Professional Documents
Culture Documents
erioperative
are
© Ogan Gurel, MD
Table of Contents
PREOP ................................................................................................................................................................... 1
Communication................................................................................................................................................ 2
Routine Preop preparations............................................................................................................................. 4
Preop rituals .................................................................................................................................................... 5
Pre-existing Cardiovascular Disease .............................................................................................................. 7
Pre-existing Respiratory Disease..................................................................................................................... 9
Pre-existing Gastrointestinal Disease ........................................................................................................... 11
Pre-existing Renal Disease ............................................................................................................................ 14
Pre-existing Hematologic Disease................................................................................................................. 15
Pre-existing Endocrinological Disease ......................................................................................................... 17
Pre-existing Neuromuscular Disease............................................................................................................. 20
Pre-existing Psychiatric Disease ................................................................................................................... 21
Miscellaneous pre-existing conditions........................................................................................................... 22
POSTOP ............................................................................................................................................................... 23
Acute Pain...................................................................................................................................................... 24
Pain Management: Pharmacology ................................................................................................................ 25
Simple Analgesic Techniques......................................................................................................................... 28
Advanced Analgesic Techniques.................................................................................................................... 30
Nausea & Vomiting........................................................................................................................................ 32
Fluids & Electrolyte Balance......................................................................................................................... 35
Bleeding & Transfusion ................................................................................................................................. 40
Feeding .......................................................................................................................................................... 44
Blood Gases ................................................................................................................................................... 46
Monitoring Devices........................................................................................................................................ 50
Hypotension ................................................................................................................................................... 52
Dysrhythmias ................................................................................................................................................. 56
Hypertension.................................................................................................................................................. 61
Myocardial Ischemia ..................................................................................................................................... 63
Pulmonary Edema ......................................................................................................................................... 65
Cardiac Arrest ............................................................................................................................................... 69
Respiratory Problems .................................................................................................................................... 72
Oliguria & Catheters ..................................................................................................................................... 81
Fever.............................................................................................................................................................. 84
Hypothermia .................................................................................................................................................. 87
CNS complications......................................................................................................................................... 89
Thrombosis .................................................................................................................................................... 95
Miscellaneous Postoperative problems ......................................................................................................... 97
Principles of Perioperative Care © Ogan Gurel, MD
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Principles of Perioperative Care © Ogan Gurel, MD
Communication
You will be judged more on your communications skills than on any other aspect
of your job
Talking to patients
Names
Learn patient’s names
Introduce yourself
Shake hands
Dress code
Tie, avoid wearing scrubs, daily shave
Make time
Avoid being curt
Shake hands & sit down (for H+P)
Make the purpose of the visit clear at the outset (“I’m here to place an IV, etc.)
Chaperones
Essential
Talking to professionals
Seniors
Get senior residents involved early in developing problems
Document your discussion with senior residents
Call senior (and have attending contacted) whenever a major (especially an
unexpected) change in patient management occurs (e.g. an admission, discharge,
ICU transfer, consult, etc.)
Other Specialists
Make personal visits when possible; (use beeps sparingly)
Visit ICU patients at least once daily
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PCPs
Send a brief note upon DC
D-SUM include: nature of surgery, any complications, drug regimen and f/u
arrangements
With deaths call PCP
Nurses
Learn their names
Treat them with respect
Ask their advice
Notes
Date and time (military)
If you put plan of action at end of note be sure to follow-through
If you talk to senior, be sure to record the fact
Sign name (print last name & beeper number)
Prescriptions
Do not put DEA number on unscheduled drugs
For scheduled drugs use a prime number (2, 3, 5, 7, 11, 13, 17, 19, 23, 29 , 31, 37,
41, 43, 47, 53, 59, 61, 67, 71 , 73, 79, 83, 89, 97, 101)
Use generic names
Put full-name, address, age & date
Write Rx for OTC meds if there is a question of compliance
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Preoperative Investigations
Screening tests
UA
CBC
Lytes, BUN, Cr
EKG (> 60, younger if smoker / major surgery)
CXR
Cross-match
BBS
T+C 2U
T+C 4U
T+C 6U
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Preop rituals
NPO
NPO/IVF pMN (avoid solids/clrs up to 4h/2h)
Do not withhold oral medications
Regular Medication
Very few drugs interfere with anesthesia/surgery
Exceptions:
1. insulin & OHAs
2. anticoagulants
3. lithium
Definitely continue cardiac meds
Bowel Prep
DVT prophylaxis
Antibiotic prophylaxis
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Principles of Perioperative Care © Ogan Gurel, MD
CHF
History
Exercise tolerance is a sensitive measure of cardiac reserve.
Ask about past history of MIs/hospital admissions & cardiac medication.
? Orthopnea/PND
Exam
rest tachycardia, LE edema, JVD, basilar rales.
Labs
EKG -> look for dysrhythmias, old MI & acute ischemia
Echo -> gives more information about fitness of the heart to tolerate
GA/Surgery than any other test. Most important: EF which is the best predictor
of outcome after major surgery. EF <40% particularly bad.
CBC -> lower than usual threshold for treating anemia
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Dysrhythmias
Atrial fibrillation is the most common abnormality
Ventricular rate in controlled AF should be 80; question the adequacy of
treatment if this is higher.
Maintain all anti-dysrhythmics
Beware of hypokalemia or changes in renal function in patients on digoxin.
Digoxin levels should be taken 6h after the dose is given.
Miscellaneous
No particular precautions for patients with pacemakers; electrocautery risk very
low.
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History
Exercise tolerance
H/O of chronic bronchitis -> purulent sputum
Check current meds (steroids, NSAIDS)
Ask about prior admissions, home oxygen, history of smoking
Exam
Cyanosis, wheeze, dyspnea at rest, right heart failure, clubbing or focal chest signs
Labs
CBC (elevated white count in PNA)
CXR
ABG (baseline for major surgery/severe disease)
PFTs (severe disease to VC, FEV1 and response to bronchodilators)
EKG
Smoking
(stopping for …
12-24hr reduces need for carbon monoxide & nicotine elimination
3-4 days improves ciliary activity
1-2 weeks reduces sputum volume
6 weeks reduces pulmonary and coronary vascular resistance and restores normal
pulmonary macrophage function
Preop preparation
stop smoking. 48hr intensive PT for sputum retainers
Asthma
Gauging severity:
ask about EW visits, previous admissions, courses of steroids, ICU stays, and
limitation of activities. Severe asthmatics are rarely wheeze-free.
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Medications/Prophylaxis
Maintain all regular medications
Avoid using bronchospastic drugs: morphine, all NSAIDs and -blockers.
Humidify oxygen, treat pain adequately and avoid creating anxiety
Consider dose of inhaler on call to OR
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Pre-existing Gastrointestinal
Disease
Obesity
BMI
weight(kg)
body mass index combines height & weight BMI
height 2 (m 2 )
Obesity = BMI > 28
Morbid obesity = BMI > 35
Cardiovascular problems
HTN, CHF, ischemia more common
Take history of snoring, day-time drowsiness
Raised bicarbonate indicates carbon dioxide retention and thus may be a
contraindication to postop oxygen
Respiratory problems
Increased work of breathing
prone to PNA
Nursing: upright position, mobilization, early PT, oxygen at night
Gastrointestinal problems
Hiatal hernias, GERD common.
Continue H2-blockers or omeprazole / Prilosec perioperatively
Metabolic issues
Screen for diabetes
Temporary insulin dependence may be a possibility
Venous access
Avoid IM injections (usually intra-adipose)
If prolonged access required think central line
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Malnutrition
Labs
Lytes, BUN, Cr especially with diarrhea or vomiting
Glucose -> chronic hypoglycemia
EKG -> weakened cardiac muscle -> CHF/dysrhythmias
CXR -> preop PNA more common due to immunocompromise/weakness.
Pulmonary edema/pleural effusions due to hypoalbuminemia
LFT/clotting: hypoalbuminemia, hypoglobulinema, prolonged PT
Management
Prone to infection, poor healing, skin ulcers, hypothermia
IM route is unreliable due to reduced muscle blood flow
Upper GI problems
Upper GI bleeding
Liver Problems
LFTs
Bilirubin (yellow pigment) function is to cause renal failure
Albumin is a protein without which you get edema & ascites
PT/INR is a measure of clotting which is impaired in liver disease
Liver enzymes are not measures of liver function at all but of liver damage
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Diarrhea
Results in hypovolemia, hyponatremia, hypokalemia and acidosis.
Replace with NS with 20-40 K (depending on K results)
Acidosis may be treated with bicarbonate
Bowel prep
Iatrogenic hypovolemia is common
Replace with 2 liters of NS over 24hr preoperatively
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Associated conditions
Medications in CRF
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Microcytic, hypochromic
MCV < 75
Most commonly due to chronic blood loss
More rarely due to failure to absorb or utilize iron
Rx with oral ferrous sulfate (will raise Hb by 2 g/dl in 2 weeks)
Transfusion will raise Hb by 1 g/dl per unit
Ideally transfuse 2 days preop to give time for stored cells to return to normal
oxygen delivery
Transfuse patients with history of ischemic heart disease more aggressively (keep
Hb > 10).
Normocytic, normochromic
Anemia of chronic disease (renal failure, severe connective tissue disease and
carcinoma).
Do not require transfusion because anemia is well-compensated by increased
intracellular 2,3-DPG which stabilizes the deoxy state allow the hemoglobin to
release oxygen more readily in the tissues.
Transfusion in renal failure may be harmful
Macrocytic (megaloblastic)
MCV > 96.
Result of either folate or B12 deficiencies due to diet, malabsorption or increased
demand (pregnancy).
Associated with heart failure; transfuse only packed cells and consider using a
diuretic,
Important to send blood for B12 and folate assays before treating with folate.
Treat B12 deficits with hydroxocobalamin 1mg IM.
Bleeding Disorders
Usually iatrogenic (rather than pathologic)
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Warfarin
Warfarin / Coumadin therapy measured by INR (2-4.5) for DVT, valve
prophylaxis
DC warfarin 2-3 days preop and replace with heparin (if necessary)
For urgent correction of coagulopathy treatment of choice is FFP (6U FFP = 1
liter)
In catastrophic cases may also consider vit K (5mg slowly IV) but it is slow-
acting, makes later AC difficult, and there is also a risk of anaphylaxis.
Heparin
Short half-life (~1hour) means that effect can be reversed by stopping 3-4 hours
preop.
Typical dose is 1000 U / hr which will achieve a 50% prolongation of PTT
Check PTT at least qD
When restarting warfarin it is necessary to overlap warfarin and heparin for 2-3
days.
Thrombocytopenia
Minimum acceptable count is 100,000
Transfusing one unit will raise the platelet count by 5,000
Hemoglobinopathies
Polycythemia
Polycythemia vera or secondary polycythemia
PV patients should undergo venesection 1-2 days preop
Secondary polycythemia due to increase erythropoeitin secondary to chronic
hypoxia. Full pulmonary work-up, possible venesection, and DVT prophylaxis
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Pre-existing Endocrinological
Disease
Diabetes
Collective term for insulin deficiency states
Principles of Management
Cardiovascular
All diabetics are at increased risk of MI, PVD and CVA. Careful PE & EKG.
Ischemia is often occult
Infectious Disease
Infection worsens diabetic control
Diabetics are immunocompromised
Consider preop Abx
Rigid exclusion of URI/UTI important
Renal
DM causes CRF
Check Lytes, Bun, Cr preop
Neurological
Autonomic neuropathy can cause hypotension
On exam:
1. Pulse rate does not change on Valsalva
2. Postural hypotension
NIDDM
Put early on for AM operations
Stop long-acting OHAs at least 18h preop
Check BS in AM and just before surgery
If hypoglycemic put in D5W; if hyperglycemic do not start insulin
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IDDM
Omit long-acting insulins the night before; continue short-acting insulins for the
evening meal. Omit all insulins on the morning of surgery.
DKA: hypovolemia, acidosis, hyponatremia and hyperglycemia. ICU admission.
Correct hypovolemia with saline (~2l/hr), give insulin bolus (20U) and replace
potassium (20 meq KCl per liter)
Thyroid problems
Hyperthyroidism
Preoperative testing
TFTs; all cases should be euthyroid
Surgery without medical control of hyperthyroidism risks “thyroid storm’.
Carbimazole and/or -blockers. Iodine sometimes given to reduce vascularity
Indirect laryngoscopy (via ENT) to exclude a pre-existing laryngeal nerve palsy.
If the other normal nerve were to be injured -> b/l palsy which could threaten
the airway.
CXR/thoracic inlet views/CT scan->tracheal compression, substernal
involvement
Preoperative calcium for baseline. To compare to post-op calcium as indicator of
parathyroid injury
Postop considerations
Airway obstruction due to hematoma, edema, nerve palsies or cartilage erosion -
> pair of scissors or staple removers at bedside
Acute hypoparathyroidism. Check postop calcium and signs of tetany. IV
calcium gluconate 10% 10ml slowly.
Hypothyroidism
At risk of heart failure, hypothermia, over-sedation and pneumonia
Adrenocortical problems
Addisonian crisis -> hypotension, hyponatremia, hyperkalemia.
Resuscitate with IV steroids and saline.
With chronic Addison’s measure preop lytes, glucose.
Patients on long-term steroids (or previous steroid therapy within one year) need
stress steroids (hydrocortisone 100 mg IV at induction and 8 hr post-op x one
day). Does halved each day until preop dose is reached.
Hydrocortisone (100 mg IV/IM) = Prednisolone (25mg PO).
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Diabetes insipidus
May follow head injury or neurosurgery
Due to failure of production or action of ADH resulting in large volumes of
dilute urine (specific gravity < 1.010).
Treat with intranasal DDAVP (synthetic ADH) 10-40 mcg/day.
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Strokes
Indication that there is underlying atherosclerosis or cardiac Dz -> preop EKG
Swallowing difficult predisposes to malnutrition & aspiration PNA
Immobility increases DVT risk & skin breakdown
Higher risk of PNA & UTI
Hypovolemia & hypoxia should be avoided
Parkinson’s disease
Possible further respiratory compromise due to rigidity of the thorax.
Continue anti-Parkinsonian drugs but watch for urinary retention + confusion
(anti-cholinergic effects).
Central dopamine antagonists [droperidol/, haloperidol/haldol,
metoclopramide/reglan] may worsen disease.
Multiple Sclerosis
Risk of UTI/PNA (aspiration) high.
Autonomic hyper-reflexia (full bladder of constipation) may lead to uncontrolled
autonomic reflex with severe hypertension, sweating and bradycardia.
Good catheter and bowel care.
Myasthenia gravis
Do not withdraw anticholinesterases or steroids.
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Benzodiazapines
Sudden withdrawal manifests as a panic attack -> severe w/d -> Sz.
Sx develop within a day to week (depending on half-life of drug).
Continue usual medications.
Antidepressants
Side-effects of tricyclics include urinary retention, constipation, blood dyscrasias,
electrolyte imbalance, dysrhythmias and confusion.
CBC, Lytes, EKG are needed preop
SSRIs are safer than tricyclics but same studies needed.
MAOIs. Do not discontinue. May not have sympathomimetics.
Antipsychotics
such as the phenothiazines (thorazine) have many side effects: Parkinsonianism,
blood dyscrasias, urinary retention, constipation, hypotension and hypothermia.
Effects are additive with other phenothiazines [prochlorperazine/compazine] or
other dopamine antagonists [metochlopramide/reglan].
Lithium
Narrow therapeutic window (0.4 - 1.0). Toxic effects may occur > 1.5.
Toxicity: mixed cerebellar signs, confusion, coma, convulsions, diarrhea and
vomiting.
Toxicity is precipitated by hyponatremia, dehydration, pyrexia and loop diuretics.
Advisable to measure serum lithium preop
Alcohol
Prevent withdrawal: alcohol or benzodiazepines
Oral diazepam/valium 30mg in divided doses on first day and reduce by 5mg/day
until maintenance of 10mg/day is reached
Consent
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Miscellaneous pre-existing
conditions
Pregnancy
Risks to fetus are teratogenesis in the first trimester and premature labor in the
third trimester. Second trimester is the safest.
After 16 weeks greater risk of aspiration -> H2 blocker/
Resting respiratory rate and heart rate higher; BP lower. Greatly increased risk of
DVT/PE. Urine output and maintenance IVF requirements are higher.
Compression of inferior vena cava -> place on left lateral decubitus position
Breast feeding
Safe medications: morphine, acetaminophen, ibuprofen, metoclopramide and
heparin.
Do not give: aspirin (risk of Reye’s), atropine (anticholinergic effects), barbiturates
(drowsiness in high doses), chloramphenicol (bone marrow toxicity in the fetus),
ciprofloxacin (large concentrations in breast milk), tetracycline (possibility of
dental discoloration)
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Acute Pain
What is the problem
Pain control is poorly managed
It is important to identify causes of pain that need a different form of
intervention (i.e. an operation).
Consequences of pain
Psychological
Secondary psychological
Respiratory
Cardiovascular
Other
Pain measurement
1-10 pain score
Important to use a series of pain scores to assess titration of therapy with response
with frequent assessment
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Actions
Analgesia
there is no such thing as more potent opioid ... just different dosages
Respiratory Depression
Assess by RR (< 8 is bad).
Never use a pulse oximeter (hypoxia is a late sign).
Respiratory depression is accompanied by somnolence.
Management of respiratory depression with naloxone / Narcan (0.2 mg IV).
Short duration of action (~10 min) so repeated doses may be required.
Addiction
Patients given opioids appropriately when in acute pain do NOT become
addicted.
Dose requirements vary enormously ... depending on severity of pain, age, prior
opioid use, psychological factors and weight.
Drugs
Morphine
Fast onset; duration 4-6 hours. Side-effects include delayed gastric emptying,
constipation, spasm of sphincter of Oddi. Histamine release which may cause
bronchospasm in asthmatics. Typical IM dose is 10mg q3 PRN
Demerol
Less spasm of sphincter of Oddi
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NSAIDs
Mode of action
Analgesic, antipyretic and anti-inflammatory actions
Mode of action (peripheral inhibition of prostaglandin synthesis) is completely
separate from opioids so are safe to use in combination
Very effective in postoperative pain relief ... so should be used in every case
where contraindications do not exist
Side effects
Gastric irritation
Hazard whatever the route of administration
Contraindicated in patients with GU/DU or predisposition to UGIB
Always prescribe NSAIDs to be taken with food
Renal effects
Reduction in blood flow, sodium & water retention
Use with caution in anyone with renal disease, hypovolemia, hypertension or gout
Check chemistries frequently
Platelet inhibition
Only becomes a postoperative problem with patients with thrombocytopenia,
dysfunctional platelets or large raw areas to bleed from.
Bronchospasm
Avoid NSAIDs in asthmatics or those with nasal polyps
strongly contraindicated in the presence of active bronchospasm
Drug interactions
Increase in anticoagulation during warfarin therapy
Specific Drugs
Aspirin
Doses 500-1000 mg q 4-6hr
Absolutely contraindicated for children
Ibuprofen / Motrin
Dose 200-400 mg q4-8hr
Causes fewer side-effects than aspirin
Ketorolac / Toradol
Powerful ... equivalent to 10mg of MS
IM form
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Combination pills
Very low risk of side-effects and high efficacy
Role of sedatives
Benzodiazepines have a weak muscle relaxant action which may improve pain
associated with skeletal muscle contraction.
Anxiolytic effects may be useful but only if anxiety is a major component of the
pain state.
Treat pain with analgesics, not sedatives
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Enteral therapy
Preferred route
Bioavailability is often less than parenteral routes
Meds per NGT require a liquid preparation
IM therapy
Use in patients who have moderate pain and who are expected to rapidly
progress to oral pain medications
Disadvantages
PRN basis … which is bad
IM therapy is time-consuming and labor-intensive
IM injections hurt … patients thus avoid them
Can result in excessive peaks & troughs
Variable absorption … contraindicated with patients in shock
Also contraindicated in patients with coagulopathy
Loading doses
Importance of loading doses
Loading doses are given IV
Use an assessment-therapy-reassessment servo loop
Start with 2 mg MS
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Epidural
Formulations
Local anesthetic
Opioids
Combination of opioid (fentanyl) + weak anesthetic (0.125% bupivicaine)
Useful for thoracotomy, major laparotomy, multiple rib Fx, high risk patients,
cancer pain & terminal care
Adverse Effects
Respiratory depression
Hypotension -> Rx with fluid bolus
Pruritis -> chlorpheniramine (10 - 20 mg IM) or decrease rate of infusion
Urinary retention
Nausea
Sedation -> reduce rate
Motor or sensory block -> reassurance
Special circumstances
Respiratory disease
Pain is definitely more dangerous than analgesia
CNS depression
Shock
Shock should be treated before analgesia is given
Fentanyl IV in increments of 25 - 50 mcg
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Narcotic addiction
Get advice from pain specialist
Children
Neurogenic pain
Does not respond to opioids
Often lancinating (shooting or electric)
Treatment may include carbamazepine/Tegretol, amitriptyline/Elavil, baclofen,
nerve blocks, neurosurgery
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Causes of emesis
Preoperative factors
Raised ICP
Bowel obstruction
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Surgical complications
Ileus
bowel obstruction
pancreatitis
Myocardial infarction (especially inferior ) may cause N/V
Complications of emesis
Physical effects
Wound dehiscence
Mallory-Weiss tear -> esophageal rupture
Physiological effects
Hypertension & tachycardia -> myocardial infarction, CVA
Treatments
General measures
Placement of NGT
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GI prokinetic agents
Metoclopramide/Reglan
Increases motility of the GI tract, blocks dopamine receptors at the CTZ
Works poorly however.
5-HT3 antagonists
Ondansetron/Zofran
Used in N/V of chemotherapy
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Normal losses
UO 1500 cc/day.
Insensible losses 0.5 cc/kg/hr.
Fever, obesity increase insensible losses.
Pre-existing deficits
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Management
IVF
Crystalloid (small particles)
Colloid (large molecules capable of exerting oncotic pressure)
Crystalloid
Distribution of IVF depends primarily on sodium content
NS/LR -> freely distributed in extracellular compartment
D5 (sugar gets pulled into cells) thus it is like giving pure water. Distributes in
the total body water
D5/saline; 20% stays in ECF, majority ends up in total body water.
Colloid
Retained within intravascular space
With shock and injury (increase in capillary permeability) colloid molecules reach
the interstitial space thus worsening edema
Assessment
History
Ask about thirst, prolonged vomiting/diarrhea
Drowsiness, headaches, dizziness, malaise, delayed mobilization
I/Os
Consider all information not charted: prior deficits, insensible loss, third space
loss, internal hemorrhage
UO 0.5 - 1ml /kg /hr. Oliguria is most commonly caused by inadequate volume,
but renal impairment and urinary obstruction must be ruled out
Exam
Dry mucous membranes
Edema
Pulse rate/pressure
warm/cold extremities
Rales
Skin turgor
Daily weights
Labs
Serial measurements of CVP
Hematocrit may point to hemorrhage ... may take several hours
Increased BUN in dehydration
CXR -> pulmonary edema indicating overhydration
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Pre-existing deficit
Treat there and then with a fluid challenge servo loop (give 250 cc NS and
reassess HD/UO.
Do not “speed up the drip” and leave
Maintenance
500 ml NS
1500 ml D5
Ongoing Losses
Usually sodium - containing so replete with D5NS, NS or LR
Potassium (20 - 40 meq/l)
Blood (keep Hct > 30)
GI losses (give NS with 20meq/l KCl); large losses should have electrolyte
content measured to ensure appropriate replacement
Nutrition
Check daily chemistries while on IV fluids
Special situations
Cardiac failure
Heart failure does not affect the rate of fluid loss so maintenance
fluid/electrolyte requirements are the same
But ... cannot cope with as wide a range of filling pressures so aggressive fluid
resuscitation should only be used with good evidence of ECF loss/deficit.
Continue diuretics
Changes in physical signs are important
Respiratory disease
Small and clinically undetectable degrees of fluid overload can dramatically
worsen pulmonary function.
Better to err on the dry side
Liver disease
Obstructive jaundice at risk of hepatorenal syndrome ... maintain high UO
Decrease sodium intake
Renal disease
Strict I/Os; daily chemistries
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Err on the wet side .. nothing will finish off a failing kidney quicker than
hypovolemia
Avoid potentially nephrotoxic drugs ... NSAIDs, aminoglycosides, loop diuretics
Diabetics
May be severely dehydrated on presentation
Renal impairment common
Other problems
Septic Shock
Often huge volumes are required
Hypothermia
Repeated bolus fluid resuscitation may be required as hypothermic patient warms
up
Hormone problems
Electrolyte disturbances
Hypokalemia
K < 3.5
Symptoms of muscle weakness
Causes include excessive K loss (diarrhea, vomiting), inadequate replacement,
alkalosis/hyperventilation, diuretic therapy
Requirements 60 meq/day
Hyperkalemia
K > 5.0
Acute changes more serious than chronic
Causes: renal failure, acidosis, hypercatabolism (malignant hypothermia)
Management
10% Ca-Gluconate
Correct acidosis
Dextrose / Insulin (50 ml D50 with 20 units insulin over 30 minutes)
Kayexelate 30mg tid po/pr
Arrange dialysis
Hyponatremia
A sign of excess water
Causes: iatrogenic (hypotonic IVF), TUR syndrome, SIADH
Acute dilutional: water restriction
Acute salt-losing resuscitate with NS+K
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Diuretic-induced
Hypernatremia
Due to lack of water
Fluid resuscitate with D5 or D5NS
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Causes
Surgical lesions
Most common reason is lack of hemostasis
A dry drain does not exclude bleeding
Bleeding disorders
Causes
Dilution of platelets/clotting factors
Inhibition of platelets/clotting factors
Consumption of platelets/clotting factors by DIC/cardiopulmonary bypass
Diagnosis
Diagnosis is a clinical one: bleeding at venipuncture sites, bruises, bleeding
mucosa, hematuria, hemarthroses. Labs are used to define cause & guide therapy
PT: Warfarin, dilution, DIC or liver disease prolong PT
PTT: dilution, DIC or heparin
LFTs liver is major source of clotting factors
FDPs fibrin degradation products seen with DIC
Chemistries: urea is a platelet inhibitor
Ionized calcium: hypocalcemia is a rare cause of coagulopathy. Tourniquet falsely
elevates serum calcium. Best assay is the ionized calcium
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Principles of treatment
Supportive treatment
Causes of death
hypovolemia (1st priority)
loss of oxygen transporting capability
Definitive treatment
Usually exploratory surgery
Bleeding in children
Physiological differences
Faster HR
Lower SBP
Higher RR
Higher UO (1ml/kg/hr)
Volume calculations
Simplest measure is weight
8% of body weight is blood
First fluid bolus is 20 ml/kg of salt
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Transfusions
Plasma products
FFP -> replacement of clotting factors
Indications
1. Massive transfusion
2. Rapid correction of warfarin / Coumadin anticoagulation
Ask for 2 U FFP whenever you ask for 4 or more units of PRBC
Platelets
Depends on platelet count.
Tx for platelets < 50,000
Preoperative cross-matching
Autotransfusion
Fluid overload
Elderly, known cardiac disease and megaloblastic anemia
Treat chronic anemia with PRBCs & give it slowly
Concomitant diuretic (furosemide / Lasix 20mg PO) with every other unit of
blood
Infection
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Immunological complications
ABO incompatibility
Other reactions
Coagulopathy (since stored blood contains very little clotting factors)
Hypothermia
Citrate toxicity -> hypocalcemia & acidosis
Hyperkalemia
Impaired oxygen delivery (stored blood progressively loses 2,3-DPG)
Other complications
Jehovah’s Witnesses
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Feeding
The effects of starvation
Liver -> 24 hr of glucose
Afterwards glucose from gluconeogenesis (from AA)
Decrease in BMR
Negative nitrogen balance which can be reversed in simple starvation but not in
starvation accompanied by stress
Enteral nutrition
Use the gut if functional
If swallowing not possible or low PO intake use NGT (or feeding tube); check
with CXR -> below diaphragm
For long-term feeding G-tube or J-tube
If slow gastric emptying -> cisapride/Propulsid 10 mg po tid or metoclopramide /
reglan 10 mg po tid
Complications of TFs: diarrhea, tube insertion, pulmonary aspiration (tube
promotes regurgitation)
Begin with low-strength ‘starter’ solution then proceed to full strength
Decrease diarrhea but reduce rate of infusion, switch to iso-osmolar solution,
treat with codeine or loperamide/Lomotil)
Parenteral nutrition
Gut dysfunction; contraindicated when gut feeding is possible
Give through central line; nothing else in line due to infection risk
Choice of regimen
Daily regimen
Monitoring
VS/fluid balance
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Complications
Catheter complications
Sepsis (C-reactive protein is a sensitive marker of line infection)
Fluid overload (esp. cardiac/renal/elderly patient)
Hyperglycemia
Electrolyte imbalance
Trace element deficiency
Carbon dioxide production
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Blood Gases
Acid-base physiology
Maintenance of pH is essential
H+ is constantly produced by the body as a product of metabolism.
Buffer systems attenuate fluctuations in pH by reducing the free H+
concentration
Most important buffer is the bicarbonate system
H HCO3 H 2 CO3 H 2 O CO2
produced by metabolism buffer removed by ventilation
Control mechanisms
Recall the Henderson-Hasselbach equation:
[ HCO3 ]
pH pK log
[CO2 ]
pH depends on the balance between bicarbonate and carbon dioxide
Whenever a physiological pH is perturbed, the body will attempt to compensate
for the abnormality
Short-term compensation (minutes) via respiratory system
Long-term compensation (days) via renal system
The body never over-compensates for an acid-base disturbance
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Interpretation
Basically two components: oxygenation & acid-base status
Oxygenation
Normal range for RA is 80 - 100 mmHg; pO2 drops with age
FIO2. You need to interpret oxygenation in the context of the inspired oxygen
concentration.
Oxygen saturation. Unless the oxygen saturation is directly measured ... trust the
pulse oximeter result
Acid-base status
Look at the pH and decide whether the changes are opposite to the pH or not.
1. Is it acidosis or alkalosis
2. Is the patient hyperventilating or hypoventilating?
Management of abnormalities
Metabolic acidosis
Causes
Failure to excrete acid: renal failure
Excessive production of acid: shock, post-MI, ketoacidosis
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Management
Directed at the cause
Respiratory acidosis
May be acute or chronic, or (acute-on-chronic … some with COPD who
decompensates)
Acute respiratory acidosis is always serious … get senior assistance.
Chronic may be subjected to “hypoxic drive” and may become apneic when
administered oxygen.
Metabolic alkalosis
Causes
Excessive bicarbonate administration
Chronic potassium loss
Pyloric stenosis (loss of acid without loss of bicarbonate) -> hypochloremic
acidosis
Management
Give sodium & water to correct dehydration
Give chloride to correct the deficit
Give potassium
NS with 40 meq /l KCl
Respiratory alkalosis
Hyperventilation is the only cause
Lung diseases (such as asthma, pneumonia, pulmonary fibrosis, mild pulmonary
edema)
Anxiety which can lead to relative hypocalcemia (numbness & tingling in the
fingers, even tetany & spasm). Alkalosis deprotonates carboxyl groups on
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albumin making more sites available for binding to calcium. Treatment: breathe
in and out of a paper bag.
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Monitoring Devices
Monitoring should never be a substitute for clinical judgment
Automated BP machines
Oscillometry
Onset of pulsations = SBP
Point at which oscillations are the greatest = MAP
Disappearance of pulsations = DBP
Arterial lines
Only used in an ICU
Used for continuous BP monitoring & blood sampling
Most important dangers are exsanguination & intra-arterial injection
Pulse oximeters
Principle
oxyhemoglobin & deoxyhemoglobin have different optical absorption spectra.
By passing two different wavelengths and measuring the relative absorption, the
proportion of oxygenated and deoxygenated blood can be estimated.
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Limitations
Poor signal (w/ poor perfusion)
Other forms of hemoglobin. Carboxyhemoglobin & methemoglobin are similar
to oxyhemoglobin
Dyes (bilirubin, methylene blue or nail varnish) will affect the reading
Ambient light (strong light sources confuse the photocell)
Venous pulsation (patients in cardiac failure, tricuspid regurgitation) may have
detectable venous pulsations
Pitfalls
Pulse oximeter should never be used as a means of detecting airway obstruction.
As the hemoglobin saturation falls, the warning will come far too late.
Is not sensitive to hypoventilation if the patient is breathing oxygen.
In comparing calculated (ABG) sats with pulse oximeter sats use the latter as it is
a measurement (unless the ABG has co-oximetry)
EKG monitoring
Detection of dysrhythmias and ischemia
For any unstable patient who you feel warrants closer monitoring use a pulse
oximeter and a Dinamap.
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Hypotension
Definitions
SBP < 90mmHg or significant drop (> 30 mmHg from recorded baseline)
Evidence of end-organ dysfunction, e.g. low UO, decreased LOC
Causes
Hypovolemic
Poor cardiac output secondary to decreased preload
Cardiogenic
Pump problem due to poor myocardial contractility,
Septic / Anaphylactic
Probably due to release of endotoxin from bacteria
Early phase warm sepsis which proceeds to hypotension and cool extremities.
Strongly associated with MSOF with a high mortality
Anaphylactic shock is caused by a type I hypersensitivity reaction leading to
massive release of vasoactive mediators such as histamine
Neurogenic
Spinal shock
Combined causes
pOP CHF may also be hypovolemic
Early sepsis there is relative hypovolemia and in more advanced sepsis there is
direct myocardial depression
Other causes
Drugs -> anesthetics, analgesics, antihypertensives
Spinal/epidural anesthesia: due to autonomic blockade
Vasovagal responses
Drug toxicity: digoxin / Lanoxin, tricyclics, lithium
Pulmonary embolus
Measurement error
Pregnancy: caval compression in late pregnancy. Heavily pregnant women
should not lie flat
Hypothermia
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Assessment
Aimed at deciding the cause and severity of hypotension
Airway: Talk to the patient. If the patient is speaking then the airway is clear.
Breathing Check breath sounds. Give oxygen. Check RR
Circulation Is there a pulse. Rate & character. Is the hypotension severe or
mild
Level of consciousness Awake & alert or comatose?
If you have determined that a cardiac arrest is not imminent, then you can revert
to a more detailed assessment
History
Age. PMH.
Surgical diagnosis - any reason for active bleeding?
Fluid history
Onset of hypotension sudden or gradual?
Recently administered drugs, especially pain medications
Any specific symptoms? CP, SOB, itchy rash?
Exam
Gen: Pallor, cyanosis; visible blood loss from drains/wounds, skin turgor.
Sweating, warm/cold extremities
VS: pulse, measure BP manually, RR
CV: JVP raised? Murmurs
Chest: Lungs clear?
Abd:
Investigations
UO (insert catheter if necessary
CBC
Lytes, BUN, Cr
BBS
EKG/CXR if suspicious of cardiogenic component
CVP
Measurement
Via central vein (subclavian, IJ or femoral) … not external jugular
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Physiology
Starling hypothesis
Contractility is a function of initial fiber length
Stroke volume varies with EDV
EDV varies with volume status
EDP varies with EDV
Right EDP varies with left EDP. True in the healthy heart … however a variety
of conditions lead to a difference in function between the two sides of the heart
including respiratory disease, mitral stenosis, cardiac failure and pregnancy.
CVP is the same as EDP
Interpretation
Normal CVP is ~ 5 cm H2O
CVP is a very indirect way of guessing left ventricular filling. Therefore absolute
values are meaningless. Do not base fluid management decisions on a single
CVP reading.
Normal CVP does not rule out hypovolemia or fluid overload
For patients with heart failure, there is a level of CVP which is optimal. This
“optimum” CVP is very unlikely to be within the “normal range”
CVP is extremely useful when monitoring trends or response to treatment.
Management
Basic resuscitation
Airway
Oxygen
Large-bore IV
Fluid Challenge
Principle
Once basic measures have been taken the cornerstone of treatment is the fluid
challenge.
The principle of the fluid challenge is an example of a servo loop.
Method
Infuse 100 - 200 ml of fluid rapidly and monitor the effects on heart rate, blood
pressure, UO and CVP.
Crystalloid vs. Colloid is not important; however, D5 or D5½NS are not
particularly useful as their effect on ECF and intravascular volume is much less.
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Caveats
Never diagnose “fluid overload” purely on the basis of a fluid balance chart.
Many important loss never get charted.
Do not base decisions on a single CVP reading
The management of hemorrhage is surgical
Blood should always be warmed when given rapidly
Opioids are only rarely the sole cause of hypotension. However, when a
hypovolemic patient is given MS for pain, the blood pressure may drop
dramatically. The treatment is fluid, not naloxone / Narcan.
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Dysrhythmias
Immediate action
Most commonly the result of pre-existing cardiac disease, but may occur as a
result of other factors such as hypoxia, hypovolemia, drug actions, electrolyte or
acid-base disturbances or a combination of these.
Ensure the ABCs: airway, oxygen, breathing, pulse, BP, consciousness level.
Hypotension in the presence of dysrhythmia is an indication for urgent, expert
help.
Get a 12-lead EKG; get preop one for comparison and attempt a diagnosis
Exclude any underlying causes: give oxygen, establish IV access and send Lytes,
BUN, Cr and blood gases
Treat the dysrhythmia with specific therapy … or get someone to do it for you.
Diagnosis
Three simple things to decide:
Is it tachycardia or bradycardia?
Is it broad-complex QRS (> 0.12 sec or three small squares) or narrow-complex?
Is it irregular or regular?
Definition
Extra beats on a background of sinus rhythm. QRS complexes are the same and
the P waves are different.
Causes
Can be precipitated by caffeine, alcohol or stress although occasionally a more
sinister underlying cause such as electrolyte abnormality or drug toxicity (e.g.
digoxin).
Treatment
Treatment is usually not necessary.
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Definition
Extra beats on a background of sinus rhythm, where the QRS complexes are
different from normal beats. The QRS complexes are wide and bizarre, and not
preceded by a P wave. They may be unifocal (where the abnormal QRS is always
the same) or multifocal, where they are different
Must be taken seriously if they are:
1. Frequent (> 5/min)
2. Multifocal
3. Occurring in runs of two or more
4. Occurring at or just before the T wave, the so-called R-on-T
phenomenon, which can precipitate ventricular fibrillation
Causes
If serious, An underlying cause such as electrolyte disturbance, ischemia or
hypoxia should be sought.
Treatment
Treatment is usually lidocaine 80 - 100 mg IV
Atrial fibrillation
Definition
Irregular, usually narrow-complex tachycardia with absent P waves. Most
common dysrhythmia
Causes
Long-standing AF is common in surgical patients.
Acute AF can occur in myocardial infarction, thyrotoxicosis, pulmonary
embolism, electrolyte disturbances and hypoxia.
A lapse in the patient’s regular digoxin dose may also cause new acute AF in the
previously well-controlled patient.
Treatment
Treat pain, hypovolemia, hypoxia
For an undigitalized patient, a full loading dose of digoxin can be given IV
For a digitalized patient, the usual problem is inadequate levels of digoxin and a
single extra dose (.5 mg orally will do the trick. Digoxin toxicity is possible,
particularly in the presence of hypokalemia.
For a shocked patient use DC cardioversion
Digoxin has a narrow therapeutic window, but undertreatment is more common
than toxicity. Almost nobody on 0.0625 or 0.125 mg qd has levels in the
therapeutic range (except for CRF patients). Loading dose is unchanged.
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Definition
Flip in and out of AF. Digoxin will not prevent paroxysms of AF, but will
reduce the ventricular response.
Treatment
The drug of choice is sotalol 120 - 240 mg/day.
Supraventricular tachycardia
Definition
Paroxysmal re-entrant tachycardia which on an EKG is a regular, narrow-
complex tachycardia with a rate usually between 140 and 250 bpm.
Abnormal P waves with a fixed relationship to the QRS complex.
Causes
Uncommon in postoperative period but may be seen in otherwise healthy young
patients who may have a history of palpitations. May occur after MI
Treatment
May respond to physiological measures which terminate the dysrhythmia by
provoking vagal activity. These include sustained valsalva maneuver or carotid
sinus massage.
Valsalva … blow into manometer of a sphygmomanometer and asked to
maintain a pressure of 20-30 mmHg for 10 sec and then breath out. On
exhalation, there is a burst of vagal activity that slows conduction in the AV
node, and may terminate the dysrhythmia.
Drug treatment: adenosine 6 mg IV followed by 6 mg, then 12 mg if necessary.
Adenosine is a powerful vasodilator, and transient hypotension is common.
Atrial flutter
Definition
Flutter waves occur instead of P waves usually a rate of 300/min and give a
sawtooth appearance to the baseline. Normally there is a 2:1 or 3:1 block. A
narrow-complex tachycardia at a rate very close to 150 bpm is highly suggestive
of flutter with 2:1 block
Causes
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Treatment
Same management as for atrial fibrillation but primarily aimed at controlling the
ventricular rate, although amiodarone or DC cardioversion may restore sinus
rhythm
Ventricular tachycardia
Ventricular tachycardia is a medical emergency
Definition
Any broad-complex tachycardia is VT until proven otherwise.
The main diagnostic difficulty occurs with other forms of tachycardia in patients
who normally have BBB, and whose QRS complexes are always wide.
Get 12-lead EKG and compare with previous traces.
The diagnosis can be confirmed if independent atrial activity can be spotted:
regular P waves superimposed on the ventricular activity.
Treatment
Conscious patient: lidocaine 100mg (10 ml of 1%) followed by an infusion of 1-4
mg/hr.
Unconscious patients: same treatment as with VF
Bradycardia
Definition
Slow heart rate
Causes
May be normal finding in fit individuals or during sleep as well as with patients
on -blockers.
May also be an ominous sign, particularly of hypoxia.
Treatment
If no underlying cause then treat with oxygen and atropine (0.5 mg IV)
Heart Block
Definition
1st degree: impulse is delayed but gets through each time. A sign of cardiac
disease but not an urgent problem.
2nd degree: impulses are sometimes transmitted but not always. There are more P
waves than QRS complexes. There are two subtypes: type I in which the PR
interval gets progressively longer until a beat is dropped (the Wenckebach
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phenomenon) and the more serious type II in which the ratio of Ps to QRSs is
more fixed (e.g. occurring in 2:1 or 3:1 pattern). 2nd degree heart block deserves
urgent attention from a physician.
3rd degree in which none of the atrial impulses are conducted. P waves are
regular but bear no relationship to the QRS complexes. The ventricular rate is
usually low. Occurs after MI, a result of degenerative changes in the conducting
system, or congenital
Causes
Problem with conduction of the impulse between atria and ventricles.
Usually a sign of significant heart disease.
Treatment
Definitive treatment is transvenous pacing, but as a temporary measure, the
ventricular rate can be improved with an infusion of isoprenaline.
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Hypertension
Sustained, severe HTN is associated with MI & CVA
Need to treat underlying cause before any antihypertensive medication is given
Definitions
DBP > 110 definitely abnormal
Sustained hypertension needs to be treated
Causes
EXCLUDE
Pain: NEVER give antihypertensives to a patient in pain
Anxiety
Drugs: inotropes
Hypercapnea/hypoxia
Full bladders (especially in elderly, confused people)
Malignant hyperthermia
Hormonal: pheochromocytoma, thyroid crisis, carcinoid …
ESSENTIAL HYPERTENSION
Undiagnosed hypertension. Brought out by surgery
Hypertension inadequately controlled before surgery
Patient mistakenly advised not to take regular medication preop
Treatment
Oxygen
Goal is short-term control
Nifedipine SL
Sublingual nifedipine 10mg.
Can be written PRN - 10 mg SL up to q2hr for systolic BP > 170
Labetalol IV
For those who cannot take sublingual medication because of sedation, poor
cognitive function on non-cooperation (consider pain or full bladder) or for
those in which nifedipine is ineffective.
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Titrate IV dose against effect, giving 5mgto start with. After 5-10 min if no
effect, give 10mg, then 15 mg etc.
Contraindicated in asthma and cardiac failure.
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Myocardial Ischemia
MI is the single biggest killer in the perioperative period.
pOP MI often does not generate the typical signs & symptoms. Chest pain may
be masked by analgesic/anesthetic medication.
pOP MI occurs most frequently 48-72 hr after surgery
Needs careful monitoring just like for DVT: identify patients at risk and employ
full range of simple measures to prevent ischemic complications.
Patients at risk
Previous MI (especially within last 6 months) or known angina
Hypertensives (especially those with EKG evidence of LVH)
Diabetics
The elderly
Vascular surgery patients (concomitant CAD)
Smokers
Those with EKG evidence of “strain,” bundle branch block or old MI
Prevention
Avoid anything that upsets the balance of myocardial oxygen supply and demand.
Avoid tachycardia, hypotension, hypertension and hypoxia.
Fluid Balance
Ensure good hydration/adequate UO. Avoid anemia (Hb > 10 mg/dl)
Analgesia
Pain is very bad for the heart
Oxygen
Patients will have hypoxia for 3 or 4 days pOP, particularly at night. Prescribe
oxygen for at-risk patients
Hypothermia
Treat accordingly
Regular medication
Continue all cardiovascular medications. Remember that NTG can be given as a
transdermal patch.
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Monitoring
The more the better. Pulse oximeter or automatic BP if feasible
DVT prophylaxis
SQ heparin & TEDs
Management
Examine for evidence of hypotension, CHF or dysrhythmia
Treat CP with increments of IV MS
Employ preventative measures above
Bed rest
Get 12-lead EKG & compare to preop EKG
Send blood for serial CKs. CK levels are normally elevated pOP so be sure to
ask for isoenzymes
Consult medicine/cardiology.
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Pulmonary Edema
Pulmonary edema is an abnormal accumulation of fluid in the extravascular
spaces and tissues of the lung.
It is not an uncommon cause of respiratory distress in surgical patients.
Physiology
Starling forces
Starling forces describe the flow of fluid in an out of the pulmonary capillary.
35 20 5 20
Arterial Venous
Most of the fluid forced out at the arterial end passes back into the capillary at
the venous end; the rest drains out via the lymphatics.
If excessive fluid leaks from the capillary, pulmonary edema results.
Interstitial Edema
Characterized by engorgement of the interstitial space.
Effects on lung function are subtle; the lungs become stiffer and the patient
usually complains of SOB.
Some radiological changes
Alveolar Edema
When fluid passes into the alveoli themselves.
Dramatic clinical effects with shrinking of the alveoli, stiffer lungs, increased
work of breathing and impaired gas exchange.
The transition from interstitial to alveolar edema tends to occur suddenly.
Mechanisms
Increased hydrostatic pressure in the capillary (e.g. LV failure)
Reduced colloid pressure (e.g. hypoproteinemia)
Increased capillary permeability (e.g. in aspiration pneumonitis or ARDS)
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Presentation
The diagnosis should be obvious clinically
History
PMH: Like to occur in a patient with known ischemic, hypertensive or
rheumatic heart disease
Associated with over-enthusiastic fluid therapy
Sx: Patient complains of sudden, severe dyspnea made worse by lying
flat.
Exam
Gen: sweating, cool peripheries, sputum is pink/frothy
VS: tachycardia, tachypnea, hypertension. Hypotension is a grave sign
indicative of cardiogenic shock.
Chest: B/L basilar rales; there may be an audible wheeze
CV:raised JVP, gallop rhythm with an S3. Murmurs may be present and a new
murmur is a significant finding.
Investigations
CXR: A normal-sized heart strongly suggests a non-cardiogenic
cause.
EKG: looking for AMI or dysrhythmia
Cardiac enzymes: for r/o MI. If the patient has had recent surgery, be sure to
ask for CK-MB (isoenzymes).
Echo To study valve function, myocardial contractility and EF.
CVP not necessary for diagnosis in the acute case.
ABG When respiratory failure is suspected.
Fluid overload
Patients with chronic heart failure cannot cope with a wide range of filling
pressures.
However, fear of this complication leads to a tendency to be excessively miserly
with IVF
Systemic vasoconstriction
Causes a redistribution of fluid from the systemic to the pulmonary circulations
as with pain, hypothermia or the wearing-off of anesthetic drugs.
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Management
Initial management
Sit up, give adequate oxygen by face mask
If there is evidence of cardiogenic shock or oliguria get help early
Titrate in some IV narcotic (MS 2mg at 2 min intervals up to a maximum of 10
mg). This reduces venous tone and alleviates agitation and anxiety
Furosemide / Lasix (20 - 40 mg IVP). The immediate effect of this drug is
venodilation which reduces preload. Later there is a diuresis.
Proceed to advanced management (with medical/ICU consultation) in severe or
refractory cases.
Advanced management
Identify and treat dysrhythmias
Consider vasodilators (e.g. isosorbide dinitrate IV)
In severe cases intubate and start mechanical ventilation
Further measures are required for cardiogenic shock (hypotension, oliguria) or
respiratory failure. These include inotropes, invasive monitoring, ventilation, and
one-to-one nursing … ICU
Causes
ARDS Final common pathway for a variety of major insults such as trauma,
shock, sepsis, pancreatitis, burns, obstetric disasters or MSOF. The basic
mechanism is an increase in capillary permeability.
Pulmonary aspiration of gastric contents
Pneumonias and sepsis
Allergic reactions to drugs or blood products
Neurogenic pulmonary edema. A rare condition in which pulmonary edema
accompanies an acute intracranial lesion such as head injury, tumor, or
hemorrhage.
Diagnosis
Suggested by an absence of specific features of cardiac failure.
Usually obvious from the history alone.
The diagnosis can be confirmed by pulmonary edema in the presence of a
normal-sized heart, or normal PCWP.
Management
ICU
Specific treatment depends on the precipitating cause
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Cardiac Arrest
Who to resuscitate?
DNR is appropriate when CPR is unlikely to succeed, where it is contrary to the
expressed wishes of a competent patient, or where CPR is likely to be followed
by a length or quality of life which is unacceptable to the patient. DNR on the
basis of age alone is not appropriate.
The decision for DNR rests ultimately with the responsible attending. The
decision should be taken as soon as possible where arrest is deemed likely. The
decision should be reviewed regularly.
When a DNR order is taken, it should be documented clearly in the chart, and a
brief rationale given.
Airway
Look for verbal response.
Open and maintain the airway with jaw thrust/chin lift and head extension
Breathing
Listen at the lips while watching the chest.
If there is no apparent respiratory effort begin mask resuscitation.
Circulation
Feel for a carotid pulse (for 5 sec). If absent, start external cardiac massage at a
rate of 80/min.
Place one hand on top of the other, on the lower sternum, and give sharp
compressions to depress the sternum by 3-4 cm each time. If alone give 15
compressions for every two breaths.
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General measures
Intubation, mask ventilation or mechanical ventilation, and securing of IV access
should be performed.
An EKG monitor should be connected.
For witnessed arrests, a pre-cordial thump is recommended.
Further treatment then depends on the heart rhythm
VF or pulseless VT
DC shock 200J, 200J, 360 J
Epinephrine 1mg IV
Continue CPR
Shock 360, 360, 360
Consider lidocaine 100 mg (= 5 ml of 2%) or bretylium
Asystole
Epinephrine 1mg IV
Continue CPR
Atropine 3 mg IV qD
Consider pacing
Electromechanical Dissociation
Differential diagnosis is hypovolemia, tension pneumothorax, pulmonary
embolism or cardiac tamponade. Consider specific therapy for each.
Epinephrine 1mg IV
CPR
Repeat as required.
When to give up
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Respiratory Problems
Effects of surgery and anesthesia on respiratory function
There are four major effects, decreased lung compliance, ventilation/perfusion
mismatch, hypoventilation and ciliary dysfunction.
2. Ventilation/perfusion mismatch
Anesthesia and surgery upset the delicate mechanisms that usually match
perfusion to ventilation
3. Hypoventilation
Central causes
Respiratory depressant effects of anesthetic agents, opioids or CNS pathology
Peripheral causes
Obesity
Abdominal distention
Tight dressings
Pain
Any lung pathology which increases the work of breathing (e.g. bronchospasm or
sputum retention)
4. Ciliary dysfunction
Giving dry gas directly to the airway has a damaging effect on respiratory mucosa
and ciliary function.
Overall effects
Common finding after surgery is hypoxemia (worse in the presence of chronic
lung disease.
Dips of oxygen saturation to < 50% are commonplace after major abdominal
surgery. Episodic hypoxemia occurs especially at night, within 72 hours of the
operation. It is known that this hypoxia is associated with episodes of severe
myocardial infarction.
Preventative measures
Identify patients at risk: abdominal or thoracic surgery, elderly, smokers,
COPDers
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Oxygen therapy
Methods
Standard facemask
Cannot deliver very high concentrations of oxygen.
The exact FIO2 depends on the pattern of breathing.
High respiratory rates will be closer to RA while deeper breathes will have higher
oxygen concentrations.
High-flow masks
Jet of oxygen is passed through the mask.
Come in a selection of concentrations 28%, 28%, 35%.
Are the preferred mode of delivery for patients with significant chronic lung
disease.
The highest concentration is 35%.
Non-rebreather masks
The reservoir bag fills up with oxygen during expiration.
Can deliver up to 85% oxygen.
Nasal cannulae
Used for comfort
Cannot give high concentrations of oxygen and are thus not suitable for very sick
patients
Complications
Respiratory depression
A small subset of patients with chronic lung disease have grossly abnormal blood
gases. As a result of long-standing lung damage, they have chronically increased
work of breathing and by consequence such hypoventilation that their central
chemoreceptors are extremely tolerant of very high levels of CO2.
Their kidneys compensate for the respiratory acidosis by retaining bicarbonate, so
the arterial pH is near normal.
Instead these patients rely on hypoxia for respiratory drive.
Giving oxygen will depress the respiratory drive further increasing the CO2
resulting in depression of consciousness and apnea. If the oxygen is
discontinued, hypoxia will return but the CO2 levels will be too high to be
overcome and unless the patient receives mechanical ventilation he will die.
Hypoxic drive is rare
Controlled oxygen delivery is the key … do not use face masks but rather use
high-flow oxygen delivery which can be titrated.
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Oxygen toxicity
Said to occur if concentrations of > 60% are inhaled for long periods (i.e. > 24
h).
Hypoxia should never be tolerated because of fear of oxygen toxicity.
Retrolental fibroplasia
See in neonates who are ventilated with high oxygen concentrations, causing
fibrosis behind the lens of the eye, and blindness.
Fire
See with inveterate, chronic smokers who can’t resist one last drag while on
oxygen therapy.
Indications
Cyanosis or documented hypoxemia (as with a pulse oximeter)
Major surgery (24 h postoperatively and at night for 3 nights)
Shock and severe hemorrhage. Any cause of shock results in a reduction of
oxygen delivery.
Myocardial ischemia or those at risk of it.
Conditions of high metabolic rate. For example, fever, rigors, thyroid crisis,
malignant hyperthermia.
Reduced consciousness or hypoventilation
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Epidural analgesia
The gold standard.
Provides the most effective pain relief available allowing movement and coughing
without pain.
The respiratory side-effects are comparatively trivial.
IV opioids
Need to titrate.
Therefore the best is PCA.
For patients with airway disease fentanyl is preferred over morphine because it
causes less bronchospasm.
NSAIDs
Are an effective adjunct to postoperative pain management and reduce the
requirement for opioids.
Significant incidence of bronchospasm; the effect is often delayed.
Sputum control
Humidified oxygen
Good general hydration.
Pain relief
Chest PT: including percussion and postural drainage.
Respiratory distress
Differential diagnosis
Asthma
Pneumonia, collapse, consolidation
Pulmonary edema
Pulmonary embolus
Pneumothorax
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Pulmonary aspiration
Pleural effusions
Investigations
CXR to exclude pneumothorax, pneumonia or aspiration
ABGs (a PaCO2 in the normal range is bad, suggesting impending deterioration).
Patients with acute asthma who are coping well usually hyper ventilate with a
PaCO2 or 25-30mmHg
Management
Humidified oxygen
salbutamol / and iptraropium / Atrovent by nebulizer
IV steroids (hydrocortisone 200 mg q6hr for average adult)
The quantity of nebulized bronchodilator that reaches the lower airways in acute
asthma is small, and if a single nebulizer has limited effect, it should be
immediately followed by another, then another. Each nebulizer then becomes
more progressively more effective. Four-hourly nebulizers are for maintenance,
not emergency management.
Sedatives are absolutely contraindicated. Opioids should also be avoided if at all
possible. Consult pain service/anesthesia if severe pain coexists.
Pulmonary edema
Pulmonary edema is a potent cause of respiratory distress, hypoxemia and
ventilatory failure.
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Pulmonary embolus
Any patient laid up in bed after surgery is at risk.
Of PEs, 40-60% are asymptomatic; 10% are fatal. The common signs are non-
specific, and the specific signs are rare, though pulmonary embolus should always
feature in the differential diagnosis of respiratory distress.
PE is a diagnosis of exclusion.
Symptoms
Dyspnea: common. Sudden onset of SOB is the most reliable indicator.
Syncope: occasionally
Pleuritic chest pain and hemoptysis: this occurs in pulmonary infarction, which is
only rarely a consequence of PE.
Palpitations: AF can occur if there is pre-existing cardiac disease.
Signs
Tachycardia and tachypnea: common
Low-grade fever: may occur
Wheeze: sometimes
Hypotension common in massive PE.
Investigations
CXR minimal change. There may be some loss of volume. Infarction
(with the classic ‘wedge’ appearance) and pleural effusion is rare.
EKG Sinus tachycardia is the usual finding. Acute-onset AF may be seen.
S1Q3T3, right axis deviation and RV ischemia are rare.
ABG may show reduced PaO2 but not always. PaCO2 is usually low.
Scans Perfusion scan can exclude; V/Q scan required for definitive proof
of diagnosis.
Diagnosis
Most patients with a PE will be dyspneic, tachycardic with a normal CXR and
sinus tachycardia on the EKG with no other signs.
Need to decide whether to heparinize.
Exclude other causes: pulmonary edema, pneumothorax, pulmonary collapse,
consolidation, aspiration.
If there are no other likely causes, then a PE can be presumed and a request for a
V/Q scan made at the earliest opportunity.
Management
Make sure there are no contraindications to anticoagulation
If not, then give 5000 U IV followed by an infusion of 20,000 - 24000 U per day.
Monitor the clotting times regularly. A PTT of 2-3 times control is required. If
clotting times fall below this, it is usually necessary to give a bolus (e.g. 2000
Units) as well as increasing the infusion rate.
If the diagnosis is confirmed with a scan, treatment with warfarin will be required
for 3-6 months.
Remember interactions with aspirin
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Pneumothorax
May be spontaneous, trauma-related or iatrogenic
Spontaneous
Occur in tall, thin males, or in those with
COPD/asthma
Trauma-related
Rib fractures, or
penetrating chest wounds
Iatrogenic
Central line insertion
Brachial plexus block
as a result of some forms of surgery (e.g. nephrectomy)
Diagnosis
Index of suspicion with a dyspneic patient
Upright CXR
Management
Large PTX managed with chest tube drainage
Small non-traumatic ones can sometimes be managed by aspiration or watched
with serial chest x-rays.
Pulmonary aspiration
Results from inhalation of gastric contents
Predisposing factors
anesthesia
emergency surgery
depressed consciousness
disorders of swallowing or cough
use of NG tubes
pregnancy and tracheostomy
Presentation
Dyspnea
Wheezing
Cough
Rhonchi
CXR changes include multilobar infiltrates which may be alveolar or interstitial
and may be unilateral
Management
Supportive including humidified oxygen, hydration and artificial ventilation.
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Antibiotics are indicated only if there is definite evidence for infection, and are
usually aimed at Gram-negative organisms.
Pleural effusions
An effusion seen on a CXR is at least 150 ml
An effusion picked up clinically is likely to be huge.
Needle drainage is indicated where respiratory function is borderline
Collapse (atelectasis)
Increased opacity of the affected lobe
Loss of volume where the three main changes seen are:
1. Raised hemidiaphragm
2. shift of mediastinal structures towards the lesion,
3. crowding of ribs on the affected side
Hyperlucency of adjacent unaffected lobes is sometimes seen, as they
hyperexpand to help fill the space left by the collapse.
Consolidation
Ill-defined margins
Irregular shape
no loss of volume (no mediastinal shift, raised hemidiaphragm, no rib crowding)
air bronchograms are common
Pneumonia
Classical picture of community-acquired “lobar” pneumonia (Strep. pneumoniae) is
uniform consolidation in a single lobe with air bronchograms and no loss of
volume.
Nosocomial pneumonias (gram-negative bacteria or Staph. aureus) may show
patchy segmental consolidation which may be bilateral and predominately affect
the lower lobes. Air bronchograms are rarely seen and there may be loss of
volume.
Pneumothorax
Two findings which are required for the diagnosis of pneumothorax:
1. loss of vascular markings at the apex, and
2. laterally a visible lung edge
On a supine film the air collects anteriorly, which is more difficult to spot, but
clues are a unilaterally lucent lung, or a translucent band parallel to the
mediastinum or diaphragm.
A tension pneumothorax is seen when mediastinal structures are displaced to
the opposite side.
Tension pneumothorax is, however, a clinical diagnosis, which must be treated
immediately.
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Pleural effusion
A large pleural effusion (300 - 500 ml) should be easy to detect on an erect chest
film.
Signs are a homogenous opacification of the lower chest, with loss of
costophrenic angle and hemidiaphragm. The upper margin is concave upwards
and higher laterally than medially.
The signs of a small pleural effusion are usually loss of the costophrenic angle.
Pulmonary edema
An excess of fluid in the lungs that is not in the intravascular compartment.
Initially the fluid is in the interstitial spaces and, as it worsens, it eventually spills
into the alveolar air spaces.
Interstitial edema
Septal lines: fluid collects in the interlobular septa which is visible as short,
horizontal lines 3-6 cm long, known as Kerley ‘B’ lines. They are best seen in the
peripheral lower zones.
Peribronchial cuffing: On normal x-rays a few bronchi can be seen end-on in
the hilar regions. In interstitial edema their walls appear thickened.
Vascular changes: Vessel shadows are seen more clearly in the upper zones
than lower, referred to as cephalization.
Alveolar edema
Irregular shadowing: Gray fluffy shadows are seen, more frequently in the
lower zones. As it progresses, the shadows become confluent and whiter.
Sometimes the hilar zones are more affected give a “bat’s wins” appearance.
Pleural effusions: commonly bilateral, but if unilateral more common on the
right. Fluid may be seen in the horizontal fissure.
Air bronchograms: common.
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Detection
Catheterize all high-risk patients: diabetics, CRF, Jaundice, Elderly, CHF, severe
CT Dz.
Catheterize all major surgeries: major trauma/crush injuries,
burns/electrocutions, hypovolemia/hypoxia, sepsis, major
abdominal/vascular/cardiac cases.
Exam: (pulse, BP, mental status, skin turgor, eye turgor, dry mouth).
Always consider the possibility of urinary retention/obstruction & examine for
full bladder. Retention is a common cause of postop confusion.
Exclude signs of heart failure or fluid overload
Consider furosemide / Lasix dependence
Management of Oliguria
Role of Fluids
Correct the fluid deficit (with 250 cc of fluid challenge) -> then reassess.
If no initial improvement then repeat the challenge; consider placing CL -> CVP
Role of Diuretics
Diuretics can only be used when there is accurate knowledge of volume status
Consider furosemide dependence
Role of Inotropes
Consider dopamine (2.5 mcg/kg/min) if volume status is normalized & UO still
low
General care
Oxygen
Check for any nephrotoxic drugs (aminoglycosides, NSAIDs, diuretics).
Diagnosis of ARF
Kidney has lost ability to concentrate urine
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ARF Hypovolemia
Dilute urine Concentrated urine, low volume
Iso-osmotic with plasma specific gravity > 1.016
High sodium content Low sodium content (< 20 meq/l)
Low urine/plasma urea ratio High urine/plasma urea ratio
Low urine urea content High urine urea content
Catheters
Indications
1. accurate measurement of UO
2. management of urinary retention
3. compromised micturition
4. bladder irrigation
Urethral catheters
Use a urojet for analgesia/lubrication; takes time to work
Antisepsis
Take weight off bladder neck by taping to leg
Clamp catheter distal to insertion of inflation channel
Replace foreskin after catheterizing males
Suprapubic catheterization
Preferred for management of acute retention
Contraindications: no distended bladder, post-TURP, in patients with bladder
tumors
Catheter problems
Blockage
Unblock with a bladder syringe & NS
Bladder washout
If unsuccessful, may need to change catheter
Acute retention
Common after major surgery, particularly in males .... associated with prostatic
enlargement
Increased with epidural analgesia
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Catheterize for painful retention only ... exception is with epidural analgesia
where pain may be masked.
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Fever
Causes
Non-septic causes
DVT, Blood transfusion reactions, malignant hyperthermia, drug reactions
Septic causes
Pneumonia
Anesthesia + surgery impair sputum clearance. Common pathogen is still Strep.
pneumoniae.
Wound/Abdomen
Staph. aureus, Gram-negative bacilli like E. coli & anaerobes.
Urine
Especially after urine catheterization/instrumentation. Gram-negatives such as
E. coli.
Lines
In any patient with a central line … especially > 1 week.
CNS
After neurosurgery - especially VP shunt
Extremities
Ischemic limbs can get infected with anaerobes. Orthopedic implants can get
infected.
Assessment
History
W/U only necessary for temperature > 38. Check oral, rectal or tympanic
measurements. Oscillating fevers are suggestive of an abscess..
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Exam
Check for other signs of sepsis: tachycardia, tachypnea, warm extremities, wide
pulse pressure, rigors, hypotension
Check clues as to focus: cough/sputum, dysuria, cloudy urine, purulent wound
drainage, peritoneal signs, meningism, long-standing central line.
Labs
Check WBC, C-reactive protein, CXR
Specimens
Key to good microbiological practice.
Take appropriate specimens before starting empirical antibiotic therapy.
Blood cultures
Blood cultures. Chance of catching bacteremia is about 60 - 70% with a 10ml
sample. False positive (contaminants) are common.
Technique: prep a wide area of skin. Let alcohol dry first. Take 10 ml of blood,
then discard needle. Place 5 ml in each bottle using a fresh needle.
The best time to take blood cultures is just before the peak of temperature.
Urine
Mid-stream urine specimen is useful.
Finding of significant WBC indicates UTI
Catheter specimen less useful as WBC may be a normal finding
Sputum
Sputum is always full of normal flora.
The only truly significant result is a heavy growth of a known respiratory
pathogen
Blood cultures are a much more productive way to investigate suspected
pneumonia
CSF
Collected by LP
Send for gram stain/.microscopy immediately
Wound swabs
Get frank pus
Wipes of erythematous areas not useful
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Treatment
Non-antibiotic treatment
Sputum clearance: good analgesia & PT
For wounds remove one or more sutures. All abscesses require surgical
exploration and drainage.
For UTI remove catheter. Increase UO. Alkalinization of urine helps alleviate
dysuria.
DC CL; send tip for Cx
Antibiotic treatment
Take cultures first
Simple
First choice is cefuroxime 1.5 g IV q8. Useful coverage for Staph. aureus, E. coli
and Gram-negatives and Strep. pneumoniae.
If you suspect anaerobes (after GI/abdominal surgery) add metronidazole /
Flagyl 500mgIV
If patient received cefuroxime perioperatively then try amoxicillin + clavulonate /
Augmentin
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Hypothermia
Definitions
Mild 35 -37; Moderate 32 - 35; Severe < 32
Causes
Anesthesia -> decreased BMR
Temperature regulation altered
Normal responses to hypothermia inhibited
Loss of evaporative heat during surgery
Use of unwarmed IVF.
Patients at risk
Extremes of age
Thoracic/abdominal surgery
Prolonged surgery
Emergency surgery
Massive blood transfusion
Hypothyroidism or malnutrition
Effects
Cardiovascular
Vasoconstriction/shivering -> increased myocardial oxygen demand
Severe hypothermia -> dysrhythmias and VF
Increased blood viscosity
Respiratory
Shivering increases oxygen consumption -> hypoxemia
Give oxygen to shivering patients
Oxy hemoglobin curve stabilized
CNS
Progressive depressed LOC
Fixed & dilated below 28
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Other
Decreased clotting function
Renal/hepatic function decreased
Hyperglycemia secondary to decreased glucose utilization
Technical problems
BP measurement difficult; automatic machines misread
Pulse oximeters may fail due to poor peripheral perfusion
Phlebotomy difficult
Management
Oxygen
Passive rewarming (remember to cover the scalp)
Active surface rewarming ... may cause vasodilatation -> hypotension; treat with
fluid
Active core rewarming (cardiopulmonary bypass or ECMO)
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CNS complications
Confusion: Definition
Delirium
Used to describe a syndrome of acute, fluctuating disturbance of attention,
memory, sleep, orientation, perception and psychomotor function.
Usually occurs in the first few days post-op, often after a lucid interval.
It is typically worse at night.
Not all patients will be agitated (some will be withdrawn)
Dementia
Differs from delirium in having a gradual onset and in being largely irreversible.
It also shows as a global cerebral impairment.
Depression
May co-exist or mimic delirium and/or dementia.
Many of the symptoms overlap and may confuse the diagnosis.
Confusion: Definition
Quick MSE
Check with a set of simple test for memory and orientation.
Ask for patients age, the time, the date, the name of the hospital and the
President.
Ask about the date of a major historical event.
Ask them to identify staff members by their uniforms
Ask them to remember an address and repeat it back to you.
Ask them to count backwards from 20.
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Causes of delirium
Metabolic
Hypoglycemia, hyperglycemia, dehydration, hyponatremia, uremia, acidosis,
hypophosphatemia, hypercalcemia, hypocalcemia, hypothyroidism,
hyperthyroidism, hepatic failure, porphyria.
Respiratory
Hypoxia, infection, pulmonary embolus, fat embolus.
Infections
Respiratory, urinary, wounds, intra-abdominal.
Cardiac
Myocardial infarct, congestive heart failure, hypotension.
Neurological
Raised ICP, brain contusion, reduced perfusion, post-ictal state, CVA/TIA, post-
cardiac bypass, infection, sensory/sleep deprivation.
Excretory
urinary retention, constipation
Drugs
iatrogenic or withdrawal
Labs
In all cases, hypoxia, electrolyte imbalance, myocardial ischemia and infection
needs to be actively excluded.
CBC anemia, leukocytosis (2o to infection)
Lytes, BUN, Cr Dehydration and electrolyte imbalance
Glucose hypo/hyperglycemia
Urinalysis both for microbiology & chemistry
Gases ± oximetry for hypoxia or acidosis.
EKG ± enzymes for ischemia, infarct or dysrhythmias
Radiology CXR, U/S, CT scans, V/Q scans
Biochemistry thyroid function, drug screening, porphyrins.
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Management of Delirium
Treatment takes two forms:
1. Dealing with the cause of the delirium
2. Supportive care to prevent deterioration or injury
Nursing care
Implement measures to minimize risk of injury.
Less experienced nurses may be inclined to rely too much on sedation and
should be politely resisted until you are sure that it is indicated.
Restraints are very rarely a good idea; they worsen the agitation and increase the
risks of injury.
Rehydration
Dehydration causes delirium and delirium causes dehydration.
Good fluid and electrolyte control is essential and is likely to need secure IV
access, repeated investigations and measurement of urine output.
This can be difficult with an uncooperative patient.
Oxygen
Hypoxia is common, especially at night.
All patients who have had major surgery should receive oxygen at night.
All delirious patients should have at least a trial of oxygen, along with serial gases
or oximetry to find if they are helped by it.
Persistent hypoxia with delirium despite oxygen is likely to mean a transfer to the
ICU.
Sedatives
Should be a last resort, not an automatic reaction to delirium.
Most sedatives can cause delirium and that many are respiratory depressants.
When sedation is essential it is best given in regular small doses.
Benzodiazepines are respiratory depressants, long-acting and disturb normal
cognitive function; unless they are specifically indicated they should be avoided.
Haloperidol /haldol is a good choice and can be given orally in doses of 0.5 -
2.0 mg q6hrs.
Thioridazine / Mellaril is an alternative in doses of 5 - 10 mg q 8hr. This dose
can be increased to a maximum of 30 mg q8hrs.
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Withdrawal
Alcohol
Benzodiazepines
Opioid
Insomnia
Rule-out pain, delirium, withdrawal or depression.
Benzodiazepines
Essential to pick a short-acting agent to avoid daytime sedation.
Try Serax 10-15mg PO.
Problems include respiratory depression and addiction.
All patients must be warned that hypnotics are extremely habit-forming and
should be used infrequently, irregularly and only in the short-term.
Reduce the dose in the elderly and avoid benzodiazepines altogether when
respiratory function is critical.
Coma
Coma is never a normal finding, nor is it safe to attribute it to anesthesia.
When there is good reason to suspect drug-induced coma a therapeutic trial of a
specific antagonist is reasonable.
Naloxone / Narcan (0.1 to 0.2 mg) reverses opioid sedation but also the
analgesia.; short duration of action and may require several doses.
Flumazenil / Romazicon (200 mcg IV) reverses the effects of benzodiazepines.
If coma persists think about ICU.
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Convulsions/Seizures
Causes
Neurological
Brain contusion, infections, raised ICP, epilepsy, CVA
Drugs
many agents in overdose including lithium, tricyclics, aminophylline, NSAIDs,
anti-emetics, local anesthetics
Withdrawal
commonly alcohol
Metabolic
hyponatremia, hypoglycemia, hypercalcemia, hypomagnesemia
Respiratory
hypoxia, alkalosis
Infection
febrile convulsions in children
Pregnancy
eclampsia
Treatment
Supportive
Maintain a clear airway
Supplemental oxygen
Prevention of injury
Medication
Emergency drug of choice is diazepam / Valium (10 - 29 mg IV slowly or 10 - 20
mg PR). This can be followed by phenytoin / Dilantin (15 mg/kg IV slowly).
Continued seizures may require general anesthesia.
The cause of the fit must be vigorously pursued with clinical and laboratory tests.
Don’t forget a pregnancy test in young women.
Extrapyramidal problems
Pre-existing Parkinsonism may worsen during a surgical admission due to
difficulty in administering the medications.
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Thrombosis
Thrombosis is a common consequence of anesthesia and surgery. Occurs in up
to 25% of all surgical procedures.
Arises from:
1. Abnormal blood flow,
2. Hypercoagulability,
3. Endothelial injury.
High-risk groups
Orthopedic surgery
Gynecological surgery
Cardiac failure
Malignancy
Obesity
Elderly, strokes & generalized immobility
Progesterone/Estrogen therapy
PVD/varicose veins
h/o DVT/PE
Unusual hypercoagulable states
Prevention
Early mobilization (with adequate pain control).
SQ heparin (5000 U SC x 5 days) -> thrombocytopenia occurs in 0.3%.
LMWH.
TEDs (TEDs + heparin may be additive).
Pneumoboots.
Epidural/spinal anesthesia.
Coumadin (especially for orthopedic surgery).
Diagnosis
DVT
DVT is commonly asymptomatic.
Calf pain (redness, swelling and engorged superficial veins). Positive Homan’s
sign.
Groin pain (with iliofemoral thrombosis).
Cyanotic discoloration of affected limb.
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Management
Calf DVT -> PE rare.
However, calf DVTs may extend proximally.
Treat with heparin ... then continue anticoagulation for 3 months.
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Miscellaneous Postoperative
problems
Thyroidectomy problems
Airway obstruction
Postoperative hematoma
May be dramatic.
Management is to remove the skin closure clips and evacuate the clot at the bedside.
Laryngeal edema
Sometimes occurs on the 2nd or 3rd day and is gradual in onset.
Severe stridor may necessitate tracheostomy.
Tracheomalacia
A very large long-standing goiter may erode the tracheal cartilages.
When the enlarged gland is removed, the trachea collapses on inspiration.
Hormonal problems
Thyroid crisis
Now rare, as a toxic gland is rarely operated on.
Clinical features include fever, tachycardia, dysrhythmias, abdominal pain and
diarrhea.
Treatment is with -blockers, iodide and steroids.
Help from an endocrinologist/ICU should be sought.
Mortality is extremely high.
Hypoparathyroidism
If all four parathyroid glands are removed, hypocalcemia will result.
It is important to check calcium post-operatively.
Severe hypocalcemia causes tetany.
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Treatment initially is with 20ml of 10% calcium gluconate given slowly IV.
TUR syndrome
Important condition that sometimes complicates transurethral resection of the
prostate.
Causes
Occurs as a result of absorption of large quantities of the 1.5% glycine irrigating
solution through open venous sinuses.
Has an incidence of up to 15% of TURPs, and is not uncommonly fatal.
Signs
The clinical effects are mainly due to hemodilution and hyponatremia.
The first signs are restlessness, headache, confusion.
Initial hemodynamic signs are a widening of the pulse pressure and increase in
SBP. This is followed by hypotension, bradycardia, dysrhythmias and, in severe
cases, cardiac arrest.
If severe, cerebral edema with convulsions or coma, and pulmonary edema.
Diagnosis
Confirmed by measurement of plasma sodium. Problems are likely when the
sodium is < 120, but any significant drop should be taken significantly.
The hemoglobin and hematocrit are usually depressed by the hemodilution.
Management
Loop diuretics
Furosemide 40 mg IV.
Given that the majority of the patients are fluid overloaded and the most serious
complications (cerebral edema) are a consequence of this. However, furosemide
causes diuresis by removal of sodium which is a curious way to treat
hyponatremia.
Do nothing
Based on the knowledge that many patients with severe hyponatremia (as low as
104 mmol/l) may be asymptomatic and spontaneously correct the problem.
Rapid correction of hyponatremia is dangerous.
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Stable patients
Receive only the usual maintenance fluid; avoid dextrose or dextrose-saline
solutions.
Hesitate to treat a low hematocrit with blood transfusion unless you are sure that
a heavy blood loss took place.
Check electrolytes regularly (q6hr).
Unstable patients
Hemodynamic instability or convulsions should be managed in the ICU.
The difficulties with the clinical assessment of volume status make invasive
monitoring with CVP or even Swan-Ganz catheters justified.
Inotropes or calcium may be indicated and coagulation studies performed as DIC
is a recognized complication.
Eye problems
Corneal abrasion
The eye is sore and red, with a gritty feeling.
Confirm diagnosis by placing a drop of 0.5% amethocaine, followed by
fluorescein. The abrasion will take up the stain.
Treatment consists of an eye pad and bandage, and chloramphenicol ointment.
Acute blindness
Rare (and often transient)
May occur due to retinal infarction from prolonged pressure on the eye, from
basilar artery spasm, acute MS or even TUR syndrome.
Although there is no specific treatment advice from an ophthalmologist should
be urgently sought.
In the case of retinal infarction, place a patch over the eye to decrease the
metabolic work and hence oxygen requirement of the ischemic retina.
Post-intubation problems
Sore throat
Common
Requires only symptomatic treatment (lozenges).
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Dental damage
Teeth should be found
early in-patient dental treatment should be offered
Arytenoid dislocation
Presents with hoarseness and odynophagia
ENT referral indicated
Musculoskeletal problems
Swollen joints
Gout
For a single joint (especially the foot), the most likely cause postoperatively is
gout.
Measure uric acid.
Involve a rheumatologist
Treat with strong NSAIDs (indomethacin 50 mg tid)
Septic arthritis
There will be signs of infection
Treatment is with immobilization, antibiotics and joint aspiration.
Nerve injuries
Occur as a result of poor positioning, injection of substances into the nerve or
use of tourniquets.
Full documentation should be made immediately a nerve injury is suspected.
Recovery is usual, but may take months.
Anaphylactoid reactions
Causes
Type 1 hypersensitivity reaction, or true anaphylaxis. In this type, prior
exposure to the drug is required. On the first exposure, lymphocytes produce
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specific IgE antibodies, which attach to the membranes of mast cells and
basophils. A second exposure leads to degranulation of mast cells on a massive
scale.
Complement-mediated reactions. Here exposure leads to activation of
complement cascade which cause mast cell degranulation. Prior exposure is not
necessary.
Presentation
Skin: characteristic urticarial rash or flushing usually appears rapidly
Cardiovascular system: hypotension to total cardiovascular collapse.
Hypotension is the result of release of histamine and other vasoactive peptides
which cause widespread capillary vasodilation and increased capillary
permeability. Leakage of fluid may cause significant ECF loss. Dysrhythmias
may occur, most commonly supraventricular tachycardia.
Bronchospasm: may be life-threatening
Glottic edema: occasionally occurs, threatening the airway.
Gastrointestinal: Immediately after recovery, the patient may complain of
abdominal pain, diarrhea, nausea and vomiting.
Miscellaneous: Other effects include conduction defects, coagulation
disorders and leukopenia.
Management
Immediate
Discontinue administration of suspected drugs, give oxygen and maintain the
airway.
Call a cardiac arrest.
Give epinephrine. The earlier the epinephrine given, the better the outcome.
Initial IV dose should be 0.1 mg (which is 1 m of 1 in 10,000) given in
increments of 0.1 mg.
Give IVF stat. 1-2 liters of saline. Good venous access is required (14 or 16
gauge). Colloid solutions may be preferable if available.
Glottic edema may require intubation or cricothyroidotomy.
Second-line
Antihistamines. The agent of choice is chlorpheniramine / Chlor-Trimeton (10-20
mg slowly IV) or diphenhyramine / Benadryl (25 - 50 mg IV/PO/IM q 6hr).
Aminophylline may be required for persistent bronchospasm particularly in the
absence of hypotension; 5 mg/kg can be given over 20 minutes.
Steroids have no place in immediate management. They may be given if the
reaction persists, for example hydrocortisone 200 mg IV.
Labs: it may be desirable to take blood samples to confirm the diagnosis and
identify the agent responsible. Two EDTA (red-top) tubes should be taken
immediately after the reaction and again at 3, 6, 12 and 24 hours.
When a drug is implicated with reasonable certainty, the patient should be
informed. Full documentation should be made. Inform the patient’s primary
care physician.
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Tracheostomy
Tracheostomy Care
Patient’s cannot speak (except with ‘fenestrated’ tubes which are placed later in
the recovery). Make sure writing materials are available.
Normal cough is not possible. Regular suctioning and PT are need to prevent
sputum retention.
Dysphagia is common due to the bulk of the cuff and to poorly coordinated
swallowing. This may be partially relieved by temporarily deflating the cuff. It is
important to assess swallowing before allowing solids. Use methylene blue, ask
the patient to swallow, observe for coughing, and then examine the tracheal
aspirate for coloration.
The presence of a foreign body is irritating and causes secretions. These may
form hard crusts and can obstruct the tube. Humidification and regular
suctioning are effective in prevention.
Pressure necrosis of the trachea is caused by a poorly positioned tube or an
overinflated cuff. This can result in stenosis or edema which make extubation
impossible. Erosion into the anterior neck can lead to fatal hemorrhage. Always
check cuff pressure regularly and do not let it exceed 20 cmH2O.
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