history of cardiac or pulmonary disease

What are indications for ordering an EKG?

>40 years of age, any history of cardiac disease

What is the most common time for post-operative myocardial infarction?

Day 3

How long should elective surgery be delayed following an MI or CABG?

6 months


How to calculate daily fluid input requirements?
First 10 kg x 100 = 1000 mL/day
Second 10 kg x 50 = 500 mL/day
Remaining kg x 20 = ___ mL/day
(e.g. 70 kg patient requires 1000 + 500 + 1000 = 2500 mL/day)

How to calculate IV fluid input rate?

―421 Rule‖ calculates IV mL/h
First 10 kg x 4 = 40 mL/h
Second10 kg x 20 = 20 mL/h
Remaining kg x 1 = ___ mL/h
(e.g. 70 kg patient requires 40 + 20 + 50 = 110 mL/h)

What other factors should be considered prior to surgery?

Is the patient on any insulin, anticoagulants, steroids, or anything else that might put them at risk
Note: any non-routine orders should be cleared with patient's primary service

What is the perioperative management for patients with diabetes?

 NPO after midnight
 Start D5W½NSS in AM
 Accu-Check
 If insulin-controlled, hold regular insulin, give ½ NPH dose, and cover with SSI
 If oral-controlled, hold oral meds and cover with SSI
 If diet-controlled, cover with SSI

What should be obtained prior to surgery on a patient with rheumatoid arthritis?

Cervical spine x-ray

What are effects of a long-term, high-dose course of steroids?

Long-term therapy suppresses adrenal function
 Risk of poor or delayed wound healing. Decreased inflammatory process.
 Risk of infection. Low WBC may mask infection.

What is the perioperative management for patients on long-term, high-dose steroids?

Peri-op IV steroid supplementation
Hydrocortisone 100 mg IV given the night before surgery, immediately prior to surgery, and then
q8h until postoperative stress relieved

What is the perioperative management for patients at risk for gout?

Begin colchicine 0.6 mg PO daily 3-5 days pre-op and continue 1 week post-op

What is the perioperative management for patients with hypertension?

If the patient has been on long-term diuretics (e.g. HCTZ, Lasix), check for hypokalemia
Avoid fluids high in sodium; may use ½NSS at low rate


When should aspirin be discontinued prior to surgery?
7 days due to irreversible binding to platelets

When should NSAIDs be discontinued prior to surgery?

3 days due to reversible binding to platelets

When should heparin be discontinued prior to surgery?

8 hours (monitor PTT)

When to Coumadin be discontinued prior to surgery?

3-4 days (monitor PT/INR)

What should the INR be for elective surgeries?


What should be done if the INR is >1.4?

If necessary, transfuse Fresh Frozen Plasma (FFP)
One unit of FFP will decrease INR by approximately 0.2
Vitamin K can be given but is slow-acting

When should a patient with an INR >1.4 be allowed to proceed to surgery?

 If the risk of not doing surgery outweighs the risk of excessive bleeding (i.e. if it is an
emergency surgery and you have anesthesia's approval)
 If the patient has PVD and the surgery is a simple debridement or amputation. Note: if
the patient has PVD, make sure you have Vascular Surgery's approval for surgery. In this
case, it is acceptable for the patient to bleed a little extra.

If a patient with a high INR undergoes surgery, what labs should be carefully monitored?
Hgb and Hct

When should a RBC transfusion be given?

If Hgb <8 or Hct<24, consider transfusing 1-2 units PRBC
One unit of PRBC will increase Hct by approximately 3 percentage points

What should be done if the patient is thrombocytopenic?

Order a six pack of platelets, which is a concentration of six pooled platelet units, and consult

Plastic Surgery
How are relaxed skin tension lines (RSTL) oriented?
Perpendicular to the long axis of the leg and foot

Should a skin incision typically be made parallel or perpendicular to the RSTL?

Parallel incisions will remain approximated and heal better while perpendicular incisions may
gap apart due to increased transverse forces


What is an anti-tension line?
S-shaped or zig-zagged incision when exposure needed is not parallel to RSTL

To close a lesion with minimal tension, what should the ratio of length to width be?
3:1 length:width

How much lengthening can be achieved with a 60° Z-plasty?


To correct a skin contracture, how should the Z-plasty incisions be oriented?

The central arm of the ―Z‖ should be parallel to the contracture

To correct a 5th digit adductovarus rotation, how should the skin incision be oriented?
Distal medial to proximal lateral

What is the order of wound graft closure?

1. Direct closure
2. Graft
3. Local flap
4. Distant flap

What are the stages of skin graft healing?

1. Plasmatic
2. Inosculation of blood vessels
3. Re-organization
4. Re-innervation

What are Blair and Humby knives?

Knives for harvesting skin grafts

What device is more commonly used to harvest skin grafts?


What is the most common complication of skin grafts?


How do you prevent it?

Mesh or pie crust graft and apply compressive dressing

What are advantages of using a split-thickness skin graft?

Donor site heals spontaneously
May cover large wounds


What are disadvantages?
Grafts are fragile
Contraction of graft during healing
May be abnormally pigmented

What are advantages of using a full-thickness skin graft?

Minimal contraction of graft
Better appearance

What are disadvantages?

More difficult to take
Must close donor site

What is an advantage of using a muscle flap?

It brings immediate increased blood supply to donor site

Fixation Devices
AO principles of internal fixation (2002)
 Anatomic articular reduction, adequate shaft reduction
 Stable/biologic fixation
 Preservation of blood supply
 Early ROM

AO principles (1958)
 Anatomic reduction
 Rigid internal fixation
 Preservation of blood supply
 Early ROM

What are the steps to inserting a fully threaded screw?

1. Overdrill near cortex
2. Underdrill through far cortex
3. Countersink
4. Measure
5. Tap
6. Screw

How much of a screw should pass the far cortex?

1 ½ threads

What is the purpose of tapping?

Creates a path for the screw threads

Why do you countersink a screw?

Prevents stress risers and soft tissue irritation
Provides even compression from screw head (land)


Describe mini fragment screws
Screw sizes of 1.5, 2.0, 2.7 – all fully threaded, cortical screws

What is the screwdriver handle made out of?

Pressed linen

What are the differences between cortical and cancellous screws?

Cortical has smaller pitch
Cortical has smaller rake angle
Cortical has smaller difference between thread diameter and core diameter

Describe a malleolar screw

For fixation of medial malleolus, partially threaded, same thread profile and pitch as cortical
screw, trephedine self-cutting tip

What screw has a fluted tip?


What are the screw sizes? What are their underdrill sizes? Overdrill? Countersink?

Mini Fragment

Sizes 1.5 2.0 2.7 All are fully threaded

Overdrill 1.5 2.0 2.7
Underdrill 1.1 1.5 2.0
Countersink 1.5 2.0 2.7

Small Fragment

Sizes 3.5 4.0 fully threaded 4.0 partially threaded

Overdrill 3.5 4.0 4.0
Underdrill 2.5 2.5 2.5
Countersink 3.5 4.0 4.0

Large Fragment

Sizes 4.5 4.5 malleolar 6.5 partially threaded 6.5 fully threaded
Overdrill 4.5 4.5 6.5 6.5
Underdrill 3.2 3.2 3.2 3.2
Countersink 4.5 4.5 6.5 6.5

What sizes are in the Synthes modular hand screw system?

1.0, 1.3, 1.5, 2.0, 2.4, 2.7


What are the cannulated screw sizes?
For Synthes 3.0, 4.0
For Smith & Nephew 4.0, 6.5, 5.5 and 7.0

What are the steps for inserting a 4.0 cannulated screw?

1. Insert 1.3 mm guide pin to far cortex
2. Measure
3. Drill near cortex with 4.0 cannulated bit (optional)
4. Drill far cortex with 2.7 cannulated bit (unnecessary for soft bone)
5. Tap (unnecessary with self tapping screws)
6. Countersink
7. Screw

What is a Herbert screw?

Headless screw – can be inserted through articular cartilage. Threaded portion proximally and
distally and smooth in between. Proximal portion has tighter pitch for compression.

What is a Reese screw?

Headless – create compression through arthrodesis. Proximal threads run clockwise, and distal
threads run counterclockwise. Smooth in between.

What are the K-wire sizes and widths in millimeters?

Size 0.028 0.035 0.045 0.062
Width (mm) 0.6 0.9 1.2 1.6

Why is there a question about K-wires in a screw set section?

K-wires can be used for the underdrill if the situation arises (e.g. underdrill bit is missing or it
fell on the floor)
The 0.062 can be used for the 1.5 underdrill (for the 2.0 screw)
The 0.045 can be used for the 1.1 underdrill (for the 1.5 screw)

What are the K wire sizes and their appropriate caps?

0.028 0.035 0.045 0.062
Yellow Blue White Green
(young boys wear green)

What are the sizes of Steinman pins?

Every one from 5/64 to 12/64 except for 11/64

What are the different types of plate fixation?

 Provides axial compression of fracture
 Pre-bend plate
 Eccentric drilling of hole adjacent to fracture; remaining holes drilled centrally
 Place plate on tension side of bone


 Protects against shear, bending, and torsional forces at the fracture site
 Interfragmental compression obtained by lag screws
 All holes drilled centrally
 Neutralization plate placed on the posterior aspect of the fibula
 Maintains alignment of unstable fracture fragments
 No interfragmental compression

Should a plate be placed on the tension or compression side of a fracture?


Is the tension side of a metatarsal on the dorsal or plantar aspect?


What is a locking plate?

Plate in which threaded screws are secured in to threaded plate holes
Does not rely on the bone for stability but rather forms a fixed-angle construct
Good for osteoporotic, comminuted fractures, or revision surgeries

What is the Hooke law?

For a material under load, strain is proportional to stress

What is the Young modulus?

After a load is removed, the material will spring back to its original shape, the resulting slope
represents the stiffness of a material or the Young modulous

Suture and Absorbable Fixation Devices

What is a Keith needle?
Straight needle

What are some common needle point configurations?

Taper point – for soft, easily penetrated tissue (subcutaneous tissue, fascia)
Cutting – cutting edge on inner curve (skin)
Reverse cutting – cutting edge on outer curve for tough, difficult to penetrate tissue

What is orthofix?
Polyglycolic acid (same as dexon)

How long for orthofix to lose strength/absorb?

Loses strength in 6-12 weeks
Absorbed in 1-3 years

What is orthosorb?
PDS (PDS=orthosorb)


How long before PDS loses its strength? When is it absorbed?
Loses strength in 4-6 weeks
Absorbed in 3-6 months

What are the two sutures that are the least reactive to tissue?
Stainless steel (least reactive), Prolene

What is Vicryl?
Polyglactin 910 (a copolymer of 90% glycolide and 10% lactide)

How is Vicryl broken down?


How long does it take to absorb Vicryl?

Tensile strength
75% @ 2 weeks
50% @ 3 weeks
25% @ 4 weeks
Absorbed completely in 10 weeks

Should you use Vicryl with an infection?

Avoid it if possible, since Vicryl is too reactive

Who first describe arthroscopy?

Who were the first podiatrists to describe a podiatric use for arthroscopy?
Heller & Vogel (1982)

What are the different scope techniques?

Scanning – side to side, up and down
Pistoning – in and out
Rotation – 360°

What are a few indications for an ankle scope?

Osteochondral lesion/fracture
Soft tissue impingement
Loose bodies

What are other uses for arthroscopy?

Endoscopic plantar fasciotomy (EPF) or endoscopic gastroc recession
Ankle fusion
Arthroscopy of STJ or 1st MPJ


What is the most common complication following an EPF?
Lateral column instability → calcaneal-cuboid joint pain

1st Ray Surgery

What is the most common indication for a Lapidus?
Hypermobile 1st ray

What is the order of the lateral release for a McBride?

1. Extensor hood
2. ADH tendon release
3. Fibular sesamoid ligament
4. Lateral collateral ligament
5. FHB
6. Fibular sesamoid excision (if performing)

What is the difference between a Vogler, Kalish, and Youngswick?

Vogler – offset V (apex at metaphyseal-diaphyseal joint)
Kalish – long-arm Austin with angles of approximately 55° for screw fixation
Youngswick – Austin with a slice taken dorsally to allow decompression and plantar flexion

What procedures correct PASA?

Biangular Austin
Offset V with rotation

What procedure corrects DASA?

Proximal Aikin

What procedure corrects hallux interphalangeous?

Distal Aikin

What are complications associated with a Keller?

Diminished propulsion of digit, loss of hallux purchase, stress fracture of 2nd metatarsal

What should be done if the capital fragment falls on the floor?

1. Rinse with saline
2. Bacitracin soak for 15 minutes
3. Rinse with saline
4. Bacitracin soak for 15 minutes
5. Rinse with saline
6. Document and inform patient


Post-Op White and Blue Toes
What are causes of a white toe post-operatively?
Arterial in nature, usually acute
Signs – pain, pale, parasthesia, pulselessness

What are treatments for a white toe?

 D/C ice and elevation
 Loosen bandages
 Place foot in dependent position
 Rotate K-wire
 Apply warm compresses proximally
 Apply nitroglycerine paste proximally
 Local nerve block proximally
 Avoid nicotine
 Consult vascular surgery

What are causes of a blue toe?

Poor arterial inflow – toe is cold and doesn't blanch with pressure
Poor venous outflow – toe is warm and will blanch with pressure

What are treatments for blue toe due to arterial insufficiency?

 (Treat like white toe)
 D/C ice and elevation
 Loosen bandages
 Place foot in dependent position
 Rotate K-wire
 Apply warm compresses proximally
 Apply nitroglycerine paste proximally
 Local nerve block proximally
 Avoid nicotine and caffeine
 Thermostat controlled heat lamp, not to exceed 90°
 Vasodilators
 Consult vascular surgery

What are treatments for blue toe due to sluggish venous outflow?
 D/C ice (but not elevation)
 Loosen bandages
 Avoid dependency
 Don’t attempt to increase vascular perfusion
 Consult vascular surgery


Rearfoot Surgery
Describe a Keck & Kelly procedure?
For Haglund deformity with cavus foot and high calcaneal inclination angle. Remove wedge
from posterior-superior aspect of calcaneus. The posterior superior prominence is moved

What are treatments for equinus?

Night splints
Gastroc recession
 Strayer
 Vulpius
 Baker
 McGlamary & Fulp
Tendoachilles lengthening
 Open/closed Z
 Hauser
 White
 Hoke
 Sgarlato
 Stewart

What is the Murphy procedure?

Achilles advancement for spastic equinus

Name surgical procedures for pes planus

 Evans
 Kidner
 C-C distraction arthrodesis
 Cotton
 Young
 Lowman
 Hoke
 Miller
 Cobb
 Koutsogiannis
 Dwyer
 Chambers
 Gleich
 Baker-Hill
 Lord


Name surgical procedures for pes cavus
 Jones
 Hibbs
 PT
 Dorsiflexory osteotomy of 1st metatarsal
 Cole
 Japas

What is an arthroereisis?
A surgical procedure to limit joint mobility (i.e. MBA implant in sinus tarsi)
Typically want 2-4° of STJ eversion with implant

What is the Valente procedure?

STJ block using a polyethylene plug with screw threads. Allows 4-5° of STJ pronation.

Who first described the triple arthrodesis?


What order do you resect and what order do you fixate the joints in a triple arthrodesis?
1. Midtarsal joints (T-N, CCJ)
2. Subtalar joint (T-C)
Fixation (opposite order)
1. Subtalar joint
2. Midtarsal joints

What are some types of fixation for a triple arthrodesis?

6.5-7.0 mm interfragmental compression screws, staples, plates

What are FDA-approved total ankle implants?

Two-component devices
 Agility
 Eclipse
 Salto Talaris
Three-component devices
 (Not FDA-approved – Buechal-Pappas, TNK, HINTEGRA)


Bone Healing
What are the stages of bone healing?
Bone heals either primarily or secondarily
Primary healing – no motion and no callus formation
1. Inflammation
2. Induction
3. Remodeling
Secondary healing – micro-motion with callus formation
1. Inflammation
2. Induction
3. Soft callus
4. Hard callus
5. Remodeling

What are some factors that negatively affect bone healing?

Smoking, antimetabolite or steroid therapy, anemia, osteoporosis

Name the types of non-unions

 Elephant foot
 Horse hoof
 Oligotrophic
 Torsion wedge
 Comminuted
 Defect
 Atrophic

What study can distinguish between a hypertrophic and an atrophic non-union?

Bone scan – positive for a hypertrophic and negative for an atrophic (avascular) non-union

What is a pseudoarthrosis?
Type of non-union in which fibrocartilaginous tissue forms between fracture fragments

What are indications for bone stimulators?

Non-union, failed fusion

What are contraindications for bone stimulators?

Pseudoarthrosis, gap greater than ½ bone diameter

What are the stages of avascular necrosis?

1. Avascular – loss of blood supply, epiphyseal growth ceases
2. Revascularization – infiltration of new blood vessels, new bone deposited on dead bone,
flattening or fragmentation of articular surface
3. Repair and remodeling – bone deposition replaces bone resorption
4. Residual deformity – restoration of epiphysis, sclerosis, deformed articular surface


What is the best study for evaluating avascular necrosis?
MRI – decreased signal intensity within medullary bone in both T1 and T2 images

Bone Grafts
What are the different types of bone grafts?
Osteogenic – able to synthesize new bone
 Mesenchymal stem cells from autologous bone or bone marrow aspirate
Osteoinductive – contains factors that induce host tissue to form new bone
 Demineralized bone matrix
 Bone morphogenic protein
 Platelet-derived growth factors
Osteoconductive – provides scaffold for host tissue to propagate new bone
 Allografts
 Hydroxyapatite
 Calcium phosphate
 Calcium sulfate

What type of bone graft is osteogenic, osteoinductive, and osteoconductive?


What are the stages of bone graft healing?

1. Vascular ingrowth
2. Osteoblastic proliferation
3. Osteoinduction
4. Osteoconduction
5. Graft remodeling

What is an early radiographic finding of bone graft healing?

Initial radiolucency of the graft due to increased osteoclastic activity which is followed by
osteoblasts laying down new bone

What is creeping substitution?

Process in which the host’s cutting cone (osteoclasts followed by osteoblasts) invade bone graft

What is the ASA classification for general anesthesia?
Class 1 – healthy
Class 2 – mild systemic disease
Class 3 – severe systemic disease
Class 4 – incapacitating systemic disease that is a threat to life
Class 5 – moribund patient who is not expected to live without surgery


What is the maximum tourniquet time?
90-120 minutes
After that, allow 5 minutes of perfusion for every half hour over

What are contraindications to using a tourniquet?

Open fracture
Sickle cell disease
Peripheral vascular disease
Recent arterial graft
Previous DVT
Skin grafts application where bleeding must be distinguished

According to Seddon, what are the different types of nerve damage?

Neuropraxia – nerve contusion resulting in conduction block that recovers promptly
Axonotmesis – interruption of axons with distal Wallerian degeneration. Supporting connective
tissue sheaths remain intact allowing regeneration.
Neurotmesis – complete severance of the nerve that is irreversible

What is the difference between an incisional and excisional biopsy?

Incisional – only a portion of the lesion is removed
Excisional – the entire lesion is removed

What are different biopsy techniques?

Punch, shave, curettage, surgical excision

How does a bone stimulator work?

Piezoelectric principle – side under compression makes a negative charge that leads to bone
growth. Therefore, placing a cathode in a non-union site will stimulate growth.

What is the direction of the cut for reverse Wilson of the 5th metatarsal?
Distal lateral to proximal medial

Who was the first to describe an arthrodesis?


What is the order for hammertoe surgery?

Note: Perform a Kelikian push-up test to determine if the next step is required
 Tendon
 Dorsal capsule
 Collaterals
 Plantar capsule
 Arthroplasty


2. MPJ
 Hood
 Tendon
 Capsule
 Plantar plate
 Arthrodesis

Why are joint implants used?

Maintain space between bony surfaces
Relieve pain

What is the lag time for presentation of osteomyelitis on an X-ray?

10-14 days

How to culture osteomyelitis?

Take one culture from the infected bone, and take a second culture proximal to the clearance
margin to ensure remaining bone is not infected

What is a Brodie abscess? What is the treatment?

Subacute osteomyelitic lesion usually found in children. It is a well-circumscribed, lytic lesion
with sclerotic borders found in the metaphysis, epiphysis, and rarely diaphysis. Painful with
periods of exacerbation and remission.
Tx: curettage and packing with autologous bone

What is in antibiotic beads?

PMMA or Poly(methyl methacrylate). Gentamycin or tobramycin are often used since they are
heat stable with good diffusion coefficiencies. Vancomycin and cefazolin may also be used.


What should be done when assessing a patient with trauma?
Primary survey (ABCDE)
 Airway
 Breathing
 Circulation with hemorrhage control
 Disability – assess neurologic status
 Exposure of patient and environmental control
Secondary survey
 Full history – medical and drug
 Thorough examination
o Evaluate tenderness and stability as well as neurovascular status of each limb
o Is there injury to joint above or below?
 X-rays and/or CT of all suspected fractures

What should always be asked with a break in the skin?

Tetanus status

Name the appropriate classification

Distal phalangeal/nail Rosenthal
1st Metatarsophalangeal Jahss
5th Metatarsal base Stewart
Lisfranc joint Quenu & Kuss, Hardcastle
Navicular Watson Jones
Posterior tibial tendon Conti (based on MRI findings)
Talar neck Hawkins
Talar body Sneppen
Talar dome Berndt-Hardy, Fallot & Wy
Calcaneus Rowe, Essex-Lopresti, Sanders
Anterior process calcaneal fracture Degan
Ankle sprains O'Donoghue, Leach, Rasmussen
Physeal ankle fracture Dias & Tachdjian
Epiphyseal fracture Salter-Harris
Ankle fracture Lauge-Hansen
Pilon fracture (distal tibia metaphysis) Ruedi & Allgower, Dias & Tachdjian
Achilles rupture Kuwada
Open fracture Gustillo
Non-unions Weber & Cech
Frostbite Orr & Fainer, Washburn

What is a clinical test for a fracture?

Point tenderness over fracture site


What are common fracture patterns?
Transverse, greenstick, torus, oblique (spiral), comminuted

Which is the most stable pattern?

Transverse is most stable

What is the weakest region of the physis?

Zone of cartilage maturation

What is the Vassal principle?

Initial fixation of the primary fracture will assist stabilization of the secondary fractures

What are possible complications of fractures?

Delayed union

What is the most common cause of non-healing for a bone fracture?

Improper immobilization

Who was Lisfranc?

He was a field surgeon in Napoleon's army

Are dorsal or plantar Lisfranc dislocations more common?

Dorsal – the plantar ligaments are stronger than dorsal

What are the Ottowa Ankle Rules?

A series of ankle X-ray films is required only if there is any pain in the malleolar zone and any of
the following findings:
 Bone tenderness at posterior edge or distal 6 cm of lateral malleolus
 Bone tenderness at posterior edge or distal 6 cm of medial malleolus
 Inability to bear weight both immediately and in ED
A series of foot X-ray films is required only if there is any pain in midfoot zone and any of the
following findings:
 Bone tenderness at base of 5th metatarsal
 Bone tenderness at navicular
 Inability to bear weight both immediately and in ED

Talar Fractures
What is the classification for talar dome lesions?
Berndt & Hardy

What stages of Berndt & Hardy are often associated with lateral ankle ligament ruptures?


What are the common locations of talar dome lesions and their mechanisms of injury?
Dorsiflexion Inversion – Anterior Lateral (unstable, shallow, wafer-shaped lesion)
Plantarflexion Inversion – Medial Posterior (deep, cup-shaped lesion)

What is Hawkins sign?

Presence of subchondral talar dome osteopenia seen 6-8 weeks after talar fracture signifying
intact vascularity. Absence of the sign implies AVN.

What is the Sneppen classification?

Talar body fractures

What percentage of fractures of the talus involve the calcaneus?


Of these fractures, how many involve the joint?


Calcaneal Fractures
What is a Mondor sign?
Plantar, rearfoot ecchymosis that is pathognomonic for calcaneal fractures

How is the Bohler angle affected by a calcaneal fracture?

Decreases with intra-articular calcaneal fracture

How is the Gissane angle affected by a calcaneal fracture?

Increases with intra-articular calcaneal fracture

What fractures are commonly associated with calcaneal fractures?

Vertebral fractures, especially L1
Femoral neck
Tibial plateau

What is the mechanism of injury for an anterior process fracture?

Inversion with plantarflexion

Ligamentous Ruptures
What are tests for ankle ligament pathology?
Anterior drawer test
Calcaneofibular-stress inversion
Abduction stress
Ankle arthrogram
Peroneal tenography


Describe the anterior drawer test
5-8 mm drawer → rupture of ATF
10-15 mm drawer → rupture of ATF + CF
>15 mm drawer → rupture of ATF + CF + PTF

Describe the talar tilt test

>10° → rupture of CFL

Describe the stress inversion test

5° inversion → rupture of ATF
10-30° inversion → rupture of ATF + CF

Achilles Tendon Ruptures

What are clinical symptoms of an Achilles tendon rupture?
Pain with history of ―pop‖
Weakness or loss of function
Palpable dell in area of ruptured tendon
Inability to perform single leg rise
Increased ankle dorsiflexion

What is the Thompson test?

A positive test results when squeezing of the calf muscle does not plantarflex the foot

What is the Hoffa sign?

Increased dorsiflexion compared to the contralateral side along with the inability to perform a
single leg rise test

What is a radiographic finding of an Achilles tendon rupture?

Disruption of Kagers triangle

Where is the most common location for the Achilles tendon to rupture?
1.5-4 cm proximal to the calcaneal insertion

Ankle Fractures
Name the fractures
Pott Bimalleolar fracture
Cotton Trimalleolar fracture
Tillaux-Chaput Avulsion fracture of anterior, lateral tibia from AITFL
Wagstaff Avulsion fracture of anterior, medial fibula from AITFL
Volkman Posterior tibial malleolar fracture from PITFL
Cedell Fracture of posterior medial process
Shepard Fracture of posterior lateral process
Foster Entire posterior process
Bosworth Lateral malleolar fracture with ankle displacement
Maisonneuve Proximal fibular fracture


What is the most common mechanism of injury (MOI) causing an ankle fracture?

What is the MOI causing a transverse lateral malleolar fracture?


What is the MOI causing a short, oblique medial malleolar fracture?


What is the MOI causing a short, oblique lateral malleolar fracture (AP view)?

What is the MOI causing a spiral, lateral malleolar fracture with a posterior spike (AP and
Lateral views)?

What is the MOI to the ankle with a high fibular fracture? What is this fracture called?
Maisonneuve fracture

What is a Lauge-Hansen Type V?

Pronation dorsiflexion
1. Vertical tibial malleolar tip fracture
2. Anterior tibial lip fracture
3. Supramalleolar fibular fracture
4. Transverse posterior tibia fracture level with proximal aspect of anterior tibial fracture

When should a posterior malleolar fracture be fixated?

ORIF when fragment is greater than 25% of the posterior malleolus

What direction should transsyndesmotic screws be inserted?

Approximately 30° from the sagittal plane from posterior-lateral to anterior-medial

Should transsyndesmotic screws be inserted using a lag technique?

No. Fully-threaded cortical screws are placed across both cortices of the fibula and the lateral
cortex of the tibia. The goal is stabilization rather than compression.

What do you test clinically test via Jack Toe Test?

Foster fracture – a fracture of the entire posterior process

What is the Thurston-Holland sign?

Epiphysis is separated from the physis with the fracture extending into the metaphysis resulting
in a triangular fracture fragment (AKA Flag sign)


Bone Tumors
What are the different patterns of bone destruction?
Geographic – well-defined, short zone of transition → benign or low-grade malignancy
Moth-eaten – more aggressive, intermediate zone of transition → benign or malignant
Permeative – poorly-defined, wide zone of transition → malignant

What are the different patterns of periosteal reactions?

Single layer – benign but sometimes malignant
Onion skin – malignant, multiple layers of periosteum
Sunburst – spiculated rays
Hair on end – parallel rays
Codman triangle – triangular elevation of periosteum

Name benign bone tumors of the foot

F – fibrous dysplasia
O – osteochondroma
G – giant cell tumor
M – myeloma
A – aneurysmal bone cyst
C – chondroblastoma, chondromyxoid fibroma, clear cell
H – hemangioma
I – infection
N – non-ossifying fibroma
E – eosinophillic granuloma, enchondroma, epidermal inclusion cyst
S – solitary bone cyst

Name malignant bone tumors of the foot

Periosteal sarcoma
Ewings sarcoma
Multiple myeloma

What is the most common, benign, primary bone tumor?


What is the most common, malignant, primary bone tumor?

Multiple myeloma


What primary bone tumors are more frequent in females?
Giant cell tumor
Parosteal osteosarcoma

What are the most common cancers that metastasize to foot?

Breast, prostate, lung, kidney

What bone tumors do not form matrix?

Bone cysts
Ewings sarcoma
Giant cell tumor

What are bone tumors typically located?

 Chondroblastoma
 Giant cell tumor (forms in metaphysis)
 Enchondroma (also diaphyseal)
 Osteochondroma
 Nonossifying fibroma
 Unicameral bone cyst
 Aneurysmal bone cyst
 Giant cell tumor (extends into epiphysis)
 Medullary osteosarcoma
 Parosteal osteosarcoma
 Chondrosarcoma
 Osteoid osteoma
 Osteoblastoma
 Enchondroma (also metaphyseal)
 Ewings sarcoma (also meta-diaphysis)
 Periosteal osteosarcoma

Centrally located
 Enchondroma
 Unicameral bone cyst
Eccentrically located within medullary canal
 Giant cell tumor
 Chondrosarcoma
 Osteosarcoma
 Osteoid osteoma
 Nonossifying fibroma


 Osteochondroma
 Periosteal osteosarcoma

What are characteristics of an osteoid osteoma?

 Benign, osteolytic lesion with central nidus (<1 cm) that may have calcifications
 1st to 2nd decades of life
 Dull pain, worse at night, relieved with ASA

What are characteristics of an osteoblastoma?

 ―Giant osteoid osteoma‖
 Benign tumor that may become malignant
 Osteolytic lesion with well-circumscribed nidus (>1.5 cm) that may have multiple
 2nd to 3rd decades of life
 Less symptomatic than osteoid osteoma, pain not relieved by ASA

What are characteristics of an enchondroma?

 Benign, well-defined, intramedullary, cartilaginous lesion
 Geographic lesions with punctuate calcified matrix
 3rd to 4th decades of life
 Painless swelling unless pathologic fracture

What is Ollier disease?

 Multiple enchondromatosis
 May become malignant
 1st decade of life

What is Maffuccis disease?

 Multiple enchondromas with soft tissue hemangiomas
 Most become malignant
 1st decade of life

What are characteristics of a chondroblastoma?

 Benign, geographic, osteolytic, lesion with sclerotic margins
 2nd to 3rd decade of life
 Pain and joint effusion

What are characteristics of an osteochondroma?

 Most common benign primary bone tumor
 Cartilage-capped, hyperplastic bone pointing away from the joint
 2nd to 4th decades of life
 Suspect malignant transformation with growth after skeletal maturity, pain, or cap >2 cm


What are characteristics of nonossifying fibromas?
 Benign connective tissue lesion with fibrous replacement of bone
 Expansive, radiolucent, medullary lesions
 1st to 2nd decades of life
 Lesions typically resolve with age
 Do not biopsy

What are characteristics of a fibrous dysplasia?

 Benign, geographic, fibro-osseous lesion with ground glass matrix
 Presents with deformity
 Sometimes painful 2° to fracture

What are characteristics of a unicameral bone cyst?

 Benign, geographic, medullary lesion that is fluid-filled
 Commonly found in calcaneus
 Fallen fragment sign – pathologic fracture in which cortex lies within lesion
 1st to 2nd decades of life
 Asymptomatic until fracture

What are characteristics of an aneurysmal bone cyst?

 Benin, expansile, lytic lesion with blood-filled cavities
 May extend into soft tissue
 Fluid-fluid levels seen on MRI
 1st to 3rd decades of life
 More common in females
 Painful, especially with pathological fractures

What are characteristics of a giant cell tumor?

 Benign but locally aggressive, lytic lesion with ground glass, ―soap bubble‖ appearance
 May destroy cortex and have soft tissue mass
 More common in females
 3rd to 4th decades of life
 Painful

What are characteristics of a multiple myeloma?

 Most common primary malignant bone tumor
 Punched out lesions or diffusely osteopenic with hair-on-end radiating spicules
 Affect 45-80 y/o
 Painful with weakness or neurologic symptoms
 Bence-Jones protein found within urine


What are characteristics of an osteosarcoma?
 Most common primary malignant bone tumor
 Sunburst periosteal reaction with Codman triangle and cloud-like, dense bone formation
 2nd to 3rd decades of life
 Dull aching pain
 Medullary
o Poor prognosis
 Parosteal
o More common in females
o Better prognosis than medullary
 Periosteal
o Slightly better prognosis than medullary

What is the most common bone tumor associated with Paget disease?

What are characteristics of a Ewings sarcoma?

 Common, malignant, primary bone tumor
 Aggressive, permeative, lytic lesion with hair-on-end, Codman triangle, and onion skin
(wings and onion rings)
 May have large soft tissue mass
 Usually under 20 y/o
 Painful with fever, weight loss, and elevated ESR
 Poor prognosis

What are characteristics of a chondrosarcoma?

 Common, malignant, moth-eaten, lesion with medullary and soft tissue calcifications
 May arise from malignant transformation of enchondromas or osteochondromas
 5th to 6th decades of life
 Painful

What study is most useful in searching for metastatic bone disease?

Total skeletal bone scan
Malignant lesions will show increased uptake


Wound Care
What are the stages of wound healing?
1. Inflammatory (lag) phase
 Days 1-4
 Initial vasoconstriction (minutes) followed by vasodilation (days)
 Neutrophils and macrophages are recruited
2. Proliferative (repair) phase
 Days 3-21
 Collagen synthesis provides tensile strength of wound
 At 14 days, tensile strength of would equals that of suture
3. Remodeling (maturation) phase
 Days 21 up to one year

In what stage of healing do chronic wounds stop progressing?


What is Santyl?
collagenase – an enzymatic debrider that digests collagen in necrotic tissue

What is Regranex?
PDGF-1 (platelet derived growth factor)

Where is Regranex made?

Puerto Rico (I was really asked this once)

What is a normal value for serum albumin?

3.4-5.0 g/dL

What is a low serum albumin level (<3.5 g/dL) associated with?

Decreased wound healing
Impaired cellular immunity
Decreased collagen synthesis
Decreased fibroblast proliferation

What minimum ABI is necessary for wound healing?

Non-diabetic patient – 0.35
Diabetic patient – 0.45

Using transcutaneous oximetry, what minimum pressure is necessary for wound healing?
Non-diabetic patient – 30 mm Hg
Diabetic patient – 40 mm Hg


How does negative pressure wound therapy (e.g. Wound VAC) assist wound closure?
NPWT applies mechanical shear stress to the wound site. This is believed to promote
granulation by decreasing bacterial bioburden, reducing edema, and inducing capillary budding.

How does hyperbaric oxygen therapy assist wound closure?

HBOT increases the partial pressure of O2 in arterial circulation, which increases diffusion of O2
at the wound site. This is believed to increase growth factors promoting angiogenesis and
collagen synthesis.

Bioengineered Tissue
What is Integra?
Bilayer graft composed of bovine tendon collagen with chondroitin-6-sulfate and a silicone layer
to control moisture loss

Extracellular graft matrix derived from porcine, small intestine submucosa

Bilayer graft derived from neonatal foreskin with dermal and epidermal layers

Extracellular graft matrix derived from human tissue with intact vascular channels

Acellular collagen matrix derived from fetal bovine dermis


Note: Although all of the classifications are important, the ones in bold and capitalized (i.e.
LAUGE-HANSEN) are the most commonly used.

Hallux Valgus
Stage 1
 Excess pronation causes hypermobility of 1st ray. Tibial sesamoid ligament gets stretched
& fibular sesamoid ligament contracts.
 Lateral subluxation of proximal phalanx occurs
Stage 2
 Hallux abductus progresses, touches against 2nd digit
 FHL & FHB gain lateral mechanical advantage
 Crista starts to erode
Stage 3
 Further subluxation at 1st MPJ, formation of IMA
 IMA increases secondary to retrograde forces from abductor hallucis
Stage 4
 Hallux subluxes & dislocates on 1st metatarsal
 Increased crista erosion

Hallux Limitus
REGNAULD (Foot, 1986)
Grade 1 – functional hallux limitus with dorsal spurring
 Intact sesamoids with no associated disease
 Joint enlargement but joint space narrowing and arthrosis
 <40° dorsiflexion and <20° plantarflexion
Grade 2 – broad flat metatarsal head with structural elevatus and significant spurring
 Pain at rest
 Osteochondral defects in metatarsal head and sesamoidal hypertrophy
 Joint space hypertrophy and narrowing
 75% decrease in total ROM
Grade 3 – ankylosis and articular hypertrophy with extensive peri-articular osteophytes
 Osteochondral defect with joint mice and extensive 1st metatarsal-sesamoid disease
 Severe loss of joint space or collapse of joint → bone on bone
 FDL contracture


Stage 1 – functional hallux limitus
 Limited dorsiflexion with weightbearing but normal ROM with non-weightbearing
 No DJD changes on x-ray
 No pain on end ROM
Stage 2 – joint adaptation
 Flattening of metatarsal head with small dorsal exostosis
 Pain on end ROM
Stage 3 – joint deterioration
 Severe flattening of metatarsal head with non-uniform joint space narrowing,
osteophytes, and subchondral sclerosis/cysts
 Crepitus on ROM
Stage 4 – ankylosis
 Obliteration of joint space with osteophyte fragmentation
 Minimal to no ROM

Drago, Oloff, and Jacobs (J Foot Ankle Surg, 1984)

Grade 1 – pre-hallux limitus
 Pain on end ROM
 X-Rays: plantar subluxation of proximal phalanx, met primus elevatus, minimal DJD
 Joint preservation/reconstruction surgery
Grade 2 – flattening of metatarsal head
 Pain on end ROM, limited ROM
 X-Rays: small dorsal exostosis, osteochondral lesion, flattened met head
 Joint preservation/reconstruction surgery
Grade 3 – severe flattening of the metatarsal head
 Pain on full ROM, crepitus
 X-Rays: large dorsal exostosis, marked flattened met head, osteophytic production, non-
uniform joint space narrowing
 Joint preservation/reconstruction surgery
Grade 4 – obliteration on joint space with joint mice
 <10° ROM
 May be asymptomatic if ankylosed
 X-Rays: loss of joint space, loose bodies
 Joint destructive surgery

Hanft (J Foot Ankle Surg, 1993)

Grade 1 – metatarsus primus elevatus, mild dorsal exostosis, and sclerosis around MPJ
Grade 2 – Grade 1 with flattening of metatarsal head, joint space narrowing, and dorsal/lateral
Grade 3 – Grade 2 with DJD findings (osteophytes, subchondral sclerosis, and cysts)
Grade 4 – Grade 2 with severe flattening and sesamoid hypertrophy
Grade 5 – Grade 3 with DJD findings


Ktavitz, Laporta, Lauton (1994)
Stage 1 – normal to mild flattening of the head
Stage 2 – minimal narrowing
Stage 3A – irregular joint space narrowing with dorsal spurring and cysts
Stage 3B – minimal joint space with loose bodies and large dorsal flag
Stage 4 – no joint space with sesamoid fusion and large exostosis formation

1st Metatarsal Dislocations

JAHSS (condensed)
Type l – dorsal dislocation of proximal phalanx and sesamoids with intact intersesamoid
Type 2 – dorsal dislocation of proximal phalanx and sesamoids
2A – intact sesamoids with ruptured of intersesamoid ligament
2B – transverse fracture of sesamoid with intact intersesamoid ligament

JAHSS (Foot Ankle, 1:15, 1980)

* Secondary to extreme dorsiflexion
Type 1 – dorsal dislocation of proximal phalanx and sesamoids with intact intersesamoid
 Tx: requires ORIF
Type 2A – dorsal dislocation of proximal phalanx and sesamoids with ruptured intersesamoid
 Tx: closed reduction and surgical shoe or BK walking cast
Type 2B – dorsal dislocation of proximal phalanx and transverse fracture of sesamoid with intact
intersesamoid ligament
 Tx: closed reduction and surgical shoe or BK NWB cast or excision of the fractured

5th Metatarsal Fractures

Stewart (condensed)
Type 1 – extra-articular fracture at metaphyseal-diaphyseal junction (true Jones fracture)
Type 2 – intra-articular avulsion fracture of 5th metatarsal base
Type 3 – extra-articular avulsion fracture of styloid process of 5th metatarsal base
Type 4 – intra-articular comminuted fracture of 5th metatarsal base
Type 5 – extra-articular avulsion of epiphysis in children

Stewart (Clin Ortho, 1960) – Stewart described only the first 4 types
Type 1 – transverse fracture at the metaphyseal-diaphyseal junction of 5th metatarsal base
approximately 1 cm from the articular cartilage. This is due to rotation of the forefoot
with the base of the 5th metatarsal remaining fixed.
 True Jones fracture (Sir Robert Jones 1902-4 fractures his own)
 This type of injury has a high propensity for non-union
 MOI: internal rotation, PF ankle, and adduction of forefoot
 Tx if non-displaced: BK NWB cast for 4-6 weeks
 Tx if displaced: ORIF


Type 2 – intra-articular avulsion fracture of the 5th metatarsal base (styloid process)
 MOI: shear force. Resulting from contraction of the peroneus brevis.
 Tx if reducible: BK NWB cast for 4-6 weeks
 Tx if non-reducible: ORIF
Type 3 – extra-articular avulsion of the 5th metatarsal base
 ―Tennis fracture‖
 Most common is 5th metatarsal fracture
 MOI: contraction of PB with DF of ankle
 Tx if reducible: BK NWB cast for 4-6 weeks
 Tx if non-reducible: ORIF (possibly tension band wiring)
Type 4 – intra-articular, comminuted fracture of the 5th metatarsal base
 MOI: crush
 Tx: BK NWB cast for 4-6 weeks
 Tx if severely displaced: bone graft and ORIF
Type 5 – extra-articular, avulsion fracture of the epiphysis (in a longitudinal direction)
 Seen in children with open growth plates
 Risk of Iselin AVN
 AKA Salter-Harris type 1
 Tx: BK NWB cast 4-6 weeks

Lawrence – Review Article (Foot Ankle, 1993)

Confusion of 3 fracture
 Jones fracture
 Diaphyseal stress fracture
 Tuberosity avulsion fracture

Shereff (Foot Ankle, 1991)

Spalteholtz tech. of 5th blood supply/nutrient artery proximal and medial 1/3 shaft
On X-ray, fracture heals medially to laterally
Fixation: tension band wire, low profile plate, screws, cross K-wires, 4.5 malleolar screw
Complications: sural nerve entrap
Apophysis fuses at 9-12 years of age

Torg (JBJS, 1984)

Type 1 – acute Jones fracture
Type 2 – delayed union of a Jones fracture or diaphyseal stress fracture
Type 3 – non-union of a Jones fracture or a diaphyseal stress fracture

Type 1A – Jones fracture
Type 1B – displaced Jones fracture with possible comminution
Type 2 – delayed or non-union of a Jones fracture
Type 3A – avulsion fracture of the styloid
Type 3B – intra-articular fracture of the styloid


Nail Injuries
ROSENTHAL (Ortho Clinics NA, 14(4):695, 1983)
Zone 1 – distal to bony phalanx
Zone 2 – distal to lunula
 Tx: V-Y advancement
Zone 3 – proximal to distal end of lunula
 If nail bed is lacerated, it is considered an open fracture
 Tx: amputation

Metatarsal Head
Freiberg Infarction
Type 1 – metatarsal head dies but heals by replacement. Articular surface preserved.
Type 2 – head collapses but articular surface remains. Peripheral osteophytes (dorsal).
Type 3 – head collapses with articular cartilage loosening. Joint is destroyed.
Type 4 – multiple heads involved

Lisfranc Dislocations
QUENU & KUSS (Rev Chir, 39:281-336,720-91,1093-134, 1909)
Convergent homolateral
 All metatarsals subluxed laterally
 All 5 metatarsals displaced laterally in the transverse plane
 1st metatarsal subluxed medially or metatarsals 2-5 subluxed laterally
 1 or 2 metatarsals displaced laterally in the transverse plane
 1st metatarsal subluxed medially and metatarsals 2-5 subluxed laterally
 Displacement in both sagittal and transverse planes

HARDCASTLE (JBJS, 64B:349, 1982)

Type A – total incongruity
A1 – homolateral
A2 – homomedial
Type B – partial incongruity
Bl – partial medial displacement
 1st metatarsal displaced medially and/or in combination with metatarsals 2-4
B2 – partial lateral displacement
 Lateral displacement of one or more lesser metatarsals
Type C – divergent
Cl – partial displacement
 1st metatarsal displaced medially with any combination of metatarsals 2-4
displaced laterally
C2 – total displacement
 1st metatarsal displaced medially with metatarsals 2-5 displaced laterally


Treatment Options
 Cast immobilization (sprains 3-5 weeks)
 Closed reduction and percutaneous pinning

Reduction Sequence
1. First realign 2nd metatarsal on middle cuneiform. Once stabilized, lesser metatarsals will
2. Next stabilize 1st metatarsal and then lateral metatarsals

Post-op Care
 BK casting for 6 to 12 weeks
 Initial NWB for 6-8 weeks
 Partial WB approximately 6 weeks
 Begin ambulation in stiff-soled shoe
 Accommodative orthotics

 Majority – post-op DJD
 Serious – circulatory compromise

Myerson (Foot Ankle, 6(5):225, 1986)

Type A – total displacement in any plane or direction
Type Bl – medial displacement of 1st metatarsal
Type B2 – lateral displacement affecting 1 or more lesser metatarsals
Type C1 – partial displacement with medial 1st metatarsal and lateral lesser metatarsals
Type C2 – total displacement with a divergent pattern and total incongruity

Navicular Fractures
WATSON-JONES (condensed)
Type 1 – navicular tuberosity fracture
Type 2 – dorsal lip fracture
Type 3 – transverse body fracture
3A – fracture of body without displacement
3B – fracture of body with displacement
Type 4 – stress fracture

WATSON-JONES (Fracture and Joint Injuries, Watson & Jones, 5th ed, p 1200)
Type 1 – navicular tuberosity fracture
 Usually an avulsion fracture by tibialis posterior tendon
 24% of navicular fractures
 Nutcracker fracture – displaced fracture with compression fracture of the cuboid between
4th and 5th metatarsal bases and calcaneus
 MOI: forceful eversion w/medial avulsion of the PT off the tuberosity or


 MOI: direct blow to the tuberosity
 Need to D/Dx Os Tibiale Externum vs. true fracture,
 Best viewed on AP and lateral oblique films
 TX: BK cast with partial WB for 4 weeks
Type 2 – dorsal lip fracture
 Most common
 Tx: BK cast with partial WB for 4-6 weeks
Type 3 – transverse navicular body fracture
3A: without displacement
o Tx: BK walking cast for 6-8 weeks
3B: with displacement
o Tx: ORIF and BK NWB cast for 6-8 weeks
Type IV – stress fracture of the navicular
 Tx if non-displaced: BK NWB cast for 4-6 weeks
 Tx if displaced: ORIF followed by BK NWB x 6-8 weeks

Accessory Navicular – Os Tibiale Externum

Geist (1914), first described by Bahin (1605)
Type l – sesamoid in tendon
Type 2 – articulating os center (Sella Clin Ortho, 1986, Foot Ankle, 1987)
2A – synchondrosis acute angle
2B – synchondrosis obtuse angle
Type 3 – fused accessory os center

Navicular Classifications
Chip, comminuted, and crush

Watson Jones
Tuberosity, dorsal lip, and transverse

Dorsal lip, avulsion, tuberosity, and fracture dislocation

Rockwood & Green

Body fracture with/without dislocation, chip, and tuberosity

Chip, tuberosity, body, displaced, and osteochondral fracture


Calcaneal Fractures
ROWE (condensed)
Type 1
1A – fracture of plantar tuberosity
1B – fracture of sustentaculum tali
1C – fracture of anterior process
Type 2
2A – ―beak fracture‖
2B – avulsion fracture of Achilles insertion
Type 3
3A – simple oblique fracture of body not involving STJ
3B – comminuted oblique fracture of body not involving STJ
Type 4 – intra-articular fracture involving STJ
Type 5 – intra-articular, comminuted, depression fracture with STJ involvement
Note: Rowe is primarily used for extra-articular fractures. Intra-articular fractures (Rowe 4 & 5)
are usually replaced by Essex & Lopresti.

ROWE (JAMA, 184:98-101, 1963)

Type 1
1A – fracture of the plantar tuberosity due to inverted or everted foot
 Tx of non-displaced: CR and BK WB cast for 6 weeks
 Tx of displaced: ORIF
1B – fracture of the sustentaculum tali due to twist on a supinated foot
 Tx of non-displaced: CR and BK cast for 6 weeks
 Tx of displaced: ORIF
1C – fracture of the anterior tubercle due to plantarflexion on a supinated foot
 Most common type 1 fracture
 Most common in females
 Tx: CR and BK WB cast for 6 weeks. If symptoms persist, excise the fragment
Type 2
2A – ―beak fracture‖ without Achilles insertion involvement
 Tx: NWB BK cast for 6 weeks in plantarflexion
2B – avulsion fracture of the Achilles tendon
 Tx: ORIF or attempt percutaneous pinning
Type 3
3A – simple oblique fracture of body not involving STJ
3B – comminuted oblique fracture of body not involving STJ
 Most common extra-articular
 Tx of non-displaced: NWB AK cast with knee flexed
 Tx of displaced: ORIF
Type 4 – intra-articular fracture involving STJ
Type 5 – intra-articular, comminuted, depression fracture with STJ involvement


ESSEX-LOPRESTI (condensed)
Type 1 – tongue fracture (vertical fracture line) without STJ involvement
Type 2 – joint depression fracture (horizontal fracture line) with STJ involvement

ESSEX-LOPRESTI (Br J Surg, 39:395-419, 1952)

Type 1 – tongue type fracture with a primary fracture line running superior to inferior with a
secondary fracture line exiting the posterior aspect of the calcaneus without STJ
1A – tuberosity fracture
1B – calcaneal-cuboid joint involvement
Type 2 – joint depression fracture with a primary fracture line running superior to inferior with a
secondary fracture line involving STJ
2A – non-displaced secondary fracture line exits posteriorly
2B – displaced secondary fracture line exits dorsally
2C – gross comminution
** 75% of all calcaneal fractures are intra-articular

Treatment of Intra-articular Fractures

Essex-Lopresti Technique
Percutaneous pinning technique placing a Steinmann pin into the tuberosity. The tongue
fragment is reduced, and a pin is placed into the anterior calcaneus or cuboid. No cast
required, and motion is performed immediately. The pin is removed in 8-10 weeks and
WB is begun. Indicated for Sanders 2C (87% success rate).

Closed reduction
Used if <2 mm displacement

Incisional Approaches
 Medial Approach: Burdeaux
 Combined Approach: Stephenson
 Extended Lateral Approach: Benirschke
 Goal is to restore the STJ and C-C articulation
 Perform surgery within 6-8 hours of the injury or wait until the swelling is reduced
 Reduction is performed by placing a Steinmann pin through the tuberosity fragment to
restore the STJ posterior facet. Once aligned, the tuberosity fragment is fixated to the
constant fragment (sustentaculum fragment). Various plates can be used as a buttress.
 Before arthrodesis is performed, CR or ORIF should be attempted

DEGAN (J Bone Joint Surg, 64:519, 1982)

Type 1 – non-displaced fracture of the anterior process
Type 2 – extra-articular, displaced fracture of the anterior process
Type 3 – intra-articular, displaced fracture of the anterior process involving C-C joint


SANDERS (Clinics Ortho, 290:87-95, 1993)
 Used for CT evaluation from coronal and axial views
 Classified by number of pieces
 Lines A and B divide the inferior portion of the posterior talar facet into 3 equal portions.
Line C separates the medial and posterior facets.
A – lateral
B – midline
C – medial (at sustentaculum tali)
1 – any number of fracture lines
 All non-displaced, extra-articular fractures
2 – one fracture line
 Two-part fracture of posterior facet
 Use one letter (2A, 2B, or 2C)
3 – two fracture lines
 Three-part, intra-articular fracture of posterior facet with depressed central fragment
 Use two letters (3AB, 3AC, or 3BC)
4 – three fracture lines
 Four-part, intra-articular fracture of posterior facet and sustentaculum fragment with high
degree of comminution

Anterior Calcaneal Process Fractures

Hannover (Clinics Ortho, 290:76-86, 1993)
CT scan evaluation based on fragments involved and number of joint fractures
1 – sustentaculum
2 – tuberosity
3 – STJ
4 – anterior process
5 – anterior STJ
* Most common is the 5 fragment/2 joint fracture

Talar Neck Fractures

HAWKINS (condensed)
Type 1 – vertical fracture of talar neck that is nondisplaced
Type 2 – vertical fracture of talar neck with STJ dislocation/subluxation
Type 3 – vertical fracture of talar neck with STJ and ankle dislocation/subluxation
Type 4 – vertical fracture of talar neck with STJ, ankle, and T-N dislocation/subluxation

HAWKINS (J Bone Joint Surg, 60A:143-156, 1978)

MOI: hyperdorsiflexion of the foot on leg
Type 1 – vertical fracture of talar neck without displacement
 Disruption of 1 blood vessel with 12% risk of AVN
 Tx: BK cast immobilization for 8-12 weeks, NWB for 6-8 wks
 Must have trabeculation across fracture site prior to weightbearing
Type 2 – vertical fracture of talar neck with STJ displacement (ankle joint remains aligned)
 Disruption of 2-3 blood vessels with 42% risk of AVN


 Tx: attempt closed reduction by pushing backward on plantarflexed foot while pulling
forward on the distal tibia. If successful, percutaneous pinning is performed. Cast in
equinus for 4 wks with subsequent casts bringing the foot out of equinus. Requires 3
months of NWB casting.
 Tx: after one unsuccessful attempt at closed reduction, ORIF is indicated. Avoid
multiple attempts at closed reduction. Longitudinal anteromedial incision along the neck
of the talus, just medial to the TA. 6.5 mm cannulated cancellous screws. Use titanium
screws to facilitate the later use of MRI to monitor the progress of osteonecrosis.
Type 3 – vertical fracture of talar neck with STJ and ankle displacement
 Disruption of 3 blood vessels with 91% risk of AVN
 25% are open fractures
 Tx: during ORIF, it is important not to dissect off deep fibers of deltoid ligament which
may remain attached to the talar body (osteotomize the medial malleolus rather than
reflect the deltoid)
Type 4 – vertical fracture talar neck with STJ, ankle joint and talonavicular joint displacement
 Disruption of 3 blood vessels with 91% risk of AVN
 Tx: ORIF

10% incidence of calcaneal fractures associated with talar neck fractures

19-28% incidence of medial malleolar fractures associated with talar neck fractures

X-rays to provide best view of talar neck

 Ankle in maximum equinus
 Foot on cassette pronated 15°
 X-ray tube directed 75° from horizontal

Sclerotic (apparent increase in density) appearance due to surrounding bones becoming

osteoporotic due from disuse and acute hyperemia

Osteonecrosis is the most common complication associated with this injury

Rates of osteonecrosis
 Type 1 (0-13%)
 Type 2 (20-50%)
 Types 3, 4 (83-100%)

MRI can define the presence and extent of osteonecrosis in the talar body as early as 3 weeks

Hawkin sign – presence of subchondral talar dome osteopenia seen 6-8 weeks after talar fracture
signifying intact vascularity. Absence of the sign implies AVN.

Up to 36 months are required for complete creeping substitution of the body after union has
occurred. Protect the patient from WB until complete revascularization occurs. A patellar
tendon brace may partially relieve the load on the talar dome once WB is initiated.


Blair fusion – if the talar dome collapses, excise the avascular talar body and place a sliding
corticocancellous graft from the anterior distal tibia into the residual, viable talar head and neck

Subchondral fenestration to increase vascularity and fibrocartilage production

Talar Body Fractures

SNEPPEN (condensed)
Type 1 – compressive fracture of the talar dome usually involving medial or lateral aspect
Type 2 – shearing fracture of the talar body
2A – coronal shearing force
2B – sagittal shearing force
2C – horizontal shearing force
Type 3 – fracture of the posterior tubercle
Type 4 – fracture of the lateral process
Type 5 – crush fracture

SNEPPEN (Acta Ortho Scand, 45:307, 1974)

Type 1 – transchondral or compression fracture of the talar dome (including osteochondritis of
the talus)
Type 2 – coronal, sagittal, or horizontal shearing fracture involving the entire body
2A – coronal shearing force
2B – sagittal shearing force
2C – horizontal shearing force
 MOA: unknown but thought to be forced dorsiflexion with the foot locked, combined
with axial compression
 Fractures displaced >2-3 mm at trochlear surface require ORIF
 75% incidence of OA of STJ
Type 3 – fracture of the posterior tubercle of the talus
 Shepherd fracture – posterior lateral tubercle fracture
 Sometimes confused with os trigonum. Bone scan can differentiate.
 MOA: hyperplantarflexion or avulsion of posterior talofibular ligament
 Tx: short leg NWB cast with foot in mild equinus. If pain persists, excise fragment.
Type 4 – fracture of the lateral process of the talus
 "Snowborder's ankle"
 MOA: dorsiflexion with inversion
 Tx: 6 weeks of NWB cast immobilization in slight equinus. Large fragments can be
internally fixated.
Type 5 – crush fracture of the talar body
 Poor prognosis
 Primary arthrodesis after 2-3 weeks due to risk of soft tissue envelope if performed

23% of open talar fractures go on to osteomyelitis and may result in future talectomy


Boyd & Knight (South Med J, 35:160, 1942)
Type 1 – coronal or sagittal shear fracture
1A – non-displaced
1B – fracture with displacement of talo-crural joint
1C – Type 1B with displacement of the STJ
1D – fracture with total displacement of the talar body
Type 2 – horizontal shear fracture
2A – non-displaced
2B – displaced

Talar Dome Fractures

BERNDT & HARDY (condensed)
Stage 1 – nondisplaced compression of talar dome
Stage 2 – partially detached osteochondral lesion
Stage 3 – completely detached, nondisplaced osteochondral lesion
Stage 4 – completely detached, displaced osteochondral lesion

BERNT & HARDY (J Bone Joint Surg, 41A:988-1020, 1959)

Mechanism: – DIAL A PIMP
Stage 1 – nondisplaced, subchondral compression of the talar dome
 Tx: conservative, off-loading patellar tendon brace
Stage 2 – partially detached, nondisplaced osteochondral fracture
 Tx: conservative, off-loading patellar tendon brace
Stage 3 – completely detached, nondisplaced osteochondral fracture
 Tx medial lesion: conservative, off-loading patellar tendon brace
 Tx lateral lesion: surgical excision of the fragment, saucerization of crater, and
fenestration to increase vascularity and fibrocartilage production
Stage 4 – completely detached, displaced osteochondral fracture
 Tx: surgical excision of the fragment, saucerization of crater, and fenestration to increase
vascularity and fibrocartilage production

Mechanism of Injury: DIAL a PIMP

DIAL – Dorsiflexion and Inversion → Anterior-Lateral lesion
 Wafer-shaped lesion, associated with trauma
PIMP – Plantarflexion and Inversion → Posterior-Medial lesion
 Small, deep, round cup-shaped fragment, 80% not associated with trauma

Stages 2-4 require lateral ankle ligament disruption to occur

 Tx of Stages 1, 2, and medial 3: NWB Short leg cast for 6-12 wks
 Tx of lateral stage 3 and 4: surgical excision of the fragment, saucerize the crater, and


Lateral Talar Process Fractures
Hawkins (J Bone Joint Surg, 47A:1170, 1965)
Type 1 – simple fracture of lateral process that extends from talofibular articular surface down to
posterior talocalcaneal articular surface of the STJ
Type 2 – comminuted fracture of lateral process that involves both fibular and posterior
calcaneal articular surfaces of the talus and the entire lateral process
Type 3 – chip fracture of anterior and inferior portions of posterior talar articular process

Posterior Lateral Talar Process Fractures

Dobas & Watson (Arch Pod Med Foot Surg, 3:17, 1976)
Stage 1 – normal posterior lateral process; no clinical significance
Stage 2 – enlarged posterior lateral process
Stage 3 – non-fused os trigonum
Stage 4 – synchondrosis of the os trigonum to the talus

McGougall (J Bone Joint Surg, 37B:257-265, 1955)

Stage 1 – line of cleavage occurs at impingement point
Stage 2 – posterior lateral process begins to separate from the main body of the talus
Stage 3 – complete separation of the posterior lateral process from the talar body

STJ Dislocations
Type 1 – medial STJ dislocation (FF moves medially and talar head moves laterally)
Type 2 – lateral STJ dislocation
Type 3 – anterior and posterior STJ dislocation

Tarsal Coalitions
DOWNEY (JAPMA, 81:187-197, 1991)
Juvenile (Osseous Immature)
Type 1 – extra-articular coalition
A – no secondary arthritis
 Tx: Badgley procedure
B – secondary arthritis
 Tx: resection or triple
Type 2 – intra-articular
A – no secondary arthritis
 Tx: resection, isolated arthrodesis, or triple
B – secondary arthritis
 Tx: triple

Adult (Osseous Mature)

Type 1 – extra-articular
A – no secondary arthritis
 Tx: resection or triple


B – secondary arthritis
 Tx: triple
Type 2 – intra-articular
A – no secondary arthritis
 Tx: isolated or triple
B – secondary arthritis
 Tx: triple

Chopart Fractures
Main & Jowett (JBJS, 57B:89, 1975)
Classification based on direction of deforming force and resulting displacement
Medial force
Type A – flake fracture of dorsal talus or navicular and of the lateral calcaneus or cuboid
Type B – medial displacement of forefoot with medial disassociation of T-N and C-C
Type C – forefoot rotates medially around interosseous talocalcaneal ligament, with T-N
disassociation and intact C-C joint
Longitudinal force
Type A – maximally plantarflexed ankle giving a characteristic pattern of through and
through navicular compression fracture
Al – force through the 1st ray crushes medial 3rd with tuberosity displaced
A2 – force through the 2nd ray crushes middle 3rd with middle 3rd and tuberosity
displaced medially
A3 – force through the 3rd ray crushes lateral 3rd with medial 2/3rd and tuberosity
displaced medially
Type B – submaximally plantarflexed ankle resulting in dorsal displacement of the
superior navicular and crush of the inferior portion
Lateral forces
Type A – forefoot forced into valgus with resulting fracture of the navicular tuberosity or
dorsal talus and a compression fracture of the C-C joint (Nutcracker Fracture)
Type B – T-N joint displaces laterally with comminution of the C-C joint
Plantar forces
Type A – avulsion fracture of the dorsal navicular to talus and the anterior process
Type B – impaction fracture of the inferior C-C joint

Ankle Fractures
1st word – position of the foot with respect to the leg
2nd word – motion that causes fracture pattern (how talus moves with respect to tibia/fibula)
* indicates hallmark sign

Supination-Adduction (SAD) – No tib-fib diastasis

Stage l – rupture of lateral collaterals or * transverse fracture of lateral malleous below level of
ankle joint
Stage 2 – * vertical fracture of medial malleolus


Pronation-Abduction (PAB)
Stage 1 – rupture or deltoid ligament or transverse avulsion fracture of medial malleolus
Stage 2 – rupture of anterior and/or posterior distal tib-fib ligaments
Stage 3 – * short fibular fracture (oblique on AP, trans, on lateral) at level of ankle joint

Supination-Eversion (SER) – most common

Stage 1 – disruption of anterior tib-fib ligament with either a tibial avulsion (Tillaux-Chaput) or a
fibular avulsion (Wagstaffe)
Stage 2 – * spiral oblique fracture of the fibula at level of ankle joint
Stage 3 – rupture of posterior tib-fib ligament or tibial avulsion (Volkmann)
Stage 4 – ruptured of deltoid or transverse fracture of medial malleolus

Pronation-External Rotation (PER)

Stage 1 – rupture of deltoid ligament or transverse avulsion of med malleolus
Stage 2 – disruption of anterior tib-fib ligament with rupture of interosseous ligament and
Tillaux-Chaput or Wagstaffe avulsions
Stage 3 – * high fibular fracture above level of ankle joint (Maisonneuve fracture)
Stage 4 – Posterior tib-fib ligament or Volkmann fracture

Pronation-Dorsiflexion (Arch Surg, 67:813-820, 1953)

Describes pilon fracture
Stage 1 – rupture of deltoid ligament or fracture of medial malleolus (oblique or transverse)
Stage 2 – fracture of anterior lip of tibial plafond
Stage 3 – fracture of fibula above the level of the syndesmosis
Stage 4 – transverse fracture of the distal tibia at the same level as the proximal margin of the
large tibial fracture

DANIS WEBER (condensed)

Describes location of fibular fracture
Type A – transverse avulsion fracture below the level of the ankle joint
(corresponds with Lauge-Hansen SAD)
Type B – spiral or oblique fracture at the level of the ankle joint
(corresponds with Lauge-Hansen SER and PAB)
Type C – fracture above the level of the ankle joint (Maisonneuve fracture)
(corresponds with Lauge-Hansen PER)

DANIS-WEBER (Ortho Clinics of NA, 661, 1980)

Type A – transverse avulsion fracture of fibula below the level of ankle mortise
 Tx: K-wire w/ tension band for fibular fracture and 2 interfrag screws for the med
Type B – fracture at the level of ankle mortise
 Tx: interfrag screws and/or plate, repair ATFL


Type C – fracture above the level of ankle mortise
 Tx: interfrag screws and plate, repair ATFL and interosseous membrane

Pilon Fractures
Pronation-Dorsiflexion (Arch Surg 67:813-820, 1953)
Stage 1 – deltoid ligament rupture or medial malleolar fracture (oblique or transverse)
Stage 2 – fracture of the anterior lip of the tibial plafond
Stage 3 – fibular fracture above the level of the syndesmosis
Stage 4 – transverse fracture of distal tibia at level of proximal margin of the large tibial fracture

RUEDI & ALLGOWER condensed

Pilon fractures – distal tibial metaphyseal fracture
Type 1 – non-displaced tibial fragments
Type 2 – intra-articular tibial fracture without comminution
Type 3 – comminution and disruption of tibial articular surface

Ruedi & Allgower (Clin Ortho, 138:105-110, 1979)

Type 1 – mild displacement, no comminution, without major disruption of ankle joint
Type 2 – moderate displacement, no comminution, with significant dislocation of ankle joint
Type 3 – "explosion fracture", severe comminution, with displacement of distal tibial metaphysis

Femoral distractor – brings tibia out to length before fixation

If Type 3 fracture, fix tibia first
40-80% failure of ankle fusion

Maale and Seligson (Orthopedics, 3:517-521, 1980)

Modification of Ruedi & Allgower
Type 1 – distal tibial compression fracture
Type 2 – external rotatory fracture with a large posterior fragment
Type 3 – spiral fracture extending from the articular surface into the metaphysis

Ovadia and Beals (J Bone Joint Surg, 68A:543-551, 1986)

Modification of Ruedi & Allgower Type II
Type 1 – non-displaced articular fracture resulting from rotational forces
Type 2 – minimally displaced fracture resulting from articular forces
Type 3 – displaced articular fracture with several large fragments due to compressive forces
Type 4 – displaced articular fracture with multiple fragments including a large metaphyseal
fragment resulting from compressive forces
Type 5 – severe comminution due to compressive forces


AO System (Ankle Fractures)
Type A – extra-articular
Type B – partially articular
Type C – completely articular
All 3 can involve:
 No comminution or impaction in the articular or metaphyseal surface
 Impaction involving the supra-articular metaphysis
 Comminution and impaction involving the articular surface with metaphyseal impaction

Destot System
Subgroup 1 – posterior marginal tibial fracture
Subgroup 2 – anterior marginal tibial fracture
Subgroup 3 – explosive tibial fracture
Subgroup 4 – supra-articular tibial fracture with extension into the ankle joint

Kellam and Waddell (J Trauma, 19:593-601, 1979)

Type A – rotational pattern consisting of two or more large tibial articular fragments, minimal or
no anterior cortical comminution, and a transverse or short oblique fibular fracture at the
level of the tibial plafond
Type B – compressive fracture pattern with multiple tibial fragments and marked anterior tibial
cortical comminution

Mast (Clinics of Ortho, 230:68-82, 1988)

Type 1 – malleolar fracture with significant axial load at the time of the injury producing a large
posterior fragment
Type 2 – spiral extension fracture
Type 3 – centrally compressive injury divided into A, B and C

Medial Malleolar Fractures

Type A – avulsion of the tip of the medial malleolus, horizontal orientation
Type B – avulsion fracture at the level of the ankle joint, horizontal orientation
Type C – oblique fracture
Type D – vertical fracture

Fibular Avulsion Fractures

Pankovich: Wagstaffe-LeFort Fracture (Clinics Ortho Rel Res, 143:138, 1979)
Type 1 – avulsion fracture maintaining attachment to both the anterior talofibular and anterior-
inferior tib-fib ligaments
Type 2 – avulsion fracture associated with an oblique fracture of the fibula originating distal to
the anterior-inferior tib-fib ligament. Spiral fracture of the fibula with a proximal fibular
spike and a transverse fracture associated with the avulsion fragment.
Type 3 – avulsion fracture of the anterior tibial tubercle followed by a Type 2


Lateral Ankle Trauma
1st Degree – rupture of the ATF
2nd Degree – rupture of the ATF and CF
3rd Degree – rupture of the ATF, CF, and PTF

O'Donoghue (condensed)
Grade 1 – partial ATF tear
Grade 2 – complete ATF tear
Grade 3 – complete ATF and CFL tear

O'Donoghue (Northwest Med, 1277, 1958)

Grade 1 – partial ATF tear with mild tenderness and swelling
 No loss of function or instability. Pt can walk, play.
Grade 2 – complete ATF tear with moderate pain, swelling, ecchymosis
 Some loss of function and moderate instability. Pt limps after injury.
Grade 3 – complete ATF and CFL tear of with severe pain, swelling, and ecchymosis
 Unable to bear weight and severe instability. Pt cannot walk after injury.

Dias (J Trauma, 19:266-269, 1979)

Grade 1 – partial rupture of the CFL
Grade 2 – rupture of the ATF
Grade 3 – complete rupture of the ATF, CF, and/or PTF
Grade 4 – rupture of all lateral collateral ligaments and partial failure of the deltoid ligament

Posterior Tibial Malleolar Fracture

Type A – large intra-articular fracture (>25% of surface area) with displacement
Type B – small intra-articular fracture (<25% of surface area) with impaction
Type C – small fracture with minimal impaction and articular damage
Type D – avulsion of posterior-inferior tib-fib ligament without articular involvement

Physeal Injuries
Salter-Harris Classification of Fractures
Site – epiphysis, metaphysis, diaphysis
Extent – complete vs. incomplete
Configuration – transverse, oblique, spiral, comminuted
Position – rotated, angulated, distracted, impacted, overriding, lateral shift
Environment – open, closed


(SMACK – Same, Metaphysis, Articulation, Continuous, Krush)
(SALTR – Same, Above, Lower, Through, Really bad)
1 – fracture through physis
2 – fracture through physis into metaphysis
3 – intra-articular fracture through physis into epiphysis
4 – intra-articular fracture through epiphysis, physis, and metaphysis
5 – crush injury

SALTER-HARRIS (Skeletal Rad, 6:237-253, 1981)

Type 1 – complete transverse separation of the epiphysis from the metaphysis through the physis
 Epiphysis separates from the metaphysis without any bone fragments
 Germ cells remain with epiphysis
 Common in infants
 Shearing force seen in pathologic fractures
 Growth is not disturbed unless there is associated avascular necrosis or premature closure
of the physis
 Tx: closed reduction if within 7 days of injury, followed by 3-4 weeks of casting
Type 2 – fracture through the physis extending into the metaphysis
 Thurston-Holland sign
 Tx: closed reduction if within 7 days of injury, followed by 3-4 weeks of casting
Type 3 – intra-articular fracture extending from the physis through the epiphysis
 Tillaux fragment
Type 4 – continuous, intra-articular fracture extending from the epiphysis into the physis and
Type 5 – comminuted fracture from impaction of the epiphysis into the physis and metaphysis
 Tx of Types 3-5: attempt closed reduction, but usually requires anatomic reduction of the
physis. Fixation should be kept within metaphysis.

Type 6 – perichondral injury produced by shearing force resulting in a cup-shaped fragment of
epiphyseal, physeal, and metaphyseal bone with possible degloving
 Tear of the ―ring of Lacroix‖

Type 7 – intra-epiphyseal fracture not involving the physis
Type 8 – transverse fracture of the metaphysis only
Type 9 – diaphyseal growth injury resulting in periosteal elevation and possible degloving of the

Type 1 – separation of the epiphysis from the metaphysis
Type 2 – partial separation of the epiphysis from the metaphysis with fracture of the diaphysis
 Thurston-Holland sign
Type 3 – partial separation of epiphysis from the metaphysis with fracture of the epiphysis
Type 4 – complete separation of the epiphysis from metaphysis with fracture of the epiphysis


Peterson (J Ped Ortho, 14:439, 1994)
Type 1 – transverse fracture of the metaphysis with extension to the physis by longitudinal
compression (15.5%)
Type 2 – separation of part of the physis with a part of the metaphysis attached (53.6%)
 Thurston-Holland sign
 Salter-Harris Type 2
Type 3 – separation of the epiphysis from the diaphysis through the physis (13.2%)
 Salter-Harris Type 1
Type 4 – separation of a portion of the physis with extension of a fracture into the joint (10.9%)
 Salter-Harris Type 3

Type 5 – fracture involving the metaphysis, physis, and epiphysis (6.5%)

 Salter-Harris Type 4
Type 6 – fracture involving a missing portion of the physis.
 Often caused by open fractures, lawn mowers, farm machinery, or other power

Type A – extra-articular
Al – separation of the epiphysis and metaphysis
A2 – fragments in the epiphysis or metaphysis
Type B – intra-articular
Bl – fracture within the physis extending into the epiphysis
B2 – fracture through the epiphysis, physis, and metaphysis

MRI Rupture
Stage 1 – 1-2 fine, longitudinal tears
Stage 2 – intramural degeneration, variable diameter
Stage 3 – diffuse swelling

Achilles Tendon Ruptures

Type 1 – partial tear <50%
 Tx: cast with foot plantarflexed
Type 2 – complete tear with <3 cm defect after debridement
 Tx: end-to-end attachment
Type 3 – complete tear with 3-6 cm defect after debridement
 Tx: end-to-end attachment and tendon flap
Type 4 – complete tear with >6 cm defect after debridement
 Tx: end-to-end attachment, recession, or graft


Radio-opaque Lesions of Achilles Tendon
Morris & Giacopelli (J Foot Surg, 1990)
Type 1 – opacities at the Achilles insertion with calcifications within tendon and partially
attached to the calcaneus
Type 2 – opacities l-3 cm proximal to insertion with lesions separate from calcaneus
Type 3A – opacities > 3 cm proximal to insertion with partial tendon calcification
Type 3B – opacities > 3 cm proximal to insertion with total tendon involvement

Peroneal Tendon Subluxations

Eckert & Davis (J Bone Joint Surg, 58A:670, 1976)
Grade 1 – retinaculum and periosteum ruptures from the cartilaginous lip and lateral malleolus
Grade 2 – distal edge of fibrous lip elevated with retinaculum
Grade 3 – thin fragment of bone with fibrous lip avulsed from deep surface of peroneal
retinaculum and deep fascia
Posterior Tendon Ruptures
1 – direct injury
2 – pathologic rupture (RA)
3 – idiopathic
4 – functional abnormality

Posterior Tibial Tendon Dysfunction

Johnson & Strom
Stage 1 – normal tendon length with mild degeneration
 Medial foot and ankle pain
Stage 2 – supple flatfoot with attenuation or PT rupture
 ―Too many toes‖ sign
 Abducted forefoot, increased talar-1st metatarsal angle, and uncovering of talar head
Stage 3 – rigid flatfoot with complete PT rupture
 Fixed calcaneal valgus with decreased STJ ROM
Stage 4 – rigid flatfoot
 Valgus tilt of talus/ankle mortise leading to lateral tibial/talar degeneration

Wilson (J Bone Joint Surg, 54B:677, 1972)

Inversion Injury
Stage 1 – lateral dislocation of 4 lesser metatarsals with divergent diastasis
Stage 2 – Stage 1 with dorsolateral dislocation of 1st metatarsal and other metatarsals

Eversion Injury
Stage 1 – medial dislocation of 1st metatarsal
Stage 2 – dorsolateral dislocation of lesser 4 metatarsals with divergent diastasis


Other Classifications
Open Fractures
Type 1 – wound <l cm without extensive soft tissue damage
Type 2 – wound >l cm without extensive soft tissue damage
Type 3 – extensive skin, soft tissue, muscle, and neurovascular damage
3A – adequate tissue coverage, high energy trauma
3B – periosteal stripping, massive comminution
3C – arterial injury

GUSTILLO & ANDERSON (J Bone Joint Surg, 58A:453, 1976)

Type 1 – open fracture with wound <1 cm without extensive soft tissue damage
 Simple, transverse or short oblique fracture with little comminution
 No crush involved
Type 2 – open fracture with a laceration >1 cm without extensive soft tissue damage
 Slight or moderate crushing injury with moderate comminution
 Moderate contamination
 Minimal foreign material
Type 3 – open fracture with extensive soft tissue damage >5 cm
 Severe comminution associated with high velocity injury
 High degree of contamination
 Significant foreign material
 Gunshot wounds, farm injuries, arterial injuries, motor vehicle accidents
3A – adequate soft tissue coverage
3B – extensive soft tissue loss/damage with periosteal stripping and bone exposure requiring
local or free flap
3C – any open fracture associated with arterial injury requiring repair. Amputation rate of

Non-Union of Fractures
Hypertrophic – hypervascular (90%)
 Elephant foot
 Horse hoof
 Oligotrophic
Atrophic – avascular (10%)
 Torsion wedge
 Comminuted
 Defect
 Atrophic


WAGNER (Foot Ankle, 2:64-122, 1981)
Grade 0 – no open lesions but bony prominence and/or structural deformity present
Grade 1 – superficial ulcer without penetration to the deep layers
Grade 2 – deep ulcer penetrating to tendon, joint capsule, or bone
Grade 3 – Grade 2 depth with the presence of infection
Grade 4 – gangrene of the forefoot
Grade 5 – gangrene of the entire foot

Wound, Ostomy and Continence Nurses Society (formerly I.A.E.T., Standards of Care, 1987)
Stage 1 – nonblanchable erythema of intact skin
Stage 2 – partial thickness loss of skin involving epidermis, dermis, or both.
 Ulcer is superficial and presents clinically as a blister or shallow crater with erythema and
Stage 3 – full-thickness tissue loss involving damage to or necrosis of subcutaneous tissue that
many extend down to, but not through underlying fascia
 Ulcer presents clinically as deep crater often with undermining, erythema, and drainage
Stage 4 – full-thickness tissue loss with extensive destruction, tissue necrosis, or damage to
muscle, bone or supporting structures (e.g. tendon, joint capsule)
 Undermining and sinus tracts often associated

University of Texas at San Antonio – UTSA (J Foot Ankle Surg, 35:528-531, 1996)
Grade 0 – completely epithelialized pre- or post-ulcerative lesion
Grade 1 – superficial wound not involving tendon, capsule, or bone
Grade 2 – wound penetrating to tendon or capsule
Grade 3 – wound penetrating to bone or joint
Within each grade, there are 4 subtypes:
A – non-ischemic, clean wound
B – infected wound
C – ischemic wound
D – infected and ischemic wound

Diabetic Foot Ulcers

Meade & Mueller (Med Times, 96:154-169, 1968)
Type 1 – diffuse, inflammatory infection of soft-tissue
Type 2 – deep plantar space infection
Type 3 – mal perforans neuropathic foot ulcers (subclassed by Wagner and USATHC)

Sanders & Freykberg
1 – IPJ, phalanx, MPJ, and metatarsals
2 – Lisfranc
3 – C-N, T-N, and C-C
4 – ankle
5 – calcaneus


Hematogenous – spread via blood starting inside the bone and working out towards the cortex
 Seen most commonly in metaphyseal region of children with open growth plates
Direct extension – secondary to trauma or surgery first affecting periosteum, then cortex, and
then marrow
 Proteolytic enzymes destroy Sharpey fibers
Contiguous – spread of infected soft tissue to underlying bone
Vascular insufficiency – PVD

Cierny & Mader

Anatomic Type
Physiologic Type
A-Host – good immune system and delivery
 Normal immune response
 Normal metabolic reserve
 Good vascular supply
B-Host – compromised locally or systemically
 Metabolic compromise
 Nutritional compromise
 Immunologic compromise
 Impaired vascularity
 Systemic illness
C-Host – no treatment because treatment is worse than disease
 Minimal disability
 High morbidity
 Poor prognosis for cure

Buckholz (J Foot Surg, 26(1):17, 1987)

Type 1 – wound induced osteomyelitis
1A – open fracture with complete incontinuity
1B – penetrating wound of injury
1C – post-op infections
Type 2 – mechanogenic osteomyelitis
2A – implants and internal fixation
2B – contact instability as bone-to-bone appositional movement
Type 3 – physeal osteomyelitis
Type 4 – ischemic limb disease
Type 5 – combination osteomyelitis, Types 1-4 as acute bone infections
Type 6 – osteomyelitis with septic arthritis
Type 7 – chronic osteomyelitis


Medicare PVD Classification
Class A
A1 – nontraumatic amputation of foot or integral portion thereof
Class B
B1 – absent posterior tibial pulse
B2 – advanced trophic changes such as (3 required)
2a – hair growth diminished or absent
2b – nail changes (thickened)
2c – pigmentary changes
2d – skin texture (thin, shiny)
2e – skin color (rubor, redness)
B3 – absent dorsalis pedis pulse
Class C
C1 – claudication
C2 – temperature changes (cold feet)
C3 – edema
C4 – parathesias
C5 – burning

Soft Tissue Injuries

Tscheme & Gotzen
Grade 0 – little or no soft tissue injury
Grade 1 – significant abrasion or contusion
Grade 2 – deep, contaminated abrasion with local contusion to skin or muscle
Grade 3 – extensive contusion or crushing of skin or destruction of muscle

Malignant Melanoma
Clark (Cancer Res, 29:705-727, 1969)
Based on histological level of invasion
Level 1 – located within epidermis or epidermal-dermal junction
Level 2 – located within papillary dermis
Level 3 – located within papillary-reticular junction
Level 4 – located down into reticular dermis
Level 5 – located within subcutaneous tissue

Breslow (Ann Surg, 172:902-908, 1970)

Based on thickness
Level 1 – <0.75 mm (99% cure)
Level 2 – 0.76-1.5 mm
Level 3 – 1.51-4.0 mm
Level 4 – >4.0 mm


Blauth & Olason
Radiographic and morphological presentation of the deformity
Describes position of duplication in both the longitudinal and transverse planes
Longitudinal Type – describes degree of duplication of the ray from distal to proximal with a
division into 5 types:
 Distal phalanx
 Middle phalanx
 Proximal phalanx
 Metatarsal
 Tarsal
Transverse Type – indicates which rays are involved in the duplication
 Classification in Roman numerals starting with the 1st ray and ending with the 5th ray

Temtamy & McKusick

Preaxial – located on the medial side of a line that bisects the 2nd digit (15%)
Postaxial – located on the lateral side (80%)
Type A – fully developed
Type B – vestigial duplication involving soft tissue

Venn & Watson

Based on degree of differentiation
 Wide metatarsal head
 T-metatarsal
 Y-metatarsal
 Complete duplication

Davis & German
Type 1 – Incomplete webbing between two digits
Type 2 – Complete webbing to ends of digits
Type 3 – Simple with no phalangeal involvement
Type 4 – Complex with abnormal phalangeal bones


Special Studies
Bone Scan
What are the phases of bone scan? When is each phase done?
Phase 1 – Immediate, early, blood flow, or angiogram (it goes by all these names)
 2-3 seconds
Phase 2 – Blood pool
 2-3 minutes
Phase 3 – Delayed
 2-3 hours
Phase 4 – Fourth phase
 24 hours

What do each of the phases of the bone scan test for?

Immediate – Blood flow
Pool – Soft tissue
Delayed – Bone activity
Fourth phase – Bone uptake for patient with PVD

What normally lights up on a bone scan?

Epiphysis of a growing child
Tips of scapula
Intercostals (ribs)

What is the half-life of Technetium-99?

6 hours

What does it mean if the bone scan lights up in Phases 1-2 but not in 3?
Cellulitis most likely

Name a way to test between Charcot disease and osteomyelitis

Ceretec scan or Indium-111

What does Indium-111 tag?

WBC’s (as does the Ceretec scan)

What does Indium-111 test for?

Highly sensitive and specific for acute soft tissue and osseous infections

What does Gallium-67 test for?

Acute inflammation and infection


How long does it take for a Gallium-67 test to work?
2-3 days
Note: it’s expensive

Why would you use a Technetium-99 scan with a Gallium-67 scan?

Acute Osteo Chronic Osteo Septic Arthritis
Phase 1 + +/- +++
Phase 2 ++ + +++
Phase 3 +++ +++ +/-
Gallium-67 Positive focal uptake Negative Positive focal uptake
Indium-111 Positive Negative Positive

Fracture Acute Cellulitis Charcot

Phase 1 +++ +++ +/-
Phase 2 +++ ++ +/-
Phase 3 +++ + +++
Phase 4 ++/+++
Gallium-67 Negative Positive diffuse uptake Negative
Indium-111 Negative Positive Negative

What causes increased signal intensity on a T1 image?

What causes increased signal intensity on a T2 image?

Fluid, Infection, Inflammation, Tumor (F.I.I.T.)

For MRI, what are the main indications for STIR imaging?
It is useful for evaluation of edema in high lipid regions, such as bone marrow.
It is also useful for evaluating cartilage.

What is fat saturation used for?

Evaluation of fat…c’mon, that’s obvious

What is Gradient Echo also known as?

Steady State Magnetization

What is Gradient Echo used for?

Joint imaging


What are 2 uses for Gadolinium?
 It will be distributed to places with increased vascularity, such as neoplasms and
 Cellulitis and walls of abscesses will enhance, but the pus will not.
 Tests cartilage integrity

What will a stress fracture show up as on MRI?

 Linear zone of decreased signal intensity surrounded by a less defined area of signal
 Linear zone of decreased signal intensity surrounded by an increased signal intensity due
to edema
 Increased signal intensity because fatty bone marrow is suppressed

How will osteomyelitis show up on MRI?

 Break in cortex, decreased signal in the bone marrow
 Break in cortex, increased signal in the bone marrow

How will AVN show up on MRI?

T1 and T2
 Decreased signal intensities
STIR and Long T2
 Double rim sign: Inner margin will show an increased signal intensity (this represents
granulation tissue). Outer margin will show decreased signal intensity (this shows

What does MRA stand for?

Magnetic Resonance Angiography

What is MRA used for in the LE?

PVD, DVT, neoplasm and anatomic studies
Most commonly ordered by a vascular surgeon for further description of occlusions/stenosis


What are the 3 planes of a CT Scan?

Which of these planes is computer reconstructed?


What does the coronal plane of a CT scan represent?

Frontal plane
(Memorization tip! 1st vowel in coronal and frontal is ―O‖)

What does the axial plane of a CT scan represent?

Transverse plane
(Memorization tip! 1st vowel in transverse and axial is ―A‖)

What must you D/C before an A-gram?
Glucophage because patient may develop metabolic acidosis

What are some tests for sickle cell anemia?

Microscope and observe
Hemoglobin electrophoresis

How many phases in a Ceretec scan?


What does HMPAO stand for?

Hexylmethypropyleneamineoxime (a.k.a. Ceretec scan)

What does MDP stand for?



Name That Surgery!
Note: This section has a variety (but incomplete list) of surgeries with some indications and brief
descriptions to help you sift through the vast amounts of procedures that are named after their
creators. If you’re going to interview or rotate with a program that has an attending in which a
procedure is named after, please know more than what is listed here! Asterisks are next to the
most common procedures you should know.

1st Ray & Tailor Bunion Procedures

* Akin
Indications: Large DASA → Proximal Akin
Long proximal phalanx → Central Akin
High hallux abductus angle >15° → Distal Akin
Procedure: Medially based wedge osteotomy of the proximal phalanx

* Austin (a.k.a. Distal Chevron Osteotomy)

Note: If you don’t know this one, stop reading this book and find a paper bag to cover your head
in shame.
Indications: HAV (IMA 12°-14°)
Procedure: V-shaped osteotomy with the apex in the center of the metatarsal head and the
arms forming a 60° angle

* Cheilectomy
Indications: Hallux limitus
Procedure: Removal of the dorsal bone spur and dorsal ⅓ of the 1st metatarsal head
OPTIONAL – Removal of bony prominences from proximal phalanx base

* Closing Base Wedge Osteotomy (CBWO, a.k.a. Louisan-Balaceau)

Indication: HAV (high IMA)
Procedure: Closing wedge osteotomy straight across the base of 1st metatarsal (difficult to

* Crescentic (a.k.a. Weinstock or Arcuate)

Indication: HAV (IMA >13°)
Procedure: Crescentic osteotomy, (with crescentic blade) concavity directed proximally

Indications: Large 1st IMA + Abnormal PASA + Valgus rotation of 1st metatarsal
Procedure: Derotational osteotomy of the 1st metatarsal head (vertical cut through metatarsal
head, cartilage is rotated for realignment, very unstable)


Note: Reverse Hohmann used for Tailor’s bunion
Indications: HAV
Procedure: Through and through transverse osteotomy at the metatarsal neck (unstable

* Juvara
Indications: HAV (IMA >15°)
Procedure: Oblique CBWO (apex prox-med, wedge laterally with the base ending in mid ⅓
of the metatarsal, direction allows for better fixation)

* Kalish
Indications: HAV (IMA ≤15°)
Procedure: Similar to Austin but with a long dorsal arm for screw fixation (angle reduced to
55° between arms)

* Keller
Note: Used in patients >50-55 years old
Indications: HAV (IMA 16° or less) + Hallux limitus/rigidus
Procedure: Resection of the proximal ¼ to ⅓ base proximal phalanx (⅓ more commonly, cut
perpendicular to long axis of bone), and cheilectomy with capsular tissue sewn
into 1st MPJ space

Indication: Hallux limitus
Procedure: Removal of a pie-shaped dorsiflexory wedge of bone from proximal phalanx

Indication: Hallux limitus
Procedure: Plantarflexory wedge osteotomy of 1st metatarsal base

* Lapidus
Indication: HAV + 1st ray hypermobility
Procedure: Fusion of 1st metatarsal base to medial cuneiform (with the resections of bone
angled to correct the deformity)

Indications: HAV (IMA ≥15° in rectus foot, 13° with adductus) + Abnormal PASA
1. CBWO (or Crescentic) → to correct HAV
2. Reverdin (or Peabody) → to correct cartilage orientation

Indications: HAV
Procedure: Transverse CBWO


Note: Opposite orientation to Mau
Indication: HAV
Procedure: Oblique bone cut diagonally (dorsal-prox to plantar-dist) through the 1st
metatarsal. Transpositional osteotomy.

Note: Opposite orientation to Ludloff
Indication: HAV
Procedure: Oblique bone cut diagonally (dorsal-dist to plantar-prox) through the 1st
metatarsal. Rotational osteotomy.

* McBride
Indication: Mild HAV (does not truly correct the HAV deformity)
Procedure: Silver plus soft tissue, capsular releases/tightening

* McKeever (a.k.a. 1st MPJ Arthrodesis/Fusion)

Indications: HAV with dislocation
Hallux limitus/rigidus
Polio, CP, previous joint surgery
1. Removal of cartilage on 1st metatarsal head and base of proximal phalanx
2. Remodel the opposing sides to be a matching cone-in-cup shape
Hallux Position: Abducted 5°-10° (or parallel to lesser digits)
DF 5°-10° off WB surface

Indication: HAV
Procedure: Distal metaphyseal osteotomy with rectangular block of bone removed and
preservation of lateral cortical ―spur‖ (width of spur varied depending on amount
of correction needed) that hangs over shaft when transposed.

* Opening Base Wedge Osteotomy (OBWO, a.k.a. Trethowan)

Indication: HAV
Procedure: Opening base wedge osteotomy (osteotomy across base of 1st metatarsal, then
insert a pie-shaped piece of bone graft into the side of the 1st metatarsal cut)

Indication: Abnormal PASA
Procedure: Reverdin done in the 1st metatarsal neck

* Reverdin
Indications: Mild HAV + Abnormal PASA
Procedure: Medially based wedge (proximal cut perpendicular to long axis 1st metatarsal and
distal cut parallel to articular cartilage surface) resection in 1st metatarsal head


* Reverdin-Green
Indications: Mild HAV + Abnormal PASA
Procedure: Reverdin osteotomy but in an L-shape (or trapezoidal) to preserve sesamoid

* Reverdin-Laird
Indications: Moderate HAV + Abnormal PASA
Procedure: Reverdin-Green with lateral shift of capital fragment to correct IMA

Indication: Hallux limitus + HAV
Allows for correction in 3 planes
Procedure: Triangle-shaped wedge removed from both the top and side of the distal 1st

* Scarf
Indication: HAV (IMA 12°-18°)
Procedure: Z-type osteotomy through the shaft of the 1st metatarsal

Indications: Medial 1st MPJ pain
Mild HAV (but does not correct the true HAV deformity)
Procedure: Isolated resection of medial eminence of 1st metatarsal head

Indication: HAV
Procedure: OBWO in medial cuneiform (wedge of graft inserted into medial cuneiform)

Indication: Hallux limitus
Procedure: Removal of angled (usually 45°) dorsal wedges from the 1st metatarsal and
proximal phalanx to increase ROM

* Vogler (a.k.a. Offset-V)

Indication: HAV
Procedure: V-osteotomy made in the neck of the 1st metatarsal (similar to Kalish but more

Indication: Hallux limitus
Procedure: Removal of closing wedge of bone from 1st metatarsal head to DF capital

Indications: Hallux limitus
Procedure: Watermann osteotomy but with a plantar shelf to preserve sesamoid articulation


Note: Reverse Wilson can be done for Tailor’s bunion
Indication: HAV (IMA 12°-14°)
HAV + Long 1st metatarsal
Procedure: Oblique (dist-med to prox-lat) through and through osteotomy at the 1st metatarsal
neck, capital fragment slides laterally on shaft (unstable and slow healing)

* Youngswick
Indications: HAV + DF 1st metatarsal
HAV + Hallux limitus
Procedure: Austin but with an extra slice taken out on the dorsal arm to allow the head to
drop plantarly and decompress the 1st MPJ

Indication: Tailor’s bunion
Procedure: Wedge osteotomy (transverse or oblique) at 5th metatarsal base. K-wire or screw

Indication: Tailor’s bunion
Procedure: Oblique wedge osteotomy at 5th metatarsal neck

Reverse Austin (or Reverse Chevron)

Indication: Tailor’s bunion
Procedure: Transverse plane V-osteotomy in distal 5th metatarsal with medial transposition
and impacted on shaft for fixation (or pin fixation)

Reverse Hohmann
Indication: Tailor’s bunion
Procedure: Transverse osteotomy in distal metaphysis of 5th metatarsal with medial
transposition of capital fragment. Fixation not usually used.

Reverse Wilson
Indication: Tailor’s bunion
Procedure: Osteotomy from dist-lat to prox-med to shorten the 5th metatarsal and medial
transposition of metatarsal head. Fixation not usually used.

Indication: Tailor’s bunion
Procedure: Oblique or transverse (most stable) wedge osteotomy at 5th metatarsal prox mid-
diaphyseal area. Fixation used.


Metatarsus Adductus Procedures
Indications: Met adductus + Age 8 years or older
Congenital absence of medial cuneiform
Procedure: Excise cuboid (to balance out lack of medial cuneiform)

Indications: Met adductus + Ages 2-6 years old
1. Transfer TP into navicular
2. Medial capsulotomy of nav-cun joint

Chondrotomy by Johnson
Indications: Met adductus + Ages 6-8 years old
1. Resect 2.5 mm lateral based wedges (apex medial) of cartilage in metatarsals 2-5, enlarge
bases medially
2. Lateral base wedge osteotomy distal to epiphysis of 1st metatarsal
3. Lengthen ABductor hallucis

See Clubfoot Procedure section

* Berman & Gartland

Note: Most popular osseous procedure for met adductus
Indications: Met adductus + Age 6 years or older
1. Panmetatarsal base wedges dome-shaped or crescentic osteotomies
a. Optional – rearfoot procedures to correct combined deformities
2. Manipulate foot into corrected position, use pin fixation in all metatarsals and cast for 6

Indications: Met adductus + Ages 2-6 years old
1. Heyman, Herndon & Strong procedure
2. PLUS ant-medial release of naviculocuneiform joint

* Heyman, Herndon & Strong (a.k.a. Tarsometatarsal soft tissue release)

Indications: Met adductus + Ages 2-6 years old
1. 3 dorsal incisions (originally one dorsal transverse incision)
2. Capsulotomies and ligament releases of all tarsometatarsal joints (metatarsals 1-5)
a. Keep plantar lateral ligaments and joint capsules intact (modification from
original to prevent dorsal subluxation)


b. Optional – syndesmotomy of naviculocuneiform joint and release of TA tendon,
also could use K-wires to maintain corrected positions
3. Manipulate metatarsals and foot into rectus position and cast for 3 months

Indications: Met adductus + Ages 2-6 years old
Procedure: Capsulotomy of 1st metatarsal-cuneiform, followed by serial casting

Indications: Met adductus + Age 8 years or older
1. 3 dorsal incisions
2. Transverse plane osteotomies in bases of metatarsals 2-4 from dorsal-dist to plantar-prox,
parallel to WB surface of foot, fixated with compression screws
3. Oblique base wedge osteotomies of 1st and 5th metatarsals, fixed with compression screws

Note: Same name as procedure for clubfoot
Indications: Met adductus + Ages 2-6 years old
To release abductor hallucis
Procedure: Sectioning of abductor hallucis through a small medial incision

McCormick & Blount

Indications: Met adductus + Age 8 years or older
1. Arthrodesis of 1st metatarsal-cuneiform joint
2. Osteotomy of bases metatarsals 2-4

Peabody & Muro

Indications: Met adductus + Age 8 years old or older
1. Excise bases of metatarsals 2-4
2. Osteotomy of 5th metatarsal
3. Mobilize and reduce subluxation of 1st metatarsal -cuneiform joint
4. Correction of any abnormal insertion of TA tendon
5. Optional – Hoke triple arthrodesis to realign rearfoot when necessary

Steytler & Van der Walt

Indications: Met adductus + Age 8 or older
Procedure: Oblique V-osteotomy (apex of ―V‖ toward rearfoot) of all metatarsal bases
Modified from original to include fixation


Indications: Met adductus + Ages 2-6 years old + hallux varus (a.k.a. hallux abductus, severe
contraction of abd hallucis)
To release abductor hallucis
Procedure: Resect abductor hallucis

Achilles Tendon Procedures

* Baker
Indication: Achilles tendon lengthening
Procedure: Tongue-in-groove cut in aponeurosis with the tongue distal, facing upward
Suture aponeurosis bands to one another in retracted position

Indication: Gastroc equinus
Procedure: Isolated gastroc recession in the deep interval between soleus and gastroc muscles

Indication: Achilles tendon lengthening
1. Incision 5 cm in length over medial aspect of tendon
2. Triple hemisection of Achilles tendon
a. Cut Achilles in half in 3 sections: posteriorly in proximal and distal aspects of
incision and anteriorly in central portion of incision
b. Modification – cuts med/lat instead of ant/post, can be percutaneous
3. Forcibly DF the foot to allow for sliding into lengthened position

Indication: Achilles tendon ruptures
Procedure: Two flaps taken proximally from Achilles and reflected distally to fill defect

Indication: Achilles tendon ruptures
Procedure: End-to-end reapproximation of ruptured Achilles (may reinforce with plantaris)

Fulp & McGlamry Modification (of Baker’s technique)

Indication: Achilles tendon lengthening
Correction of non-spastic gastroc equinus
Procedure: Tongue-in-groove cuts in aponeurosis with the tongue distal, facing downward
(inverted version of Baker’s technique)

Note: Makes a 3 joint muscle into a 2 joint muscle
Indication: Achilles tendon lengthening
1. Release the gastroc heads at their attachments to the femoral condyles (above knee joint)
2. Reinsertion into the posterior proximal tibia area (below knee joint)


* Sliding ―Z‖ Lengthening
Indication: Achilles tendon lengthening
Procedure: Cuts most commonly done in frontal plane but can be in sagittal plane
Usually percutaneous, recommended open in McGlamry
DF the foot after cutting to separate and lengthen ends of the tendon
If open procedure, suture ends of ―Z‖ together in lengthened position

Indication: Gastroc equinus
1. Distal recession with the complete transverse cutting of gastroc aponeurosis
2. Proximal retracted portion of gastroc is sutured into the deeper soleus

* Vulpius & Stoffel

Note: Originally a transverse cut in aponeurosis
Indications: Gastroc equinus
Procedure: Distal resection of gastroc aponeurosis using an inverted ―V‖
But DON’T suture to soleus

Indication: Achilles tendon lengthening
1. Section anterior ⅔ of distal Achilles and medial ⅔ of Achilles (5-7.5 cm proximal to this
2. This lengthens the gastroc in relation to its twisting before its insertion

Pes Planus and PTTD Procedures

Baker & Hill
Indications: Pes planus (to restore alignment of STJ and reduce heel valgus and excess
Cerebral palsy
Procedure: Horizontal osteotomy inferior to posterior facet of STJ (in calcaneus, medial
cortex intact as hinge) and a wedge-shaped graft inserted

Indication: Flexible pes planus (more often in children, <8 years old)
Rarely performed anymore
1. TAL
2. Bone graft under sinus tarsi (similar to location of arthroereisis to block translocation of
talus on the calcaneus)


Indication: Pes planus
1. Silver (opening wedge calc osteotomy from lateral side) with TP advancement
2. TA tenodesis to TP

Note: Good procedure because FDL preserved
Indications: PTTD
Pes valgus
1. Hemi-section of TA (more medial portion released, other half left intact at insertion near
ankle level)
2. Lay released portion of TA along TP tendon and suture together

* Cotton
Indications: Pes planus
Medial column repair (to get structural PF of medial column)
1. Medial (and sometimes intermediate cuneiforms) osteotomy dorsal to plantar
(maintaining plantar cortex intact)
2. Triangular shaped bone graft (base measuring 4-7mm) inserted in osteotomy. No
fixation necessary.

* Dwyer
Indication: Pes planus
To produce calcaneal varus
Procedure: Closing wedge osteotomy from medial side (difficult due to possible nerve

* Evans Calcaneal Osteotomy

Note: Same name as procedures indicated for clubfoot and lateral ankle instability
Indications: Pes valgus foot deformity
To lengthen calcaneus
1. Incision over C-C joint, reflect EDB
2. Osteotomy of calcaneus parallel and 1-1.5 cm (dist ⅓) prox to C-C joint
3. Wedge of graft inserted into osteotomy (lateral side of graft up to 1 cm in kids and max 7
mm in adults)

Indication: Pes valgus foot deformity (especially frontal plane dominant)
Procedure: Oblique calc osteotomy (posterior calc osteotomy) displaced anteriorly (to
―restore the normal angle of the long axis of the calc to the floor‖)


* Hoke Arthrodesis
Note: Not to be confused with the Hoke Achilles procedure
Indication: Pes planus
Medial column repair
Usually done in conjunction with ankle equinus correction and calcaneal
osteotomies or arthroeresis
1. TAL
2. Fusion of navicular to medial and intermediate cuneiforms

* Kidner
Indications: Pes planus
Kidner foot type (accessory navicular and/or enlarged navicular)
Medial column repair
1. Detach TP from navicular medially
2. Resect accessory navicular and/or bump from navicular
3. Reattach TP to navicular more plantarly (tendon bone anchors commonly used)

* Koutsogiannis (nickname ―Kouts‖)

Note: Sometimes combined with Evans osteotomy for PTTD
Indication: Pes valgus foot deformity
Restores heel valgus, less so in restoring medial longitudinal arch. Also shifts the
functional insertion of the Achilles medially.
1. Medial displacement of an oblique osteotomy of calcaneus from lateral incision
a. Posterior portion of calcaneus ―slides‖ medially ⅓ to ½ the width of calcaneus
until it sits just below sustentaculum tali
2. K-wire, Steinmann pins, or lag screw fixation

Indication: Pes planus
Procedure: A Gleich (oblique calcaneal osteotomy) displaced anteriorly, medially, and

Indications: Pes planus
Medial column repair
1. TAL
2. Talo-navicular wedge arthrodesis
3. Reroute TA under navicular and suture into spring ligament
4. Tenodesis of medial arch by taking slip of TA and reflect downward (leave its insertion
to the calcaneus intact) along medial arch


Indications: Pes planus (more often appropriate in adults than children)
Medial column repair
1. TAL
2. Medial column fusion (navicular to medial cuneiform to 1st metatarsal)
3. Resect hypertrophy of navicular (use as bone graft for fusion sites)
4. Advance medial soft tissues

Peroneus Brevis Tendon Transfer (PBTT)

Indication: Type 1 vertical talus
Severe pes planovalgus
Procedure: Detach PB and reroute dorsally to talar neck
ALT – Detach PB and transfer to lateral cuneiform or 3rd metatarsal

Indication: Flexible pes planus + Ages 5-9 years old
Congenital vertical talus (flexible/supple deformity) + Ages 5-9 years old
1. Osteotomy and grafting of sustentaculum tali
a. Osteotomy performed midway between interosseous talocalcaneal ligament and
post margin of sustentaculum tali
b. Wedge bone graft inserted to redirect the middle and anterior facets
2. Tightening of medial structures (tightening redundant spring ligament and repositioning
of the TP)
3. Reroute half or all of TA into navicular

Silver or Opening Wedge Dwyer

Indication: Pes planus
1. Opening wedge calcaneal osteotomy from lateral incision
a. Oblique osteotomy from just post to post facet inferiorly to just prox to C-C joint
b. The more proximal and anterior the osteotomy, the greater correction
2. Graft insertion into osteotomy
a. Average wedge size ¼ inch, no fixation needed

* STJ Arthroereisis
Indication: Flexible pes valgus + patient not yet at skeletal maturity (or if arthrodesis not
appropriate in older patient)
1. Incision 2-4 cm long parallel to relaxed skin tension lines over sinus tarsi. Incise deep
fascia to expose lateral talar process, post facet and sinus tarsi floor.
2. Further steps of dissection depend on the specific device you are using
a. MBA (Maxwell-Brancheau Arthroereisis) implant, STA-peg device


Young Tenosuspension
Note: Often done in conjunction with other procedures
Indications: Pes planus + Age 10 years or older
Patients with navicular-cuneiform fault but no DJD yet
Helps to PF 1st ray (takes away TA antagonist action against PL)
1. TAL
2. Reroute TA through keyhole in navicular (do not detach TA from insertion)
a. Alternate – detach TA from insertion and reattach after passing through a trephine
hole in navicular
3. TP reattachment beneath navicular (creates a powerful plantar navicular-cuneiform

Lateral Ankle Instability Procedures

* Brostrom-Gould (or just Brostrom)
Note: Common procedure used, see Special Surgery Section for details
Indication: Lateral ankle instability
For primary repair
1. Incise lateral ankle capsule 2-3 cm distal to lateral malleolus
2. Evert foot and tighten capsule including ATFL and CFL in pants over vest fashion with
non-absorbable suture
3. Mobilize extensor retinaculum, pull it over capsule and suture down

* Christman & Snook

Note: Could use PL instead of PB for this procedure
Indication: Lateral ankle instability
To reinforce ATFL and CFL
1. Detach half of PB from its insertion
2. Reroute it through a drill hole in the talar neck and distal lateral malleolus (through
widest part, anterior to posterior). Suture graft tendon to periosteal flap at level of CFL.
3. Distal half of PB then sutured to proximal half

Indication: Lateral ankle instability
To reinforce ATFL and CFL
Procedure: Tensor fascia lata routed through calcaneus, then lateral malleolus, then talus,
back through lateral malleolus and back through calcaneus

Note: Same name as osteotomies indicated for pes planus and clubfoot. Similar to Nilsonne but
with an osseous tunnel instead of subperiosteal tunnel.
Indication: Lateral ankle instability
Reinforces ATFL only (this does not reconstruct ATFL or CFL anatomically)


1. PB is detached proximally
2. Reroute it through fibular drill hole (anterior-most and distal-most → post-prox location).
PB secured posteriorly at prox aspect of superior peroneal retinaculum.
3. Prox PB is attached to PL

Indication: Lateral ankle instability
Reinforces ATFL and CFL
1. Split PL
2. Reroute into talus (or attached through it), through a lateral malleolus drill hole (anterior
to posterior), through calcaneus and attached to the other half of the PL

Indication: Lateral ankle instability
Reinforces ATFL and CFL
1. Isolate the plantaris tendon
2. Reroute it from the calcaneus into lateral malleolus through a drill hole (posterior to
anterior), back through the calcaneus then sutured on itself

Indication: Lateral ankle instability
Reinforces ATFL only
1. PB detached proximally
2. Reroute it through lateral malleolus drill hole (post → ant) and sutured upon itself
(peroneal anastomosis)
3. Periosteal flap from dist fibula reinforces new ligament
4. Prox PB attached to PL

Indication: Lateral ankle instability
Reinforces ATFL only
1. PB detached proximally at musculotendon junction
2. Reroute it through subperiosteal groove through fibula (post-superior → ant-inferior),
CFL primarily repaired if necessary
3. PB secured in subperiosteal tunnel (this approximates ATFL course)
4. Prox PB attached to PL

Indication: Lateral ankle instability
Reinforces ATFL and CFL


1. Use a hemi-section of PL
2. Reroute it from talus into lateral malleolus and into calcaneus

Indication: Lateral ankle instability
Reinforces ATFL only
1. PB detached proximally
2. Reroute it through lateral malleolus (drill hole posterior to anterior ~2 cm from distal tip
of fibula) into talar neck (vertical drill hole dorsal to plantar), then back through lateral
malleolus (along ATFL course) and sutured on itself posterior to fibula
3. Proximal PB attached to PL

Indication: Lateral ankle instability
Reinforces ATFL and CFL
1. PB detached proximally while maintaining distal attachment
2. The detached portion is rerouted through a lateral malleolus drill hole (anterior to
posterior) and inserted into calcaneus

Clubfoot Procedures
Baja Project
Indication: Clubfoot
1. Cuboid decancellation procedure
2. Laterally based triangular wedge of bone removed from cuboid and lateral cuneiform

* Dwyer
Note: Indicated also for pes planus but wedge done laterally instead of medially (calcaneus goes
into varus)
Indication: Clubfoot
Cavus foot deformity
Procedure: Opening wedge medial calcaneal osteotomy
Calcaneus goes into a more valgus position

* Evans
Note: Same name as procedures indicated for pes planus and lateral ankle instability
Indication: Clubfoot
Procedure: Shorten lateral column by calcaneal-cuboid fusion


Note: Often done in conjunction with other procedures, especially if more rigid deformity
Indications: Residual clubfoot deformity
Cavovarus deformity
Met adductus + Age 8 years or older
Bone graft inserted into medial cuneiform with opening wedge osteotomy to lengthen medial
Modification – closing wedge osteotomy of cuboid and lateral cuneiform, then use this bone
as the graft for the opening medial cuneiform osteotomy. Good with ages 3-10 years old,
residual adduction, or varus deformity in forefoot/midfoot.

Note: Same name as a procedure for met adductus
Indication: Clubfoot
Procedure: Closing base wedge osteotomy of anterior calcaneus (base of wedge lateral,
shortens lateral column)

Indication: Clubfoot (neglected or arthrogryphotic neuromuscular type) + Ages 2-5 years old
(ideally, occasionally in adults)
Talectomy (foot posteriorly displaced allowing for correction in sagittal and frontal planes)
Optional – portions of navicular and fibula may need to be resected. Also may use
midfoot wedges adjunctively. Often multistaged.
Fixation with Steinmann pin from calc to tibia for pseudojoint space. Long leg casting for 1
month to BK cast for 4 months.

Miscellaneous Procedures
Indication: To decrease MPJ buckling and increase DF
1. EDL is detached from insertion and reattached to lateral cuneiform or 3rd metatarsal
2. Distal stubs of EDL are attached to EDB at metatarsal head area

* Hoffman
Note: Often done with Keller arthroplasty
Indications: MPJ subluxation secondary to rheumatoid arthritis and fat pad atrophy
Procedure: Resection of metatarsal heads 2-5

Indications: MPJ subluxation secondary to rheumatoid arthritis and fat pad atrophy
Procedure: Resection of metatarsal heads 2-5 and bases of proximal phalanxes


* Jones
Indications: Cock-up hallux
Weak TA (procedure enhances DF)
1. EHL is detached and inserted into 1st metatarsal head via a med → lat drill hole
2. IPJ fusion
3. Stump of EHL is attached to EHB

Indication: Spastic equinus
Procedure: Anterior transfer of TA into calcaneus
Modification – route under FHL

OATS (Osteoarticular Transfer System)

Indication: Posterior medial talar dome osteochondral lesion
1. Take a plug of bone with articular cartilage from the knee
2. Through a trans-tibial approach, insert it into the talus (matching the contours of cartilage
on graft to dome of talus)

Peroneus Longus Tendon Transfer (PLTT)

Indication: Drop foot
Anterior muscle weakness
Flexible cavus deformity
1. Cut PL near PB insertion site, suture distal PL to PB
2. Reroute it dorsally to 3rd cuneiform

Silver & Simon

Indication: Spastic equinus
1. Proximal release of gastroc without reinsertion of heads
2. Neurectomy of tibial branches to medial head of gastroc

* Split Tibialis Anterior Tendon Transfer (STATT)

Note: Same as TATT but only half the tendon is used. See Special Surgery Section for details.
Indications: To increase true ankle DF and decrease long extensor swing phase
To decrease adductovarus forefoot
1. Detach half of TA from its insertion
2. Reroute and insert it into peroneus tertius (or cuboid, if peroneus tertius isn’t present)

Indication: Correction of spastic muscular forms of ankle equinus
Procedure: Selective denervation of tibial nerve


Note: Grice procedure = STJ arthrodesis
Indications: Congenital convex pes planovalgus (vertical talus!) + Ages 4-6 years old
1. First stage: TAL with posterior ankle and STJ capsular release
2. Second stage: (3 weeks later) STJ extraarticular arthrodesis

Tibialis Anterior Tendon Transfer (TATT)

Note: The STATT is slightly preferred due to fewer complications. See Special Surgery Section
for details.
Indications: To decrease forefoot supinatory twist
To increase true ankle DF
1. TA is detached from its insertion
2. Reroute and insert it into lateral cuneiform or 3rd metatarsal (or inserted into peroneus
tertius if present)

Tibialis Posterior Tendon Transfer (TPTT)

Note: See Special Surgery Section for details.
Indications: Drop foot
To eliminate flexor substitution
1. TP is detached at its insertion site on the navicular
2. It is then rerouted through the interosseous membrane of the tibia and fibula, brought
anteriorly and then inserted into the lateral cuneiform


Special Surgical Section
This section is based on my notes on how to do a select few rearfoot and ankle cases. Basically,
the outlines are a combination of McGlamry’s, Coughlin’s, and Kitoaka that I used in my third
year to prepare for the cases. Obviously, my notes are only one of many ways to do the cases.

I have included my notes here as a quick outline reference. As always, it is up to the reader to go
to the original sources to learn the material.


We also used McGlamry and Coughlin & Mann to prepare for cases. We have included a few
additional notes that we found helpful.

--Hubert & Sandi


Achilles Tendon Rupture
 Frequently in ―Weekend Warriors‖ men 30-50 yrs old
 Location of tear usually occurs in the ―watershed area‖ (2-6 cm proximal to the Achilles
insertion) though avulsions and myotendinous junction ruptures are also possible
 Clinical Exam
o Patient can PF because of posterior tibialis but can’t do a one-legged heel raise
o Positive Thompson test (squeezing the calf reveals an absence of ankle plantarflexion)
o Palpable gap, although this may be less obvious with edema after 24 hours
 Surgery vs Conservative Tx
o Younger people tend to do better and recover faster with surgery over conservative
o Older, non-active people tend to do better with conservative methods
 Conservative Treatment
o PF cast for 2 weeks NWB
o Increase DF (but still PF) for 2 more weeks. Continue NWB.
o At 4 weeks, if can cast in neutral, pt can WB
o At 8 weeks, D/C cast and use CAM boot for 4 more weeks. A 2-2.5 cm heel lift can be
put in shoes. Begin passive ROM.
o At 12 weeks, start active exercises in regular shoe (with ¼‖ to ½‖ heel lift)
 Pre-op Tx
o Jones compression dressing with mild PF of foot

 Procedure
o Patient set-up
 Prone
 General or spinal
 Thigh tourniquet
1. Incision: medial aspect of the Achilles tendon from just above the myotendinous
junction to insertion on calcaneus. Incision is down to paratenon.
a. Use very careful dissection as this area is very avascular
b. Watch out for:
i. Plantaris medially
ii. Sural nerve perforates the Achilles tendon centrally at the myotendinous
junction and then courses laterally
iii. Lesser saphenous vein may also run with the sural nerve
2. Incise the paratenon. The paratenon should be opened as part of the full thickness
flap. Get good exposure to the tendon.
 For End-to-end or mid-tendon ruptures
3. Irrigate, debride the mop-top ends of tendon
4. Reapproximate using Bunnel, Kessler or Krackow type of suture using 3-0 or 2-0
Ethibond or other non-absorbable polyester suture
5. Reinforce site with 1-0 or 2-0 Vicryl in a circumferential stitch. Irrigate again.
6. Close paratenon with 3-0 Vicryl, subcutaneous, then skin


 For Myotendinous junction ruptures (Reverse Lindholm’s technique)
3. Rather than inverted strips of tendon being raised from prox → dist (as in Lindholm’s
technique), go dist → prox
4. Weave inverted tendon into place
5. Suture with Bunnel, Kessler or Krackow technique, similar to end-to-end repair
6. Reinforce with Vicryl circumferential suture, close subcutaneous and skin
 For Avulsion ruptures
3. Extend incision distally past insertion of Achilles onto calcaneus
4. Debride calcaneus of fibrous tissue, debride down to cancellous bone
5. Make 2 drill holes longitudinally to each other and put non-absorbable suture in
tendon (i.e. half a Kessler) bring suture through drill holes and tie over itself or (more
commonly now) use suture bone anchors
6. Close

 Post-op
o Jones compression dressing for 7-10 days
o NWB BK cast for 2-3 weeks
 Cast in 20° PF for avulsion and mid-tendon ruptures
 Cast in neutral for myotendinous ruptures
o After the PF cast, cast in neutral position (have the patient rest foot on a footrest for 15-
20 min to gently allow the foot to go to neutral or close). WB BK cast for 2-4 weeks or
CAM boot (removable walking cast) here instead. Pt may also start passive ROM.
o After casts, return to regular shoes with a 1‖ heel lift
o Aggressive walking may begin around 10 weeks post-op
o Return to sports at 14-16 weeks post-op
o Note: Pt may not be able to get full DF of foot for 3-6 months


Delayed Repair of Achilles Tendon
 Clinical Presentation
o At time of rupture, pt feels as if struck in the back of the calf
o Pt complains of weakness in PF
o If pt has progressive degenerative changes to Achilles tendon, insidious onset
o Often rupture is not palpable
o Tendon tends to be thicker as it progressively gets longer
 Areas of Ruptures
o At tendon 2-6 cm from insertion
o At myotendinous junction
o Calcaneal avulsion
 Conservative Treatment
o Heel lifts, lace up shoes, MAFO, braces
o BUT…these won’t restore normal push-off
 Indications for Surgery
o Restore normal push-off power
o Take X-rays and MRI
 If >3 cm defect and >3 months → end-to-end suture (as in Acute Achilles repair)

 Procedure
o Patient set-up
 Prone
 General or spinal
 Thigh tourniquet
o For mid-tendon tear
1. Posterior medial incision over Achilles from just above myotendinous junction to
past calcaneal insertion. Make full thickness incision to paratenon.
2. Incise paratenon, reflect with full thickness flap
3. Irrigate, clean up mop-handle like edges
o If >3 cm tear
4. Kessel, Bunnel or Krackow type suture with 3-0 Ethibond
5. Reinforce ends circumferentially with 2-0 or 3-0 Vicryl
o If gap is approx 3 cm → inverted V-Y advancement is done
4. Inverted V-Y – leaving underlying muscle attached to the paratenon
5. Advance the distal flap distally
6. Close the defect via Kessel, Bunnel, or Krackow with 3-0 Ethibond
7. Reinforce ends circumferentially with 2-0 or 3-0 Vicryl
o If gap is much greater than 3 cm → V-Y advancement, close end-to-end, reinforce
with FHL
 Inverted V-Y will have to be done at an acute angle and will make the tendon
very thin…which is why you have to reinforce with FHL
 FHL Transfer
1. Incision is on medial border of midfoot, from the navicular to head of 1st
metatarsal, just above the level of the abductor muscle (approximately
where plantar skin meets regular skin)


2. Dissect down to the layer of the abductor hallucis fascia. Reflect the muscle
downward. Retract with Weitlaner.
3. FHB is reflected plantarly
4. Identify the FHL (medial) and FDL
a. These are usually covered by a fatty layer
b. Flex the IPJ of the hallux, and the FHL can be identified
5. Section the FHL as distally as possible, generally at midshaft of 1st
6. Tag prox part of FHL. Suture distal FHL to FDL with the toes in neutral
o Posterior Medial Incision
1. Posterior medial incision over Achilles from just above myotendinous junction to
past calcaneal insertion. Make full thickness incision to paratenon.
2. Incise paratenon, reflect with full thickness flap
3. Irrigate, clean up mop-handle like edges
4. Incise the fascia overlying the FHL. By pulling on the suture from the FHL, you
can identify the muscle.
5. Retract the tendon through post-medial incision
6. Make transverse drill hole into posterior calcaneus just distal to insertion of
calcaneus halfway from medial → lateral
7. 2nd drill hole goes from prox → dist to intercept the holes in calcaneus. A large
towel clip is used to connect the 2 holes.
8. A suture passer is inserted in the dist-medial hole upward. The FHL is attached
to it and the FHL tendon is passed from prox → dist-medial.
9. The FHL is then woven into the Achilles tendon from dist → prox and repeated
to use the full length of FHL tendon.
10. The tendon is secured with Ethibond
11. Repair paratenon, then close in layers

 Post-op
o Jones compression dressing and plaster splints with foot in 15° PF until first post-op
visit (7-10 days)
o BK cast with foot in 15° PF for 4 weeks
o Cast foot in neutral with BK walking cast or removable cast boot for 4 weeks
 Put foot on footrest with hip flexed. Allow foot to passively go to neutral.
o At 8 weeks post-op, begin strength training and ROM exercises
o Patient remains in removable cast boot until the 10° of DF and 4/5 PF strength is
o Half-inch heel lift is added to their shoe. Home exercises are performed at this period.
o Athletic activity restricted for 6 months


Excision of Calcification of Achilles Tendon
 Procedure
o General or spinal
o Prone is ideal
o Thigh tourniquet
 Have Mitek anchor or other kind of anchor in room
1. Incision: from the superior-medial of the Achilles tendon (can go 1 cm medial to
tendon and 3-4 cm proximal to spur or tuberosity)lateral (2-3 cm distal to spur or
tuberosity), with the horizontal part over the spur
a. Note: can go the other direction which may keep away from sural nerve
2. Dissect in layers, tag paratenon
3. Incise Achilles tendon longitudinally (Lateral ½ = Medial ½). Keep distal attachments
of Achilles, if possible.
a. If total resection of Achilles tendon must be performed, remove all bony
prominences and treat it like a ruptured Achilles tendon
i. Can drill holes and use non-absorbable suture (ie fiberwire) or Mitek
bone-tendon anchor
4. Reflect Achilles tendon side to side, remove any intra-tendon calcification
5. Deepen incision—remove retrocalcaneal bursa
6. Release any paratenons fibrosing or scaring
a. Expose any posterior calcaneal exostosis
b. Can resect calcaneal exostosis with an osteotome
7. Repair Achilles tendon with 2-0 Vicryl in running suture
8. Close

 Post-op
o 3-6 weeks NWB in cast (if necessary)
o 3-6 weeks in a WB boot


Murphy Procedure – Achilles Tendon Advancement
 Indication
o Spastic equinus
o Plantarflexory force of gastroc-soleus complex at ankle joint is weakened with minimal
decrease of toe-off force

 Procedure
1. Incision 5 cm slightly medial to midline of Achilles tendon
2. Dissect down to deep fascia and paratenon. Incise and tag the paratenon. Do not
dissect in layers because this will lead to soft tissue necrosis.
3. Detach TAL from its insertion to the calcaneus
a. If child, careful not to disturb the calcaneal apophysitis
4. Reroute the TAL under the FHL (if desired)
5. Divide the fat over the calcaneus, then resect a 0.5 cm wedge of bone from calcaneus
just posterior to posterior facet
6. From that wedge, make 2 drill holes, one exiting medially, one exiting laterally
7. Use a Bunnell technique to the distal end of the TAL with either an absorbable (1-0
Vicryl) or non-absorbable (1-0 Ethibond) suture
8. Bring one of the loose end strands through the medial drill hole, and bring the other
strand laterally
9. With the foot in neutral, guide the tendon into the wedge and tie the sutures over the
dorsal surface of the calcaneus, anterior to Achilles tendon
10. Close, cast in AK cast with knee slightly flexed, foot in neutral


Ankle Arthrodesis
 Ideal position
o Ankle neutral (no DF or PF)
o 5° valgus
o External rotation equal to opposite limb

 Procedure
o Patient set-up
 Prone with sandbags
 Thigh tourniquet
 General or spinal

 Lateral approach
1. Incision is curved starting approx 10 cm proximal to fibula to base of 4th metatarsal
a. Avoid sural and intermediate dorsal cutaneous nerves
2. Create skin flaps
3. Strip periosteum from fibula (reflect anteriorly and posteriorly)
4. Incision is carried down to expose posterior facet of STJ and sinus tarsi
5. Use a periosteal elevator to strip the tibia, ankle joint and prox talar neck (med →
a. Do NOT dissect talar neck except for prox portion. You don’t want to strip off
the blood supply to the talus!
6. Osteotomize the fibula approx 2 cm prox from ankle joint
a. Bevel the cut proximal-lateral to distal-medial so you don’t leave a sharp edge
b. Remove distal portion of the fibula
c. Reflect peroneal tendons posteriorly
7. Make incision through deep fascia at post tibia. With a periosteal elevator, strip the soft
tissues off the tibia.
a. This is visualized after fibula is removed
8. The initial cut in the tibia is with the short wide blade, then complete with the long
wide blade
a. Cut is perpendicular to long axis of bone
b. Remove as little bone as possible
c. Stop cut where the tibia curves for the medial malleolus

 Medial approach
1. Incision is 4 cm over the anteromedial aspect of the medial malleolus and directed
slightly inferior so that the medial tip of the medial malleolus can be exposed
2. Strip soft tissue anteriorly
a. Do as little damage to deltoid ligament as possible
3. With a size 10 osteotome, cut along the medial malleolus to finish the initial tibial cut
while freeing up the initial portion


 Lateral incision
1. With a broad osteotome, wedge out the tibial cut using gentle levering
2. In the talus, cut 3-4 mm from the superior surface
3. Check alignment and remove more bone if needed

 Fixation
1. Temporary fix with 0.062 K-wire
a. Check position relative to patella
b. Place two 3.2 drill bits, one in sinus tarsi and one just above lateral process
c. Check position
2. Insert two 6.5 mm screws from lat-distal → med-prox
a. Note: There are multiple specialty plates available specifically for this procedure
that may change the way you do your fixation
3. Be sure to engage medial cortex of tibia
4. If soft bone, use a washer
a. Check rigidity of arthrodesis site
b. Optional – Can put 3rd screw through medial incision
c. Optional – Fixation of fibula with 4.0/4.5 mm cancellous screw
5. Closure
a. Use a drain
b. Deep closure, etc.
c. Administer marcaine block
d. Compression dressing and splint

 Post-op
1. Leave post-op dressing in place for 10-12 days, change and remove stitches
2. Put patient in BK cast, NWB
3. Do not use removable cast because they don’t provide enough support
4. At 6 weeks, X-ray. If healing begins to appear, use BK WB cast.
5. At 12 weeks, if satisfactory healing, can WB
6. Avg fusion time: 14 weeks
7. Avg shortening: 9 mm


Tibial-Calcaneal Arthrodesis
 Procedure
o Patient set-up
 Supine with bump under ipsilateral hip
 Thigh tourniquet
 General or spinal

 Lateral Approach (similar to lateral approach in Tibiotalar arthrodesis)

1. Incision 10 cm proximal to tip of lateral malleous across the tip of the lateral malleolus
and toward the 4th metatarsal base
a. Watch out for sural nerve and superficial peroneal nerve
2. Strip the periosteum from the anteroposterior aspect of the fibula, the lateral aspect of
the talus, and the calcaneus
3. The distal portion of the fibula is removed approx 1.5 cm above the level of the distal
4. Dissect over the anterior portion of the tibia to the medial malleolus
5. An incision is made over the posterior aspect of the tibia, and the periosteal elevator is
passed along the back of the tibia to the level of the calcaneus
a. The entire lateral aspect of the ankle joint and talus is now exposed
6. Using a saw, cut the talar neck, from lat → med just distal to the dorsal articular
cartilage of the talus
7. Remove the talus body
a. The calcaneal articular surface can now be visualized
8. Remove the articular cartilage of the tibia perpendicular to the long axis of the tibia
a. Starting approximately 2 mm above the cartilage, remove as little bone as
9. With the foot in plantargrade position, remove the dorsal aspect of the calcaneus.
This creates a flat surface for the arthrodesis.
a. This includes the posterior and middle facets but leaves the sinus tarsi intact
b. Do not violate the C-C joint or the anterior process of the calcaneus

 Medial approach
1. Incision over the anteromedial aspect of the joint and carry it out distally past the tip of
the medial malleolus for about 2cm to the TN joint
2. Strip the periosteum from the medial malleolus (the portion uncut from the
3. Remove this portion of the medial malleolus, usually by osteotome
a. Be careful of the neurovascular bundle at the posterior medial portion of tibia

 Remember your alignment (5° of dorsiflexion and 5° of valgus)

1. If necessary, remove bone from tibia or calcaneus to achieve it
2. The fusion site should be posterior enough for normal posterior curvature of the heel
3. Make cut in anterior aspect of the tibia parallel to the cut made in the talar neck
4. Drill surfaces of arthrodesis sites


 Internal Fixation
1. Use 0.062 K-wires for temporary fixation
a. Check alignment
2. Insert 7.0 or 7.3 cannulated screws from posterior calcaneus to anterior portion of tibia
a. If possible, insert two screws
b. The screws are more plantar than in a subtalar arthrodesis, even if this means you
are on a WB surface
c. Can throw a third screw from tibia to calcaneus post → ant or apply a blade plate
3. Fixate the talus to tibia with two 4.0 screws
4. Note: There are multiple specialty plates available specifically for this procedure that
may change the way you do your fixation
5. Check alignment with C-arm
6. Close


Subtalar Arthrodesis
 Procedure
o Patient set-up
 Prone
 Thigh tourniquet
1. Lateral incision over sinus tarsi from tip of lateral malleolus to 4th metatarsal base
2. Free the EDB from its attachment to calcaneus
3. Incise the fatty plug longitudinally
4. Retract the peroneals plantarly
5. With lamina spreader, spread the sinus tarsi.
6. Remove articular cartilage with rasp, curette, osteotome or rongeur
a. Preserve the shape and contour of the bones
b. Be careful not to violate the tibio-talar joint
7. Make a stab incision. Put guide wire in calcaneus.
8. Put heel in 5˚-10˚ of valgus
a. After the heel is in good position, advance wire into talus
b. X-ray and advance 7.0 mm cancellous screw with 16 mm thread length
9. Test strength of fusion
10. Optional – 2nd screw through same incision.
11. If not stable, remove hardware and insert a screw through talar neck into calcaneus.
12. If bone graft is needed, you can take part of the anterior process of calcaneus. Or use

 Post-op
o First 48˚ Jones compression dressing with splint
o Then BK cast NWB for 6 weeks (remove stitches at 3 weeks)
o BK WB cast for 4-5 weeks until radiographic evidence of healing
o Eventually rehab with or without PT


Talo-Navicular Fusion
 Good results in low activity patients
 High demand patients should probably add a C-C fusion (double arthrodesis)
 Indications
o Primary arthrosis secondary to trauma or rheumatoid arthritis (main indication)
o If instability secondary to PT dysfunction or collapse of TNJ from rupture of spring
ligament, isolated T-N fusion is indicated (but Coughlin usually does triple)

 Procedure
o Ideal position of foot
 5° valgus
 TNJ in neutral
 Forefoot 0-5° varus
o Patient set-up
 General or spinal
 Thigh tourniquet
 Patient supine
1. Incision just distal to medial malleolus to 1 cm beyond the navicular-cuneiform joint,
curved slightly dorsal (especially if large dorsal osteophyte is present)
2. Strip joint capsule with periosteal elevator or sharp osteotome
3. Remove osteophytes with rongeur or osteotome
4. Identify articular surfaces, remove with curette or osteotome
a. Can use towel clip in medial navicular for exposure
b. Visualization can be improved with lamina spreader if bone is hard
c. Difficult to see laterally, but this must be exposed and debrided
5. Joint surfaces are heavily feathered and foot is manipulated into anatomic alignment
6. Stabilize calcaneus and place STJ in 5° valgus
a. Manipulate midtarsal joint into a few degrees abduction
b. Forefoot into a plantigrade position that is perpendicular to long axis of tibia
c. Forefoot should not have a residual of more than 7-10° varus or valgus
7. Internal fixation—can use two 4.0 or 4.5 mm canulated cancellous screws. For large
person, can use 7.0 mm screw. If bone is soft, can use multiple staples.
8. Hold foot in corrected alignment, drive guide pin into navicular starting at navicular-
cuneiform joint and drill obliquely across navicular into head and neck of talus
9. Check alignment of foot, C-arm
10. Add second guide wire, C-arm
11. Overdrill navicular, insert 40 to 50 mm long threaded cancellous screw. Screw threads
must pass the intended fusion site. If soft bone, use washer. C-arm
12. Check stability of foot
13. If bone is soft or the fusion is not stable, use staples. This is also useful if there is a
fracture of the navicular.
14. Close
15. Marcaine at the end


 Post-op
o Compressive dressing with two splints
o NWB for at least 6 weeks
o Add cast on 1st visit
o After sutures are removed, place patient in short leg removable cast
o After 6 weeks, and x-rays look good, patient can ambulate with short leg cast
o 3 months after surgery, if x-rays ok, patient can d/c the short leg cast

 Complications
o Non-union—Rate is higher than in CCJ or STJ probably because of inadequate exposure
to joint. Also because navicular is avascular.
o Flatfoot—Results from placing the STJ in too much valgus and forefoot in too much
 Correct with a triple arthrodesis

 Items needed for surgery

o Periosteal elevator, osteotome, curettes
o Possible saggital saw
o Wire driver
o Towel clips
o Lamina spreader
o 4.0, 4.5 or 7.0 canulated cancellous screw (probably 40-50 mm)
o Possible washers
o Possible staples
o 3-0, 4-0 Vicryl, 5-0 Monocryl or 4-0 prolene
o Splints for stirrup/posterior split


Triple Arthrodesis
 Procedure
o Patient set-up
 Prone
 Thigh tourniquet
 General or spinal
1. See Subtalar Arthrodesis for subtalar steps
2. Lateral incision
a. Incise over sinus tarsi from lateral malleolus to base of 4th metatarsal
i. Avoid superficial peroneal nerve and peroneal tendons
b. Reflect EDB off calcaneus
c. Longitudinally incise sinus tarsi fat plug
d. Find bifurcate ligament → this will show you the entry point to debride the
talonavicular (TNJ)
e. Spread with lamina spreader
f. Mobilizing the soft tissues is necessary for reducing the pes planovalgus
3. Calcaneal-Cuboid joint (C-C joint)
a. From the above incision, reflect down to the C-C joint
b. Distract with a Hohmann spreader
c. Reflect the soft tissues
4. Talonavicular joint
a. Find the bifurcate ligament and resect it
b. Resect the soft tissues of the TN joint
5. After all the soft tissues are released, the deformity can be corrected → minimally
resect the articular cartilage of the joints
a. Resect TN joint, then C-C joint, then the talocalcaneal joint
6. Dorsomedial incision
a. Incision is centered over TNJ and extends proximally up talar neck
b. Resect the soft tissues and then the cartilage
7. Fixation: Order TC → TN → CC
a. From talar neck aimed post-lat, a 6.5 mm partially threaded cancellous screw
i. Avoid placing the screw too far posteriorly into the talar neck because it will
cause ankle impingement
ii. Could also go from calcaneus into talus.
b. A 4.5 mm cortical screw is placed from the navicular to talus
i. Screw should measure less than 40 mm
c. C-C joint is fixated with a 4.5 mm cortical screw placed from calcaneus to cuboid
i. Screw should measure less than 40 mm


Calcaneal Slide Osteotomy
 Can slide medially for flatfoot, or laterally for ankle instability

 Procedure
o Patient set-up
 General or spinal
 Supine
 Thigh tourniquet
 Bump hip
1. Incision is1 cm posterior to fibula and 2 cm proximal to superior aspect of calcaneous
(behind peroneal tendons and anterior to Achilles tendon). Stay posterior to peroneal
tendons. Ends at junction of plantar and lateral skin at level of peroneal sulcus.
2. Sharp dissection down to bone, careful of peroneal tendons and sural nerve.
3. Bone cut: perpendicular to calcaneous. From the midpoint of tuberosity to 1 cm past
the plantar weight bearing portion of the calcaneous. ***Careful about cutting too far
medial because your nerves and arteries are over there.
a. Score your cut first
b. Get a wider, longer blade than usual.
c. May have to finish with osteotome.
4. Displace tuberosity:
a. If laterally so that midaxis of tibia is slightly medial to the midpoint of the
calcaneus. The lateral wall of calc should be just lateral to the lateral malleolus.
b. If medially, displace approx 1 cm.
c. Can displace with an osteotome or lamina spreader without teeth.
5. If needed, can use a Dwyer wedge for added valgus. A Dwyer wedge is generally 1 cm
6. Fixation: angled plate, one (or two) 6.0 or 7.0 partially threaded cannulated screws, or
two 4.0 partially threaded screws.
a. For the screws: insert just off the heel pad posteriorly (about 1.5 cm above
plantar surface). If sliding medially, insert screw just laterally. If sliding laterally,
insert just medially.
b. C-Arm for position.
7. Marcaine post-op block
8. Close.

 Post-op
o Posterior splint in OR, compression dressing
o Cast application after 1st visit for 5 weeks.
o Removable cast: ROM exercises until osteotomy site is healed.


Evans Calcaneal Osteotomy
 Mark out tendons and CC joint before surgery

 Procedure
o Patient set-up
 General or spinal
 Supine
 Thigh tourniquet
1. Get bone graft in saline and starting to reconstitute.
2. Incision is oblique over distal half of calcaneous (cut will be 1-1.5 cm from CCJ)
3. Dissect to bone. Careful of Intermediate Dorsal Cutaneous Nerve (Dorsal) Sural N
and Peroneal Tendons (Plantar)
4. Expose to osteotomy site 1-1.5 cm from CCJ
5. Free up EDB
6. Pass a probe thru the anterior and middle facets.
7. Make cut with sagital saw parallel to CCJ, aimed slightly distal to emerge in between
the anterior and middle facets. Don’t go too far medially or you may damage vital
soft tissues medially. Can use osteotome to finish the medial cut
8. Lamina spreader is put in place of the osteotomy site.
9. The osteotomy site is opened by loading the fifth met and putting foot in adduction.
Load until the hind foot valgus is corrected as well as the forefoot varus.
10. Insert bone graft. Bone graft is probably going to be twice as wide on the outside as
the medial side. Most likely the graft will be about 1cm in width at the widest side
(maximum). Don’t forget to keep the cortical sides with the other cortical sides.
11. Can fixate with staple, or screw. Screw is placed distal dorsal to proximal plantar.
a. Very often no fixation is used.

 Post-op
o NWB BK cast. For adults 6-8 weeks, for adolescents 5-6 weeks.


Peroneal Brevis Tendon Repair and Reconstruction
 Non-operative management—BK cast in neutral to slight inversion for 6 weeks.
o Associated with 30-40% rate of redislocation.

 Procedure
o Pt supine
o Sandbag under hip or lateral decubitous.
o General or spinal
o Thigh tourniquet
1. Incision-curvilinear, approx 5-7 cm behind the fibula, inline with the peroneal tendons.
Half of incision above malleolus, half below.
2. Full thickness flaps, identify superior peroneal retinaculum
3. Inspect peroneal tendons for subluxations, partial or complete tears and tenosynovitis
4. Retract PL anteriorly to visualize PB and often reveals a central split and subluxation
over posterior ridge of fibula
a. If PB tear is found and degenerative tissue is <50% of tendondebride
degenerative tissue. Then tubularize the remaining tissue using a running,
absorbable suture.
b. If peroneus tertius or low-lying muscle belly is presentexcise it.
c. If lateral ligament instabilityuse Brostrom or Chrisman-Snook
d. If PB tear is >50% then resect the whole tendon (not sure about this personally)
and attach to PL.
5. Inspect floor of peroneal groove. If too shallow make larger groove (pg 303)
6. Use rongeur to prepare fresh-bleeding fibular bed, then reattach the superior peroneal
retinaculum through drill holes in lateral ridge. Go from deep thru holes to dorsal.
Suture the rest of superior peroneal retinaculum with pants over vest style.

 Post-op
o NWB splint for 1 week
o BK walking cast for 4-6 weeks


Posterior Tibial Tendon Repair-Substitution
 Stages
o I: Normal length with tendonitis or peritendonitis
 Surgical options: Debridement or repair
o II: PT is elongated, but RF is still flexible
 Surgical options: FDL transfer
o III: PT is elongated, RF rigid
 Surgical options: Triple arthrodesis
 Tendon is usually worse than you thought
 Always try conservative first-rest, arch supports, PT, oral anti-inflamatories, immobilization
with cast or brace
 Steroid injections are contraindicated.

 Procedure
o Almost always done with an osseous procedure
1. Incision is 10 cm proximal to tip of tibial malleolus and 1 cm posterior down behind the
medial malleolus to the navicular tuberosity’s plantar portion. (Follows the TP tendon)
2. At the upper end of the incision, the deep fascia is incised and the TP is exposed.
a. The TP lies very close to the posterior margin. Trace the tendon distally to its
insertion while leaving a 2 cm pulley just posterior to medial malleolus at the
level of the tibial plafond.
3. Determine the length of the TP tendon.
a. If TP is normal length, it’s stage Ithen do tendon debridement,
tenosynovectomy and sheath resections are done and close wound
b. If tendon is elongated, it’s stage II and FDL transfer is needed.
4. For debridement of tendon:
a. If fraying—smooth edges leaving major portion of tendon intact
b. If bulbous enlargement just tip of medial malleolus-an ellipse is removed from
bulb and tendon is sutured burying the knot
c. If longitudinal split exists-clear inner side of tendon of scars and approximate
2. Tenosynovectomy—the outer portion of the tendon sheath distal to the pulley is
removed to prevent a possible reformation of stenotic tendon sheath
3. Inspect tendon for area of tear. Proximal to the region involved, the tendon will be
dull and white if the tear is old. Sometimes there is a transverse tear.
4. Transfer of the FDL: Detach FDL distal to the crossover area of FDL and FHL. Cut
the FDL under direct vision.
a. Optional: Suturing of distal end of FDL to FHL
5. Tag FDL with strong, non-absorbable suture in zigzag suture
6. Identify tuberosity of navicular and expose the inferior and superior surfaces of the
7. With 0.25 or 0.375 inch drill bit, a drill hole is done from superior to inferior. The drill
hole should come out inferior to the main surface of the PT
8. Leave FDL in its own sheath. Bring FDL into navicular drill hole from inferior to
superior. Pull through as tightly as possible with foot PF and supinated.


9. Suture the FDL with its non-absorbable suture into the capsule dorsally. Reinforce the
tendon by suturing the inferior portion of FDL (under navicular) into the TP tendon.
10. Assess the proximal TP muscle. Often the muscle will become fibrotic and stiff after a
TP dysfunction. Test the muscle by pulling on the proximal portion of the tendon.
a. If there is some elasticity (the muscle still has some function)—then do a side-to-
side suturing of FDL to TP with non-absorbable sutures, buried knot.
b. If the muscle is stiff—don’t suture the two muscles together.
11. Optional: Advancement of the spring ligament and the TN capsule
12. Alternative method: TP tendon repair with side-to-side suturing.
a. Limitations-cannot restore significant flatfoot deformity to normal alignment, but
it should relieve pain and improve function
b. Identify and resect the diseased section of the TP tendon. Suture tendon ends
together with non-absorbable suture
c. Then do a side-to-side repair with the FDL with non-absorbable suture.

 Post-op
o Without FDL transfer
 Jones compression cast with foot in PF and inversion for 1-2 days
 BK WB cast for 3 weeks
 Post op shoe and gradually move into shoe. May take months
o With FDL transfer
 Jones compression cast with foot in PF and inversion for 1-2 days
 NWB BK with foot in adduction and inversion for 3 wks.
 Remove sutures, NWB BK with foot in neutral for 3 more weeks
 Progress to WB as tolerated, PT


Tibialis Posterior Tendon Transfer (TPTT)
 Procedure
o Patient set-up
 Prone
 Thigh tourniquet
 General or spinal
o Four incisions
 One at TP insertion site on navicular
 One at middle distal 1/3 of leg, medial to tibial crest
 One at middle distal 1/3 of leg, 1 cm lateral to tibial crest
 One at lateral cuneiform-3rd metatarsal insertion site
1. First incision – at TP insertion on navicular
a. Release the TP from its insertion on navicular
2. Second incision – at middle distal 1/3 of leg medial to tibial crest
a. Pull TP up through this incision
3. Third incision – at middle distal 1/3 of leg 1 cm lateral to tibial crest
a. Separate TA from tibia
b. Expose interosseous membrane and make a window in it
c. Compress the posterior muscle mass. This will expose TP
4. Gently pull TP from medial incision through window in interosseous membrane with
blunt curved Kelly forceps and moist sponges
a. Be careful of NV bundle which lies under TP
b. Often there are muscle fibers attached distally from the window → gently pull
them free
5. Fourth incision – over lateral cuneiform or 3rd metatarsal
a. Insert tendon passer, Bozeman forceps or uterine packing forceps into insertion
site incision and retrograde up extensor sheath. Grab TP and retrograde.
b. Fixate TP to lateral cuneiform with foot in neutral position


Split Tibialis Anterior Tendon Transfer (STATT)/
Tibialis Anterior Tendon Transfer (TATT)
 Procedure
o Patient set-up
 Prone
 Thigh tourniquet
 General or spinal
1. Three incisions
a. One over TA insertion of medial cuneiform-1st metatarsal
b. One over anterior surface of leg just proximal to transverse cruciate ligament
c. One over peroneus tertius insertion
i. If the peroneus tertius is not present, the tendon can be inserted to cuboid or
sutured to the PB
2. Split the tendon with umbilical tape with a tendon passer in leg incision through to TA
3. Cut the lateral ½ of the TA tendon and retrograde that through to the proximal
4. Insert to peroneus tertius tendon

 Procedure
o Patient set-up same
o Note: Usually with TATT, the 3rd incision is over the lateral cuneif-3rd metatarsal and
the TA is transferred to this bone. However, it is possible to transfer the TA all the way
to the peroneus tertius sheath.
1. Three incisions
a. One over TA insertion of medial cuneiform-1st metatarsal
b. One over anterior surface of leg just proximal to transverse cruciate ligament.
c. One over lateral cuneiform
2. Tendon is separated from its insertion
3. Tendon is drawn up through insertion onto leg incision
4. With a tendon passer, bring tendon up through peroneus tertius sheath (same as the
EDL tendon sheath)
a. Be sure to be under extensor retinaculum
5. Insert TA into lateral cuneiform via hole and button


Note: These sections on Ankle Fractures are based on my notes from my personal experiences,
the texts I have previously referenced and from my lectures from the AO course in Davos,
Switzerland. The first thing they stated at the AO Course in Fracture Management was that they
used the Weber Classification and not the Lauge-Hansen system because the Lauge-Hansen was
too complicated. Therefore, the surgical choices are broken down by the Weber Classification.
However, you still want to learn the Lauge-Hansen system because that is what you will most
likely be quizzed/tested.


Weber A Surgical Procedures

 Screw Placement
o Patient set-up
 Supine with bump under hip
 Thigh tourniquet
 General or spinal
1. Small incision at tip of lateral malleolus
a. Expose tip of malleolus by splitting calcaneofibular ligament longitudinally
b. Avoid tilting lateral malleolus toward the talus
2. Insertion point for medullary fixation is at lateral surface of malleolar tip
a. 4.0 cancellous screw (or malleolar screw) is inserted across fracture into the
proximal medial cortex of fibula above the fracture site
b. Insertion of a long screw (4.0 mm) across the fracture line into the medullary
canal of the proximal fragment
3. Avoid rotation or displacement of distal fragment as screw is inserted
a. K-wire can be added as temporary fixation
b. Note: Since the medullary device (screw) is straight, the lateral malleolus may be
inadvertently tilted toward the talus – this will result in narrowing of ankle
mortise and reduced motion
4. Close

 Tension Band Wiring

o Patient set-up
 Supine with bump under hip
 Thigh tourniquet
 General or spinal
1. Skin incision vertical and parallel to long axis of tibia directly over lateral malleolus
a. Note: A straight incision is often used because it can be extended. Try to avoid J-
shaped incision because they cannot be extended.
2. Dissect sharply down to bone
a. If undermining is necessary, do it just over periosteum


3. With a periosteal elevator or #15 blade, elevate the periosteum 2-3 mm proximal and
distal to the fracture line
a. Remember, be good to the soft tissues
4. Curette and irrigate fracture fragments to remove all hematoma
5. Inspect joint
6. Reduce fracture with towel clip on fracture fragment and guide it with periosteal
7. Insert two 0.045 or 0.062 K-wires. Insert from dist → prox from tip of lateral
malleolus across the fracture line, up the diaphysis of the fibula.
a. Insert at right angles to the fracture (this is pretty vertical)
b. Be careful not to violate the joint
8. 20-gauge wire is then passed through a transverse drill hole above fracture site and
placed in a figure-8 fashion around bent tips of protruding K-wires. The fragment
should be well-aligned and held securely in place with the wires.
a. Twist the 20-gauge wire and trim the excess wire off and make sure the twisted
tips lie flat against the bone
b. Note: Instead of a transverse drill hole above the fracture site, a screw may be
placed at the same level above the fracture line with a washer and tightened down
after the figure-8 of wire is wrapped around it.
9. Close


Weber B Surgical Choices
 Fixation Options
o 2 lag screws
o Posterior anti-glide plate
o Lateral plate with lag screw
 Weber B Ankle Fracture Characteristics
o Fracture at the joint line
o Corresponds with PAB or SER
 Lateral Malleolus Anatomy
o PB and PL posterior to fibula
o Superficial Peroneal Nerve anterior/medial to fibula
o Sural Nerve and Short Saphenous Vein is posterior and plantar to fibula
o FHL is posterior and mainly muscular at this level
o Proximally incision is between peroneus tertius (anteriorly) and PL and PB (posteriorly)
o Generally safe with an incision centered over fibular fracture site

 Fixation With 2 Lag Screws

o Indications to use 2 Lag Screws
 If fibular fracture is spiral (2x diameter of bone) + not comminuted + not
osteoporotic → then sufficient fixation can be achieved with only 2 lag screws
o Advantages
 Allows for a smaller incision
 Hardware is not prominent and usually does not have to be removed
 Will not interfere with syndesmotic screws (if they are needed)

o Procedure
1. Incision is made slightly anterior to midline of fibula
a. Incision is down to bone without too much layered dissection
2. Irrigate and clean up wound edges
3. Restore fibular length
a. Hold with reduction clamps
b. Check with C-arm
4. Insert two 3.5 screws (or 2.7 if small pt) from ant → post using AO lag
a. C-arm to confirm position
5. Close

 Lateral Plate and Anterior-to-Post Lag Screw

o Most common surgical approach for Weber B fibular fracture
o Ideally, you want to cross 5 cortices of fixation proximally and distally. If using a
buttress plate, only unicortical screws are used and most likely only 3 cortices will be
fixated distally.


o Procedure
 Patient set-up
 Supine with lateral bean bag/bump
 Thigh tourniquet
 General or spinal
1. Incision directly over fibular fracture site. May make incision slightly anterior to
midline. (If posterior malleolus fracture is present, then make it posterior.)
a. Do not do too much dissection. Make incision down to periosteum
preserving soft tissues. Any undermining should be done at the periosteum
2. Elevate periosteum 2-3 mm from the fracture line. The full anterior and
posterior portions of the fracture line must be exposed.
3. Curette and irrigate fracture fragments and hematoma
4. Explore talus for any osteochondral defects
5. Reposition fracture (increase deformity, distract, reposition) using towel clip and
periosteal elevator to assist
6. Hold fracture in anatomical position with bone clamps
7. Reassess anatomical position
a. Can use bone clamps, lobster claw, or K-wire across fracture to stabilize it
b. Note: Keep in mind the next step with the lag screw, your clamp will most
likely be in the way, so position it thoughtfully!
c. Can use posterior spike of fracture as guide for adequate reduction
d. C-arm for verification of position
8. Insert lag screw (3.5 mm cortical) ant → post, as perpendicular as possible
across the main fracture line
a. Screws must engage posterior cortex, but should not extend so far as to
disrupt the peroneal tendon sheath
9. Apply ⅓ semi-tubular plate laterally
a. Bend plate to appropriately contour of fibula
b. Plate size is based on the number of screws around fracture site and
position on fibula
i. 3 proximally (3.5mm cortical screws)
ii. 2-3 distally 4.0 cancellous screws
iii. Run distal screws short so to avoid violating fibular-talar joint
10. C-arm to check position
11. Close

 Posterior Antiglide Plate

o Advantages
 Achieves strong fixation even in osteoporotic bone
 Hardware generally does not cause symptoms or wound necrosis (or at least less
than a straight lateral plate would)
 Does not interfere with syndesmotic screw insertion
 Distal screws obtain better purchase, because they engage a thicker part of distal


 Engage 2 cortices without risk of joint penetration (essentially no risk of intra-
articular screw insertion because of plate placement)
 Biomechanically, this construct is stronger than lateral plate fixation, especially in
osteoporotic bone (i.e. good in elderly!)
 Loss of fixation is rare due to the stability of the construct
 Posterior plate provides better fixation with posterior comminution
 Posterior incision allows access to the posterior malleolus, when direct fixation is
o Disadvantages
 Technically more challenging
 May irritate peroneal tendons in minority of patients, but this often spontaneously
resolves in 4-8 weeks
 Peroneal tendon subluxation
 Should not be a problem is the tendon sheath is left intact

o Procedure
 Patient set-up
 Supine with lateral bean bag/bump
 Thigh tourniquet
 General or spinal
1. Incision is made along the most posterior border of the fibula at fracture level
a. The plate often lies slightly posterolaterally (rather than directly post), thus
the incision will be away from the plate
b. Incision is carried down to peroneals, but does not violate the peroneal
c. Incision proceeds over the lateral edge of peroneals which are usually
retracted posteriorly
2. Some of proximal retinaculum may need to be released to expose distal fibula
a. Clear periosteum off fibula
3. Fracture reduction – Ideally, anatomic reduction should be achieved prior to
plate application
a. Reduction can be held with a single K-wire or lag screw
b. Apply lag screw from ant → post so not interfere with plate application
4. Plate application – ⅓ tubular plate is applied to posterior surface of the fibula
a. 4-hole plate – Classically
b. 6-hole plate – More recently
c. Because posterior surface of fibula is straight, contouring of the plate is
usually not necessary
d. Due to the lateral bow of fibula, the plate sits best posterolaterally
5. Proximal screw insertion
a. 1st 3.5 mm cortical screw is placed proximally, through the plate, 2 mm
above posterior fracture line
b. Plate helps prevent proximal gliding of the distal fragment
c. If anatomic reduction is achieved, the proximal screw can be tightened


d. If anatomic reduction has not been achieved, then do not fully tighten the
screw yet
i. Apply bone clamps to both fracture fragments and distract out to
ii. Apply slight internal rotation to distal fragment
iii. Proximal screw is now tightened, and fragment should be properly
6. Remaining proximal 3.5 mm cortical screws are inserted
7. Lag screw insertion
a. Lag screw is then inserted post → ant through the first plate hole which is
distal to the posterior fracture line
i. Because the posterior cortex is thin, lag screw must be inserted
through plate (which serves as solid posterior cortex)
b. The screw must be angled slightly proximally in order to be perpendicular to
the fracture site
i. Remember to remove initial lag screw (inserted ant → post) if used
c. Note: Lag screws improve fracture reduction but do not significantly improve
anti-glide strength
d. Okay to leave screw slightly long because screw is directed away from the
peroneal tendons
e. If possible, a 2nd lag screw can be inserted using the same technique
8. Optional – Insert distal screws: Technically the more distal screws are not
necessary, but 4.0 mm cancellous screws may be inserted. Because there is no
risk of joint penetration, longer screws can be used to get a better hold on bone.
9. Close


Medial Malleolar Fractures
 Fixation Options
o 2 Lag Screws
o Medial Plate
o Tension Band Wiring
 Patient set-up for all types
o Supine
o General or spinal
o Thigh tourniquet

 Two Lag Screw Procedures

o Two methods
 Two Screw Fixation either open or percutaneous (a.k.a. two stab incision)
 Lag Screws: True lag screws are used to counteract and neutralize a tension
failure on the medial side
 Brett Chicko Note: I prefer to do an open procedure over a stab incision because
with a fracture of the medial malleolus, there usually is some soft tissue in-
between the fracture fragments

 Two Stab Incision Procedure (Percutaneous)

o Most common procedure for medial malleolus fracture
1. Two stab incisions at tip of medial malleolus
2. Blunt dissect (with hemostat)
3. K-wire from distal tip across fracture line at right angles into proximal section
a. Aim somewhat vertically to avoid the ankle joint
b. C-Arm to check position
4. Insert two 4.0 mm cancellous partially-threaded cannulated screws
a. C-Arm to check position
5. Close

 Open Procedures (Screw/Plate or Tension Band)

o Indications
 For plate insertion
 For two screw insertion with better visualization
 Comminuted fractures
 Difficulty in reduction with percutaneous method

o For Screw Fixation or Plate Insertion

1. Incision – vertical and parallel to with long axis of tibia directly over medial
a. A straight incision is often used because it can be extended. Try to avoid J-
shaped incision because they cannot be extended.
2. Dissection sharply down to bone. If undermining is necessary, do it just over
the periosteum.


3. With a periosteal elevator or #15 blade, elevate the periosteum 2-3 mm from the
fracture lines
a. Remember to be good to the soft tissues!
4. Curette and irrigate fracture fragments to remove all hematoma
5. Inspect joint
6. Reduce fracture with towel clip and guide it with periosteal elevator
7. Stabilize with 2 K-wires
a. Insert from distal → proximal from tip of malleolus across the fracture
b. Insert at right angles to the fracture (this is pretty vertical) with care not to
violate the joint
8. Insert two 4.0 mm cancellous bone screws
a. Cannulated screws may be used
b. If not cannulated, remove K-wire and insert screw in K-wire hole
9. If using a plate, insert with 3.5 mm cancellous screws. Run the proximal screws
short so they don’t violate the ankle joint.
a. Other options: ⅓ semi-tubular, DCP, T, Clover Leaf
b. Note: For a "push off" (shear) fracture, the purpose of the plate is to provide
an anti-glide or a buttressing effect
10. Close

o Tension Band Wiring

 This can be used for the very small medial malleolar fragments or comminuted
 Studies differ onto effectiveness of tension band
 Tension bands are rarely used now for medial malleolus
 If you always place two screws, you are going to comminute a few medial
malleoli and you’ll to be very unhappy. Then you will need this tension band
technique for salvage.
 Also, pts hate these wires. Anytime you do a tension band wire and leave a wire
long (in an area where there is movement) patients will hate you a lot.
1. Incision – vertical and parallel to with long axis of tibia directly over medial
a. A straight incision is often used because it can be extended. Try to avoid J-
shaped incision because they cannot be extended.
2. Dissect sharply down to bone. If undermining is necessary, do it just over the
3. With a periosteal elevator or 15 blade, elevate the periosteum 2-3 mm from the
fracture lines
a. Remember to be good to the soft tissues!
4. Curette and irrigate fracture fragments to remove all hematoma
5. Inspect joint
6. Reduce fracture with towel clip on fracture fragment and guide it in with
periosteal elevator
7. Two parallel K-wires (0.045 inch or 0.062) are inserted at distal end of fibula
and engage the proximal medial cortex above fracture site


8. 20-gauge wire is then passed through transverse drill hole (or a cortical screw
may be placed instead at this level, which you would wrap the wire around and
tighten the screw down after the wrapping) above fracture site and placed in a
figure-8 fashion around bent tips of protruding K-wires
a. Twist end of wire and trim. Make sure to bend it so it sits close to bone.
9. Let the first year close


Posterior Malleolar Fracture
 When to do an ORIF?
o When > 25% of posterior articular surface is involved as seen on lateral view
o Fracture is displaced >2 mm
o There is posterior subluxation of talus
o If fracture prevents reduction of tibia

 Procedure
o Patient set-up
 Use a posterior lateral approach (similar to the one used for a fibular antiglide
 Lateral or prone
 General or spinal
 Thigh tourniquet
1. Incision is at posterior border of fibula, if fibula needs to be reduced, do that first
a. Hold with temporary fixation
b. Brett Chicko Note: According to Coughlin – Do the definitive fixation of fibula
after the post malleolus because of lack of exposure after fibula is fixated.
However, I have seen the fibula fixated first and then the post malleolus was
2. Bluntly dissect between the PB/PL and the FHL (muscular at this level) to the
posterior surface of the tibia. Must get exposure of entire fracture fragment.
3. Reduce fracture
a. The fracture reduction is determined by palpation and visualization of extra-
articular fracture line and C-arm. Cannot directly visualize the intra-articular joint
because talus is in the way.
b. Note: Reduction of fibular fracture most likely will reduce the posterior malleolus
because of firm attachment of post tibiofibular ligament. Ligamentotaxis!
c. If difficulty reducing fracture, DF foot may give slack to ligaments and posterior
4. Hold reduction with large reduction clamp
5. Insert 2 K-wires to the fragment in place (for 4.0 mm partially threaded cancellous lag
cannulated screws)
6. Insert screws post → ant
a. Insert at right angles to the fracture
7. Alternate fixation: Stab incision anteriorly, insert 4.0mm cortical screw ant → post
a. Check C-arm for position
8. Let the 1st year close

 Post-op
o NWB until union is solid. This may take up until 3-4 months.


Syndesmotic Repair
 After every ankle fracture repair, evaluate the syndesmosis with intra-op stress exam
 Syndesmotic separations are unstable and should be stabilized
 Remember the AO principle of stable fixation if non-articular
 Indications for Syndesmotic Fixation
o Irreparable medial joint injury w/ disruption of syndesmosis
o High fibular (Weber C) fracture >15 cm above the joint line
o Medial ligament injury, syndesmotic disruption, talar shift w/o fracture of fibula
o Widening of the tibiofibular "clear space" as a result of disruption of the syndesmosis.
The clear space is normally < 5 mm wide.
 Injury Patterns
o Isolated
o Syndesmotic injury with fibular fracture
o Syndesmotic injury with medial injury
 Choices of Syndesmotic Screws
o 4.5 mm screw (most common) x2 or 3.5 mm screws in smaller patients
o Bioabsorbable fixation (polylevolactic acid)
o Fiberwire (Tightrope or others like this…technique as per manufacture’s guidelines)
 Proper level for a Syndesmotic Screw
o Screws should be parallel to joint line
o 1 cm prox to syndesmosis or 4 cm prox to ankle joint
o If too low, can pass through distal tib-fib articulation causing pain
o If too high, may cause tip of fibula to go outward

 Procedure
o Patient set-up
 Prone with hip bump
 General or spinal
 Thigh tourniquet
1. Stabilize the fibular fracture before the syndesmosis
a. Use a plate on the fibula
b. Fibula should be reduced posteriorly into the tibial sulcus
c. The syndesmosis should be reduced before the screw(s) are inserted
2. Dorsiflex foot 5°
3. Stab incision on fibula
a. Use C-arm to find correct level: 1cm proximal to syndesmosis and/or 4 cm prox
to ankle joint
4. Insertion of screw (4.5 mm cortical fully-threaded)
a. Because fibula is posterior to tibia, aim screw through posterior-lateral fibula
to anterior-medial tibia at an angle of 25-30° anteriorly
b. Perpendicular to long axis of bones, parallel to the ankle joint
c. Engage 3 cortices or 4 (depending on doctor preference)
d. Do not lag! Do not over-tighten!


 Post-op
o Screws generally will not loosen or break if the ankle does not dorsiflex past neutral
o Patients are allowed to WB after 6 weeks in a short leg cast or walking boot
o Routine removal of screw 8-12 weeks after surgery


ORIF Calcaneus
 Indications
o Injuries that would do poorly without surgery, such as severely displaced intraarticular,
widening of heel, horizontally oriented talus, severe soft tissue injury, and high-energy
 Contraindications
o Severely comminuted
o Impaired vascularity
o Infection
o Severe neuropathy
 Essex-Lopresti Classification
o Primary fracture line runs from ant-lat → post-med through the STJ (mostly through
the posterior facet). As the primary fracture line progresses, this will lead to lateral
wall blowout and decrease in calcaneal height.
o Both Essex-Lopresti types start with the primary fracture line
o Type 1 – vertical force will lead to tongue type
o Type 2 – more horizontal force will lead to joint depression

 Procedure
o Patient set-up
 Lateral decubitus position
 General or spinal
 Thigh tourniquet
o General order of reduction
 Anterior process
 Medial wall
 Posterior facet
 Lateral wall
1. Incision is curved behind the lateral malleolus. The proximal portion is halfway
between the anterior portion of the Achilles and the peroneal tendons. The line
progresses distally, around the lateral malleolus, and then runs parallel to the bottom of
the foot, ending up roughly at the C-C joint.
a. Watch out for sural nerve and peroneal tendons
2. Sharply dissect down to bone, create a flap with the CFL and the peroneals and flap that
3. Insert two 0.062 K-wires into the talus and bend K-wires upward to hold this flap up
4. Expose STJ, remove hematoma and small fracture fragments via irrigation and rongeur
5. Identify the fracture lines in the anterior calcaneus that extend medially
a. Determine if the fracture line progresses to the C-C joint
6. The anterior process is typically elevated. Therefore, the anterior process needs to be
retracted plantarly. Use a retractor or lamina spreader between the talus and the
anterior process. Fix with K-wire.
7. Identify the fracture line progressing from ant-lat → post-med (the primary fracture
lines), separating the posterior facets from the anterior and middle facets


8. The posterior facet is usually PF. With the use of a periosteal elevator, lift up the
posterior facet. Hold with K-wire directed from the anterior process laterally to the
posterior facet medially.
a. The lateral part of the posterior facet is retracted laterally or removed. This allows
visualization of the medial posterior facet
9. A 4.0 Shantz pin is inserted into the tuberosity fragment from post → ant (from the
back of the heel into the posterior tuberosity). This is used as a lever to reduce the
fragment plantarly, medially, and into slight valgus.
10. When the medial wall of the tuberosity lines up with the medial wall of the facet
fragment, it is held with two 0.062 K-wires. The K-wires are inserted from the
posterior aspect of the tuberosity and directed to the sustentaculum tali (be careful not
to damage articular cartilage). Use C-arm for this.
11. After the anterior process and the medial wall are reduced, the posterior facet is
reduced. Match the lateral fragment to the medial fragment. Insert 0.062 K-wires
into the anterior and posterior margins.
12. Get intra-op X-rays. If alignment is good, insert a 2.7 mm cortical lag screw below the
subchondral surface.
a. Reconstruct the lateral wall if necessary. Bend and insert plate.
b. Best bone for a plate is subchondral bone deep to the C-C joint, the subchondral
bone near Achilles tendon insertion, and the dense bone of the sustentaculum tali
c. May need to fill in deficit with bone chips, Grafton or other bone substitute
13. Insert drain and close

 Post-op
o Course depends on the amount of damage
o If minimal displacement, 6-8 weeks ROM exercises and NWB
o If severe displacement, >12 weeks ROM exercises and NWB

 Complications
o Relatively common
o Infection
o Delayed wound healing
o Sural nerve
o Tibial nerve problems (more likely from injury rather than surgery)


ORIF Talar Neck Fractures
 ORIF should be done even if Hawkins type II was close reduced because this type of fracture
will inevitably develop an equinus contracture that happens with prolonged casting in PF

 Talar neck fracture WITHOUT dislocation

o Procedure
 Patient set-up
 Supine with bump under ipsilateral hip
 Have C-arm ready
1. Anterior-medial incision – made from anterior aspect of the medial malleolus to
the dorsal aspect of the navicular tuberosity
a. Dissect carefully down, go dorsal to TP tendon. Don’t disrupt deltoid
ligament because this might disrupt some of the vasculature to the talus.
2. Remove hematoma. Don’t dissect the soft tissues off the talus dorsally and
plantarly because this might disrupt the blood supply to the talar neck.
3. Anterior-lateral incision – starting from anterior margin of lateral malleolus to the
base of the 3rd or 4th metatarsals
a. This allows confirmation of the reduction of the talar neck
b. It also permits removal of foreign bodies
4. Incise inferior retinaculum
5. Retract EDL and peroneus tertius. Retract EDB dorsally.
6. Remove all fragments. Probe STJ blindly for fragments.
7. Reduce the fracture
a. Careful not to have comminution or reduce into varus position.
8. Insert two 2.5mm titanium screws (can be used with MRI). Do not lag! A lag
screw might send talus into varus.

 Talar neck fracture is displaced (as in Hawkin’s Type III – STJ and Ankle joint)
o Procedure
1. Anterior-medial incision – extend the incision over the medial malleolus and the
distal aspect of the tibia
2. Go into the space between tibia and Achilles. The body of the talus will be
3. A femoral distractor may be needed. Put pins in the tibia and calcaneus.
4. Manually place the body of the talus back into mortise
a. If the talus will not return to the mortise, a medial malleolar osteotomy
will have to be done
i. For medial malleolar osteotomy
1. Identify the ankle joint for tibia
2. Make 2 retrograde 2.5 mm drill holes in the medial malleolus
across the osteotomy site
3. Release the anterior portion of the capsule off the deltoid
ligament as well as a portion of the TP sheath. Protect the TP
4. Incise the periosteum about 5-10 mm superior to the ankle joint


5. With oscillating saw, cut the transverse portion, then the 2
vertical portions
6. Reflect the medial malleolus distally. Don’t damage the deltoid
7. Manually place the talus back into its place
5. Anterior-lateral incision – as above
a. Fix medial malleolus with two 4.0 mm cancellous titanium screws

 Post-op
o Post-splint or boot
o Do not do ROM exercises until wound healing is done
o NWB for 8-12 weeks until trabeculae cross the fracture

 Complications
o Arthrofibrosis
o Malunion, nonunion
o Skin necrosis


Tibial Periarticular Fx Reduction & Fixation
 Indications
o Pilon or Tibial Plafond fractures
o Articular displacement of >2mm or unacceptable axial alignment
o Open fractures
o Neurovascular injury due to fracture
 Pre-op planning
o Check NV, compartment syndrome, soft tissue injury
o Radiographs: AP, Lat, MO
o Whole tibial shaft
o Foot radiographs
o CT can be useful

 Procedure
o Staged surgery—First part immediate once the patient has stabilized (usually 12-18
hours) with ORIF of fibula and external fixator for tibia. Kitaoka recommends EBI or
o 1st Stage
1. Fibular incision-slightly posterior-laterally to increase the width of the skin bridge
with the later anterior incisions.
2. Do not do calcaneal skeletal traction- (even with a Bohler-Braun frame) this
pulls patient out of bed and displaces foot posteriorly
3. Fix Fibula fracture
4. Apply Ex-Fix onto tibia
5. When the soft tissue edema has subsided (usually 10-21 days), ORIF can be
o 2nd Stage
 Patient set-up
 Pt supine
 General or spinal
 Thigh tourniquet
 Take frame off tibia but don’t remove the pins. Have circulator sterilize the frame.
This may be used later in the case for distraction.
 Anterior-medial incision
1. Locate the fracture fragment. If the fragment is anterior-medial: incision
begins just lateral to the medial crest of tibial shaft. Extend the incision
distally across the ankle joint, staying just medial to tibialis anterior
2. Identify the anterior tibia tendon sheath. Once identified, create a full
thickness flap by incision the tendon sheath and the extensor retinaculum.
Bring this incision down to bone/joint down to the periosteum. Do not strip
the periosteum or remove any fat unnecessarily
3. Identify fracture ends, debride and irrigate. Remove all clots
4. Reduce the fracture. This incision works well with a medial pilon plate


 Anterior Midline Incision
 Use this incision when the fracture is a pure anterior crush injury. This
injury gives good exposure and will allow for easy placement of low profile
anterior tibial plate
1. Incision is made between the TA and the EDL
a. Identify the superficial peroneal nerve, the artery and the deep
peroneal nerve. Retract all of this laterally
 Anterior-Lateral Incision
 Use this with large lateral fragments, such as the Tillaux-Chaput avulsions.
Careful with this incision because it may jeopardize the skin from the fibular
 This is why you usually use a posterior lateral incision for the fibula.
1. Incision starts proximal to the ankle joint and slightly medial to Chaput’s
tubercle and extends distally in a strait line toward the base of the 3rd and 4th
a. Superficial peroneal nerve is protected
2. Incise through the superior and inferior extensor retinaculum
3. Mobilize the peroneus tertius and EDL, the deep peroneal nerve and the
anterior tibial/DP artery
4. Distally the EDB is seen and can be retracted laterally or detached
5. Protect the lateral branch of deep peroneal nerve and the lateral tarsal artery
 Fixation
o Fix the jigsaw puzzle, then use reduction clamps followed by 1.6 mm k-wire
o Canulated screws are rarely used
o If a piece is small, a bioabsorbable pin can be used
o Once the screws are in place, a cancellous graft can be used
o Apply plate. Options are:
 Medial pilon plates for rotational and varus valgus injuries
 Anterior pilon plate for anterior crush plates. Note Dr Lutz states to always use an
anterior plate.
 Supplemental washer plates may be needed. Ex: spider washer plate
 Closure
o Small drain, close etc.

 Post-op
o Jones compression dressing and splint
o At 1 week change to compression stocking and removable boot and start ROM.
o Pt is to wear the boot at all times, even sleeping or the patient may develop equinus
o Start formal PT about 4-6 weeks, only after the wounds have healed
o WB at 3 months if radiographic evidence of healing
o Outcome is based on the fracture at presentation


 Technical Pearls
o Joint surface should be reconstituted first because anatomical malalignment is not
acceptable. The ankle will accept some axial malalignment, but not articular.
o Shaft reconstruction is performed second
o Reconstruct the joint with isolated lag screws followed by neutralization plate of the
metaphyseal-diaphyseal component
o Joint surface needs to be anatomic reconstructed. If there are centrally depressed pieces,
the perimeter fragments need to be retracted and the central ones need to be elevated
 Technical Pitfalls
o Doing definitive surgery too soon because fracture patterns are not clear with all of the
soft tissue swelling
o Unstable EX-FIX
o Failure to stabilize the fibula
 Complications
o Infection
o Wound complications
o Malunions
o Post-traumatic complications at 1-2 years


Ankle Arthroscopy
 Portals
o Most commonly used – Ant-med, ant-lat, and post-lat
o Anterior-medial port
 Medial to TA
 Lateral to saphenous vein and nerve
o Anterior-lateral port
 Lateral to Peroneus Tertius
 Medial to intermediate dorsal cutaneous nerve
o Posterior-lateral port
 Lateral to Achilles tendon, 1-2 cm distal to anterior ports
o Anterior-central port
 Just lateral to FHL
 Medial to DP and deep peroneal nerve, medial dorsal cutaneous nerve crosses
over FDL at this level and may be lateral
 Due to all of the potential complications, this port is usually contraindicated
o Posterior-medial port
 Medial to Achilles tendon
 Also in this area: FHL, FDL, posterior tibial nerve and artery, calcaneal artery
 Due to all of the potential complications, this port is usually contraindicated
o Posterior-central port
 A.k.a. ―trans-Achilles‖ because it is through the Achilles
 This is usually contraindicated…

 Procedure
 Insertion of scope
1. Mark anatomic landmarks (medial and lateral malleolus, superficial peroneal nerve, TA
and peroneus tertius, if this is not present use EDL)
2. Use 2.7 or 4.5 scope
 For Anterior-medial and Anterior-lateral ports
3. Find the ankle joint, insert 18-gauge needle into joint. Fill the joint with 20 cc of NSS
or Lactated Ringers
4. Incise the skin only, use blunt dissection down to the capsule
5. Insert cannula and blunt obturator. Insert scope.
6. With direct vision of scope, insert 18-gauge needle into lateral port, find the needle
with the scope (―Triangulate‖ your position!). Be careful of the superficial peroneal
7. Incise the skin over the 2nd port hole, blunt dissect and use obturator to complete the
 For Posterior-lateral port
8. Go lateral to Achilles tendon approx 1-2 cm distal to anterior port levels (this will be
just distal to posterior syndesmotic ligament)
9. Cannula is used for dedicated inflow


 Joint examination
10. Look for anterior joint synovitis and shave with 2.9 or 3.5 shaver
11. Always remember to do a good irrigation, often times this may be all that is needed
 Anterior ankle exostosis approach
12. Reflect the capsule by putting the shaver against the osteophyte and lifting the capsule
off of it
13. Use a 4 mm burr from the ant-lat port while viewing from ant-med port. You may
also use a rongeur or osteotome.
14. Switch portals and do lateral portion
15. C-arm or intra-op radiographs may also be used
 Anterior medial exostosis approach at tip of medial malleolus
16. Make secondary port approx 1-2 cm medially and slightly distal to ant-medial port
17. Be sure to suture close all ports used


 Procedure
o Patient set-up
 General or spinal
 Thigh tourniquet
 Pt heel is resting over edge of bed
1. Incision over sinus tarsi
2. Blunt dissect to sinus tarsi
3. Insert guide pin so it abuts the anterior aspect of the body of talus. Advance pin until it
tents the skin medially. Can C arm here, or at any step.
a. Axis: distal lateralprox medial. Proper insertion of probe should cause the distal
aspect of the probe to exit just superior to the tibialis post tendon and anterior and
slightly inferior to medial malleolus—this is the direction you’re aiming
1. The torpedo shaped probe is inserted until it tents the skin. Make incision.
4. Rotate probe clockwise and counterclockwise to dilate the tarsal canal.
5. The guide pin is then placed within sinus tarsi.
6. Most often the 8 and 10 mm implants will be used. Use the sizers, the correct size
should allow 2-4° of subtalar eversion.
7. Next, use the trial implant of the above size. Check ROM, and clinical correction are
assessed. Use C-arm at this point.
8. Now use actual implant on screw driver with nose cone. Apply over guide pin. Screw
in clockwise. Insert no more than 1 cm medial to calcaneal wall and no more than ½
way across talus
9. Once inserted, the implant should be resting on floor of sinus tarsi. Take x-ray
10. When satisfied, remove guide pin and inserter. Irrigate with NSS. Re-valuate motion,
close in layers.

 Post-op
o WB in cast for 2 weeks, gradual return to shoe gear.


Arthrosurface 1st Metatarsal Head Implant
 Indications
o Hallux limitus/rigidus + Good bone stock!
o Also a good procedure if arthrodesis is not an option
 Contraindications
o Significant bone demineralization or inadequate bone stock
o Inadequate skin, musculotendinus or NV system status
o Inflammatory, rheumatoid arthritis, sepsis, infection and osteomyelitis
o Pts known to have sensitivity to metal alloys typically used in prosthetic devices

 Simple Technique Guide Steps

o Step 1 – Drill Guides, match with Articular Component
o Step 2 – Cannulated Pin, Drills
o Step 3 – Tap
o Step 4 – Driver
o Step 5 – Tap Cleaner
o Step 6 – Trial Cap
o Step 7 – Centering Shaft
o Step 8 – Contact Probes
o Step 9 – Circle Cutter and Surface Reamer
o Step 10 – Sizing Trial
o Step 11 – Implant Holder, insert Articular Component and Impactor
o Size is usually 15

 Procedure
1. Dissect down and expose 1st metatarsal head (similar to an exposure for a bunion)
2. Use Drill Guide to locate the axis normal to the articular surface and central to the
a. Be sure to choose a Drill Guide where the diameter circumscribes the defect
3. Confirm Articular Component diameter by matching it to the Drill Guide
4. Place Guide Pin through the Drill Guide into bone
a. Make sure its central to defect
b. It is very important to verify that Drill Guide is seated on the curved articular
surface such that four points of contact are established. A normal axis and
correct Articular Component diameter are necessary for proper implant fit.
5. Place Cannulated Drill over Guide Pin and Drill until the proximal shoulder of drill is
flush to the articular surface
6. Tap hole to etched depth mark on tap
a. Optional – insert bone cement into pilot hole
7. Place Driver onto the Taper Post over the guide pin and advance until the line on the
Driver is flush with the height of the original articular cartilage level
a. Optional – advance the Driver further to decompress the joint
8. Remove guide pin
9. Clean taper in Taper Post with Taper Cleaner


10. Place Trial Cap into taper post to confirm correct depth of Taper Post
a. The peak height of the trial cap must be flush or slightly below the existing
articular cartilage surface to avoid the articular component from being place
above the surface of the defect
i. Adjust depth using the driver to rotate the taper post (clockwise to
11. Place Centering Shaft into Taper Post
12. Place Contact Probe over Centering Shaft and rotate around Centering Shaft. Read
contact probe to obtain offsets at four indexing points.
a. Superior/inferior and medial/lateral
b. Select appropriate Articular Component using Sizing Card
13. Remove Centering Shaft and replace with Guide Pin. Advance Circle Cutter back
and forth.
a. Don’t bend guide pin
b. Score articular cartilage down to subchondral bone
14. Choose appropriate Surface Reamer based on the offsets. Drill Surface Reamer over
Guide Pin until it contacts the top surface of Taper Post.
a. Begin rotation of Surface Reamer prior to contacting bone to avoid chipping
articular rim
15. Remove Guide Pin and clean Taper Post to remove any debris from implant bed
16. Place the Sizing Trial into the defect that matches the offset profile selected
a. Confirm that the Sizing Trial is equal or slightly recessed to edge of articular
b. If the Sizing Trial is proud at the edge of articular cartilage, ream with the next
appropriate sized reamer and matching Sizing Trial
17. Use the Implant Holder (attached to suction wall tubing) and align the Articular
Component on the holder with appropriate offsets
18. Insert implant into Taper Post
19. Tap the Impactor gently against the implant to seat it against the bone.
20. Check ROM of 1st MPJ and close in appropriate layers


Brostrom-Gould Repair
 Indications
o Chronic ankle instability unresponsive to conservative treatment
o Athlete with ankle instability
 Contraindications
o Fixed varus heel type (need to correct with Dwyer)
o People over 200-225 lbs (use Evans with PB repair)
o Peroneal weakness (i.e. CMT)

 Procedure
o Patient set-up
 Supine with bump (to internally rotate leg)
 Thigh tourniquet
 General or spinal
 Optional – Bump under foot
2. Incision curvilinear over anterior border of fibula, stop at peroneal tendons
a. Be careful of sural nerve, intermediate dorsal cutaneous nerve, peroneal tendons
b. You will may have to ligate lesser saphenous branch of nerve
3. Dissect down to capsule, incise it from 2-3 mm from border of fibula
a. Leave a cuff for later attachment
4. Find CFL by reflecting peroneals and incise it
5. Put foot in neutral DF and slight eversion
6. Resect necessary capsule, reapproximate using 0 or 2-0 absorbable (or non-absorbable)
suture starting with the CFL then ATFL (extend incision if necessary)
7. Test for full range of DF and PF (gently)
8. Identify extensor retinaculum (should be distal), its fibers run perpendicular to ATFL and
CFL (extend incision if necessary)
9. Mobilize extensor retinaculum. Pull it over the repaired capsule and attach to the tip of
the fibula using 2-0 absorbable suture.
10. Check again for ROM and stability
11. Close

 Post-op
o Posterior splint 3-5 days
o BK walking cast for 3-4 weeks
o Air-type stirrup for an additional month with ROM exercises


Fibular Derotational and Lengthening Osteotomy
 General
o Tramatic displacement of talus is associated with displacement of lat malleolus
o Malalignment is characterized by distal fibular shortening, lateral shift or malrotation
o Increases pressure in mid-lateral and posterolateral quadrants of the talar dome
o Goal of Fibular Derotational and Lengthening Osteotomy is to restore the sensitive WB
area to normal anatomic relationship
 Radiographs (Can also use CT and MRI)
o Abnormalities of talar position is seen on x-rays. Check for (compared to other side)
 Widening of medial joint space
 Talar tilt
 Fibular shortening
o Mortise View—Check for:
 Equidistant and parallel joint space with no medial widening
 Shenton’s line of the ankle
 A dense subchondral supporting bone creates a radiographic line that can be
followed over the syndesmotic space from tibia to fibula (Kitoaka pg. 501)
 This should be even and continuous between the two bones
 Unbroken curve between the lateral part of the articular surface of the talus and
the distal fibular recess
 Talar tilt.
 This should be parallel or within 3° of parallel
 Abnormal seating of fibula in the incisura fibularis of the tibia. (Pg. 501)
 Normal is less than 6mm as measure 1 cm above tibial plafond
 If internal fibular rotation-increase in this measurement
 If external rotation of fibula-measurement is normal or decreased. This is
more common
 Check for DJD
o If no DJD—Fibular Derotational and Lengthening Osteotomy
o If severe DJD-ankle arthrodesis
 Contraindications
o Infection
o Neuropathy
 Surgical choices
o Oblique osteotomy—can only gain 3-5 mm in length
o Transverse osteotomy of fibula, uses iliac bone graft, with plate and syndesmotic
screws through plate


Ilizarov Method
 Insertion of wires
1. Place wire with the frame already built
2. Make stab incision
3. Blunt dissection (with a hemostat)
4. Wire is inserted via safe tract via clamp
5. Remember to pulse the drill to avoid overheating
6. Use a wet Ray-Tec sponge to keep wire cool and stabilized
 Positioning the frame
o Proximal: 2 fingers between the frame and tibia
o Distally: 3 fingers (to allow for swelling)
o Frame should be 2-3 cm from the surface of the ground to allow for WB
 Tibial wire insertions
1. Break the tibia into 6 segments (1st being most proximal and probably out of our scope
of practice)
2. At the 2nd segment
a. Put half pin perpendicular to subcutaneous surface of tibia (pretty much the
general rule for insertion of half pin at the tibia)
b. For the wire, try to engage the widest portion of the tibia. This means inserting
the wire slightly oblique to the transverse plane of the tibia, thus exiting a little
more ant-medial when compared the plane of tibia.
3. At the 3rd and 4th segment
a. Similar to 2nd segment
4. At the 5th segment
a. Wire is inserted almost perpendicular to frontal plane of tibia.
i. Note: Often the tibial wires will be parallel so that the frame can be slid both
medial and lateral
5. At the 6 segment
a. Wire options
i. Directly med → lat
ii. More ant-lat → post-med
iii. Through fibula and into tibia


Osteochondral Lesions of the Talus
 Conservative treatment indicated for Stage 1-2 and Stage 3 medial lesions
 Surgery indicated for Stages 3 lateral and Stage 4 lesions

 Procedure
o Patient set-up
 Supine
 Thigh tourniquet
 General or spinal
1. Get scope portals
2. Use 2.7 mm scope, both 30˚ and 70˚. Examine the joint.
3. With a probe, evaluate the articular cartilage. Look for any loose bone fragments
beneath articular surface and the extent of the lesion over the talar dome.
4. Type of surgery is dependent on type of osteochondral defect
a. Acute fracture is usually ant-lat, more substantial bone base and better for
internal fixation
b. Chronic post-med lesion is more likely to have fragmented necrotic bone and
poor articular cartilage. These lesions must be removed.
c. In young patients without skeletal maturity, simple drilling may be enough if
articular cartilage remains intact
5. For drilling, use 0.062 K-wire to depth of 1-1.5 cm
 For post-med lesion
o Old method was to use trans-tibial approach.
o New method is to use a guide and go through sinus tarsi into post-med portion
 For articular cartilage that is fragmented, loose and necrotic
1. For post-med lesions, use post-lat port for 70˚ scope
2. Use probe to lift cartilage
3. Remove cartilage with forceps
4. Use angled cervical curette to debride lesion to healthy, bleeding bone
a. Stopping the inflow will demonstrate bleeding
5. If good bleeding, just remove all remaining bone fragments
6. If not good bleeding, drill as previously described
 For bone grafting
o If cartilage is good and intact, but either there is a viable bone fragment or there is
only edema of the underlying cancellous bone
o Insert in the trans-talar approach (like drilling through subtalar)
o OATS Procedure
 For post-med lesion
 Take a plug of bone with articular cartilage from knee and through a
trans-tibial approach, insert into the talus


Tarsal Tunnel Release
 Most often occurs in the fibro-osseous tunnel (bound by lacinate ligament), most often at the
distal edge of the ligament.
 Division of nerve of medial and plantar nerve occur deep to lacinate ligament in 93% of
people, and proximal in the other 7%
 The nerve is in the third channel (Tom, Dick and A Very Nervous Harry.)
 Need ―peanuts,‖ posterior splint, and Penrose drain.

 Procedure
o Patient set-up
 General or spinal usually
 Thigh tourniquet, deflate before closure.
 Don’t esmarch the foot, just elevate it.
1. Incision 10 cm proximal to the tip of the medial malleolus and 2 cm posterior to the
tibia. After the medial malleolus, gently curve plantar to the level of the talonavicular
joint (plantar to TNJ). This should be about the midpoint of the abductor hallucis
a. McGlamry—2cm proximal to superior edge of lacinate ligament and gently
curving to the proximal margin of the abductor hallucis.
2. With hemostats, blunt dissect the SubQ. A moistened 4x4 can be used. When in the
SubQ, be careful of the medial branch of the nerve as it punctures the lacinate ligament.
3. When at the lacinate ligament, feel for the pulse of the PT artery. Also palpate for the
tendons of the PT and FDL. The FHL (4th compartment) can be palpated by moving the
big toe.
4. From proximal to distal, make incision of the roof of the third canal. May want to use
hemostats and split them, or may use groove channeler/director.
5. Isolate the Tibial Nerve and all 3 branches (medial and lateral plantar nerve, and the
calcaneal branch) of its branches from all tissues.
6. Remove any neoplasm. Be careful!
7. Move varicose veins. Ligate veins if necessary, but make sure that you aren’t ligating
an artery.
8. Follow nerve distally through the abductor canal. Section the abductor canal stricture.
9. Go proximal and follow nerve upwards.
10. Deflate tourniquet.
11. Closure—but don’t reapproximate the lacinate ligament (McGlamry says only partially
reapproximated) and the subQ and skin are closed. If a lot of ooze, then use a drain.
12. Marcaine at the end

 Post-op
o Below the knee compression dressing is applied.
o NWB or partial WB for two weeks.
o Begin DF and PF of ankle after 2 weeks.


Case Study 1
A 23 y/o male presents to the ED with foot trauma.

What should you do first?

Obtain a quick history and check neurovascular status
HPI – patient had foot run over at work. He complains of 10/10 pain and that his toes feel cold
and numb.
PE – pulses are present. Toes feel cold. Patient cannot feel you touching his toes. Toes are
changing color (purple or white). Patient cannot move his toes.

What is your diagnosis?

Compartment syndrome

What is compartment syndrome?

Condition with increased tissue pressure within a limited space which compromises the
circulation and function of the tissues. It can lead to ischemia of the tissues.

Is this a surgical emergency?

Yes. Compartment syndrome is a clinical diagnosis, according to the AO Principles course. It is
better to get the patient up to surgery than to find an instrument to measure the pressure.

What are some causes of compartment syndrome?

Fractures, crush injuries, prolonged limb compression, post-ischemic swelling. Practically any
injury can result in compartment syndrome.

What are the signs of compartment syndrome?

 Pain out of proportion (most important)
 Paresthesia
 Pallor
 Pulses present
 Poikilothermia
 Paralysis

What are some techniques for measuring pressure?

Wick catheter, slit catheter, Synthes catheter, needle technique, continuous infusion technique.
But as stated before, this should be a clinical diagnosis.

What is the treatment?

Fasciotomy of the compartment. In the leg, surgical access should be made to all four
compartments. To do a leg fasciotomy, make one incision medial to the tibia and one lateral.
From the medial incision, open the superficial and deep posterior compartments. From the
lateral incision, open the anterior and lateral compartments.


What are some absolute indications for a fasciotomy?
 Tissue pressure above 30 mm Hg (normal 4 ± 4 mm Hg)
 Sensory and motor loss
 Pain out of proportion


Case Study 2
A patient who you prescribed pain medications has wheels, hives, itching, and trouble
breathing after taking the medication.

What is most likely going on?


What is anaphylaxis?
Rapid, generalized immunologically-mediated event that occurs after exposure to foreign antigen
substances in previously sensitized persons. This syndrome can affect any organ in the body, but
it most commonly affects the pulmonary, circulatory, cutaneous, neurologic, and GI systems.

What are the clinical symptoms of anaphylaxis?

Mild (common)
 Urticaria, weakness, dizziness, flushing, angioedema, congestion, sneezing
 Upper respiratory tract obstruction, hypotension, vascular collapse, GI distress,
cardiovascular arrhythmias, cardiac arrest

What is the difference between anaphylaxis and anaphylactoid reaction?

Clinically, they present the same, but anaphylactoid reaction is not mediated by the IgE antibody
and does not necessarily require previous exposure to the inciting substance

What is the treatment for anaphylaxis?

Stop the offending agent, and if necessary, D/C all meds
If the patient is having life-threatening problems, get them to the ED
Treat the symptoms
 Airway – bronchospasm
o O2 40-100%
o Epinephrine 0.3-0.5 mL 1:1000 soln SC or IM q15min
o Albuterol 0.5 mL 0.5% in 2.5 mL NS nebulized q15min
o Benadryl 50 mg PO q4-6h
o Methylprednisolone 2-60 mg PO daily
 Cardiovascular – hypotension
o IV fluids 1 L q20-30min prn
o Maintain systolic pressure >80-100 mm Hg
o Epinephrine 1 mg 1:1000 in 500 mL D5W IV at rate of 0.25-2.5 mL/min
o Norepinephrine 4mg in 1 L D5W IV at 0.5-3 mL/min
o Benadryl 50 mg PO q4-6h
 Cutaneous reactions
o Epinephrine 1:1000 0.3-0.5 mL SC or IM q15min
o Benadryl 50 mg PO q4-6h
Document offending agent and educate patient on future avoidance


What is the best way to prevent anaphylaxis?
Thorough history and elimination/avoidance of the offending substance


The Interviews
For some people, the social interview is harder than the academic interview. In my opinion, the
reason that it is harder is because people don’t prepare for the social interview. After sitting
through 2 years of interviews, I’m amazed at how some people don’t seem ready for the social
questions. Many of these ideas are from my past as a salesperson on a job interview. Essentially
that is what you are…a person selling themselves for a job.

-Brett Chicko

The amount of Social vs. Academic Interviewing will vary from program to program. Some will
only ask social questions (but pimp you when you rotate with them) and some may ask only one
social question and a battery of academic questions. Review this section so you have some
baseline answers for common social questions and review the rest of the book for common
academic questions. Overall: be yourself and relax!

-Hubert & Sandi

Hint #1 – Look and dress appropriate!

 Men
o Wear a pressed shirt, tie, and suit. (Suggest a dark suit with a blue or white shirt.)
o Hair should be neat and combed and facial hair clean cut.
 Women
o Wear a conservative suit. Keep the skirt length and shirt neckline appropriate.
o Hair should be neat and combed.
 Sitting in the interview chair
o When you sit in the chair, sit back with good posture. NO SLOUCHING!
o Your hands should be in your lap (when you’re not talking to them).
o Keep your feet flat on the floor for men or legs crossed for women.
o Do not lean your arms on the table in front of you…you’re not at your desk at

Hint #2 – Proper entrance/exit from interviews

 Do not be late for your interview!
 When you enter the room, sit in the chair and give a proper greeting.
o Say hello at least.
o Say ―nice to see everyone again‖ or something similar if you’ve rotated with the
 Make sure to make eye contact with everyone in the room and SMILE! (But don’t be too
cheesy about it.)


 When you leave the room, it is appropriate to only shake hands with the director unless
the other members of the room offer to shake their hands.
 Thank the interviewers for their time.

Hint #3 – Do your homework

 At the end of many interviews, the host will ask the interviewee if he/she has any
o Brett says: You should not. ―You should have done your homework by this point.
Why would you spend your money and time to interview at a place you don’t
have any information about (other than what is in the CASPR book)? To ask
questions in the interview that should’ve been asked on a visit makes you look
unprepared and uninterested.
o Hubert & Sandi say: It is okay to ask any burning questions you may have about
the program (rumors about taking 4 residents instead of 3, or hearing a program
may be closing next year). Avoid simple questions that may be answered by
reading a program’s handbook or website.
 By the time of your interview, you should have visited the program (and in theory
asked all your questions at that time)
o If you live and attend school near a program you’re interviewing with by golly
you BETTER HAVE VISITED there by the time of the interview!
o If you live too far away (airplane ride distance) then a phone call to one of the
residents will work (track down a resident’s pager number or contact info through
the number given in the handbook for each program)
 During this phone call, get your questions answered.
 As always, be prepared and have a good list of questions for the resident.
 If any questions do arise after the visit/phone call then it is perfectly
acceptable to call or re-page or email the resident.
 A good response to this question: ―Do you have any questions about our program?‖
o ―No Sir/Ma’am, all of my questions were thoroughly answered by Dr. So-and-So
on my visit (or phone call). I feel as if I have a good understanding of the
opportunities of your program.‖

Hint #4 – Ask for the program

 Brett says:
o I know some people feel that by showing up for the program their presence alone
means they want the program. I still feel like one should go the extra yard and
ask for the program. I do not mean suck up to them, but state to the interviewers
that you want the program in a mature and professional manner.
o By asking for the program or stating that you want the program it shows the
program that you want to be there and that this is not a practice interview
o I know personally that if there are 2 women I want to date, the one who expresses
an interest me versus one that is indifferent, I will always choose the one who
expresses an interest
o Proof? All the interviews I’ve been a part of, only 4 people asked for the program
(over a 3 year span) and all 4 have gotten the program.


 Hubert & Sandi say:
o Getting a good program’s spot (like Crozer’s) is highly competitive, and many
students have learned to sneak in ―I love your program‖ or ―I definitely want to
come here‖ as many opportunities as they can.
o Proof that this doesn’t always work? Since this book was written, the occasional
student who has said they wanted the program has turned in to more like 60-75%
of the students coming through with visits or externships that ―ask for the
program.‖ Trust us, your actions speak way louder than your words…
o But if it makes you feel better to say this as a parting goodbye, you wouldn’t be
the first or the last!

Hint #5 – Be enthusiastic
 Don’t be one of those people that walk around looking like they have a hangover or just
took a sleeping pill.
 Get a good night’s rest so your tiredness from studying/drinking doesn’t overcome your
alertness and enthusiasm.
 But don’t be a cheeseball or act unnaturally.

Hint #6 – Act like someone you would want to work with

 If you’ve rotated with the program for a whole month, no matter how you act in the
interview, they already know your personality. But acting like a big goof can hurt your
 Continuing on Hint #5 and think about #7, be like a mature, responsible adult, or at least
act like one.
 If you’re picked, you’d be the one representing the program so you need to show you’re a
good person to work with.

Hint #7 – Remember you’re in a formal interview

 Even if you joked around a lot on a visit or on a rotation, especially when answering
academic questions, keep the ridiculously silly answers to yourself.
 Although you may have spent a month at a program, not everyone at the interview may
have met or remember you. Make sure your first impression with them a positive one.
 You want to do well because sometimes a good or bad interview makes or breaks your
chances with a program.

Hint #8 – Prepare for the social interview

 Go over some of the sample social questions and formulate some answers for a couple of
them. Go over these answers with a classmate, a resident you’re working with or are
friends with, your mom, anyone really.
 Practice, practice, practice…
 Be creative, but please read your answers out loud to another human being so your
creativity is not interpreted wrong or sound ridiculous.
 Don’t ignore this part because you have a thousand other things to study for the academic


Hint #9 – Have fun
 Seriously, this is the only way to get through these types of questions.
 This will show the program you are applying to a part of your personality and how you’re
handling the stress of interviewing.

Hint #10 – Don’t over think things

 With nerves and anywhere from 2 to 15 people interviewing and watching you, even the
most confident person can show some nervousness.
 With a few exceptions of certain known hard-core academic programs, most programs
just want to see your scope of basic knowledge and reasoning when working up a case
study or working through the questions.
 If it looks like a dog, smells like a’s probably a dog. Meaning, if you think you
know the answer, you probably do!
 And if you hear hoofbeats, think horses – not zebras…

Hubert & Sandi’s Bonus Tips

 The Match for students with programs is designed to work in favor of STUDENTS NOT
 Rank programs the way YOU want them. Don’t let rumors influence how you rank
your programs. (Ex: If you rank a program you really want and they don’t end up
picking you, it just bumps you down to your #2 pick, but at least this way, if you’ve put
them #1 you’ve given yourself the strongest chance of matching with your first pick!)
After all, no one knows how you ranked programs except YOU (or the people you
 When evaluating a residency program, in addition to making sure you’d get the cases
and experience you’re looking for, evaluate the senior resident class and how they’re
performing. Think about it...if they’re good, that’s how you would be if you graduated
that program! (Ex: Are they excellent surgeons who are confident doing a variety of
cases? Are they getting skin-to-skin cases? Are they having trouble getting their
numbers? Are they knowledgeable? Are they happy they went there??)

Sample Social Questions

Tell us about yourself
 Keep this one short. Three sentences is a good length (i.e. who you are, what you are and
what you like to do).
 Keep this to the point and under 15 seconds.

Who is your hero?

 Obviously, besides ―Jazzy‖ Jeff Lehrman, DPM (Crozer attending extraordinaire and
graduate of the Crozer program).
 It’s probably not wise to say someone in your class or a cartoon superhero…but anything
else is probably appropriate.

Why did you pick podiatry?

Foot fetish is NOT okay.


Why should we take you over the other applicants?
Just don’t personally call out any of the other applicants when answering this.

What do you know about our program?

What did you learn on your externships?

What is your favorite externship and why?

Yup, what you’re thinking is correct…it is not wise to name a different program than the
program that asks this silly question.

Did you visit our program?

 If yes, what did you learn (or like) about our program?
 If no, why didn’t you visit our program?
o If you live close to the program (i.e. Temple students and our program), there
really aren’t many good excuses that sound acceptable. The ―I didn’t have time‖
or ―My schedule didn’t allow it‖ just don’t cut it…

Tell us about some of the current events

Just a question to make sure you don’t live in a bubble.

What was the last book you read?

But please have read the book, cause if it’s some unknown title, someone may ask you what it’s
about and it’s kinda strange to say ―I’ve just started it so I don’t know yet.‖

Tell us a joke
 Keep it clean!
 Brett’s joke:
o Sherlock Holmes & Doc Watson were camping. They went to sleep and were
sleeping soundly until Sherlock woke up Watson. Sherlock said ―Watson, look
up. What do you see?‖

Watson looked up at the sky and saw millions and millions of stars and the moon.
Realizing that The Sherlock Holmes asked him the question, Watson wanted to
give an impressive answer.

Watson thought about it for a second and answered:

―From an astronomical point of view, I see the Milky Way and many different
constellations to the North.
―From a holographic point of view, I see the clouds are coming from the East and
we may have a chance of rain tomorrow.
―From a theological point of view, it shows how vast and powerful God is and
how insignificant we are when compared to God.
―From an astrological point of view, I see that the moon is in Jupiter and if you
are a Scorpio, you are going to have a good day tomorrow.‖


Watson then asked, ―Why, what do you see Sherlock?‖

Sherlock took a drag on his pipe and replied, ―Someone stole our tent.‖
 Hubert & Sandi say: Good luck remembering a long joke like that, but only tell a joke if
you can tell the whole thing and remember the punch line. Please!

What do you do in your free time?

 Usually the program isn’t looking for a geeky answer like ―I read podiatry articles.‖
 Mention a hobby or activity you like to do on the weekend (like back in undergrad, when
you had a life…and no, going to frat parties is not an acceptable answer).

Be prepared to answer a question about one of your lower grades (if you have any)
Especially if you have to re-test or re-take a class to pass.

Who was your favorite resident? Who is your least favorite resident?
Proceed to think of an answer with mucho cuidado (much caution)!

What is your favorite color?

Wouldn’t advise you to say black or white, cause technically those aren’t colors and it’s totally
lame if you do say them.

If you can be any animal, what would it be and why?

Who is your favorite clinician in school and why?

Who is your mentor?

Please don’t say someone in your class!

Who is our director?

Please don’t ever mess this one up!


A Surgery
(& a few other important
items for externships)

Officers of 2005

Re-typed, Edited, Updated by the JPMSA in 2009

All pictures came from class notes / handouts.
Most of the pictures were referenced from Dr. Hetherington’s book.

Table of Contents:

Topic Page #
Surgical Consult 6
Pre-Op Note 6
Post-Op Order 6
Admission Order & Note 6
Post-Op Note 7
Post-Op Visit 7
Layers of the Foot 8
Key Lab Values 8
Hospitalization Indications 9
Post-Op Fever Etiologies 9
Types 10
Selection 11
Technique 11
Classification Systems
Stewart, Salter-Harris 12
Gustillo-Anderson, WatsonJones, Freiberg 13
Berndt-Hardy, Hawkin 14
Sneppen, Watson & Dobas, Kuwada 15
Rowe, Sander’s 16
Hardcastle, Dias, Danis-Weber 17
Lauge-Hansen 18
MRI 19
Anesthetics 20
Dosing 20
Onset/Duration 20
Increasing Comfort 21
Ankle Block 21
Hemostasis = Tourniquet Pressures 21

Table of Contents (Continued):
Topic Page #
Corticosteroid Injections
Types 22
Side Effects 22
Cocktails 22
Radiographic Data 23
Joint Deformities 24
Proximal 25-27
Shaft 29-30
Distal 31-33
Internal Fixation
Principles 34
Rule of 2’s 34
K-Wires 34
Steinmann Pins 34
Monofilament Wire 35
Tension Band Wiring 36
Staples 37
Anatomy 38-39
Types 40-41
Fixation Technique 42-43
Selection 44
Soft Tissue Anchors 45
Plates 45-46

Table of Contents (Continued):

Topic Page #
External Fixation
Principles 47
Complications 48
Types 48-49
Dynamics 50
Care & Management 50
Forefoot Pathologies / Surgical Procedures
Hallux Limitus/Rigidus 51-52
Hammertoes 53-56
Etiologies for Contracted Digits
5 Digit Arthroplasty 57
Rearfoot Surgery
Plantar Fasciotomy 58
Haglund’s Deformity 59
Keck & Kelly Osteotomies 59
Tendon Transfers & Indications
Adductor Hallucis 60
Abductor Hallucis 60
Extensor Hallucis Longus 60
Jones Suspension 60
Hibbs 60
Tibialis Anterior 61
Cobb 61
Tibialis Posterior 62
Peroneus Longus 62
Bunions based on Angles 63
Other things to know… 67

1. Chief Complaint 8. Primary Care Dr
2. HPI (NLDOCAT) 9. Hospitalizations
3. Allergies 10. RoS
4. Medications  Vitals / Vascular / Neuro / Derm /
5. Social History Musculoskeletal
6. Medications 11. Ancillary (x-rays, labs, ect…)
7. Family History

Surgeon Medications
Pre-Op Dx Allergies
Planned Procedure Diagnostic Data – Labs, x-rays, EKG, ect…
Consent Form: Describe Procedure & Care / Complications /
Alleviations / Expected Outcomes / Arrange Pre-Op Testing
“Consent form was reviewed with patient, signed and placed in chart.” “All
risks, possible complication and alternative treatments have been
discussed with the patient in detail. All patients’ questions have been
answered to satisfaction. No guarantees to the outcome have been made.”


Date/Time/Signature Date/Time/Signature Activities
Vitals Admit to Allergies
Activities Dx Nursing
Nursing Condition Diet
Diet - Ins/Outs
Ins/Outs Labs
Meds Meds
Ancillary Ancillary
X-ray X-ray

Surgeon Hemostasis – type Findings
Assistants Estimated Blood Loss Pathology
Pre-Op Diagnosis Materials – sutures/hardware Prophylaxis
Post-Op Diagnosis Injectables – any post-incision Complications
Procedure Condition
Anesthesia – type /
how much
“Patient tolerated procedure and anesthesia well. Patient transported to
recovery by anesthesia with vitals stable and vascular status intact.”
Also may include.. Pathology – bone, ST; Condition – stable, guarded,
fair, poor; Prophylaxis


1. POV # ______, PVD #_______
2. Procedure
3. N,V,C,F,SOB
4. Activity status
5. Pain / How controlled
6. Other Complaints
1. How patient presents – walking, wheelchair
2. Vascular, Neuro, Derm, Musculoskeletal
1. Status Post-Op
2. Compliance
1. Treatment
2. Dr & Residents


1st Layer
1. Abductor Hallucis M.
2. Abductor Digiti Minimi M.
3. Flexor Digitorum Brevis M.
2nd Layer
1. Quadratus Plantae M.
2. Lumbricales M.
3 Layer
1. Flexor Hallucis Brevis M.
2. Flexor Digiti Minimi M.
3. Adductor Hallucis M.
4 Layer
1. Dorsal Interossei M. (4)
2. Plantar Interossei M. (3)


Chem 7
(136-145mEq/L) (97-107mEq/L) (5-20mg/dL)
Na Cl BUN Glucose
(3.5-5mEq/L) (23-29mmol/L) (M: <1.2 W: <1.1mg/dL)

CBC (M: 14.4-16.6g/dL)

(W: 12.2-14.7g/dL)

(4500 - Platelets
11,000/L) HCT (150,000-450,000μL)
(M: 43-49%)
(W: 37-43%)


1. Fever >101.6o
2. Ascending Cellulitis / Suspect Osteomyelitis
3. Lymphangitis / Lymphademopathy
4. Immunosuppressed
5. Virulent / Resistant Organisms
6. Need for I&D Procedure
7. Need for IV Antibiotics
8. Failed response to outpatient therapy
9. Need a consult


1. Wind – Pulmonary
a. Aspiration / Pneumonia
b. Occurs 24-48h
c. Get chest x-ray

2. Water – UTI
a. Occurs in 2-6d

3. Wound
a. Occurs in 3-5d

4. Walk – DVT / Pulmonary Embolism

a. Within 1st week
b. Virchow’s Triad
i. Hypercoagulation
ii. Venous Stasis
iii. Endothelial Damage

5. Wonder – drugs / fever / benign / medicines


Absorbable Sutures Filament Type Total Absorption

Chromic Gut 70d
Monocryl Monofilament 90d
Maxon Monofilament 90-120d
Vicryl Monofilament 56-70d
or Braided
Dexon Mono- or 90-120d
Dexon Plus Mono- or 90-120d
Dexon S Multifilament 90-120d
PDS Monofilament 180d
Non – Absorbable Sutures Filament Type Advantages
Stainless Steel Mono- or High strength, low
Multifilament tissue Rxn
Ethilon Nylon Monofilament Elasticity/Memory
Prolene Monofilament Minimal Tissue Rxn
Novafil Monofilament Elasticity/Tensile
Silk Multifilament Good Handling
Nurolon Nylon Multifilament
Mersilene Multifilament Consistent Tension
Ticron Braided Minimal Tissue Rxn
Ethibond Multifilament Good Handling

1. Bone 5. Subcutaneous Fat
a. Stainless Steel a. Vicryl
2. Tendon 6. Subcuticular
a. Prolene a. Monocryl
b. Ethibond b. Vicryl
c. Nylon 7. Capsule
d. Polyesters a. Vicryl
3. Muscle 8. Skin
a. PDS a. Nylon
b. Vicryl b. Silk
c. Prolene
4. Fascia Deep Tissue  taper needle; 3-0 suture
a. Prolene Subcutaneous Tissue  taper needle; 4-0 suture
b. PDS Dermal Layer  precision needle; 5-0 suture
Capsule  2-0 or 30 suture
Subcutaneous  4-0 suture
Subcuticular  5-0 clear suture
Skin  4-0 clear suture

1. Simple Interrupted
Good for infected wounds
Individual know for each throw
2. Horizontal Mattress
Everts skin edges well
3. Vertical Mattress
Everts tissue edges well
4. Continuous Running
Good to save time
Good for large wound areas
5. Subcuticular (Running Intradermal)
Leaves the best scar
Type I Supra-articular @ metaphyseal-diaphyseal junction
True Jones!
Type II Intra-articular avulsion, 1 or 2 fracture lines
Type III Extra-articular avulsion, PB tears small fragment from the
styloid process
Type IV Intra-articular, comminuted fracture, assoc. with crush injury
Type V Extra-articular avulsion @ of physis in children (SH Type I)


Type I
Epiphysis is completely separated from metaphysic
Type II
Epiphysis, and the growth plate, is partially separated from the
metaphysis, which is cracked
Type III
Fracture runs through the epiphysis, across the growth plate from
the metaphysic
Type IV
Fracture runs through the epiphysis, across the growth plate, and
into the metaphysic
Type V
The end of the bone is crushed and the growth plate is compressed
Type VI
(Rang’s Addition) Avulsion of peri-chondral ring
Type VII
(Ogden’s Addition) Avulsion fracture of the epiphysis without
involvement of the physis

Type I
Fracture with open wound <1cm in length
Clean, minimal soft tissue necrosis
Usually traverse or short oblong
Type II
Fracture with open wound >1cm in length
Clean, minimal soft tissue necrosis
Usually traverse or short oblon
Type III
Fracture with open wound >5cm in length
Contamination and/or necrosis of skin, muscle, NV, & ST
 Type IIIa
 Adequate bone coverage
 Type IIIb
 Extensive soft tissue loss with periosteal stripping and bone
 Type IIIc
 Arterial injury needing repair
Type I Navicular tuberosity fracture
Type II Avulsion fracture of dorsal lip
Type III A: Transverse body fracture – Nondisplaced
B: Transverse body fracture – Displaced
Type IV Stress fracture
Type I No DJD Articular cartilage intact
Type II Peri-articular spurs Articular cartilage intact
Type III Severe DJD Loss of Articular Cartilage
Type IV Epiphyseal dysplasia; multiple head involvement

Stage I
Compression lesion or non-visible lesion
Stage II
Fragment attached
Stage III
Non-displaced fragment without attachment
Stage IV
Displaced fragment


Type I
Non-displaced talar neck
Disrupts blood vessels entering dorsal talar neck and intra-osseous
20% chance AVN
Type II
Displaced talar neck fracture with subluxed or dislocated STJ
Disrupts dorsal neck arterial branches and branches entering from
inferiorly from sinus tarsi & tarsal canal
40% chance AVN
Type III
Displaced talar neck fracture with dislocated STJ & ankle joint
Disrupts all 3 major blood supplies
100% chance AVN
Type IV
Displaced talar neck fracture with complete dislocation of STJ
Ankle joint + subluxation or dislocation of the talonavicular joint
Disrupts all 3 major blood supplies
100% chance AVN


Group I Transchondral / Compression fracture of the talar dome

Group II Coronal/Sagital/Horizontal shearing fracture of the entire body
Type I Coronal or Sagital
A: Non-displaced
B: Displacement of trochlear articular surface
C: Displacement of trochlear articular surface with
associated STJ dislocation
D: Total dislocation of the talar body
Type II Horizontal
A: Non-displaced
B: Displacement
Group III Fracture of posterior tubercle of talus
Group IV Fracture of lateral process of talus
Group V Crush fracture of the talar body
Stage I Normal Lateral talar process with no clinical significance
Stage II Enlarged posterior lateral tubercle of the talus (Steida’s Process)
Stage III Accessory bone / Os Trigonum that may be irritated by trauma
Stage IV Os Trigonum + cartilaginous/synchrondrotic union with talus
Type I Partial rupture
Type II Complete rupture <3cm gap
Type III Complete rupture 3-6cm gap
Type IV Complete rupture >6cm gap

Type I A Medial Tuberosity fracture
B Sustentaculum Tali fracture
C Anterior Process fracture

Type II A Posterior break fracture without Achilles involved

B Posterior break fracture with Achilles involvement

Type III Extra-articular body fracture

Type IV Intra-articular body fracture without depression

Type V A Comminuted, Intra-articular fracture with depression

B Comminuted fracture with severe joint depression


* Fractures are classified according to the number of intra-articular
fragments and location of fracture lines
# of Fractures
Type I Any non-displaced intra-articular fracture
Type II 1 fracture through posterior facet creating 2 fragments
Type III 2 fractures through the posterior facet creating 3 fragments
Type IV 3+ intra-articular fracture lines

Location of Fracture Lines:

Type A: Total or Homolateral
– Disruption of the entire Lisfranc joint
– Transverse or Sagital plane
– Most common type
Type B: Partial
B1 – Medial incongruity with the first met forced medially
– Involves 1st met OR mets 2,3,4 but NOT 5
B2 – Lateral incongruity with lesser mets forced laterally
Type C: Divergent
C1 – Partial divergence with the 1st met medial and 2nd met laterally
C2 – Total divergence with the 1st met displaced medially and lesser
mets displaced laterally
Grade I  Partial rupture of CFL
Grade II  Complete rupture of ATFL
Grade III  Complete rupture of ATFL, CFL, &/or PTFL
Grade IV  Complete rupture of all 3: ATFL, CFL, & PTFL
+ Partial rupture of the Deltoid Lig

Type A Transverse avulsion fibular fracture BELOW…

Type B Spiral fracture AT…
(SER or PAB)
… the level of
Type C Fibular Fracture ABOVE…
the syndesmosis



¤ Stage I Transverse avulsion of fibula @/below AJ level
Rupture of the Lateral Collateral Ligament
¤ Stage II Oblique to Vertical fracture of the Medial Malleolus


¤ Stage I Transverse avulsion fracture of Medial Malleolus
– or – Rupture of Deltoid Lig
¤ Stage II Rupture of AITFL & PITFL
– or – Tillaux-Chaput / Wagstaffe fracture
¤ Stage III Short oblique fracture of the fibula @ lvl of syndesmosis


¤ Stage I Rupture of AITFL
– or – Tillaux-Chaput / Wagstaffe fracture
¤ Stage II Spiral/Oblique fracture of fibula @ lvl of syndesmosis
¤ Stage III Rupture of PITFL
– or – Avulsion fracture of Posterior Malleolus
(Volkmann’s Fracture)
¤ Stage IV Transverse fracture of Medial Malleolus
– or – Rupture of Deltoid Lig

PRONATION EXTERNAL ROTATION (PER) *** Longest healing time!

¤ Stage I Transverse fracture of Medial Malleolus
– or – Rupture of Deltoid Lig
¤ Stage II Rupture of AITFL & Interosseous membrane
– or – Tillaux-Chaput / Wagstaffe fracture
¤ Stage III High Spiral Oblique fracture (Maisonneuve Fracture)
¤ Stage IV Rupture of PITFL
– or – Avulsion fracture of Posterior Malleolus


T1-Weighted  good for showing anatomical detail

+ Short TE + TR
+ Tissue with short T1 are brighter
+ Fat

T2-Weighted  good for highlighting areas of pathology

+ Long TE + TR
+ Tissue with long T2 are brighter
+ Water, Edema

STIR  Short Tau Inversion Recovery

+ Fat suppression
+ Heavily water–weighted image
+ Very Sensitive for Bone Marrow abnormalities

Gadolinium (best for infection)

+ Contrast–enhanced chemical agent
+ Shortens T1 relaxation times  Increases signal intensity on T1
weighted images
+ Usually used in conjunction with fat suppression
+ Good for identifying ST masses, inflammation processes, & for
staging bone and ST infection

TE = Time to Echo dec TE + dec TR = T1-Weighted

TR = Time of Repetition inc TE + inc TR = T2-Weighted


 Higher incidence of allergies
 Metabolized in Blood (Cholinesterase in plasma)
 Types
~ Cocaine
~ Procaine
~ Cholorprocaine
~ Tetracaine

 Metabolized by CYP450 system in Liver
 Types
~ Lidociane / Xylocaine (0.5, 1, 1.5, or 2% solutions)
~ Bupivicaine / Marcaine (0.25, 0.5, or 0.75% solutions)  C/I <12y/o
~ Mepivicaine / Carbocaine (1, 1.5, 2, or 3% solutions)

0.25% solution = 2.5 mg/cc drug 1cc = 1mL
0.5% solution = 5 mg/cc drug
1% solution = 10 mg/cc drug

Ex: 5cc of 1% Xylocaine (lidocaine) = 50mg of Xylocaine given

Ex: 3cc of 0.5% Marcaine (bupivicaine) = 15mg of Marcaine given

Toxic Doses: Onset & Duration:

Lidocaine Plain = 300mg Onset: 5min
w/ Epi = 500mg Duration: 1-2h

Marcaine Plain = 175mg Onset: 10-15min

w/ Epi = 225mg Duration: 6-8h

6 Ways to Increase Comfort of the Injection: Draw up with 18G
1. Quick Stick Inject with 25 or 27G
2. Slow Injection
3. Small Gauge Needle (large # = small gauge)
4. Small Syringe (less pressure)
5. Cold Spray
6. Warm the Solution (to body temp)

Ankle Ring Block:

Superficial = Saphenous N., Sural N., Superficial Peroneal N. (IDCN, MDCN)
Deep = Posterior Tibial N., Deer Peroneal N.
** Fact: If you mix Fibular N.
Lidocaine and Marcaine, you
will only have partial Saphenous Superficial
anesthesia deep into surgery. N. Fibular N.
Only mix to avoid toxic M Trochlea L
doses. M M

** Fact: If you need to inject Post. Tibial Sural N.

more volume, use a small
percent of drug solution.
Achilles Tendon

Ex: 30cc of 1% gives more anesthesia than 15cc of 2%

Saphenous N .5-1cc
Posterior Tibial N 1-3cc give the most here since this N is the largest
Sural N .5-1cc
Deep Peroneal N .5-1cc between 2 Long Extensor Tendons
Superficial N .5-1cc plantarflex & invert

Hemostasis = Tourniquet Pressures:

Ankle: +100 over systolic ~250mmHg
Thigh: +200 over systolic ~ 350mmHg
Corticosteroid injections are used to control local inflammatory reactions

Phosphates: short-acting (clear)

Acetates: long-acting (cloudy)

All corticosteroids are collagenilytic and therefore should not be injected

into the same area of soft tissue more than 3-4 times per year.

Side Effects:
~ Soft tissue atrophy
~ Tendon rupture
~ Skin discoloration (lightening)

Cocktails Commonly used in Podiatry: Always draw up the Lido/Marc 1st

1. Plantar Fasciitis followed by Dex or Kenalog!
a. 1cc Kenalog-10 (10mg/mL)
b. 0.75cc 1% Lidocaine
c. 0.75cc 0.5% Marcaine

2. Joint Injections
a. 0.2cc Dexamethasone Phosphate
b. 0.5cc 1% Lidocaine

3. Intermetatarsal Neuromas
a. 0.3cc Dexamethasone Phosphate
b. 0.5cc 1% Lidocaine


Angle: Normal:
Hallux Abductus Angle 0-15o
Proximal Articular Set Angle (PASA) 0-8o
Distal Articular Set Angle (DASA) 0-7o
Intermetatarsal Angle
1-2 0-8o
2-5 16o + 4o
4-5 8o + 2o
Hallux Interphalangeal Angle (HIA) 0-10o + 2o
Metatarsal Length + 2mm
Metatarsus Adductus 0-8o
Tibial Sesamoid Position Positions 1-3
1 = Medial to midline of hallux
2 = Touching midline medially
3 = 2/3 medial + 1/3 lateral to midline
4 = 1/2 medial + 1/2 lateral to midline
5 = 1/3 medial + 2/3 lateral to midline
6 = touching midline laterally
7 = lateral to midline of hallux
Calcaneal Inclination Angle 18-22o
Talar Declination Angle 21o
TaloCalcaneal Angle (Kite) 17-21o
Böhler’s Angle 25-40o
Angle of Gissane 125-140o
Calcaneal Fracture resulting in
Joint Depression  Böhler’s Angle ↓
Angle of Gissane


Positional Deformities:
PASA and DASA within normal range (0-8o)
Joint is Subluxed

Structural Deformities:
PASA and DASA abnormal
Joint is Congruous

Combined Deformities:
PASA and DASA abnormal
Joint is Dislocated

IM between 15-22 , normal PASA
NOT for a short metatarsal

I. Closing Base Wedge

1-1.5cm from met-cuneiform joint
4-6weeks NWB

 Structural Lg IMA
 Splayfoot
 Juvenile/Recurrent HAV
 Met Primus Elevatus
 HAV + MetAdductus
 C/I in Elderly

II. Juvara – Types A,B,C

A: Oblique, distal lateral to proximal
medial with an intact medial cortical hinge
B: same as A but the medial hinge is
sectioned after wedge resection
C: Oblique, without wedge resection


III. Opening Base Wedge

Good for a short metatarsal
Use medial eminence for the graft

IV. Crescentic
1.5cm from met-cuneiform joint
Easy traverse plane correction
Good for short metatarsal


V. Double Osteotomy
IM and PASA correction

VI. Proximal V
Good screw fixation
Unlikely to get elevates

VII. Lapidus
IM > 18o
Fusion of the base of 1st met to the medial
 Pain with motion at met-cuneiform joint
 Hypermobility of 1st met-cuneiform joint

** Troughing is unique to midshaft osteotomies

I. Ludloff Osteotomies
IM 1-2 angle: 13-20o
Abnormal HAA
Normal to short 1st metatarsal
Elevatus is a risk

II. Mau
IM 1-2 angle: 13-20o
Abnormal HAA
Normal to short 1st metatarsal
Due to cut, decreases elevates


III. Scarf – “Z”

Dorsal to Plantar – 50:50 or 66:33 cut
Very Stable, technically difficult
2 screw fixation

IV. Off-Set “V”

Modification of the Austin
Cut angled <55o

HAV angle – 35 o

IM angle -- 16 o
Some PASA correction

I. Reverdin
Some PF possible

II. Hohmann
Very unstable; Rigid Fixation necessary
Shortening occurs with fragment removal


III. Mitchell – “Step-down Osteotomy”

Used for long 1st metatarsal
Good visualization of possible change

IV. Wilson
Dramatic shortening possible


V. Austin / Chevron / Distal “V”

Transpositional – PASA, IM, DF/PF possible
Joint preserving
Possible of Juvenile HAV
Displace capital fragment ¼ to ½ bone width

VI. Reverdin Green / Distal “L”

Cut 2/3 way through bone, then plantar cut


4 Main Principles of Internal Fixation:

1. Anatomical Reduction
2. Rigid Internal Fixation
3. Atraumatic Technique
4. Early active RoM

Rules of 2’s:
Fracture / Osteotomy site should be 2x’s the diameter of the bone
2 points of fixation is better than 1
2 threads should purchase the distal cortex
2 finger tightness

Kirschner Wires (K-wires):

Steel wires used as permanent or temporary fixation
Dependent on diameter
Available in both smooth and threaded
Threaded wires provide more stable purchase
BUT are weaker & harder to remove
Both are measured by outer diameter
ONLY maintain compression
Sizes: 0.028, 0.035, 0.045, 0.062 inches

Steinmann Pins:
Very similar to K-wires
Larger diameter than K-wires
Provide Inc Stability
Measured in 64ths
Sizes: 8/64 (1/8), 7/64, 6/64…


Monofilament Wire:
Malleable Steel
Provide interfragmentary compression
Measured in Gauges (small gauge = large diameter)
 Cerclage fashion
 circling around a bone
 Interfrag fashion
 placed in between 2 fragments
 always pull on the proximal fragment
 most stable


Monofilament Wire Continued…

 Box Wire fashion
 2 boxes at 90o to each other
 One wire is placed medial to lateral
 Other is placed dorsal to plantar

Tension Band Wiring:

Combines K-wire with MF wire
Requires that there is a soft tissue structural component
Two K-wire’s placed the parallel fashion across fracture site with the
MF wire in a figure 8 pattern around the K-wire on the site opposite to
the tendon’s anatomical pull.
Size of wire measured in gauges -- Lower gauge; thicker wire
26 & 28 are common in Podiatry


Primarily used for fractures, osteotomies & fusions
Inserted manually or with pneumatic gun
Provide compression, distraction or maintain compression
Be careful about thickness of bone – DO NOT use if cortical bone is
greater than 2-3mm, may cause cortical fractures or not seat in bone



Compression  = Divergent Lines

Distraction  = Convergent Lines

Richards Staple: GOLD STANDARD for major fusion

Os Staple: Heat activated
Uniclip: Has an aperture
Requires a tool to compress the legs after insertion


 These features can differ depending on the function of the screw.

Head Has various configurations; hexagonal, cruciate, slotted…

Land The curve-contoured underside of the screw head

Increases the surface contact between the screw and the bone
Reduces the chance from stress-risers

Shaft/Shank Area of the screw that is void of the thread pattern

Thread The means by which the screw purchases the bone

Thread Diameter The diameter across the thread width

Measurement is the value used to describe the screw size

Core Diameter Diameter between the thread patterns

Pitch Distance between the adjacent threads

Run-Out Junction where the shaft meets the thread

Weakest point on the screw
Avoid placing the run-out near the fracture / osteotomy site

Lead Distance that the screw advances with each turn (360o)

Rake Angle Thread to axis angle

Tip Angle Tip to axis angle

Tip Either rounded (needs pre-tapping) or fluted (self-tapping)


Screw Diagram:


Types of Screws:
1. Cortical Screws
Threaded the entire length of the screw
Have smaller pitch for greater number of contacts between the
screw and the dense cortical bone
2. Cancellous Screws
Partially threaded
Larger pitch to provide greater distance of contact between the
screw and the less dense, porous cancellous bone
3. Cannulated Screws
Hollow center down the length of the screw to be used over a guide
Offers easier placement and less complications
May have decreased pullout strength
4. Herbert Screws
Ho head and two set of threads proximally not distally
Proximal threads have greater pitch than the distal threads
Indicated for intra-articular fractures
Compressive strength of Herbert screw are less than conventional
5. Interference Screws
Fully threaded, headless screw
Does not provide interfragmentary compression but resists axial
displacement of one fragment on another
Indicated for stabilization of tendon grafts to bone and tendon


Types of Screws Continued:

6. Absorbable Screws
Available in natural / synthetic polymers
Most common absorbable polymers used are based on alpha-
hydroxy acids such as L-lactic acid, glycolic acid, & para-dioxanone
Need to be able to last 6-8 weeks

Basic Properties for the Ideal Absorbable Implant:

~ Posses and initial strength to meet biomechanical demands
~ Degrades in a predictable manner over time
~ Undergoes complete absorption without harm to surrounding tissues


General Screw Fixation Technique:

~ Place one screw perpendicular to the fracture / osteotomy line for
maximal compression. Place the 2nd screw perpendicular to the
longitudinal axis of the bone this provides greatest resistance to the axial
loading forces on the bone.

~ If only a single screw placement is allowed – place the screw in an

angle that is halfway between the angle that is perpendicular to the
fracture line and perpendicular to the long axis of the bone

A. 2 Screw Technique
B. 1 Screw Technique


General Screw Fixation Technique Continued:

Load Screw Technique
This technique is commonly used in plate fixation.
Involves placement of 2 screws in the plate that is closest to the
fracture line to be drilled offset away from the fracture line.
As the screws are advanced the bone segments between the two screws
are further compressed.

Lag Screw Technique

Placement of the screw so that ONLY the thread engages the distal
cortex of the bone.
Thus further advancement of the screw results in approximation and
subsequent interfragmentary compression.
Most effective in fracture / osteotomy that is 2x’s the width of the
bone or has a fracture angle that is less than 40o.

Partially Threaded Screw Insertion Technique

1. Thread / Pilot Hole
2. Countersink (increases surface contact between screw head and the bone)
3. Depth gauge (measures distance between the proximal and distal cortex)
4. Tap
5. Insert Screw

Fully Threaded Screw Insertion Technique

1. Thread / Pilot Hole
2. Countersink
3. Glide Hole
4. Depth gauge
5. Tap
6. Insert Screw


Screw Selection Chart:

Thread Diameter Thread Hole Gliding Hole Tap Diameter

1.5 1.1 1.5 1.5
2.0 1.5 2.0 2.0
2.7 2.0 2.7 2.7
3.5 2.5 3.5 3.5
4.0 (partial/cancel) 2.5 NA 3.5
4.0 (full/cancel) 2.5 NA 3.5
4.5 3.2 4.5 4.5
4.5 (mall) 3.2 NA 4.5
6.5 (partial/cancel) 3.2 NA 6.5
6.5 (full/cancel) 3.2 NA 6.5


Soft Tissue Anchors:

 Used for reattachment of tendons or ligaments
 2 basic types: Expandable / Screw type
 Complications: Improper Placement / Failure of Suture / Pullout

 Various size and shape – allow alignment of the bones and stability
across the fracture / osteotomy site
 Stability allows for early passive RoM
 Adequate screw fixation is important for the plate to function properly
 Plate designs include semitubular, 1/3 tubular, ¼ tubular, T – plate, L
– plate, calcaneal plate…

Types of Plates:
1. Neutralization Plate
a. Prevents torsional / bending forces from acting on the lag
b. The ridge extension of the plate on the bone proximal & distal
to the fracture / osteotomy site helps neutralize any extra forces
along the bone segment

2. Compression Plate
a. Generate compressive forces along the fracture / osteotomy site
by either placing the plate on the tension side of the bone, off-
set drilling (AKA load screw technique) or pre-bending the plate.


Plates Continued…

3. Dynamic Compression Plate (DCP)

a. Employs the concepts of offset drilling with unique plate
designs to optimize the compressive forces of the plate
b. Disadvantage is it increases periosteal damage and decrease
intramedullary blood supply to the area, decreasing the overall
strength of the bone segment

4. Limited Contact Dynamic Compression Plate

a. Has a series of recessed undercuts on the undersurface of the
plate which allows limited contact between the bone and the
b. Generates less disruption to the vascular supply

5. Buttress Plate
a. Anchored to the main stable fragment
b. Supports the load-bearing bone
c. Indicated in impacted fracture that results in comminution (e.g.
tibial plateau and the tibial pilon fractures)

6. Bridge Plate
a. Useful in unstable comminuted fractures by spanning the
length of the comminution
b. Frequently used with bone grafts to fill the voids in the bone

External fixation implements the use of wires, pins, and rods to keep
bone segments in alignment or compression. Furthermore they allow
distraction of bone segments by the principle of tension-stress effect.

 Use in open fractures, acute, fractures, infected fractures and non-
 Requires minimal tissue dissection
 Allows compression, neutralization, or fixed distraction of bone
 Length can be maintained in a comminuted fracture
 Allows access to the wound site for care, monitoring and dressing
 Full weight bearing is allowed immediately post-operatively

 Requires skin and pin tract care
 Difficult frame construction
 Bulky frame
 Fracture through the bone is possible
 Refracture possible after frame removal
 Expensive

Basic Principles of External Fixation:

1. Frame should avoid and respect all vital structures in the area
2. Allow access to the wound site
3. Frame must meet the mechanical demand of the patient and injury


 Pin irritation – avoid pin placement in muscle
 Pin tract infection – most common complication (30%)
 Neurovasculature Impalement – Anterior Tibial A. & Deep Fibular N.
and they are most commonly involved
 Delayed Union / Non-Union – due to faulty frame construction
 Compartment Syndrome – due to increase in the intracompartmental
pressures (mmHg)
 Refracture – once the frame has been removed due to tension
shielding, a rare complication

Types of External Fixators:

1. Unilateral Fixators
 Produces compressive or distraction forces
 Used to fixate fractures, fuse joints, and lengthen
 Available in small or large, it is attached to the bone by multiple
half-pins screwed into the bone and attached to the fixator with the
 Main disadvantage – not create any sagital plane stability &
therefore should not weight bear immediately post-op


Types of External Fixators Continued…

2. Circulator Fixators
 Produces compressive and distraction forces
 Used to fixate fractures, treat non-unions, limb-lengthening , soft
tissue lengthening, and correction of congenital deformities.
 Utilizes trans-osseous wires with half-pins to position the wires in
different plane stability
 Limited by the circular frame’s ability to fit the extremity and
patient’s comfort of wearing the apparatus

3. Hybrid Fixators
 Combination of unilateral and the circular fixator
 Used to treat tibial plafond fractures and pilon fractures
 Utilizes trans-osseous wires and half-pins and footplate to allow
early weight bearing

4. Taylor Spatial Frame Fixators

 Newest external fixation device
 Allows for reduction and stabilization of fracture
 Its unique feature allows for reduction of complex triplane


After removal of the plate, the bone may be prone to re-fracture during
weight-bearing because of weakening of the bone from disuse
osteopenia. To prevent this complication it is important to gradually
release tension in the trans-osseous wires and loosen the pins to allow the
bone to gradually strengthen as it bears weight.

Fixator Care & Management:

Pin sites need to be kept clean with sterile solution and applied antibiotic
cream in order to prevent infection and seal the opening around the pins.
Avoid applying Betadine around the pins in order to avoid corrosion.


Hallux Limitus / Rigidus

Decreased or absent RoM at the 1st MPJ
Normal RoM = 90o (20-25o PF + 60-65o DF)

Radiographic Appearance
AP Lateral
 Focal joint space narrowing  Dorsal Flag Sign
 Joint mice  Spurring
 Spurring  Sclerosis
 Asymmetry  Metatarsus Primus Elevatus
 Squaring of metatarsal head

Etiologies = TIN-MAC
Neoplasm of bone or soft tissue
Structural = short/long 1st ray, Met Primus Elevatus
1. Meary’s Angle deviation (b/s talus should b/s 1st met)
2. Parallelism between 1st & 2nd metatarsals
3. Metatarsal parabola / protrusion deviation
Biomechanical = pronation, hypermobile 1st ray


Hallux Limitus / Rigidus Continued…

Joint Procedures:
Joint Preserving
1. Cheilectomy = Valenti (V-cheliectomy)
2. Osteotomies
 Proximal Phalanx = Bonny-Kessel (proximal DFWO)
 1st Metatarsal
Waterman = Distal DFWO
Mitchell = step-down shortening procedure
Youngswick = chevron double dorsal cut elevates
Sagital Z = corrects for elevates
Lambernudi = diaphyseal PFWO, for elevatus
Joint Destructive
1. Keller = Proximal Phalanx arthroplasty / for elderly / less
 Complications – transfer metatarsalgia, stress fracture of 2nd,
proximal migration of sesamoids
2. Implant = Hemi or Total – must cover cortical surfaces
3. McKeever = 1st MPJ arthrodesis – positioned dorsiflexed and
abducted with no rotation
 DF = 10-15o off weight bearing – one finger under toe
 5-10o of abduction
 Toe will no longer bend so patient cannot squat down

Joint Distraction with External Fixator:

1. Cheilectomy, mini rail
2. 7mm distraction intra-operatively, 2 weeks rest, then 1mm
distraction qd for 7d = Total 14mm Distraction


Function of Lesser Digits:
 Decelerate the foot
 Stabilize the forefoot
 Aid in propulsion
 Provide kinesthetic sensation

Function of Musculature:
 EDL / EDB = dorsiflex MPJ – passive flexion at PIPJ / DIPJ
 FDL / FDB = actively plantarflex MPJ, PIPJ, DIPJ
 Interossei = prevent buckling
 Lumbricales = hold digits rectus (plantarflex MPJ, dorsiflex PIPJ /

Types of Deformities:
Hammertoe Extension Flexion Extension
Claw Toe Extension Flexion Flexion
Mallet Toe Rectus Rectus Flexion

Etiologies for Contracted Digits:

1. Flexor Stabilization (Most Common)
 Weakness of intrinsic Interossei Ms
 Adv. of Quadratus Plantae
 Pronated foot type – flexors fire longer and harder
 Causes AdductoVarus deformity on 4th and 5th
 Late stance phase biomechanical abnormality
 Tx = Derotational Arthroplasty


Etiologies Continued:
2. Flexor Substitution (Least Common)
 Weakness of Triceps Surae – Flexors gain mechanical advantage
over extensors
 Supinated foot type – late stance phase abnormality
 Tx = suture FDL to Achilles tendon to strengthen muscles
 Must perform Arthrodesis

3. Extensor Substitution
 Weak Tibialis Anterior – extensor gains mechanical advantage
over Lumbricales
 Begins flexible and becomes rigid  reduce early w/ weight
 Pes Cavus / Ankle Equinus / TA weakness / EDL spasticity and
pain are frequent symptoms
 Swing phase biomechanical abnormality
 Tx = Arthrodesis if Rigid
Hibb’s Tenosuspension if Flexible


Hammertoes Surgical Procedures:

1. Tenotomy = stab incision medial or lateral to tendon deformities only
 PF digit with blade in place – flexible deformities only
 Older population only – lose strength & stability
2. Capsulotomy
3. Tendon Transfer
4. Girdlestone
 Transfer FDL & FDB to dorsal head of proximal phalanx to restore
intrinsic function
5. Hibbs
 Transfer EDL to base of proximal phalanx or met head
6. Kuwada & Dockery
 Modification of Girdlestone – drill hole in base of proximal phalanx
and bring tendons up through it
7. Lengthening
8. Z-Plasty at level of MPJ
9. Percutaneous stab incision and splint
**Complications: Muscle spasm caused by overcorrection, tenosynovitis,
scarring, adhesion, weakness, bowstringing, and nerve entrapment

1. Arthroplasty
 Post – resection of base of proximal phalanx
 Gotch & Kreuz – resect base of proximal phalanx and syndactylize
2. Arthrodesis
 Lambrinudi – fusion of PIPJs and DIPJs
 Young-Thompson – Peg-in-Hole Fusion (Peg from Prox.Phalanx)
 High amount of shortening
3. Taylor – PIPJ fusion using K-Wire


Sequential Reduction:
1. Z-Plasty
2. Arthroplasty
3. Extensor Hood Release
4. MPJ Capsulotomy
5. Volar Plate Release
6. Tendon Transfer (Girdlestone, Kuwanda & Dockery, Hibbs)

** Kelikian Push-Up Test: Performed between each step to determine if

sufficient correction has been established. If you get dorsiflexion when
placing GFR on the met head then do the next step.

Hallux Hammertoe:
 Muscle imbalance
 Iatrogenic after sesamoid removal or detachment of FHB
 IPJ sesamoid binding FHL tendon

Flexible – IPJ fusion with EHL lengthening
Rigid – IPJ fusion with Jones Tendon Transfer
~ Cut EHL distally from insertion
~ Drill hole transversely through 1st med head
~ Insert tendon through drill hole and suture back on itself

1. Lazy “S” Incision
 Lateral condylectomy of distal and middle phalanges with resection
of head of proximal phalanx

2. Derotational Arthroplasty
 Distal Medial  Proximal Lateral Incision

3. Complications
 Floppy Digit
 Edema (sausage digit)
 Floating Toe with Metatarsalgia
 Regeneration of Proximal Phalanx
 Infection
 Decreased sensation
 Blue toe

Spurs are incidental findings only and are rarely the cause of pain.
1. May be painful if directed plantarly
2. Must be present to be approved for orthotics

Conservative therapies should be used for the first 3-9 months

Plantar Fasciotomy:
1. Plantar L shaped incision at the medial midfoot
2. Release of the medial band of the plantar fascia
3. NWB for 3 weeks
4. Sutures out after 3 weeks

Endoscopic Plantar Fasciotomy:

1. Small incision in the medial rearfoot 3 fingers from the posterior
heel and 2 fingers up from the plantar foot
2. Blunt dissection to the fascia
3. Insert spatula across plantar aspect of foot, dissecting fascia from
plantar fat pad – remove spatula
4. Insert trochar into slotted tube and insert through dissected incision
– remove trochar
5. Insert scope into tube laterally and blunt probe medially – separate
medial and central bands of plantar fascia
6. Insert cutting tool into medial tube and cut medial band of plantar
fascia while pulling instrument out of the tube
7. Visually observe abductor hallucis muscle belly before removing
tube and irrigating incision site


Haglund’s Deformity:
Philip-Fowler Angle = normal 44-69o, >75o pathological
Total angle of Ruck = Philip-Fowler + Calcaneal Inclination Angle –
Normal up to 90o, pathological if > 110o
Parallel Pitch Lines – most objective method of determining a
Haglund’s deformity

Longitudinal incision lateral to TA
Dissection down to posterosuperior Calcaneus
Aggressive removal of pathologic bone, but don’t chase the bump
If you need to reflect the TA, reattach with a soft tissue anchor and
remain NWB for 3 weeks

Keck & Kelly Osteotomy:

Indicated for increased CIA angle with no Haglund’s deformity
Dorsal wedge osteotomy of the posterior Calcaneus
Rotate posterior aspect of Calcaneus dorsally after wedge removal –
Secure with cancellous screws
NWB for 6 weeks


Tendon Transfer – detachment of the tendon from insertion then relocate

to new position

Tendon Transplantation / Translocation – rerouting the tendon without

detachment from its insertion

1. Adductor Hallucis
 Resect at insertion, pass under the joint capsule and reattach at
medial aspect of the capsule
 Indicated in HAV to realign the sesamoid apparatus
2. Abductor Hallucis
 Transected at insertion, rerouted inner 1st met head and fixated at
lateral base of proximal hallux
 Indicated in Hallux Varus with an osteotomy
3. Extensor Hallux Longus
 Transected at origin, rerouted under DTIL, fixated to lateral base
of proximal hallux
 IPJ needs fused
 Indicated when have sagital component with Hallux Varus
4. Jones Suspension
 EHL excised from insertion, drill a hole transversely through 1st
met head, rerouted through hole and sutured on itself
 Indicated with cock-up deformity, flexible cavus, lesser
metatarsalgia, chronic ulcers, weak TA, flexible plantarflexion of
1st met
5. Hibb's Tenosuspension
 EDL detached from insertion, bundled together and placed
through midfoot at the base of the 3rd met or lateral cuneiform
 Indicated to release retrograde buckling at MPJs, met equines,
flexible cavus, claw toes


Types Continued...
6. Tibialis Anterior Transfer
 3 incisions at (1) proximal dorsal leg, (2) TA insertion at medial
plantar cuneiform / tubercle 1st met, and (3) the new area of
insertion in the midfoot
 Release from insertion, reroute out the proximal incision, with
tendon, with tendon passer brought to new insertion (usually 3rd
 Indicated for recurrent clubfoot, flexible forefoot equines,
dropfoot, tarsometatarsal amputation, Charcot Marie Tooth

7. Split Tibialis Anterior Tendon Transfer (STATT)

 3 incisions at (1) base of 1st met, (2) anterior leg over TA just
lateral to medial malleolus and (3) over peroneus tertius at base of
5th met
 Split tendon through proximal insertion, lateral slip passed
through peroneus tertius sheath and sutured to tendon fixated to
 Indicated for spastic RF equines, spastic equinovarus, fixed
equinovarus, FF equines, flexible cavovarus deformity, DF
weakness, excessive supination in gait

8. Cobb Procedure
 STATT but reroute to TA to PA tendon
 Indicated for PT dysfunction


Types Continued...
9. Tibialis Posterior Tendon Transfer
 3 incision (1) insertion of the PT at navicular tuberosity, (2)
anterior leg, middle 1/3 just lateral to tibial crest and (3) one at
new insertion at dorsal midfoot
 Tendon released from navicular Tuberosity, dissected free at the
medial leg insertion to expose the IM and the PT pulled through
this opening then brought to new insertion level (usually 3rd
 Indicated for weak anterior muscles, equinovarus, spastic
equinovarus, recurrent clubfoot, dropfoot, complications from
Charcot Marie Tooth, peroneal nerve plaste, leprosy, Duchenne’s
 Muscle goes from a stance to a swing muscle during gait

10. Peroneus Longus Tendon Transfer

 3 incisions (1) lateral, lower leg, (2) lateral cuboid and (3) base of
3rd met/lateral cuneiform
 Suture the Peroneus Longus to the Brevis , cut the longus at the
level of the cuboid and the tendon is brought through the
proximal incision and back through the medical incision to the 3rd
 Indicated for anterior muscle weakness, dropfoot


IM Angle 12-16o Distal Austin

Osteotomy Hohman (Neck) -- Trapaziodal
Normal: 0-8 Mitchell (Neck)
Wilson (Neck)
Reverdin Laird (Distal L)
Short Z
>16 Proximal Base Wedge
Osteotomy Lapidus (Met-Cuneiform Fusion)Hypermobile
Proximal V of Kotzengerb
Comments: with a thin Met shaft  may need to use a proximal procedure
Mitchell – shortens the length of met shaft  used in Long Met Length
( >2mm longer than 2nd met)
Taylor’s Bunion = Symptomatic when IM4-5 >9o
Splayfoot = IM1-2 + IM4-5 >20o

DASA >8o Proximal Proximal Akin

Osteotomy -- cylindrical akin w/ long prox phalanx
Normal: 0-8o -- oblique
-- transverse
-- Bonnel-Kessel  DF wedge

PASA >8o Distal Reverdin

Osteotomy Reverdin Green PASA
Normal: 0-8o


Abnormal IM:12-16o Distal Biplane Austin
PASA + Abn P Osteotomy Reverdin Laird (Distal L)  PASA + IM
+ Reverdin Green
IM Angle Biplane Mitchell  Roux
Shaft Mau
Osteotomy Ludloff
Scarf / “Z”
IM: >16o Proximal Lapidus w/ Reverdin
+ Abn P Osteotomy V Osteotomy
Logroscino (Base Wedge Reverdin)
Proximal V of Kotzengerb

HAA > 16o Silver

Normal: 0-16o Adductor Hallucis Tenotomy
Lateral Capulotomy
Comments: ST or Osseous Abnormality
↑ HAA + IM1-2 13-20o = Lodloff + Mau
(+ ↑ PASA) = Scarf Z

HIA > 10o Distal Akin

Normal: 0-10o

Tibial Sesamoid Position 4-7 Fibular Sesamoidectomy
Fibular Sesamoid Release
Normal: 0-3

Lateral IM: 8-12o Distal Osteotomy Reverse Austin

Deviation Normal 2  exostectomy Reverse Mitchell
Angle Slight  dist. Reverse Hohmann
Normal: 2.5o Increase metaphyseal Reverse Wilson
+ osteotomy Reverse Mercado
IM4-5 LDA: Inc
Normal: 0-8o IM: > 15/16o Proximal Base Wedge
Marked Inc Osteotomy

LDA: ↑
Severe Lat

Other Important Things
to Know for 3rd Year
Rotations & Externships
Dr. Bodman’s Drugs p. 68
Dr. Caldwell’s Drugs p. 74
Dr. Caldwell’s Wound Care p. 84
Ankle Scopes p. 90

Penicillin V (PO)
G+: Strep
G–: Eikenella corrodensHuman Bites
Penicillin G, Aqueous (IV)
** Tx: Clostridium Tetani if Nisseria gonorrheaSTD Septic Joint
allergic to Tetanus Toxoid Anaerobes: Clostridium perfringens
Penicillin G, Procaine (IM)
** Tx: Treponema Palidum
(Syphilis) HELPS2:
Tx: Strep Throat & Otitis Media Haemophilus
G+: Strep E. coli
G–: Eikenella corrodens Listeria
Proteus mirabellus
Amoxicillin Nisseria gonorrhea Shigella
** Used in kids instead
of Augmentin!
HELPS2 Salmonella
M Methacillin (IV)
** Toxic, not used!

O Oxacillin (Bactocil)(PO)
β–Lactamase Resistant Staph Aureus
N Nafcillin (Unipen)(PO)

D Dicloxacillin (PO)
If resistant to this = MRSA!


Carboxypenicillins Carbenicillin
High Na+ loads 
avoid pts w/ HTN
Broad SpectrumDo NOT cover β–Lactamase
Beware of Hypokalemia! Ticaricillin
G+: Good Coverage
G–: ↑ Coverage
Ureidopenicillins Mezlocillin Anaerobes: ↑ Coverage

** Tx: Pseudomonas aeruginosa

Piperazine Penicillin Piperacillin
DRUG INTERACTIONS: Warfarin, Oral Contraceptives, Probenecid, Aminoglycosides
C/I with pts on Methotrexate Rheumatiologist
75 Docs tell pts they are C/I!
Pt must take all 10d of meds or else get post-strep glomerulonephritis
Piperacillin / Tazobactam (Zosyn)(IV)
Tx: Pseudomonas aeruginosa & Proteus mirabilis
 Needs 4.5g q6h for pseudomonas
Amoxicillin / Clavulanic Acid (Augmentin)(PO) Broad Spectrum
**Staph aureus is susceptible to G+: Strep, Staph aureus
Augmentin ≤ 35% due to MRSA
G–: Neisseria gonorrhea…
Ticarcillin / Clavulanic Acid (Timentin)(IV) Anaerobes: 

Ampicillin / Sulbactam (Unasyn)(IV)

**Unreliable against G– infections!

Zosyn = 3.375g q6h
Augmentin = 875mg q12h
Timentin = 3.1g q6h
Unasyn = 3.0g q6h

Cephalexin (Keflex)(PO) G+: Good Staph aureus
Staph epidermidis
Cephadroxil (Duricef)(PO) Strep HEN – PEcKS:
Haemophilus influenza
G : Some PEcK

Enterobacter aerogens
Cefazolin (Ancef)(Parenteral) An: Some not B.fragilis Neisseria species
< 80% susceptibility to Ancef Proteus mirabilis
E. coli
2ND GENERATION Klebsiella pneumonia
Cefuroxime (Ceftin)(PO) G+: Almost as good as 1st G
(Zinacef)(Parenteral) G–: Extended HEN – PEcKS
Cefoxitin (Mefoxin)(Parenteral) An: 

Cefixime (Suprax)(PO)
G+: Significantly ↓↓↓
Cefpodime (Vantix) (PO)
G–: Superior Coverage
Ceftriaxone (Rocephin)(Parenteral) (Fortaz  Pseudomonas)
*Not good for Staph (Rocephin  Neisseria)
Ceftazidime (Fortaz)(Parenteral)
An: 
Cefdinir (Omnicef)
*Covers Staph & Strep better than 1st G.  MIC levels are superior to Cephalexin
4x’s better for Staph // 7x’s better for Strep
Omnicef = 300mg q12h
Cefipime (Maxipime)
G+: More active against Staph aureus than 3rd G
G–: Good Coverage
(+ Pseudomonas)
An: 
Ceftobiprole G+:  – Active against MRSA
G–: 
An: 

DRUG INTERACTIONS: Avoid Cephalosporins if pt allergic to Penicillin!

Cefdinir(2ndG) & Cefuroxime(3rdG) are allowed for Penicillin allergy!
 Due to different structure. 77


Imipenam–Cilastin (Primaxin)
*ID specialists ONLY! Broad Spectrum
G+:  – Most
G–:  – Most (pseudomonas – resistant)
(mycoplasma – resistant)
An:  – Excellent

Meropenam (Merrem)
*Mostly ID specialists G+: Staph & Strep only (Inferior to Imipenam)
G–:  (Superior to Imipenam)
↓ Seizure Risk! An:  

Ertapenam (Invanz)(IV/IM) DOSAGE BOX:

Invanz = 1g qd
G+:  CrCl < 30ml/min = 500mg 6h pre-dialysis
G–: Limited
An:  

Broad Spectrum
G+: 
G–:  (pseudomonas)
An: 

C/I in pts with Penicillin allergy
C/I in pts with Seizure History
Ertapenam interacts with Probenicid.


Aztreonam (Azactam)(IV/IM) G+: 

*OK for Penicillin Allergy G–:  (?pseudomonas)
No major renal toxicities; only
dose adjust for renal insufficiency
An: 
or dialysis



G+:  MRSA
Tobramycin Ototoxicity (Irreversible)
G–:  Proteus mirabilis
Amikacin Nephrotoxicity (Reversible)
* NOT use on Diabetics or MyGravis Klebsiella HypoK+ ––– Gentamycin
E. coli HypoMg+ –– Amikacin
Peak (30min post dose) & Trough
(30min before next dose) levels are Salmonella
recommended Shigella
An: 

Vancomycin (PO/IV) G+:  IVMRSA

Tx: Endocarditis Prophylaxis G–:  POClostridium difficile

for pts allergic to β-lactams An: 
- Keep for reserve cases! DOSAGE ADJUSTMENT BOX:
50kg: 750mg
DOSAGE BOX: Normal Trough = 5-10mg/dL
50-74kg: 1000mg If trough range >15mg/dL 
Vancomycin = 1g slow push IV 75-90kg: 1250mg double the dose time interval
(over 60min) >90kg: 1500mg

2ND GENERATION G+:  -- MRSA, VRSA, Strep, C.difficile

Dalbavancin(PO/IV) G–: ?
Ototoxicity (Reversible)
3RD GENERATION Nephrotoxicity (Reversible)
Telavancin G+:  -- MRSA, VRSA, Strep Red Man Syndrome
G–: ? Vestibular Imbalance
An: ? Thrombophlebitis
Absorption is limited by:
~ Antacids ~ Iron

Doxycycline G+:  Staph aureus

* Some Anti-Inflammatory
properties seen on OA MRSA
Minocyline G–:  E. coli
Methacycline Vibrio vulnificansSalt Water
Tetracycline HCL Chlamydia
An:  
NonSpecific GI Issues ~ Don’t give Doxycylcine before bed  erosive esophagitis
Photo-Onycholysis (Doxycycline)
?Acute Pancreatitis
No Pregnant / Kids ~ tooth discoloration in kids under 8y
C/I for pts on Digoxin -- ↑ Toxicity
C/I for pts on AccutaneAcne -- ↑ ICP, Pseudomotor Cerebri Risk

* Erythrasma  Coral Red Woods Lamp

Erythromycin G+:  Staph / Strep / Corynebacterium minitussimum*

Rarely used -- poor
ST penetration
G–: 
An:   GI Upset
Oral Dose = 2x Risk of Sudden Death Prolonged Heart Depolarization ~ Torsades de Pointes
Combined with Ca2+ Chanel Blockers DRUG INTERACTIONS: Potent Inhibitors of CYP 3A4
= 5x Risk of Sudden Death Cyclosprine / Sirolimus / Tacromilus
(Verpamil, Diltiazam) C/I for pts on Carbazepine & Theophyline
(Zithromax) G :  Staph / Strep
Detox in Liver G–:  GI Upset
Excreted in Bile An:   Prolonged Heart
DRUG INTERACTIONS:Potent Inhibitors of CYP 3A4
DOSAGE BOX: ↑Digoxin // ↑Coumadin
Zithromax = 500mg 1st Day
(z-pack) 250mg qd next 4 days HMGcoA Reductase ↑

Clindamycin (Cleocin) G+:  Fulminate Group A StrepNecrotizing Fasciitis

* Good Bone Penetration
* Poor CNS Penetration Group B Strep ~ may show resistance
MRSA ~ may show resistance
Cleocin = 600mg 1hr pre-op Staph Aureus** *Staph Aureus resistant to
Given as prophylaxis for G–:  erythromycin on C&S can
bacterial endocarditis An:  B. fragilis develop inducible resistance to
*C&S of organism is sensitive
to Clindamycin but resistant to
ADVERSE DRUG REACTIONS: erythromycin  do NOT give
Diarrhea Clindamycin because it will
Pseudomembranous Colitis develop resistance
↑Respiratory Paralysis with m. relaxants (Baclofen / Diazepam)



G–:  Gray Baby Syndrome
An:  Serious Infections Severe Bone Marrow Toxicity
Aplastic Anemia
. Last resort for VRE


Trimethoprim–Sulfamethoxazole (Bactrim / Septra)* Beware in pts over 50 year old


MRSA Acute pancreatitis
An:   T–S + Methotrexate = ↑ Bone Marrow Suppression
T–S + Coumadin/Digoxin = ↑ Toxicity of C/D
T–S + Oral Sulfonylureas = Hypoglycemia


Metronidazole (Flagyl) G+:  ADVERSE DRUG REACTIONS:

* Tx Pseudomembranous Colitis Peripheral Neuropathies
G–: 
N/V with Alcohol Consumption
An:  B. fragilis Dark Brown Urine
Flagyl = 15mg/kg loading dose ↑ Anti-Coagulation effects of Warfarin
7.5mg/kg q6h IV -or- 500mg tid


Ciprofloxacin (Cipro) G+:  CONTRAINDICATIONS:

DOSAGE BOX: G–:  most active Under age 18
Cipro = 750mg bid Pregnant / Nursing
against P. aeruginosa * Attacks joints
infection of bones & joints *Can cause Tendonitis / Rupture
An:  
Levofloxacin (Levaquin)
DOSAGE BOX: G–:  N. gonorrhea GI / Headache / Phlebitis all are rare!
Levo = 500mg qd (po/IV)
An:  
* Post antibiotic effects (G+)

Moxifloxacin (Avelox)
Broad Spectrum
* Good in ST
* Good for diabetic foot G+:  Staphsome resistance
infections with inoperable Strepenhanced
atherosclerosis G–: 
* May work against TB
An:  B. fragilis

Not give within 2hr of: Multivitamins, Antacids, Sulcralfate
MANY interactions! – Theophyline, Caffeine, Warfarin, NSAIDs, ddI (HIV)
May see… Torsades de Pointes & Ventricular Fibrillation

**May produce a false (+) on viral assay for opiates

Broad Spectrum DOSAGE BOX:
* Turns fluids Orange
Not given alone  Give with Cipro / Bactrim
* CYP 450 system G+:  Staph aureus
* Tx Leprosy Strep epidermidis
* Tx Vanco Resistant MRSA
G :  N. gonorrhea

An:  

Dalfopristin/Quinopristin (Cipro) ADVERSE DRUG REACTIONS:
* Reserve this drug!!! G+:  VRE Arthralgia / Myalgia
MRSA Nausea
MRSE Thrombophlebitis
G–:  ↑ LFT’s
An:   Injection Site Reaction

Linezolid (Zyvox)
* Good bone penetration G+:  VRE ADVERSE DRUG REACTIONS:
* Check weekly CBC’s MRSA Mylosuppresion
VRSA N/V lactic acidosis
G–:  Optic Neuropathy Tx >1mo
An:  

Daptomycin (Cubicin)
* Check weekly CPK’s G+:  MRSA DRUG INTERACTIONS:
VRSA Tobramycin
Statins  Myopathy
4mg/kg qd G–: 
An:  

Tigecycline (Tygacil)
* Check weekly CPK’s Broad Spectrum ADVERSE DRUG REACTIONS:
G+:  MRSA N/V
Tooth Discoloration
IV: 100mg Loading Dose VRSA
50mg bid G :  An: 83 

Itraconazole (Sporanox)
Candida GI upset / Rash / Headache
Tinea pedis(off label) 
Molds  Hepatotoxicity  LFT’s ALT & AST
DOSAGE BOX: Statins Ca2+ Channel Blockers
Pulse Dosing = 2x 100mg tabs in AM & PM with food Tikosyn Erythromycin
Take for 1 week of the mo. for ___ months
Patient with CHF!
Terbinafine (Lamisil) Dermatophytes ADVERSE DRUG REACTIONS: Rare
Onychomycosis  Headache / Abnormal Taste
Tinea pedis(off label)  Green Vision
Pulse Dosing = 250mg qd 1 week/mo over 2mo Cimetidine Cyclosporine
Normal = 250mg qd 3mo Rifampin Nortriptyline

Fluconazole (Diflucan) Dermatophytes ADVERSE DRUG REACTIONS:

DOSAGE BOX: Candida Severe Skin Rash
Pulse = 300mg/week Molds  Alopecia
Drug Interactions: CYP450 3A4

Griseofulvin (Gris-PEG)
Chronic Tinea pedis  Paresthesia / Rash / Headache
250mg tid (x4-8 weeks) Oral Contraceptives

Thiabendazole (Mintezol) DOSAGE BOX:
* Cutaneous Larva Migrans Mintezol = 10% aqueous solution qid
Ivermectin Ivermectin = 200μg/kg po x1dose for 1-2days


ACTICOAT = Nanocrystalline Silver (antimicrobial effect up to 7days)

 Reduces Exudates while maintaining a moist wound environment
 Moisten with sterile water (NOT SALINE!!! Silver reacts with Saline)
 Effective against VRE & MRSA

IODOSORB GEL / IODOFLEX DRESSING = Absorbent Iodine Cadexomer

 Slowly releases small amounts of a 0.9% elemental iodine

 Moderate to High Exudate
 Never use the adhesive type!

 Adhesive, non-woven fabric
 Hold post-op dressings / catheters / drainage tubes in place

HYDROGEL SHEETS = ElastoGel, Nu-Gel, Vigilon, Amerigel

 Low Exudate
 Re-Epithelializing wounds
 NonAdhesive
 Gas permeable
 (+) Provides Moisture
 qd change for infected wounds
 (+) No trauma upon removal
 (–) Potential to macerate surrounding skin

HYDRO-GEL = Duoderm Gel, Nu-Gel, Restore, Hypergel

 Low Exudate
 Partial  Full thickness wounds
 Use once granulation tissue is present
 (+) No trauma upon removal
 (+) Provides Moisture
 (–) Potential to macerate surrounding skin

TRANSPARENT FILMS = Opsite, Tegederm, Bioclusive, Epivew
 Adhesive, Polyurethane film
 Low Exudate
 May be used over absorptive wound filter or hydrogels
 Superficial Wounds (Blisters)
 (+) Up to 7d wear time (semi-permeable)
 (+) Allows visual assessment
 (+) Provides Moisture
 (–) Potential to macerate surrounding skin with excessive drainage
 (–) NOT absorptive
 (–) Adhesive may tear healthy skin

HYDROCOLLOIDS = Duoderm, Duoderm CGFControl Gel Formula, Tegasorb, Restore

 Adhesive, Occlusive
 Low Exudate
 Granulating & Epithelializing Partial Thickness Wounds
 May be used over absorptive wound filter or hydrogels
 Cover @ least 1inch of surrounding skin
 (+) Up to 3d wear time
 (–) May tear healthy skin
 (–) Potential to macerate surrounding skin with excessive drainage
 Change dressing before it leaks
 Odor/Drainage are Normal

FOAM = Acticoat Moisture Control, Allevyn, Polymem, TeilleAdhesive Border

 Polyurethane
 Adhesive or NonAdhesive
 Moderate to High Exudates
 Varying Thickness
 Infected wounds if changed daily
 Venous Leg Ulcers
 (+) Up to 7d wear time
 (–) May tear healthy skin

ALGINATE = Sorbsan, Dermacea Alginate, Kaltostat, Curasorb
 Seaweed Polymer
 Gel formed when fibers interact with wound fluid
 Pad or Rope Form
 Partial/Full Thickness Granulating Wounds
 Moderate to High Exudates
 (+) Haemostatic effect
 (+) Up to 7d wear time
 (–) Requires 2o dressing
 Infected wounds if changed daily
 Tan mucoid appearance upon removal
 90% Collagen, 10% Alginate
 Sheets, Rope, Paste, Granules, Powder made of Starch Polymers
 Deep Wounds
 Heavy Exudate
COLLAGEN BASED PRODUCTS: Medifil Particles/Pads/Gels, SkinTempNylon Mesh over
 Use Collagen Gels for Dry Wounds collagen membrane

 Use Sheets for Low  Moderate Exudative Wounds

 Use Powders, Particles, Pads for Moderate  Heavy Exudative Wounds
 Actions: Absorbent, Hemostasis, Chemotaxis, Provisional Matrix in wounds
for Granulation tissue formation
 PRISMA  colonized or contaminated wounds
 55% Collagen // 44% ORC Oxidized Regenerated Cellulose
 1% Silver
 55% Collagen // 44% ORC
 Only matrix proven to bind & reduce MMPs Matrix MetaloProtinase
 ORC/Collagen combo binds more MMPs in the dressing the ORC or
Collagen alone
 PEGASUS = Unite Biomatrix
 Enzyme resistant collagen scaffold -- Fenestrated

 REGRANEX = Becaplermin
 Recombinant PDGF platelet-derived growth factor
 Attracts monocytes & fibroblasts -- inflammatory phase
 Stimulates granulation tissue
 Refrigerate
 Regranex Gel 0.01%
 15g tube, apply qd, spread evenly and thin (1/16th inch)
 Cover in moist saline gauze dressing
 PROCURAN = Thrombin–Induced Platelet Releasate
 GF from patients own blood
 50-200cc of blood drawn from patient
 Spin down, separate, activate the thrombin
 1 blood draw = 3mo of daily application

 APLIGRAFT = Bilayered Skin Equivalent
 Epidermis & Dermis Dermis side down
 Newborn foreskin
 FedEx in 24hr in petri dish – use immediately
 Place a compressive wrap over it
 DERMAGRAFT = Human Dermal Replacement
 Newborn foreskin
 Cover with Allevyn & Hypofix tape
 DO NOT use with any other topical agent
 Small Interstine Submucosa Pig/Porcine
 SIS scaffold attracts patients cells
 Store @ room temp up to 18mo
 Collagen–GlycosAminoGlycan Biodegradable Matrix Cow/Bovine
 Porous Matrix of cross-linked bovine tendon collagen/GAGs
 Semi-Permeable Polysilxane (Silicone) layer
 Sterile Preperation

 Processed Human Dermal Membrane
 3-D Bioactive Frame – supports granulation tissue
 Deep Wounds
 Irradiated human skin allograft
 Epidermis & Dermis
 Store @ room temp
 After 24hr in place -- remove secondary covering and allow area to air-
dry for 2-3hr  once dried in place there is no need to recover it
 (+) Patients can do this at home
 SANTYL = Collagenase
 Digests collagen in necrotic tissue
 Collagen in healthy tissue or in newly formed granulation tissue is not
 May be used as an Antibiotic Powder
 Stop use when granulation tissue is well established
 Accuzyme, Gladase
 Papain Proteolytic enzyme from papaya
 Urea  Protein denaturing agent
 May have a burning sensation in patients RARE
 Cleanse with normal saline, NOT water
 Panafil
 Papain
 Urea
 Chlorophyllin Copper Complex Sodium  Inhibits hemagglutinating &
inflammatory properties of protein degradation products in the wound
 Elase = FibrinolysinDesoxyribonuclease RARE 2 Find
 Balsum of Peru  Increased blood flow to wound site
 Castor Oil  Creates a moist environment
 Trypsin  Maintains moist wound bed
 Aluminum Magnesium Hydroxide Stearate  Fluid Repellent

 Anterior
o AnteroMedial
 Medial to Tibialis Anterior
 Visualize: medial gutter & medial transchondral margins
 Caution: TA, Saphenous V & N
o Accessory AnteroMedial
o AnteroLateral
 Lateral to EDL or Peronial Tertius
 Visualize: lateral gutter
 Caution: EDL, Peronial Tertius, Superficial Peroneal N
o Accessory AnteroLateral
o AnteroCentral
 Lateral to EHL
 Caution: AntTibial A, Deep Peroneal N, EHL & EDL tendons
o Medial Midline Portal
 Posterior
o PosteroMedial
 Medial to the Achilles Tendon
 Caution: Sural N, Lesser Saphenous V
o Accessory PosteroMedial
o Modified PosteroMedial
o PosteroLateral
 Lateral to the Achilles Tendon
 Visualize: the posterior process of the talus & posterior media talar dome
 Caution: T-D-A-N-H
o Accessory PosteroLateral
o TransAchilles  6 Central Points
o Coaxial Portals o Med / Central / Lat – TibioTalar Artic
o Posterior Inferior TibioFibular Lig
21 POINT EXAM: o Transverse TibioFibular Lig
 8 Anterior Points o Capsular Reflection of the FHL tend
o Deltoid Lig  7 Posterior Points
o AntMed Gutter o PostMed Gutter
o Med / Central / Lat – Talar Dome o Med / Central / Lat – Talar Dome
o Ant TibioFibular Articulation o Post TibioFibular Artic
o AntLat Gutter o PostLat Gutter
o Anterior Gutter 90 o Posterior Gutter
PODIATRIC RADIOLOGY also leave epiphyseal scars which may look like stress fxs.
These occur in predictable anatomical areas. Epiphyseal
INTERPRETATION OF PEDAL RADIOGRAPHS plates tend to close from medial to lateral in teenagers.
X-ray interpretation is a written notation of pathological Talar beaking is a finding on lateral of the distal neck of the
findings made in objective terminology. Correlation of talus that occurs secondary to capsular pressure.
radiographic findings along with clinical and lab findings Trabeculae in some circumstances may be accentuated, and
allows a physician to arrive at differential diagnoses. X-ray look possibly like a fx.
interpretation follows the 5-step approach: The calcaneal apophysis is located at the posterior aspect of
1. Quality of Film the calcaneus, and has irregular margins. It is often mistaken
for a fracture. It also may be normally bifid.
• Too light or too dark (background/film density)
Compact bony islands are normal and benign variants.
• Proper projection
A simulated fracture may occur in any bone w/ more than
• Proper positioning one ossification center.
• Adequate contrast The silver dollar navicular is a normal (small) variant of
2. Soft Tissue Assessment navicular development – be sure to r/o Kohler’s dz.
• Increased ST density (edema, obesity) A pronated foot may cause the spaces between bones in the
• ST calcification (vascular, traumatic, chronic) midfoot to be accentuated, causing a simulated lisfranc’s fx.
• ST contour – thicker medially and proximally A pseudo-epiphysis is a secondary ossification center.
• Foreign bodies (r/o artifact w/ multiple views) The gun-barrel effect is seen when a bone (usually phalanx)
3. Bone Assessment is perpendicular to the film plane. It may look like a cyst.
• Number of osseous structures – start distally and Distal phalangeal condyles are normal variants.
work proximally Cone-shaped epiphyses may be normal but are frequently
• Integrity and morphology of osseous structures – are syndromic as well.
cortices intact? Are there structural changes?
• Density of osseous structures – evaluate 2nd MT ACCESSORY OSSICLES AND SESAMOIDS
o Rule of 1/3s – in individuals <40 y/o, middle 1/3 Accessory ossicles and sesamoids are normal variants in
should be medullary, outer 2/3 should be cortical anatomy that occur in predictable locations. Accessory
o Rule of 1/2s – in individuals >40 y/o, half bone ossicles usually arise earlier, are larger, and irregular
should be cortical, half medullary compared to sesamoids (which are usually present in tendons.)
o 1/3 of bone is lost before apparent on X-ray Os Trigonum (2-8%) – occurs posterior to the lateral tubercle
o Cortical bone lost at a rate of 2%/year (>35 y/o) of the talus. When fused (~18 y/o) is called steida’s process.
o Medullary bone lost at a rate or 1% per year Os Tibiale Externum (3-12%) – secondary ossification center
4. Joints and Joint Spaces of the navicular tuberosity. The pre-hallux type is pyramidal
• Is there narrowing? Is it symmetrical/asymmetrical? in shape, while the accessory navicular is in the PT tendon.
• Absence of joint = coalition/joint fusion Os Intermetatarsium (1-10%) – occurs btw the 1st cuneiform
• Increased space is due to joint effusion and 1st and 2nd MT bases. May fuse.
5. Biomechanical Assessment Os Supranaviculare (1%) – located on the dorsal aspect of
• Measure of angular relationships for treatment goals the TN joint (may look like fx/osteophyte).
• Determines surgical procedure and post-op correction Os Calcaneus Secundarius (1%) – located at the anterior
process of the calcaneus – may be confused w/ rowe fx.
• Performed in angle and base of gait
Os Sustentaculi (<1%) – is located posterior to the
• Serial radiographs to check progression of healing
sustentaculum tali, often fused. Is assoc w/ STJ coalition.
Conclusion – use systematic approach to avoid missing
Os Supratalare is located on the dorsum of the talar head.
details. Review the entire film. Do not let your eyes be drawn
Os Vesalinum (<1%) – occurs at the proximal 5th MT base.
to the obvious. Cite only differentials which make sense and
Usually confused w/ apophysitis, or a stewart/jones fracture.
are defensible to you.
Accessory ossicle of the Hallux occurs usually at the base of
the distal phalanx at the medial or lateral aspect.
Os Subtibiale/Subfibulare (4%) - occur distal to the medial
Identification of variants requires knowledge of normal
and lateral malleoli. R/o trauma
anatomy. Often normal variants are mistaken for pathology.
Hallux IPJ Sesamoids (50%) – located at the IPJ of the
The simplest error in this regard is structural overlap due to
hallux, may remain cartilaginous. Assoc w/ plantar HPKs.
wrong projections ordered.
Lesser IPJ Sesamoids occur in the joint capsule and short
Benign fibrocortical defect – small area of discontinuity
flexor tendons of the lesser digits. Does not occur in the 3rd.
usually in long bones. Eventually fades away over time.
Os Peroneum (20%) - a sesamoid in the PL tendon near the
Nutrient foramen – may look like a fx, but discontinuity
cuboid. Often is not ossified.
“stops” halfway through the cortex.
Constant Sesamoids occur in the MPJ of the hallux and
Ward’s triangle – area of low trabecular density in the
ossify around 10-12 y/o. The tibial sesamoid is larger and is
anterior inferior portion of the calcaneus.
commonly bipartite. Partitions occur in cardinal body planes,
Epiphyseal plates can look similar to fractures, if the X-ray
and their combined size is greater than a single sesamoid.
passes through the plane of the plate. Closed epiphyseal plates
You must r/o fx when dxing a bipartite sesamoid.
lymphatic channels), inflammation, surgery, burns, infection,
or helminthic infestation. Inflammatory edema is associated
with systemic disorders, particularly arthridites and metabolic
disorders. D/Dx include A vitaminosis, RCPS, melorheotosis,
collagen vascular diseases, dilantin use, reynaud’s disease, and
thyroid dysfunction (thyroid acropachy – nodular myxedema.)
THE 5 STEP APPROACH TO PLAIN FILM ANALYSIS Traumatic edema will be localized to the site of trauma and
STEP 2: SOFT TISSUE ANALYSIS should be consistent with the history. Besides direct trauma,
The soft tissue analysis of plain film incorporates two main this type of edema is seen in stress fractures, infection, and in
features: surgical sites post-op. Of particular clinical significance is
1. Tissue Density edema in the posterior triangle (bordered by the posterior
2. Tissue Contour flexor hellucis longus, the anterior tendo Achilles, and the
First you want to determine what kind of view you posterior-superior calcaneus.) Edema or hematoma from
are looking at. The most common is of course the DP view of injury to the tendo Achilles will cause this triangle to
the foot, which may be taken WB or NWB. To tell the disappear, which is a pathologic finding. Another pathologic
difference, look at the joint spaces and see if they are clearly finding is the teardrop sign of the ankle, which is visible as
visible. If the MPJs are clearly visible the view is probably increased tissue density surrounding the ankle joint. This is
WB, which is taken at 15 degrees as opposed to NWB, which caused by extravasation of fluid to the ankle joint subsequent
is shot at 0. You may also look to see the ankle position (90 in to trauma. Ligamentous sprain is visible as diffuse edema
WB.) The view is important because WB views will show the surrounding the area of the affected ligament.
soft tissue somewhat distorted due to pressure. On the DP this Burns and frostbite cause areas of devitalized tissue
presents as extra thickness of the S.T. on the lateral column, to show up on radiographs as areas of increased density.
and on the lateral it presents as flatness on the plantar surface. Small localized areas of increased density are visible in the
The first point, density evaluation, requires case of focal gigantism associated with acromegaly. Bony
knowledge of different tissue densities to be of any use. The growth is also affected in this disorder and diagnosis should be
least dense material is of course gas or air, which is easy to make if it has not been made already.
pathologic. The next higher density is fat, typically seen in Heel pad thickening is a finding associated with a
kager’s/bohler’s/toygar’s triangle, as well as on the plantar number of pathologies, and as such measuring the heel pad is
surface. Next dense from fat is water, which is the primary recommended in routine analysis of NWB views. Possible
composition of the soft tissues including muscle and tendon. D/Dx include acromegaly, dilantin use, plantar edema, plantar
Muscular compartments of the foot as well as the tendo infection, obesity, trauma, myxedema, and thyroid acropachy.
Achilles will be of this density. Next dense is atrophied or The accepted limit for normal heel pad thickness is 25mm.
devitalized tissue, which is somewhat dehydrated. Like gas, Soft tissue emphysema is a decrease in radiodensity
tissues of this density are pathologic and should be explained due to the presence of air or gas in the tissues. Always
fully. Next dense is calcific density, which is the density of pathological and often the sign of an emergent situation, S.T.
calcium deposits in the tissues. This is most often pathologic. emphysema is a worthy finding. Gas is almost always
Next dense is ossific density, which is the density of bone. produced by bacteria, especially clostridium perfringens,
Bones are only slightly denser than calcified structures – they which may produce superficial emphysema (radiographic
are normally differentiated by their internal architecture. emphysema) or deep emphysema (deep intramuscular
Finally, the densest structures radiologically are metallic or emphysema). The only non-emergent emphysema finding is
glass structures, which are almost completely radioopaque. of a gas abscess which is a localized ulceration containing gas
Objects of this density are almost always foreign bodies, which does not spread to other areas. Gas abscesses are
although in many cases they simply represent fixation or typically found only in the distal part of the digits. It is
implants from prior surgery. important to distinguish emphysema from the decreased
Pathologic changes in soft tissue density may be radiographic density caused by a sinus tract leading to an
either an increase or decrease in character. Edema causes ulcer. A sinus tract will always track back to the surface of
generally an increased radiodensity which matches that of the skin, whereas emphysema is contained within the soft
muscle or tendon, usually in areas where fat density is normal. tissues.
This is important in the posterior triangle as well as on the Some disorders which affect only soft tissue contour
plantar surface of the foot as extravasation of blood or fluid are worthy of note as well. Ainhum’s disease is a thickening
will show up as an obliteration of normal fat anatomy on film. of fascial bands about the base of the proximal phalanges of
Edema also causes an increase in soft tissue contour, which is the digits, causing a constriction of the underlying tissues that
the second point to evaluate in soft tissue analysis. Edema is is visible on x-ray. This constriction eventually leads to
normally classified by its cause. Obstructive edema is autoamputation, and although it is easy to diagnose from X-
caused by obstruction of the lymphatic channels draining the ray, there is no known treatment for this disorder. The
affected area. This may be normal for the individual with sullivan’s sign sometimes seen on radiograph is a splaying of
congenital lymph blockage, as in lymphedema praecox, but digits which are abducted away from each other at the level of
with insidious onset of obstructive edema a previously the MPJ. This is caused usually by a space-occupying lesion
undiagnosed pathology may be at work. D/Dx include tumor, like a neuroma or interstitial fibrosis following surgery.
trauma, radiation (repeated exposure to radiation damages Sometimes, however, the etiology is biomechanical, due to the
unequal pull of flexor tendons that can result from DM motor particularly CREST syndrome. Calcinosis circumscripta
neuropathy, or simply from closely positioned metatarsal associated with frank scleroderma is termed thiberge-
heads. weissenback syndrome. These distal calcifications
Vascular calcification is seen in varicose veins, predispose the digit to ulceration. Tumoral calcinosis is not
monckeberg’s sclerosis, ASO, thrombophlebitits, and DVT. associated with cancer as the name implies, but rather is a
They appear on X-ray as thin parallel or curvilinear lines. descriptive term referring to the presentation of the
Phleboliths are small round or oval calcifications that appear calcification. Seen in renally compromised patients (usually
within superficial veins. DM type II), these calcifications begin near joints as small
Dracunculosis is a rare finding that is seen in nodules that eventually grow in size to possibly impinge
patients who have had a history of filiaria medinasis infection. neurovascular structures, limit ROM, and cause ulceration.
These helminthes, which burrow into the dermis of the foot, The typical presentation is near the 5th MPJ. This type of
remain after death as bits of foreign tissue that sometimes growth is benign.
calcify. The dracunculosis is the radiographic finding of these The last form of calcinosis is calcified bursa
calcified helminthes, which present as curvilinear lines of secondary to irritation (usually posterior heel, medial 1st MPJ,
radiodensity that do not follow any vascular anatomy. lateral 5th MPJ.)
Hemosiderin deposits may calcify in tissues Soft tissue ossification is distinguished from soft
following the trauma or disease state that caused them. This tissue calcification by the degree of organization within the
type of increased radiodensity is typically seen in periarticular ossified segment, typically with trabecular patterns.
tissue, arthritic joints, or the subcutaneous area of the ankle. Additionally, ossifications that occur near bone
General calcification of the soft tissues can be characteristically do not cause periosteal reaction.
distinguished from ossification by the degree of organization Progressive myositis ossificans (aka fibrodysplasia ossificans
seen in the radiodense area. Calcification is non-homogenous progressive) is a rare childhood disorder in which there is
and disorganized, giving a “salt and pepper” appearance. extensive and unexplained muscular ossification which causes
Ossification, in contrast, is highly organized, often exhibiting extraarticular ankylosis and disuse osteoporosis.
a trabecular pattern, and may have a cortex. In general, soft Neurological myositis ossificans has a similar presentation
tissue calcification is much more common that ossification. but occurs in conjunction with a neurogenic lesion (stroke,
Calcification etiologies are organized into three broad spina bifida, encephalitis, syphilis, brain trauma,
categories: metastatic, dystrophic, and calcinosis. myelomeningocoele, spinal cord hemisection, tuberculosis,
Metastatic calcification is systemic calcification of a and poliomyelitis). The calcifications occur at levels below
metabolic derivative, such as hyperparathyroidism, the neurogenic lesion. Finally, myositis post-traumatica
hypervitaminosis D, renal osteodystrophy, sarcoidosis, or (circumscripta) is an area of localized ossification secondary
cancer. The calcifications are caused by an imbalance in to acute trauma. Ossification begins soon after the traumatic
calcium or phosphorus metabolism. The calcifications may incident, but cortical formation is only seen 6-8 weeks after
appear vascular, but are typically more numerous and less the incident. Ectopic bone within the muscle may also be seen
organized than vascular calcifications. Advanced parallel to the muscle fibers. On X-ray the mass appears
hyperparathyroidism causes chunky calcification, in which similar to an egg, with well-defined borders. Histologically it
separate calcifications conglomerate into calcified patches that contains the same sections as an epiphyseal plate.
are prone to ulceration. Foreign body analysis in soft tissue is vital to
Dystrophic calcification is calcification of localizing the foreign body for surgical removal. Analysis of
devitalized tissues without metabolic imbalance. the film typically calls for the ”tunnel technique” in which a
Theoretically calcium precipitates in devitalized tissue, giving piece of paper is rolled up into a tube, which is used to analyze
rise to this type of presentation. Examples of possible small segments of the film at a time. Often needles are placed
etiologies include ehlers-danlos syndrome, pseudoxanthoma in three planes near the affected area so that when films are
elasticum, fibromatosis, tumor, cyst, hematoma, focal taken the exact location of the object can be triangulated. For
necrosis, trauma of any kind, and vascular disease. One some foreign bodies, particularly wood, advanced imaging
peculiar finding is that of hemarthrosis, which is calcification modalities (ultrasound, CT, MRI, xerogram) should be
of blood exudate in a joint space. These calcifications may employed.
aggregate as “pebbles” within the capsule, visible on x-ray,
that can limit ROM of the affected joint (common in the
Calcinosis is the term applied to califications that are
idiopathic in nature. There are four syndromes associated
mainly with calcinosis. Calcinosis interstitialis universalis
presents as a calcification of subcutaneous structures,
progressing deeper with time. It may affect any soft tissue,
but calcifications are generally laid down in linear
aggregations parallel to the long axis of the limb. This
condition is very rare and is diagnosed in youth. Calcinosis
circumscripta is a distal subcutaneous calcification that is
normally associated with collagen-vascular diseases,
THE 5 STEP APPROACH TO PLAIN FILM ANALYSIS progressive onset of pain, stiffness, swelling, and atrophy
STEP 3: BONE EVALUATION distal to the site of injury over a 3-6 month period. The cause
is hyperactivity of the sympathetic nervous system. In type I
OSTEOLYTIC DISORDERS RCPS no specific nerve damage can be identified. In type II
Osteoporosis is an absolute reduction in bone mass RCPS direct nerve injury has occurred. In 70% of pts, the
and density. Osteopenia is a generalized term to denote a disease can spread up the extremity, sometimes even to the
relative loss in bone density regardless of any etiology. opposite limb. RCPS can also be staged.
Osteoporosis is the most common skeletal pathology, common Stage I describes localized edema, muscle pain, joint stiffness,
in smaller older individuals who are less active. Females are and vasospasm with duration of about 3mos. Additionally,
affected more commonly then males overall. (Age-related, or trigger points form where touch causes pain out of character to
“senile” osteoporosis affects men and women equally.) the stimulus (causalgia.) Osteopenia is noted on x-ray distal to
Environmental factors that contribute to osteoporosis include the lesion.
smoking, alcohol intake, estrogen deficiency, and the use of Stage 2 includes increased pain and area of involvement,
certain medications. The most common presentation of brawny edema, hair loss, brittle nails, and spotty osteopenia.
osteoporosis is vertebral fracture, followed by hip fracture. (Osteopenia w/ areas of normal bone.)
Bone loss in osteoporosis is mostly cortical (80%), Stage 3 trophic damage becomes irreversible at this stage, w/
but 33-50% of bone must be lost before the disease is evident intractable pain, muscle atrophy, joint weakness, flexor tendon
on x-ray. Peak bone mass is realized at age 35, with contracture (producing deformity) and deossification.
involutional bone loss due to age beginning at age 35-40. Tx for RCPS includes pain tx (NSAIDs, opiates), nerve
Cortical bone is lost at a rate of about 1% per year after this blocks, physical therapy, and sx sympathectomy.
point. Bone has a gray appearance on x-ray w/ the primary Osteomalacia is a lack of calcium in osteoid matrix
trabeculae accentuated and the secondary trabeculae reduced. laid down by osteoblasts, resulting in improper bone
Primary osteoporosis is that which has no underlying mineralization. Symptoms include muscle weakness, bone
disorder. Secondary osteoporosis is caused secondary to a pain on palpation, and bone deformity. X-ray shows osteoid
pathology like steroid tx, myeloma, metastasis, gastric sx, seams, lines of unmineralized bone that appear as pseudofxs
anticonvulsants, hyperparathyroidism, heparin, DM, (aka increment fx, looser line, umbua zonen, milkman
alcoholism, disuse, hypogonadism, amenorrhea, and anorexia. syndrome). The cortex is thin and blurs into the medullary
Generalized osteoporosis affects all bones, particularly of the bone (endosteal blurring.)
axial skeleton, and may be post-menopausal or senile. Post- Rickets is osteomalacia seen in children, usually due
menopausal osteoporosis affects females aged 51-75, and is to vitamin D deficiency (but also due to renal dz.) It typically
caused by the increased osteoclastic action present in states of affects children 6-12 months old, and will be accompanied by
estrogen deficiency. Mainly only medullary bone is lost, with muscle tetany, irritability, and weakness. Physical
coarsened trabeculae. It is particularly associated with development is impaired, bone growth is impaired and
vertebral, hip, and colle’s fx (wrist.) Lab values for this type deforms. Cartilage in the epiphyseal plates hypertrophies and
of osteoporosis are normal except for a decrease in PTH. is surrounded by edema. CXR shows a rachitic rosary about
Senile osteoporosis has about an equal distribution btw males the costo-chondral junctions. Proximal calcification of the
and females over 70 y/o. There is a proportionate loss of metaphyses is absent, and margins are frayed and cupped.
cortical and trabecular bone due to generalized loss of Pseudofractures are also seen in rickets as well as
osteoblast activity. Lab values show increased PTH. The tibial/femoral bowing.
most common presenting symptom is extra-capsular hip fx. Scurvy is a disease caused by long-term deficiency
Regional osteoporosis occurs only in a particular segment, of vit. C. It takes 4 months to be apparent on X-ray, and
usually due to disuse atrophy. Localized osteoporosis affects typically affects infants aged 4-8months. Scurvy is
one part of a bone, and is due to tumor, arthritis, or infection. characterized by improper collagen formation, leading to
Diagnosis of osteoporosis is preferred with a device spontaneous capillary hemorrhage, osteopenia, and poor
called a DEXA scanner, or dual-energy x-ray absorbiometry. cartilage. Radiographically, there is a dense zone of
This measures the absolute density of bone via penetrance of provisional calcification (line of frankel), ring epiphyses
x-rays. CT can also be used to diagnose this disease. (wimberger’s sign), irregular metaphyseal margins (corner
Osteoporosis is graded using the calcaneal index: sign), metaphyseal protuberance (pelken’s spurs), scorbutic
Grade V (normal) – all trabeculae are uniformly present zones (trummerfield zones), and sub-periosteal hemorrhage.
Grade IV (normal) – posterior compressive trabeculae are Hyperparathyroidism is ostepenia due to
divided into two separate columns overactivity of the parathyroid gland. Primary
Grade III (borderline) – posterior tensile trabeculae are lost hyperparathyroidism is caused by parathyroid
Grade II (osteoporotic) – anterior tensile trabeculae lost adenoma/carcinoma/hyperplasia, or an ectopic PTH-secreting
Grade I (severe) – all tensile, most compression trabeculae tumor. Secondary hyperparathyroidism is caused by renal
are lost disease. Typical presentation is female, 30-50 y/o, weakness,
Regional Complex Pain Syndrome (RCPS) also lethargy, polydipsia/uria, hypercalcemia and kidney stones.
known as the “great mimicker,” manifests on x-ray as an acute Serum calcium and phosphate are elevated. The radiographic
painful regional osteopenia following minor trauma. Males hallmark is sub-periosteal bone resorbtion (1), followed by
and females are equally affected, and patients are typically accentuated trabeculae and reduced medullary bone (2), and
over age 50 and of type A personality. Presenting s/sx are formation of brown tumors. (3) Bone resorbtion typically
occurs first in the phalanges, and soft tissue ossifications may Hypervitaminosis D presents with nausea, anorexia, polyuria
also be seen. Brown tumors are “holes” in the bone that are and polydipsia. X-rays show extensive calcification of blood
filled with osteoclast-laden fibrous tissue, seen in both primary vessels, soft-tissue, kidney, and peri-articular spaces.
and secondary forms.
Melorheostosis of Leri – “flowing hyperostosis” that looks
like candlewax dripping down the bone. Etiology unknown. BONE AND FRACTURE HEALING
No gender predilection. Joint effusion w/ decreased ROM and Bone Characteristics: Bones support our frame as well as
contracture, one limb (monomelic) affected, muscle wasting, protect the vital organs, provide a source of calcium, a site of
lymphedema all are symptoms. X-ray shows wavy cortical insertion for tendons and ligaments, and provide the rigidity
thickening, narrowing of endosteal space. needed for movement against gravity. Bones comprise 1/10th
Osteopathia Striata – “Voorhoeve’s Disease” most of our body weight. They resist axial stresses very well but
commonly seen in the hip metaphysic. Seen as a linear band are weak against rotational forces. Tubular bones are built for
of bone density of unknown etiology, typically coexisting with axial support and locomotion. Flat bones are built for
sclerosing dysplasias. protection of vital organs.
Osteopetrosis – “Albers-Schoenberg Disease” also known as Bone Healing: Consists mainly of spontaneous regeneration.
“brittle bone disease.” Medulla is completely destroyed – all Tubular bone forms by endochondral ossification, flat bones
bone is cortical. Existing bone thus has no shock absorbing by intramembranous ossification. The periosteum surrounds
ability and is very brittle. It is a hereditary disorder in which and protects the bone, and is made up of an outer fibrous layer
the osteochondroid tissue of developing bone fails to mature and an inner “cambium” layer which contains osteocytes. It is
into medullary and lamellar bone. There are 2 types: this inner layer of the periosteum as well as the endosteum that
osteopetrosis tarda (benign, a dominant trait) and osteopetrosis are most closely associated with bone healing.
congenital (malignant, recessive trait w/ neck LAD and HSM.) FRACTURE TERMINOLOGY
Lack of bone remodeling results in long bones having an Avulsion Fx – pulloff fx consisting of a fragment of bone
Erlenmeyer flask deformity (flared metaphysis.) Variably, pulled off by a muscle, tendon, or ligament.
some persons present with a spotty osteopetrosis which Butterfly Fx – triangular shaped cortical fragment that is part
appears like a “bone within a bone” or as striations of normal of a communuted fracture.
bone with osteopetrotic bone. Chip/Corner Fx – small fragment of bone from a joint
Osteopoikilosis – “Osteopathia condensans disseminata” or margin. Distinguish from a joint mouse, which is a piece of
“spotty bone disease” is a hereditary disorder that presents as osteophytic bone that breaks off into a joint space.
multiple compact bone islands existing within normal bone. Closed Fx – does not penetrate the skin.
The disease is asymptomatic and is usually an incidental Comminuted Fx – consists of more than 2 pieces.
finding. Turnover is also very high, such that two radiographs Fleck Sign – avulsion fx by the lisfranc’s ligament of the base
taken in the same year may show completely different of the 2nd metatarsal.
presentations. 25% of patients have a coexisting Impaction Fx – telescoping of bone segments (also called
dermatological problem (dermatofibrosis, scleroderma, “bayoneting”) that results in shortening of a segment.
syndactyly), 20% have arthralgia. X-ray shows multiple Greenstick Fx – incomplete fx in which one cortex is affected
compact bony islands in long bones with uniform density. and the fracture line follows down the axial line of the bone.
Rarely, bone islands may have a radiolucent center. Torus Fx – trabeculae are buckled inwards with a cortical
Compact Bone Islands are normal variants seen in regular bulge around the fracture site
radiographs. They appear as small areas of radiodensity, Insufficiency Fx – aka pathological fx, caused by normal
usually in flat or tubular bones. What may appear normally as physiological stresses through diseased bone.
a compact bone island can rarely be a osteoid osteoma. Oblique Fx – fx is 45 degrees from the long axis of the bone
Osteoid Osteoma is a painful benign tumor that is typically Occult Fx – see also stress fx; subtle and difficult to identify
<1cm, appearing as a compact bone island with a radiolucent Open/Compound Fx – skin is penetrated
center. They are usually located near the cortex. Symptoms Simple Fx – two bone fragments are involved
include pain at night, relieved by ASA. Dx w/ bone scan. Spiral Fx – fx is circumferential and longitudinal in bone
Heavy Metal Poisoning can be by lead (plumbism), Stress Fx – due to repetitive stresses, no fx line is apparent but
phosphorus, or bismuth. Lead lines at the metaphyses are bony callus forms 10-14d on X-ray. Must rely on clinical Sx.
visible on radiographs one month after exposure. Lead Transverse Fx – fx at 90 degrees to the long axis of bone.
deposition may also be seen at the distal ends of the digits. FRACTURE REPAIR
Lead line density is determined by the amount of lead Displacement/Distraction – requires reduction
ingested, the width is the single-time duration of exposure, and Closed Reduction – realign fragments through manipulation
the number equals the number of exposures. What may of ST, stabilize w/ cast
appear as lead lines in a 4 y/o or younger is actually a normal Open Reduction – realign fragments surgically, using ORIF
finding. Lead foreign bodies do not cause plumbism (unless Inflammatory Phase – Periosteum, haversian system
located within a joint space.) damaged, bleeds to form hematoma. Osteocytes die from
Hypervitaminiosis A presents with dermatitis, pruritis, ischemia, creating necrotic tissue that induces the
alopecia and skin yellowing. X-rays show solid periosteal inflammatory response of vasodilation, edema, and
bone at the ulna and metacarpals. macrophage attraction.
Reparative Phase – governed by vascularity, the reparative This is a variant of non-union characterized by scar tissue and
phase involves the formation of a callus which is mainly fibrin false joint formation. Congenital pseudoarthrosis is present
from inflammation invaded w/ pluripotent cells for healing. A at birth and is assoc w/ neurofibromatosis. It typically occurs
collar callus forms around the bone to stabilize, dictated by in the distal tibia/fibula. Acquired pseudoarthrosis causes
the periosteum, while the internal callus is dictated by the pain, instability, and bowing, with sclerotic bone ends and
endosteum and dictates bridging and union between the two lucency between fragments. It is most common in the distal
segments. Compression encourages bone rather than fibrous tibia.
tissue formation. Necrotic tissue is simultaneously removed. Malunion
Clinical Union – the goal of reduction, clinical union is the Bone healing that occurs in non-reduced fx, in which bones
resolution of symptoms w/ palpable rigidity to the affected are in improper position. It can spontaneously correct in peds.
bone. Clinical union precedes radiographic union. THE 5 STEP APPROACH TO PLAIN FILM ANALYSIS
Remodeling Phase – begins while the reparative phase is STEP 4: EVALUATION OF JOINT SPACE
winding down, in the remodeling phase the callus is resorbed
and the trabecular bone remodeled along lines of stress, PEDAL COALITIONS
resulting in a bone that is stronger than when it broke. A coalition is a union of separate things into a single body or
Cancellous bone heals faster than cortical bone, and has a group; true coalitions are intra-articular fusions of bones,
smaller callus. Cortical healing is limited by vascularity and and bar/bridge coalitions are extra-articular fusions of bone.
the amount of movement permitted during the healing phase. A complete coalition is osseous and limits all motion. An
COMPLICATIONS OF FRACTURE REPAIR incomplete coalition is a union by fibrous or cartilaginous
Delayed Union – union is not achieved w/in the expected time tissue. A rudimentary coalition is an osseous projection
(6 wks.) This is due to inadequate reduction, soft-tissue which limits motion but does not produce a union of parts.
imposition in the fx, excess ST destruction, vascular A synchondrosis is a cartilaginous union, a synostosis is a
disruption, inadequate immobilization, fragment distraction, or bony union, and a syndesmosis is a fibous union of two parts.
inadequate fixation. AO principles dictate that bone healing Coalitions are caused by accessory ossicles (os trigonum, os
fails in tension and heals in compression. sustentaculi proprium), failure of mesenchyme to segment in
Non-Union – complete arrest of bony repair, replaced instead development, trauma, DJD (causing a fibrocartilaginous
by fibrous, cartilaginous, or synovial compensation for the fx fusion), inflammatory rheumatoid conditions, and fxs.
site. It is variably classified as being diagnosable 6-8 months Tarsal coalitions occur in 1-2% of the population and consist
post-fx. Others say non-union is dx if no radiographic healing of the talo-calcaneal coalition (most common), calcaneo-
changes are seen for 3 months. Classification of non-union is navicular, and talonavicular (least common.)
by Weber and Cech, and are divided into two major Ossification of coalitions in the tarsus occur at different times.
categories, hypertrophic and avascular (or hypotrophic.) The age of ossificiation determines when symptoms occur.
Hypertrophic Non-Union may be of the elephant’s foot type, Talonavicular coalitions 3-5 y/o
the horse’s hoof type, or the oligotrophic type. Elephant’s Calcaneonavicular coalitions 8-12 y/o
foot type is usually due to early WB and inadequate Talocalcaneal coalitions 12-16 y/o
stabilization. Horse’s hoof is caused by inadequate internal S/Sx of coalitions include stiffness, decreased ROM, pain,
fixation that has allowed a small amount of movement. peroneal spasm, anterior/posterior tibial spasm, local POP,
Oliogotrophic non-union has poor callus, and is usually due to pronation, cavus deformity, and fixed RF valgus.
inadequate alignment of fx ends. Peroneal spastic flatfoot is characterized by restricted STJ
Avascular Non-Union – consists of four types; torsion motion, RF valgus (in OKC), FF abduction, bowstrung
wedge, comminuted, defect, and atrophic. Torsion wedge is peroneal tendon, and extensor digitorum longus spasm.
incomplete healing of a fx in which there are three or more D/Dx of coalitions include RA, JRA, trauma, neoplasm,
pieces, in which some pieces fuse together but others do not acromegaly, CCPV, casting (causing peroneal contracture),
because of inadequate vascularity. It is sometimes seen with extra-articular arthrodesis, overcorrected flatfoot,
plate fixation, usually in the tibia. Comminuted non-union is osteochondral dystrophy, infection, and N/M disease.
the presence of one or more fragments that become necrotic, Plain film analysis of coalitions is cheap and able to identify
the callus fails, and any involved fixation may break from most symptomatic coalitions.
stress. Defect non-union is the loss of a devitalized fragment IPJ coalition can be viewed on AP projection.
of cortical bone that leaves a dead space within the bone Synphalangism is a congenital fusion of the IPJs.
which cannot be bridged. Atrophic non-union is a long-term Intermetatarsal coalition may be viewed on AP and oblique
result of insufficient vascularity that causes fx ends to become views. Diaphyseal fusions are typically the result of trauma.
osteopenic and atrophic. Metatarsal cuneiform coalition may be viewed with AP,
Radiographic Findings of Nonunion med oblique (medial column), or lat oblique (lateral column.)
Sclerosis of the fracture ends, failure of changes of healing, Navicular cuneiform coalition may be viewed with the AP
progressive bowing, increased bone atrophy above and below and medial oblique projections.
fx site, excessive callus formation, and absence of remodeling. Navicular cuboid coalition may be viwed w/ AP or oblique.
Bone scans show up “hot” in non-union; increased uptake at Calcaneocuboid coalition may be viewed on lateral or lateral
the fracture ends may be indicative of pseudoarthrosis oblique views (typically it is osseous and easy to pick up.)
formation. Talonavicular coalition can be viewed on AP and medial
Pseudoarthrosis oblique. AP shows a “putter sign” of the fusion.
Calcaneonavicular coalition can be viewed on lateral and Conclusion – correlate coalitions w/ pts age. Be suspicious of
lateral obliqe, and shows an “anteater sign” on lateral. These changes in plain films. Consider advanced imaging to
fusions are more commonly cartilaginous or fibrous in nature. investigate further. (Special views, CT, MRI.)
STJ coalition is the most common tarsal fusion, and usually is
the middle facet (the posterior facet is least common.) Fusions
of the sustentaculum tali or posterior process are also possible
(though not common.) Anterior facet coalitions can be seen
on lateral oblique isherwood projections but are most
commonly dx though lateral CT. Middle and posterior
facets are viewed on harris and beath axial projections (30, 35,
40, and 45°) or broden views. The posterior and middle facets
should be parallel to one another, and the posterior facet
should be about 2/3 the width of the calcaneus. Posterior
fusion may be secondary to trauma involving the os trigonum.
(Achilles pain, end ROM plantarflexion, deep ankle pain.)
Radiographic Features of STJ coalition (lateral projection) ARTHRIDITIES
Talar beaking Inflammatory arthridities are RA, erosive arthritis, psoriatic
Posteior TC joint space narrowing arthritis, reiter’s disease, ankylosing spondylitis, and
Rounding of lateral process of the talus enteropathic arthritis.
Obscured middle facet Non-Inflammatory arthritis is degenerative joint disease.
“Halo” effect (Wait a minute – doesn’t arthritis mean joint inflammation?)
Do not confuse talar beaking w/ dorsal hyperostosis, which is Metabolic arthritis is gout and CPPD disease.
caused by pathomechanics. Talar beaking occurs at the Neuropathic arthritis is neuropathic joint disease.
distalmost aspect of the talar neck, near the TN joint. It is Miscellaneous arthridities are DISH, PHO, and pigmented
caused by stress on the talonavicular ligament and nodular synovitis.
impingement of the navicular on DF. The halo sign is a subtle
finding, which is a ring of trabeculae that form around the PSORIATIC ARTHRITIS
coalition secondary to altered compressive forces. Seen in 7-15% of pts w/ psoriasis (80% if pt has nail changes.)
Computerized Tomography is the modality of choice for Typically affects 20-50 y/o, M:F equal. HLA-B27 frequently
evaluation of coalitions (b/c of cortical definition.) It allows positive, particularly w/ SI involvement. Distribution is
planar analysis which may be used to determine the extent of asymmetrical and is most common in the DIPJs. Often
coalition and change to surrounding osseous structures. confused w/ RA (for some reason.)
Nuclear Imaging is not very useful for the diagnosis of Classic radiographic features
coalition. Increased uptake is seen adjacent to areas fusing, Joint margin erosions working in to the center (similar to RA)
and decreased uptake in already fused areas. – eventually leads to “pencil in cup” appearance
MRI allows planar and oblique analysis to more fully explore Increased synovial fluid w/ increased intracapsular pressure
the nature of a coalition. T2 weighted images are particularly Apparent wide joint space (due to erosions)
useful to note presence or absence of synovial fluid in an area. Acroosteolysis – resorbtion of the distal phalangeal tuft
Syndromes associated with coalitions may aid in the Sausage digits
diagnosis of a bony union, and vice versa. Common coalitions Abundant periosteal activity (resulting in “whiskering”)
typically are axial, i.e. distal to proximal fusions, whereas Ivory Phalanx – due to abundant endosteal activity
syndromic coalitions tend to be medial to lateral in position. Osteopenia secondary to reduced activity
Apert’s Syndrome results in massive tarsal synostoses, as Main-en-lorngette (telescoping) – long standing disease
well as cranial synostoses and midfacial hypoplasia (“mouse” process resulting in collapse of diaphyses on themselves.
facies). The distal phalanx of the hallux and pollux are broad. Posterior/Inferior calcaneus hyperostosis (not heel spurs.)
Feet tend to have valgus attitude. Footwear is a problem
Nievergelt-Perlman Syndrome typically has synphalangism REITER’S DISEASE
and carpal fusion, moreso in the hands than feet. This Classic clinical triad – conjunctivitis, urethritis, arthritis.
syndrome may also present with an atypical clubfoot and Also 4th – derm lesions (keratoderma blenorrhagicum)
tarsal fusions, which causes a ball-and-socket type of ankle Usually preceded by diarrhea.
joint. Other findings include congenital dislocation of the Typically males, 18-40 y/o. HLA-B27 positive almost always.
radial head and conduction deafness due to ear ossicle fusion. Asymmetric distribution, primarily lower extremity.
Phocomelia is defective development of the arms or legs, Attributed to chlamydial infection (endemic) or dysentery
resulting in “flipper” extremities. Hemimelia is (epidemic) which are the two main types of Reiter’s.
underdevelopment of a specific extremity, usually a below- Epidemic form may affect women and children as well.
knee deformity. These conditions cause unusual fusions. Arthritis long-term symptom; conjunctivitis/urethritis resolves
Tx of coalition includes immobilization and supportive in weeks. Arthritic changes may also become chronic.
therapy, orthotics, NSAIDs for pain, and possible surgical Acute Stage - weight-bearing joints are more commonly
intervention (resection or arthrodesis.) affected. In the acute stage there is peri-articular ST edema,
deossification of opposing articular structures, Achilles
inflammation/widening, and periosteal reaction (metatarsal crystals are weakly positive birefringent and simulate gout
metaphyses, phalangeal diaphyses, inferior surface of the attacks when precipitated in joint spaces. The typical pt is
calcaneus.) Retrocalcaneal bursitis is also common. over 30 y/o (usually ~60) and there is no gender predilection.
Infracalcaneal exostoses (poorly defined or “fluffy”) form The problem is associated with hyperparathyroidism,
bilaterally and cause heel pain. pseudogout, acromegaly, DJD, and DM. The typically
Chronic stage – periarticular deossification, small marginal affected joint is the knee, where the menisci as well as the
erosions, symmetrical loss of joint space, ankylosis. articular cartilage may calcify as a result. It also can be seen
Specific findings – heel spurs in young men, Achilles edema, in the wrist, hand, ankle, symphysis pubis, and elbow.
small joint space periosteal reactions, primarily foot s/sx. True chondrocalcification is sometimes seen after trauma or
with hyperparathyroidism.
Affects pelvic and spinal joints, ligaments, and tendons. DEGENERATIVE JOINT DISEASE
Affects 15-25 y/o, usually males. Almost always HLA-B27 Also called osteoarthritis, DJD is a local, mechanically
positive. Characterized by lower back pain due to arthritis at caused degeneration of joint function that occurs in
the sacroiliac joint, bony proliferation at enthesiopathies, conjunction with age and trauma, resulting in degradation of
spinal osteophyte formation, and lateral syndesmophytes. the articular cartilage. Primary DJD is the most common form
and is due to aging. Secondary DJD is early onset due to
ENTEROPATHIC ARTHROPATHY trauma or injury to the joint. Joint space narrowing is
Joint changes secondary to GI disease. Seen in young adults, asymmetric in DJD, the subchondral bone exhibits
w/ malaise, anorexia, wt. loss and arthritis. Typically eburnation (pathologic sclerosis), the articular surface
sacroiliac, bilateral periostitis. X-ray findings are nonspecific. becomes broad and flat, and osteophytes form at joint
margins, often breaking off to become joint mice within the
GOUTY ARTHRITIS articular space. Osteophytes typically bend towards the joint
Gout is the result of an inborn error of purine metabolism. It space, which causes locking of the joint in areas where there
typically affects men age 40-50 y/o, and is characterized by are osteophytes on either side of the articulation. Pseudocysts
elevated serum uric acid and negatively birefringent crystals in may also form in the subchondral bone in areas where the
the synovial fluid. The most commonly affected joint is the 1st cartilage is completely worn away. It is important to note that
MPJ due to relative avascularity and lower temperature. the disgnosis of hallux rigidus and limitus, which are seen in
Women only get gout after menopause. Characteristic of gout patients with DJD of the 1st MPJ, cannot be diagnosed
is extreme paroxysmal pain in the middle of the night. radiographically and are purely clinical diagnoses.
Primary gout is hyperuricemia due to over-production of uric Additionally, the hands of patients with DJD clinically may
acid or under-excretion of it by the kidneys. Secondary gout present with enlarged IPJs which are called bouchard’s nodes
is due to medications (particularly HCTZ) and (PIPJ) or heberden’s nodes (DIPJ) that are simply the result
hyperparathyroidism. Urate deposits in relatively avascular of extensive osteophytosis in long-standing disease.
tissues like cartilage, synovial tissue, ligaments, bursae, and Erosive osteoarthritis is a variant of DJD which
subQ tissue. Hyperuricemia may never become symptomatic, affects primarily females aged 40-50 y/o. Clinically an
and in fact may be reduced during an acute phase attack. A 24 increased ESR may be seen because there is an inflammatory
hour urine collection is needed to diagnose accurately. component to the erosive component. The presentation is
X-ray findings of gouty arthritis only occur after several symmetrical and bilateral, and most commonly affects the IPJs
attacks. Thus radiographs in an early attack function mainly of the hands. Radiographically erosive osteoarthritis appears
to r/o other pathologies (septic arthritis.) There is peri- like DJD except that the erosions are symmetric and take on
articular swelling of the joint margins, erosions of the joint the characteristic gull wing appearance that is specific to EO.
margins, punched-out lesions resembling RA, and complete
lysis of bone in the acute stages. Large tophi may form at RHEUMATOID ARTHRITIS
joint margins and produce “rat bite” erosions peri-articularly RA is an inflammatory seropositive joint disease affecting
that leave overhanging shelves of bone called martel’s sign. primarily females between the ages of 20-40 y/o, but affect
This is not seen for 5-10 years after the attack and merely men and women equally beyond the age of 40. 70% of pts w/
signifies that a pt has had gout in the past. Tophus formation RA are seropositive for rheumatoid factor. The small joints of
can occur in the absence of an acute gout attack, and the hands and feet, and articulations of the spine are typically
subsequent erosions can cause subQ calcification and affected. Early presentation in the foot can easily be mistaken
pathological fxs. The joint space is preserved in gouty for gout – most commonly small, C-shaped erosions appear at
arthritis. DJD may accompany the process, and the joint may the base of the proximal phalanges. Radiographic changes are
be somewhat narrowed due to subchondral cyst formation, but seen in 65% of pts who have had some disease process for at
is otherwise unaffected. Metastatic tumors of bone are an least 3 months (85% for >6 mos.) However, no clinical s/sx
important d/dx to r/o when considering asymptomatic gout. may appear until the disease has been present for 3 years.
Early radiographic findings in RA include peri-
CHONDROCALCINOSIS articular edema that is fusiform in shape around the joint,
Pseudogout, or calcium pyrophosphate dihydranate disease, is typically in IPJs and MPJs. Inflammation of the synovium
a symptom similar in presentation to gout that causes the creates pannus which results in bone deossification peri-
radiographic finding known as chondrocalcinosis. CPPD articularly, which progressively extends proximally over time.
Secondary trabeculae are resorbed while primary trabeculae DISH is a disorder of ligamentous ossification and
are enhanced. Fibular deviation of the digits occurs calcification that affects the spinal and extra-spinal
secondary to bony deossification that destroys the medial articulations. Typically it affects males over 50 y/o. It is
collateral ligaments of the MPJs (except on the 5th MPJ.) associatied (20%) w/ DM. 40% are HLA-B8 positive. All
Early on the joint space becomes noticeably widened as parts of the spine, particularly the SI joint, are affected.
effusion and pannus formation characterize the disease Radiographically flowing hyperostosis is seen over 4
process, and often this is the only presenting sign in consecutive vertebral bodies, usually in the area of the anterior
undiagnosed RA. Joint space changes are most easily seen in longitudinal ligament. In any case, the disc is preserved,
the ankle joint radiographically. Near the joint periosteum differentiating this process from syndesmoses seen in
may become irritated and periosteal elevation in the ankylosing spondylitis. Extra-spinal presentations may be at
epiphyseal/metaphyseal region is seen. This creates any enthesis, producing whiskering at the bony attachment and
lamellations which enlarge the bone near the articulation. ossification of the tendon or ligament while preserving the
Entheses and bursae near the joint may also become inflamed joint space.
and enlarge. Localized bony erosions occur near the joint due
to herniation of the pannus through capsule, producing an area PULMONARY HYPERTROPHIC OSTEOARTHROPATHY (PHO)
of radiolucency with poorly defined borders. Erosions seen en PHO is a disease caused by bronchogenic carcinoma that is
face may appear completely within the bone, while laterally described by the triad of digital clubbing, symmetric
they may have a dot-dash appearance. Medial-plantar arthritis, and linear periostitis. It typically affects males 40-
erosions of metatarsal heads 1-4 are most common. Later 60 y/o. The arthritis in this process, like many seronegative
symmetrical joint narrowing is seen, particularly in the IP and diseases, is nondescript in its clinical and lab findings. The
TN joints (but never the CC joint.) arthritis is specific to the extremities only. Periostitis in long
RA-induced subluxations of MPJs and IPJs following bones occurs in the metaphseal/diaphyseal region, appearing
ligamentous involvement cause the characteristic swan-neck as a “double strip sign” on bone scans (dual cortices.)
(like mallet-toe) and boutonneire (like HDS) deformities. PIGMENTED VILLONODULAR SYNOVITIS
These deformities are also seen in SLE and post-rheumatic This disorder is a proliferative pathology of joints that does
fever (jacoud’s) arthritis. Other deformities seen in RA not produce arthritis, but rather a mass within a joint or tendon
include main-en lorgnette deformity (“opera-glass hand”) sheath which may affect the joints secondarily. Typically it
that is also seen in psoriatic arthritis. affects young males. Joint involvement is asymmetric.
Late radiographic findings in RA have obviously Radiographically there is a soft-tissue mass evident with
no diagnostic value, but are used to track the progression of localized bony erosions that have well-defined sclerotic
the disease. Characteristic features include subluxation and borders. Calcification is unusual.
dislocation of the joints, ulnar deviation of the digits,
destruction of joint space, and finally bony fusion and SYSTEMIC LUPUS ERYTHEMATOSUS
ankylosis of the joints altogether. Pathological fxs secondary SLE is a connective tissue disorder involving nearly every
to osteopenia may be seen. Overall, the MPJs are most organ system in the body. It is most common in females 20-
severely affected in RA, with the IPJs of the 1st and 5th digits a 40 y/o, and is characterized by elevated ESR and ANA titer
close second in frequency. levels. Radiographic features are most readily assessed in the
hands, and are characterized by reversible subluxation,
NEUROPATHIC JOINT DISEASE dislocation, and varied deformity. Calcification and atrophy
More commonly known as charcot foot, neuropathic joint can occur secondary to deformity. Most radiographic findings
disease is a destructive disease that occurs secondary to loss of are non-specific and there is no articular degeneration.
proprioception, seen in DM (5%) and syphilitics (20%.)
Clinically there is no protective sensation; instability and SCLERODERMA
crepitation are present in the joint, and neurologically the pt Scleroderma is a connective tissue disease that also involves
suffers from ataxia and loss of DTRs. Besides the more many organ systems and affects females predominantly (30-60
common pathology, neuropathic joint disease can occur y/o.) Radiographic changes in scleroderma are most readily
iatrogenically secondary to administration of indocin or appreciated in the CREST syndrome, in which soft tissue
steroids over long periods of time (notable because of the tx calcification and acro-osteolysis may be seen. (r/o psoriasis)
protocols for RA and gout recommend this.) The hypertrophic
form of the disease affects large, WB joints, while the
hypotrophic (atrophic) form affects NWB joints. Clinically
both undergo 3 stages; fragmentation, coalescence, and
reconstruction. Radiographically the hypotrophic form is
characterized by bone resorption, diabetic osteolysis, and a
“licked candy stick” appearance. The hypertrophic form is
characterized by the six D’s: joint distension, density
increase, debris production, dislocation, disorganization, and


line drawn from distal inferior aspect of calcaneus to
anteriormost weight-bearing point of calcaneus

Lesser Tarsal Angle = GTA + LTA
Metatarsus Angle = LTA + MTA
Used to evaluate for metatarsus adductus
Digitus Angle = DA + MTA of measured digit
Forefoot Angle = GTA + MTA
Used to evaluate metatarsus adductus in peds
Talo-Calcaneal Angle = collum tali + collum calcanei axes
Used to evaluate pronation/supination
Cuneo-Metatarsal Angle = MTA(1-3) + long axis of
proximal cuneiform
Used to evaluate hypermobility, lisfranc’s injury
Calcaneocuboid Angle = Collum calcanei axis + line CD of
Used to evaluate lateral column integrity
Talometatarsal Angle = column tali axis + 1st MTA
Called Simmons Angle on AP
Used to evaluate pronation/supination
Intermetatarsal (IM) Angle = 1st MTA + 2nd MTA
Used to evaluate bunion deformity
Hallux Abductus (HA) Angle = hallux axis + 1st MTA
Used to evaluate bunion deformity
THE 5 STEP APPROACH TO PLAIN FILM ANALYSIS Hallux Interphalangeus Angle = hallux axis + bisection of
STEP 5: BIOMECHANICAL EVALUATION distal phalanx of the hallux
The biomechanical evaluation of radiographs is used for pre- Metatarsal Break Angle = line between center of 1st and 2nd
op planning and post-op assessment of correction as well as metatarsal heads + line between center of 2nd and 5th
for the evaluation of orthopedic pathology. Biomechanical metatarsal heads.
readings are most sensitive to positioning errors, and so great Tibial Sesamoid Position
care must be taken to ensure proper positioning in patients 1 = Tibial sesamoid medially clear of 1st MTA
needing a biomechanical evaluation. 2 = Tibial sesamoid laterally abuts 1st MTA
AXES 3 = Tibial sesamoid laterally overlaps 1st MTA
Greater Tarsal Axis (GTA) 4 = Tibial sesamoid bisected by 1st MTA
Line drawn parallel to the distolateral border of the calcaneus, 5 = Tibial sesamoid medially overlaps 1st MTA
most easily identifiable on AP radiograph. 6 = Tibial sesamoid medially abuts 1st MTA
Lesser Tarsal Axis (LTA) 7 = Tibial sesamoid medially clear of 1st MTA
Point A is placed on the distomedial aspect of the medial Proximal Articular Set Angle (PASA) = line btw medial and
cuneiform. Point B is placed at the medial proximal aspect of lateral borders of metatarsal head articulation + line
the navicular articular surface. Point C is placed at the perpendicular to MTA.
proximal lateral aspect of the cuboid and point D at the distal Distal Articular Set Angle (DASA) = line btw medial and
lateral aspect of the cuboid. The midline between points A & lateral borders of proximal phalanx MPJ articulation + line
B and C & D are found and a line drawn between them. The perpendicular to digital axis.
line per