JONAH COHEN

SURGERY CLERKSHIP CASE LIST

JANUARY 2009

CASE LIST:
1.) Appendicitis
2.) Colon cancer
3.) Diverticulitis
4.) Bowel ischemia
5.) Bowel obstruction
6.) GI Bleed
7.) Hemorrhoids/Perianal pain
8.) Pancreatitis
9.) Gallbladder disease
10.) Hernia
11.) Breast mass
12.) Thyroid mass
13.) Melanoma
14.) Abdominal trauma
15.) Abdominal Aortic Aneurysm
16.) Carotid bruit
17.) Peripheral Vascular Disease
18.) Hyperparathyroidism / Hypercalcemia
19.) Soft Tissue Sarcoma
20.) Carcinoid tumor

1.) Acute Appendicitis (1)

1.) History: Age, GENDER? (important w/ ALL Abdominal pain) Classic chronology: visceral referred periumbical pain
(intermittent/crampy) > N/V> Anorexia > migrates to RLQ mcburneys point (parietal peritoneal constant/intense) w/in 24 hrs.
(Appendicitis = PAIN FIRST/BEFORE VOMITTING/Change in bowel habits vs. Gastro vomit/change in bowel habits then pain)
PMH: IBD, DM, previous surgeries, etc. SH: sexually active?
2.) Physical Examination: Vitals: low-grade fever (high grade if perf).
As listed above: must do complete Physical examination including Cardiac and Lung exam > Focusing on Abdominal exam including
pelvic (if female)/genital exam and rectal exam. May see peritoneal irritation signs: like a log (vs. renal colic = cant sit still)
involuntary/voluntary guarding, rebound tenderness, obturator sign (flex knee/hip, internally rotate leg seen in pelvic appy), psoas sign
(extend hip with knee extended classically in retrocecel appy), rovsing (palp of LLQ elicits pain in RLQ).
3.) Laboratory / Other tests: CBC w/ diff (elevated WBC w/left shift), C7, U/A-UCx, UPreg (female) - (CCUU) Abnl UA does not
rule out A.Appy cause periappendicieal inflammation can cause pyuria and microscopic hematuria.
4.) Imaging: Only if unclear from H&P and Labs - AXR (upright/supine looking for calcified fecalith, free air, scoliosis away from
pain), CT (periappendiceal fat stranding, appy diameter >6 mm, periappy fluid), U/S (large noncompressible appendix). Could order
CXR R/O RLL PNA.
5.) Differential Diagnosis: GI: Crohns, Mesenteric adenitis (viral or yersinia enterocolitica), Meckels diverticulum, gastroenteritis,
pancreatitis, constipation, intussuception, cecal volvulus GYN: listed above, GU: listed above, Non-surg: listed above, perforated
gastric/duodenal ulcer (RLQ pain from succus draining = Valentinos sign).
6.) Treatment options both medical and surgical: ADMIT, Pre-op: NPO, IVFluids (LR - or Normal Saline if Vomitting! > NaCl will
improve contraction alkalosis whereas Bicarb from LR is not good for this), ABx w/ anaerobic coverage. Laparoscopic appendectomy
(women so you can see adnexa) or if patient needs to quickly return to physical activity. OR Open appy.
**Non-perf: prompt appy, 24 hrs. ABx (Unasyn or Cipro/Flagyl), D/C POD#1. **Perf: IVF and appy, drain all pus and send for Cx,
ABx (Zosyn) for 3-7 days (when WBC drops and is afebrile, ambulating w/ reg. diet), leave wound open after closing fascia > 2ndary
intention or delayed primary closure). **Abscess: PCT drainage + ABx, w/ elective interval Appy 6 weeks later.
***If you suspect PERFORATION, NO CT, go STRAIGHT TO THE OR. Might suspect perforation if WBC > 15-16,000
-Some same Classic 1.) HX, 2.) Vitals/Exam 3.) Labs w/ plain films (ie. Hx, Fever, WBC) is enough to go to Surgery.
7.) Complications: of appendicitis = free perf, (Risk of perf. 25% by 24 hours. 75% by 48 hours.) pelvic abscess, liver abscess. of
appendectomy: wound infection, SBO, EC fistula.
8.) Follow-up: Path report: R/O CROHNs Dz.
9.) Misc/PP: 50% present w/ classic sxs. U/S best to assess pelvic pathology while CT best to asses non GYN abdominal process.
Diagnostic laparoscopy is most accurate test to asses for acute PID and visualize appendix. Pathophys: obstruction of lumen,
inflammation/infection, ischemia/necrosis, perforation secondary to Lymphoid hyperplasia/fecalith/tumor.

2.) Colon cancer

Name it, Stage it, Treat it for all cancers.
1.) History: AGE, HPI: most present asymptomatically. DOE, angina, Constitutional Sxs: ie. rectal bleeding, anorexia, wt. loss, change
in bowel habits: decrease caliber in stool, diarrhea, post-prandiel bloating, distention, constipation, blood in stool, hematochezia (L),
melena (R). Classically Right sides bleed (Anemia), Left sides obstruct. PMH: IBD (UC), Hx. Colon cancer/polyps, last colonoscopy.
Previous Hx of Colon cancer! MEDS: aspirin, NSAIDs FH: Hx. Colon ca? HNPCC, FAP, Turcots, Garnders (desmoid tumors), IBD

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2.) Physical Examination: Vitals: tachycardic, General: pale? Complete physicial exam, signs of anemia? Ie. conjunctival pallow, loss
of red in palmar creases. Focusing on Abdominal exam: tenderness, measses, RECTAL exam: masses (10% palpable), gross blood,
heme-occult blood (10% guaiac positive have CRC)
3.) Laboratory / Other tests: CBC (Hb? Compare w/ last Hb), low MCV, Iron studies (low ferritin, high TIBC), C7 (hypokalemia from
villous adenoma)
4.) Imaging: endoscopy upper (EGD) and lower (colonscopy). Lower most likely.
STAGING: Get CT of Chest/Ab/Pelvis. TNM, T1 subm, T2 musc prop, T3 thru musc prop, T4 thru perit. N1 =1-3 regional nodes. N2
>3 regional nodes, N3=regional nodes along major vascular structure. Lymph node involvement > Stage III.
5.) Differential Diagnosis: Adenocarcinoma, carcinoid, lipoma, leiomyoma,, leiomyosarcoma, lymphoma, diverticular disease,
Ulcerative colits, Crohns, peutz jagers, hyperplastic polyps.
6.) Treatment options both medical and surgical:
Polyps: endoscopic resection and follow-up.
Invasive adenocarcinoma: pre-op bowel prep for elective surgery = cathartic (ie. GoLytely) + BSAbx IV (ie. Unasyn) and oral
nonabsorbable ABx (neomycin). Requires segmental resection with margins > 2-5 cm. Find the tumor, resect the blood supply, then the
bowel. Must get at least 12 nodes to say its negative w/ high sensitivity. W/ positive Lymph nodes, you get chemo.
PREOP- Metastatic workup: CXR, LFTs, CEA (get PRE-OP, <5=normal, smoking can increase CEA to around 7, not a good screen
but for baseline and recurrence), CT AP. Adjuvent chemo for Stage III improves survival: FOLFOX4= 5-FU, leucovorin, oxaliplatin. 5
year survival = I (90), II (75), III (50), IV (5).
With METS, Stage IV, if isolated Liver met, some can do surgical resection or RFA.
7.) Complications:
8.) Follow-up: N.B. Surveillance for occurrence of metachronous CRC. Post CRC, @ 3 months: PE, stool guaiac, CEA (every 3
months for 3 years (90% recur within 3 years of surgery), then every 6 months for 2 years) Some say colonscopy at 6 month intervals up
to 1 year, then Q2 years and then Q3 years. Plus yearly H and P with serial CEA measurements.
SCREENINGw/ hx of polyps, place on surveillance for 3 years later, then every 5 years. Standard screening = ACG: Annual DRE and
FOBT starting at 40, colonoscopy Q 10 years beginning at 50. With strong family hx, age 40 or 10 years before youngest family
member with it. FAP ~ 10 y/o (also EGD for duodenal cancer). HNSPCC 25 y/o. UC ~ having it for around 8 years and bx Q1 yr.
Turcot (head CT). Some say 75% recur within in FIRST YEAR. 95 percent by 5 years.
9.) Misc/PP: 5% lifetime risk, 5% less than 40 y/o. 70% develop from adenomatous polyps. Size of polyp associated with risk of CA. >
2cm = 46% . No serosa in Esophagus and middle/distal rectum. Main colon function = water absorption and stool storage. Risk starts to
increase at 40, peaks at 70-80 (but can still happen at any age!). Any polyp youll resect if >1cm generally, but Tubular (pedunc), TV,
Villous (sessile). Thought is it takes ~ 8 years for a polyp to becomes cancer. Even if Bx is normal, if Tissue grossly looks bad, remove
it. Risk of cancer w/ polpy size = 1 cm> 10%, 2 cm>30%, 3 cm>50%

Related topic = RECTAL Cancer:

-has mesorectum, and envelop of fat THEREFORE can use RADIATION in treatment. Major difference from COLON CA.
-can Stage rectal w/ 3-D U/S pre-operatively.
-Presents w/ hematochezia, or mucus; tenesmus, feeling of incomplete evacuation.
-30% CRC. Same mets workup + endoscopic U/S to assess perirectal LNs and depth of invasion.
-Treatment: (all resections include removal of rectal mesentery and LNodes)
Abdominoperineal (AP) resection: for tumors near the sphincter complex = (of rectum and anal canal including anal sphincter complex)
for low-lying rectal carcinoma > give permanent colostomy.
Low Anterior (LA) resection: for rectal tumors above anal sphincter = resection of rectum to level of levator ani muscle leaving anal
canal and anal sphincter muscles intact.
STAGE III, reduction in tumor recurrence if receive NEOadjuvent chemo (5-FU radiosensitizes) plus Radiation pre-op of surgical
resection.

3.) Diverticulitis
1.) History: Age, HPI: Constitutional: F/C/S, Anorexia, NV, Diarrhea, pneumaturia, fecaluria PMH: diverticular dz? Recurrent UTIs,
2.) Physical Examination: Vitals (fever, tachycardia, hypotension), General, complete CP exam focusing on abdomen, peritoneal signs
(localized? Generalized?), pelvic/genital exam/r/o scrotal pathology torsion/hernia + rectal exam.
3.) Laboratory / Other tests: CBC w/ diff (white count, left shift, anemia), C7 (lytes, BUN/Cr), U/A > DIAGNOSIS can often be made
clinically (H and P) and treated as an outpatient (can they tolerate oral meds?)
4.) Imaging: If signs of obstruction, diffuse tenderness to palpation w/ history of no stool or gas, > AXR to look for A/F, dilated loops,
free air. **Confirm suspicion especially if systemic toxicity signs w/ abdominal CT (showing A. diverticula, B. colonic wall thickening,
C. mesenteric fat stranding). CT (w/ oral/PO contrast) can help to R/O abscess. NO Colonoscopy acutely, nor barium study. ON CT,
normal colon generally 2-3mm in width. > or equal to 5 mm = increases chances and >1cm, makes it even more likely.
5.) Differential Diagnosis: (4 Is) IBS, IBD, Ischemic colitis, Infections (C.Difficile, Pyelonephritis), lactose intolerance, colon
cancer, sigmoid volvulus, endometriosis, PID, rupture ectopic (age)
6.) Treatment options both medical and surgical:
Uncomplicated: non-operatively managed. Mild cases as outpatient, but with dehydration, hospitalize for observation and NPO
(bowel rest), IVF, NG (as needed), Broad spectrum ABx with Anaerobic coverage (ie. Cipro + Flagyl) .
Complicated: typically requires surgery. Ie. Perforated diverticulitis w/ peritonitis > urgent surgical exploration. > If HD unstable, resect,
colostomy, and close rectal stump (Hartmann). Reanastomose 2-3 months later.
N.B. Small mesenteric abscesses usually resolve w/ ABx, but large ones may require CT-guided drainage + ABx. If patient fails to
improve clinically after 72 hours w/ nonoperative treatment > surgery. If second time or more, elective surgical resection with primary
anastomosis (and pre-op bowel prep)! Or for patients younger than 40 or immunocompromised with first episode, may need resection.

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7.) Complications: without treatment = (PFAO) perforation, fistulas, abscess, obstruction. Fistulas = sigmoid and bladder, vagina or
skin.
8.) Follow-up: colonoscopy 4-6 weeks later to confirm diverticular dz and R/O colon cancer. (unless already had one w/in 3-5 years
previously)
9.) Misc/PP: Classic = Left-sided appendicitis in an older person, ie. 1 week hx. of LLQ pain and diarrhea, N/V/ fever. Most common
location is sigmoid colon. Pathophys: underlying diverticulum (actually false diverticulum as only mucosa/submucosa herniated through
bowel musculature where blood vessels enter increase intraluminal pressure, ie. 2/2 low fiber diet) > obstruction by fecalith,
inflammation, and microperforation.
-2/3rd of cases handeled by internists as Outpatient. Therefore CT off the bat may not be needed. As outpatient, might do clear liquids,
PO ABx, F/U in 2-3 days. If no improvement, do/repeat CT.

4.) Bowel ischemia

CHRONIC MESENTERIC ISCHEMIA
1.) History: AGE, HPI: OPQR(to back), S (where is pain) T (get good pain assessment), significant weight loss (ie. ~40 lbs. how much
over how long), EPISODES of: inability to eat 2/2 diffuse abdominal pain (mesenteric angina) w/ meals/postprandial > sounds more like
chronic M.I. as opposed to acute. Food anxiety = sitophobia. Related: diarrhea following fatty meals w/ chronic back pain and
steatorhea, greasy stools, stools float? (chronic panc), pass stool/gas? PMH: afib?, recent MI, Atherosclerotic dz? HTN? DM, FH: ,
SH: smoking? EtOH,
2.) Physical Examination: Vitals: RRR? Or afib? Hypotension?, General: , Complete physical paying attention to vascular exam: bruits
(carotid, renal, femoral, aortic/abdominal), pulsatile mass, distal pulses. Focus on abdominal exam: tenderness? Peritoneal signs, Rectal:
guaic may be positive.
3.) Laboratory / Other tests: CBC (white count, left shift?, anemia?), C7 (lytes 2/2 poor nutrition and BUN/Cr volume status), LFTs,
amylase, could ck LFTs, Bilis if concerned for Biliary Dz. Blood gas looking for acidosis /w gap.
4.) Imaging: May consider endoscopy to R/O gastric causes, Duplex U/S before and after food challenge can R/O proximal mesenteric
artery vascular Dz. MRAngiography > Celiac and SMA. Gold standard is selective arteriography. Could get CT to R/O pancreatic
malignancy, chronic itis. If worried about Biliary stuff, could get RUQ U/S.
5.) Differential Diagnosis: gastritis, gastric cancer, pancreatic stuff (chronic itis, cancer), IBD, bowel obstruction, chronic mesenteric
ischemia, acute mesenteric ischemia, acute nonocclusive MI (low flow state in critical illness or vasospastic meds), mesenteric venous
thrombosis (hypercoaguable state).
6.) Treatment options both medical and surgical: Bypass, endarterectomy, angioplasty, stenting (BEAS). Operative
revascularization. High risk patients: angioplasty can be useful. BUT, definitive revascularization with anterograde aortomesenteric
bypass OR perivisceral aortic endarterectomy are best options. Retrograde bypass from altervative source (ie. Iliac artery) also possible
with higher risk patients. Higher risk = advanced age or other CP co-morbidities.
7.) Complications:
8.) Follow-up:
9.) Misc/PP: Chronic Mesenteric Ischemia: 2/2 occlusion of mesenteric arteries related to atherosclerotic changes. Rule out other
sources of upper/lower abdominal pain. Celiac: hepatic, splenic, L gastric, SMA: Small bowel and up to 2/3 of Transverse colon, IMA:
distal colon and rectum. Generally requires 2 of 3 artery occlusion w/ disease in remainder.

ACUTE MESENTERIC ISCHEMIA:

-SURGICAL EMERGENCY. Usually no history or chronic symptoms. Acute embolus in SMA or celiac. Or acute thrombosis (acute
plaque change). Afib? Recent MI, endocarditis, mechanical valve? Can be nonocclusive: hypotension, hypovolemia, CHF.
History: TRIAD: 1.) acute onset of pain, 2.) vomiting/diarrhea/both, 3.) Hx of AFib or heart disease.
MEDS: coumadin., digitalis=assoc. w/ AMI
EXAM: pain out of proportion to physical exam, no peritoneal signs until necrosis,
Dx: mesenteric arteriography (but may delay treatment!)
-Therefore clinical judgement > emergent laparotomy. (frank necrosis or dusky/nonmotile).
Tx: ADMIT patient. NPO, IVFs, embolectomy (Fogarty catheter embolectomy) w/ resection of necrotic bowel +/- second look
laparotomy if bowel doesnt appear perfectly viable (24-72 hrs later). Catheter trial of thrombolytics may be attempted, but be ready for
emergent lap. If acute thrombosis, +/- Papaverine = vasodilator until patient is in OR.
-Post op: systemic heparinization (prevent extension of clot if still there) if AFib. may give ABx to prevent sepsis depending on
clinical picture (lactate, WBC (cortisol effect? demargination)

ISCHEMIC COLITIS (subset of Bowel ischemia):

-often resolves on its own.
-clinical entitiy resulting from inadequate blood flow in the colon often causes mild to moderate transient colitis majority of cases
resolve spontaneously, most patients >60.
Sx: sudden, crampy, mild left-sided abdominal pain, urge to deficate and passage of red or maroon blood mixed w/ stool.
-Cause: most cases none identified, often attributed to nonocclusive vascular process, or small vessel disease. COULD be mesenteric
artery embolus, thrombosis, vasospasm, systemic circulatory insufficiency, digoxin, volvulus.
-Location depends on cause = low flow> Right colon. Local non-occlusive = watershed splenic flexure =MCC.
-DX: Hx, physical, GENTLE COLONOSCOPY (or sigmoidoscopy, and gentle barium enema if needed (thumbprinting
nonspecific.). Colonoscopy may show erythema, ulceration, edema.
-Mgmt: acute ischemic colitis = w/o evidence of perfor/ peritonitis, MGMT= conservative: IVF, NPO, BSAbx w/ anaerobic coverage.
NG tube if ileus. Treat identifiable causes if exist: ie. CHF. IF HIGH WBC, fever, worsening abdominal pain and bloody stool, > OR w/
laparotomy and bowel resection.

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-Prog: most Sx resolve in 24-48 hrs, colon heals in 1-2 weeks.

5.) Bowel obstruction

SMALL BOWEL OBSTRUCTION:
1.) History: HPI: intermittent, crampy, abdominal pain, bilious vomiting (lots of vomiting may suggest proximal obstruction, distal may
be more distention and less vomiting). No passage of stool/ flatus. Bowel movement might happen w/ onset of pain and thus does not
rule out proximal obstruction. Had this before? If pain is persistent > might signify severe bowel distention (venous congestion,
decreased perfusion and necrosis) or bowel ischemia 2/2 strangulation. PMH: recent surgeries (makes ADHESION more common
than Hernia), MEDS: narcotics? Anticholinergics?
2.) Physical Examination: Vitals (fever- how high?, hypotension, tachy?), General, complete PE focusing on Abdominal exam: inspect
for scars, distention, auscultate (hypoactive with occasional high pitched rushes), incarcerated hernias?, peritoneal signs, often will be
mild diffuse tenderness. Rectal exam: little or no stool in rectal vault. (lots of stool may suggest ileus rather than mechanical obstruction.
3.) Laboratory / Other tests: CBC + diff (white count?), C7 (hypokalemia is MC lyte deficiency causing ileus, BUN/Cr), U/A, (Upreg
if woman) Amylase, ABG (A.G. acidosis may reflect ischemic bowel or dehydration) (CCUUAA / T), Type and Screen, lactate maybe.
May see hypovolemic, hypochloremic, hypokalemic metabolic alkalosis w/ proximal obstruction and lots of vomiting. (JMC>might
mask hypoperfusion acidosis)
4.) Imaging: AXR (supine and upright): distended loops of bowel (upright), air-fluid levels, abdominal free air? Complete obstruction >
usually paucity/no colon gas vs. partial ***Without visible hernia or history of abdominal surgery > CT scan (can help R/O
malignancy, gallstone ileus, or internal hernia) (thickened bowel wall, free fluid, mesentery edema) require PO contrast > (if etiology
obscure - can reliably identify transition point from dilated to decompressed bowel =Dx for mechanical obstruction vs. ileus).
UGI/SBFollowThrough (req. PO contrast > can aggravate Vomitting>Asp): can differentiate between mechanical obstruction and ileus.
GOAL = diagnose obstruction/location and identify factors indicating progression to STRANGULATION.
5.) Differential Diagnosis: mimics SBO = paralytic ileus (AXR gas distention throughout, including the colon), MI, DKA,
hypokalemia, pancreatitis, large bowel obstruction,
partial or complete. No gas = complete. gallstone ileus, volvulus, internal hernia,
If in Kid/young adult: cause likely = hernia, malrotation, meconium ileus, meckel diverticulum, intussusception
In adult: ABC (adhesion (postop), bulge (hernia), or cancer/crohns) or gallstone.
6.) Treatment options both medical and surgical:
If no hernia present, and positive history of surgery> indications of complications? NONE > try NON-Op. If yes, resusc and early
operative treatment.
NPO, IVF (critical to restore intravascular volume), NG (prevent further vomiting/aspiration), Foley (monitor Urine output and
assess response to fluid resus), (NINF), and serial exams, w/ radiologic follow up. 6-24 hours, most who improve w/ non-op will
improve = decrease discomfort and distention, decrease in NG aspirate, and radiologic improvement of distention.
Without early improvement > CTscan/ UGI/SBFT (can distinguish complete from partial)
UNCOMPLICATED: Non-operative therapy is frequently successful for SBO 2/2 adhesions. > however inappropriate if exhibiting
warning signs below (of existing/impending bowel ischemia/necrosis) Close observation.
COMPLICATED: Signs of HIGH-GRADE (COMPLETE) mechanical SBO =
persistent pain, fever, tachy, WBC, increased serum Amylase, and AXR findings.
be PRO-ACTIVE for EARLY INTERVENTIONespecially w/ elderly patients(persistent leukocytosis after hydration therapy) If
real sick> BSAbx pre-laparotomy. Likely Tx: EXPLORATORY Laparotomy after FLUID resus. (especially before general anesthesia
which promotes hypotension). If adhesive, bands are divided and (LOA) necrotic bowel resected.
7.) Complications: Mechanical SBO > strangulation, necrosis, perf, SEPSIS. Vomiting> aspiration pneumonitis.
Unrecognized/untreated fluid loss (2/2 3rd spacing and vomiting) pre-renal azotemia and Acute Renal insufficiency.
8.) Follow-up:
9.) Misc/PP: Mechanical vs. NON mechanical (ileus), MCC in adults = adhesion, MCC in kids/adults without previous surgery: hernias.
small bowel pain often refers periumbically. IVascular Fluid loss: in bowel lumen (2/2 to loss of absorptive function, inflammatory
increase in permeability and venous congestion) and 3rd spacing. Zebra cause = SMA syndrome: seen w/ females and weight loss, SMA
compresses duodenum causing obstruction.

EARLY POST OP SBO and Ileus (within 30 days of abdominal surgery):

-SBO Causes = Adhesions (most resolve spontaneously w/ NG, IVF, NPO), incarcerated hernia (internal or fascial/dehiscence),
intraadbominal infection.
-Ileus: Laparotomy, hypokalemia, narcotics, intraperitoneal infection
-signs its resolving = Flatus, stool
-order of recovery post-op = Small intestine, Stomach, Colon

LARGE BOWEL OBSTRUCTION:

-if suspicious for large bowel obstruction > go straight to CT scan after initial labs and AXR.
-Most common causes of Large bowel obstruction in adults = Cancer, Volvulus (sigmoid), Diverticular disease (CVD)
-Olgilvies syndrome: acute pseudoobstruction of colon without mechanical obstruction in criticall ill patient. Massive diltation of colon.
-Sigmoid volvulus (high fiber diet), seen most commonly in bedridden elderly patients, AXR: bent inner tube, with necrosis = free air,
pneumotosis (air in bowel wall). Diagnosis made w/ Sigmoidoscopy or if no Dx, Rads + gastrografin enema= birds beak. Initial
treatment = non-operative. In no strangulation, sigmoidoscopy = Dx and Tx (reduction) is successful in 85% of cases. If strangulation >

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emergent surgery (Hartmann resect rectosigmoid colon, and close rectal stump plus proximal colostomy). If cecal volvulus> most
patients require surgical reduction.

6.) GI Bleed
Q1: is the patient Stable* or Unstable?
HR >100 = best first indicator> Class II shock (15-30% BV) better to say Hemodynamically Normal Caveat = BBlocker, young
athlete. Can then also check, BP, RR, UOP, Mental status)
Q2: Upper or Lower (ligament of Treitz marks the end [technically 3/4th of duodenum] of duodenum and the end of the foregut, end of
Upper GI tract)? (Upper>hematemesis, melena* = *classically upper) (Lower> BRBPRFast upper can also be BRBPR)

UPPER GI HEMORRHAGE:
1.) History: Male? HPI: acute onset of upper abdom pain w/ hx PUD might suggest perf ulcer. Tarry stools? Lightheadedness,
hematemesis? Vomiting/retching? GERD sx? (epigastric pain, related to meals?), PUD? Duodenal classically gets better w/ meals (cause
increased acid). Gastric ulcer (increase w/ pain). Ever had this before? Recent trauma, burn,
ACUTE: hematemesis, coffee-ground emesis, melena (>50cc), or BRBPR=hematochezia.
CHRONIC/OCCULT: signs/symptoms of anemia +/- melena. Systemic sx: wt. loss, anorexia, F/C/S.
PMH: PUD?, Bulemia, Cirrhosis, AAA repair? HIV/Immunocompromised (infectious esophagitis) Medications: aspirin/plavix, advil
(how much?), coumadin, steroids, PPI?, FH: SH: Alcohol, tobacco?
2.) Physical Examination: VITALS: Temp, HR, BP +Orthostatics (HR up 30, syst. down 20, diastolic down 10 = 2 min. after lying to
standing), RR, O2sat, >ASSESS WHICH CLASS OF HEM. SHOCK they may be in.
GENERAL: pale, PE: complete PE focusing on CP (anterior mediastinal crunch = Hammons crunch = Boerhaaves syndrome, esoph
rupture), and abdominal (w/ rectal + Guaiac). Rule out acute abdomen ie. peritoneal signs. Stigmata of cirrhosis/portal hypertension:
Ascites, telangiectasias, palmar erythema, thin extremities, caput medussiae, fetor hepaticus, asterixis. Signs of hypovolemia.
3.) Laboratory / Other tests: CBC (anemia? MCV? Leukocytosis in perf, platelets), C7 (BUN/Cr-BUN might be elevated due to
absorption of blood by GI tract), LFT, PT/PTT, TYPE AND CROSS, amylase, Order platelets/FFP is coagulopathy or TCP found.
4.) Imaging: AXR (free air? Anterior duod perf), Endoscopy (EGD) > If no source identified > selective ANGIOGRAPY (Dx and Tx).
5.) Differential Diagnosis: PUD = 50% (Dr. Roye says TOP 3 = AVMs, Cancer, PUD> Cirrhosis)
VARICEAL (Esophageal varices (veins)-look for Stimnata of Cirrhosis) high risk of re-bleeding (60%) vs. NON-VARICEAL:
Esophagitis, Mallory-Weiss (Dx by History: post retching/vomiting longitudinal mucosa and submucosa tear > 3/4 in stomach, near GE
junction- 85% hematemesis), Gastric ulcer/Duodenal ulcer (ZE syndrome?) duodenal ulcers are 2x more common than gastric,
Gastritis/gastric erosions, Perforated peptic ulcer, Dieulafoys lesion, AVM, neoplasms (benign and malignant > esophageal cancer.
gastric cancer=more likely wt. loss, anorexia, but hematemesis less likely- more chronic blood loss). Aortoenteric fistula, hemobilia,
duodenal diverticula, Boerhaaves syndrome (more pain than bleeding), epistaxis. R/O MI w/epigastric pain. Panceatitis (perf post. Duod
ulcer > GD artery, high amylase, pain radiates into back), Trauma? (blunt/perf)
6.) Treatment options: 1st STEP = A, B, C > then IVF resuscitation = 2 periph (antecubital fossa) IVs, 14/16 gauge, FOLEY. IF
MASSIVE UGI bleed/agitation/impaired respiratory status = ET INTUBATION. (w/ monitoring of patients response by UOP, clinical
appearance, BP, HR, serial Hb/Hct, +/- CVP monitoring > NG tube following resusc (to determine if actively bleeding and rate? Warm
saline irrigation until clear aspirate appears)> UGI

**IF PATIENT unstable> following ABC-IV-O2-Monitor (high-flow oxygen, cardiac monitor) > THEN ATLS = 2 liters NS/LR>
followed by BLOOD (while T/Cross is sent to lab > when in doubt, can give Type O negative). N.B. Blood to FFP ratio generally is 1:1
and may need to give platelets eventually 2/2 dilutional effects. > Give DDAVP (vasopressin-increases vWF release from endothelium
and megakaryocytes) + IV protonix. > Endoscopy
Endoscopy to identify source/etiology = Dx and Tx. (if high suspicion of PUD > PPI empirically). UGI ENDOSCOPY establishes
diagnosis in > 90% cases! ENDO THERAPY includes electrocoagulation, epinephrine injections, thermal therapy. If non-variceal,
permanent hemostasis occurs in 80-90% cases w/ such treatment. Even w/ varices, endoscopic injection of sclerosing agents control
bleeding in most cases. Other options include variceal ligation (banding), vasopressin or octreotide (lowers portal pressure by splanchnic
vasoconstriction > but with CAD, must give w/ NITRO to prevent CA vasoconstriction and MI). With PERF, need ABX and surgery.
IF NO SOURCE > can do ANGIOGRAPHY (Dx /Tx in 70% > gel foam/sclerotherapy, metal coil springs or embolization).
*** Bleeding tends to be self-limited in 80% of all acute UGI bleed.
Overall mortality = 10%. (higher mortality w/ re-bleeding, age >60, shock, >5 units PRBCs, inpatient bleeding)
SURGERY INDICATED if Refractory, or recurrent bleeding and site known. > 3U PRBC to stabilize, or >6 U PRBCs overall. (10%
require surgery) PUD w/ massive, recurrent bleeding or w/ ulcers > 3cm. (MUST BX all gastric ulcers to R/O cancer). May require
vagotomy and pyloroplasty (drainage procedure needed w/ truncal vagotomy cause w/o vagus, pylorus wont open). Oversew bleeding
vessel in ulcer. Duod perf> graham patch (if poor surgical candidate), Truncal vagotomy and antrectomy (higher mortality, lowest
recurrence).
Dr. ROYE: > 6 U PRBCs in 2hrs OR, in 2 days >VIR
-Mallory weiss = generally self limiting, mild and amenable to supportive care/ endoscopic management if needed > Dx and Tx. 90%
people stop bleeding w/ room temp. water lavage. Surgery if >6 Units PRBCs needed.
-Last resort for Varix = tamponade balloon tube. TIPS (increased encephalopathy).
-Boerhaaves= postemetic esophageal rupture (no serosa in esophagus), may see Hammans sign, subq emphysema, fever, tachypnea,
tachy,, neck crepitus, widened mediastinum on CXR. Left PTX/Pleural effusion. Macklers triad: Emesis, lower chest pain, Cervical
emphysema (SubQ air) > Esophogram w/ water soluble contrast. Tx: Surgery w/in 24 hours to drain mediastinum and surgically close
perf. BSABx. MCC of esoph perf=iatrogenic >cervical esoph (in EGD?)

5
7.) Complications:
8.) Follow-up: Long term PPI/H2 blockers if necessary (most ulcers heal in 4-6 weeks) if not heal in 6 weeks, re-biopsy gastric
ulcers). H.Pylori testing/ treatment (Amox, Omeprazole, Clarith/Flagyl. Discontinue NSAID. Or can add misoprostol or COX-2
selective. Varices > consider TIPS, propranolol,
9.) Misc/PP: Dieulafoys lesion: rare, submucosal artery in stomach, requires prompts diagnosis by endoscopy and
endoscopic/operative treatment. AVM: small mucosal lesion, bleeding = abrupt but rate of bleeding usually slow and self-limiting.
Varices: 2/3 w/ portal HTN get Varix, 2/3 w/ Varix bleed. Bases are worse than Acids for caustic ingestion because they are more
difficult to buffer. VIR is NOT a good place to have a sick patient.

LOWER GI HEMORRHAGE:
1.) History: AGE, HPI: BRBPR (hematochezia), could be melana (tarry stools), acute? Chronic (might classically present w/ Iron
deficiency anemia, fatigue, and +Guaiac).? How much blood in stood? Mixed in? or coating? Maroon colored stool and blood clots >
> more classic for LGI bleed. Assoc sx/ change in bowel habits? Painless?/Painful? Last colonoscopy? PMH: colon cancer?
Coagulapathy? Cardiac Disease (morea at risk for demand ischemia 2/2 hypovolemia) Diverticular dz?, Aortic stenosis? (Heydes
syndrome- AVMs w/ Aortic Stenosis and acquire vWF deficiency) MEDS: Aspirin,? Other NSAIDS? Plavix, Coumadin
Surg Hx: AAA repair? (AEnteric fistula-painless hematochezia ~1 year s/p AAA repair)) FM: colon cancer SH:
2.) Physical Examination: VITALS: hypotensive, tachycardic, orthostatics GENERAL: pale, obtunded, PE: Complete PE focusing on
(Aortic stenosis?) abdominal exam and rectal: gross blood?/occult (guaiac)
3.) Laboratory / Other tests: CBC (Anemia? MCV> Iron studies?, WBC, Platelets), C7 (BUN/Cr), PT/PTT, Type and Cross,
4.) Imaging: See Tx!
5.) Differential Diagnosis: If seems acute, may still need to RULE OUT brisk upper GI Bleed.
MCC of Acute/overt LGI bleed in
Children/adolescents = M.I.P. = Meckels diverticulum (gastric mucosa/heterotopic rest and adjacent ileal ulceration), IBD, Polyps.
Age 20-60 = D.N.I. = Diverticuluosis, Neoplasm, IBD
Age > 60 = D.A.N. = Diverticulosis, Angiodysplasia (vascular ectasia/AVMs), Neoplasm (all generally PAINLESS). If +pain,
possibly ischemic bowel IBD, and intussuception.
-Also include INFECTIOUS causes of colitis= shigella, salmonella, EHEC, entamoeba histolytica.
-rectal bleeding generally formed stools streaked w/ blood or fresh blood coating them or at end of normal bowel movement.
-if anorectal source considered (ie. internal hemorrhoids), rigid proctosigmoidoscopy should be considered after rectal exam.
6.) Treatment options: (BETWEEN 80-90% STOP bleeding w/ resuscitative measure only > at least temporarily).
If acute, patient seems hypotensive, tachy, etc. then 1st STEP = A, B, C > then IVF resuscitation = 2 periph IVs, 16 gauge, FOLEY
(monitor response to resuscitation). Give crystalloid, ie. LR or NS (isotonic). D/C Aspirin.
MUST R/O UPPER GI BLEED: to R/O gastric bleed, place NG tube following resuscitation, and if nonbloody, bilious material,
unlikely gastric source (not 100% sensitive). If any question exists, do EGD! (definitively Rules/Out duodenal source). >Then,
Anoscopy/Protoscopic exam. > SLOW Bleed > Colonoscopy. SIGNIFICANT BLEED > Tagged RBC> A-gram.
-IF MASSIVE bleed/agitation/impaired respiratory status = ET INTUBATION. (w/ monitoring of patients response by UOP, clinical
appearance, BP, HR, serial Hb/Hct, +/- CVP monitoring
FOLLOWING RESUSCITATION> LOCALIZE bleed
1. Tagged-isotope RBC scan (for >active bleeding > 0.1cc/minute. (therefore RBC scan is better than angiography for SLOWer bleed).
May not be very accurate. Some recommend this as initial screen before angiography to guide location for angiography.
2. Mesenteric angiography (SMA/IMA, higher specificity than TRBC scan, can be BOTH Dx and Tx vasopressin/gel foam
injection, requires bleeding> 0.5-1.0cc/min.
3. Colonoscopy can consider as FIRST STEP IN HD stable patients. Can be very SPECIFIC successful at locating bleeds, but may not
catch intermittent sources. Can also be Dx and Tx: ie. w/ angiodysplasia, can treat w/ epinephrine/coagulation. (Dr. Roye said it is not
as helpful as upper Endoscopy in GI bleed).
-May require SURGERY (only ~10%) (segmental resection) as last resort, but only when bleeding site is KNOWN. TRY TO AVOID
Ex Lap until SOURCE identified! BUT IF ALL ELSE FAILS, can do EX LAP +/- small bowel enteroscopy and total abdominal
colectomy w/ primary anastomsis of ileum to rectum (ileorectostomy) as last resort.
7.) Complications:
8.) Follow-up: must exclude GI malignancy in these patients (ie. CRC).
9.) Misc/PP: means distal to ligament of Treitz, MOST OCCURS IN COLON.
-angiodysplasia: MC in cecum/ascending (RIGHT) colon > 50 y/o. MOST p/w low-grade, self-limiting bleeding!
-Melana= tarry stools, Hb breakdown by bacteria and forms > 14 hours in GI tract. Usually associated w/ UGI bleeding (above lig of
treitz, but can be see w/ Small intestine and ascending colon). W/ ischemic colitis> not full thickenss necrosis (which doesnt really
bleed) > it is not full thickenss, so you just slough off mucosa and thus get bleeding from submucosal vessels.

7.) Hemorrhoids/Perianal pain

1.) History: HPI: OPQRST, specific questions about symptom duration and prior treatment? associated w/ bleeding, defecation?
Constipation, F/C/S?, happened before? PMH: Meds? OTC? DM, Last colonoscopy? Consider sexual history. FH: IBD?
2.) Physical Examination: Vitals: febrile? tachy, General: , PE: Complete PE focusing on abdominal and rectal exam (LLDecub):
inspection for lesions, skin tags, erythema, discharge, masses, Palpation: tenderness in buttocks or perianal region. DRE masses,
sphincter tone, bleeding, tenderness? Severe pain prevents complete anal exam from being done > topical, regional or general anesthesia
3.) Laboratory / Other tests: CBC (white count?, anemia),
4.) Imaging: anoscopy (visualize dentate line=rectal and anal mucosae)
5.) Differential Diagnosis: anal fissure (tear in anoderm in posterior midline position and if chronic > associated w/ sentinel skin tag,
anorectal pain w/ defication/maybe blood, hx. constipation, no fever, perianal skin tag w/o erythema or swelling. N.B. A nonhealing

6
fissue anywhere other than posterior area of anus, consider Crohns or malignancy > consider Biopsy), hemorrhoids (blue or purple mass
at anus), fistula (from rectum to perianal skin, usually painless, purulent, mucous drainage, fluctuant mass, consider Crohns), peri-rectal
abscess (perianal fluctuant-[fluid filled], mass/ulcer w/ erythema and tenderness in perianal and buttock region+/- fever), crohns,
ulcerative colitis, anal SCC (MC sx=bleeding, 25% w/o sx, Tx: NIGRO protocol= Chemo, Rads, postrads scar Bx), anal melanoma
(WLE or APR), pilonidal cyst, perianal warts
6.) Treatment options both medical and surgical:
Anal fissures: try non-op if acute problem and not yet chronic w/ Sitz (for Fizzure) bath, stool softener, suppositories, bulking agents
(fiber), topical nitroglycerin ointment (vasodilator> improves blood flow to posterior ischemic anal canal). If chronic/recurrent, local
BoTox or operative therapy (lateral internal sphincterotomy> 35% risk of incontinence, therefore last resort) to reduce resting sphincter
tone.
Hemorrhoids: tx by grade> I=diet changes (increase bulk and fluids), II=diet/banding/infrared coag, III=ruberband ligation and
hemorrhoidectomy, IV=hemorrhoidectomy
-Thrombosed external hem: treat w/ excisional thrombectomy NOT I&D.
Fistula: draining and/or fistulotomy (fillet tract open). Seton loop> plastic vessel loop placed thru fistula when sphincter muscle
involved, in place for weeks to months until drainage resolves and fistula closes. Wound care, Sitz bath.
Abscess: I and D under local anesthetic if small or under sedation if large. +/- ABx (must w/ DM)
7.) Complications: of hemorrhoidectomy = exsanguinations, pelvic infection, incontinence, anal stricture. C/I in Crohns.
8.) Follow-up:
9.) Misc/PP: Lower GI bleed believed to be caused by hemorrhoids, MUST R/O COLON CA (ie. colonscopy or proctoscopy).
Anal fissure: 2/2 trauma during defication of large firm stool and regional ischemia of mucosa 2/2 hypertonic internal sphincter
(elevated tonic pressures).
Hemorrhoids = abnormally enlarged hemorrhoidal venous plexus 2/2 constipation/diarrhea/obesity/increased intra abdom pressure.
Internal: above dentate line, painless, prolapse, bleed, INTERNALs are GRADED I-IV (I=painless bleeding, NO PROLAPSE,
III=prolapsed but reduceable, IV=nonreduceable)
External: below dentate line, painful, thrombose
Fistulas: draining sinuses > end result of perianal abscesses (2/2 obstructed crypts). Inter/trans/supra/extra-sphinteric. GOODSALLs
rule: used to find internal opening of fistula. When exterior opening is.Anterior - track Straight to dentate line, Posterior track
Curved toward Posterior midline (AS PC)
-Pilonidal cyst: aka. Sacrococcygeal fistula: contains hair and skin near natal cleft of buttocks. Painful. Caused by ingrown hair. Tx:
Abx, hot compresses. Severe: surgical excision w/ flap reconstruction. High odds of recurrence. DDx: sacrococcygeal Teratoma.
-Bowens: SCC in situ (Tx: WLE), Pagets: AdenoCA in situ (Tx: WLE)
-All abscesses are drained except simple amebic liver abscess.

8.) Pancreatitis
ACUTE PANCREATITIS:
1.) History: HPI: severe epigastric pain, radiates to back, constant. FOLLOWING PAIN > nausea/vomiting, Had before? PMH: hx of
gallstones, FH: SH: alcohol
2.) Physical Examination: Vitals: (Febrile?, tachy, bp, RR, O2 sat) General: Exam: complete P focusing on abdominal exam.
Epigastric tenderness, decreased bowel sounds (adynamic ileus), hemorrhagic pancreatitis signs = Grey Turners: flank ecchymosis,
CUllens: peri-Umbilical bluish discoloration (retroperit hem. tracking to anterior abdom wall thur fascial planes)
3.) Laboratory / Other tests: Pancreatitis = LAB-FEST:
CBC (white count, Hct hemoconcentration initially, then if hemorrhagic > may drop), C10 (lytes, BUN/Cr, gluc), (Calicum), LFTs
(AST), Bili, Amylase/Lipase, LDH ABG (hypoxemia?, acidosis), Type and Screen, Lipids,
4.a) Imaging: CXR, AXR: diffuse ileus, sentinel loop: Single dilated jejunal loop in upper abdomen. Colon cutoff (no air after certain
point in colon 2/2 inflammation) Calcification. CT w/ contrast: when diagnosis is in question or if no Clinical improvement w/in 3-5
days or high Ranson score to look for NECROSIS (nonenhancement). + U/S (RUQ) especially if no history of alcohol and possible
gallstone Hx.
4.b) PROGNOSTIC CRITERIA (ie. Staging): is it more MILD or more SEVERE:
Ranson criteria: meant to reflect severity of retroperitoneal inflammation (other systems = APACHE and C-reactive protein levels)
On admission (FIVE = GA LAW) = Glucose>200, Age>55, LDH>350, AST>250, WBC>16000. (WITH THREE or MORE = more
severe disease/risk of death > but previous mortality rates of initial criteria DONT APPLY TODAY).
48 hours later (SIX =BBC HPF) BUN increase of 5, Base excess of 4, Calcium<8 (fat saponification= fat necrosis binds to calcium),
Hematocrit fall of 10%, PO2 <60, Fluid requirement of >6L
5.) Differential Diagnosis: SBO, mesenteric ischemia/infarction, Gastritis/PUD, Acute cholecystitis, perforated viscus, ruptured AAA,
inferior MI, pneumonia.
6.) Treatment options: In summary, resuscitative measures = IVF and O2. Focus on FLUIDS, OXYGENATION/VENTILATION,
RENAL PERFUSION. Ie. NINFA (NPO, IVF, NG (if N/Vomit), FOLEY, ANALGESIC (IV-demerol, not morphine = less sphincter of
Oddi spasm). > 85% will improve!!! Manage Electrolytes and nutrition (TPN) as well.
In SEVERE pancreatitis, most important element to prevent M.O.S.F. = fluid resuscitation and intensive monitoring (ICU). IF
NECROSIS by CT scan > 50% of pancreas, PPX ABx as infection will occur 50% of time. Good penetration and enteric coverage =
Iminpenem/Cilastatin.
May need to drain fluid collections or necrotic areas> CULTURE for infection. If infected, operative debridement and drainage
indicated. STERILE necrosis generally improves w/ ABOVE regimen > if no clinical improvement> Surgical exploration!
If GALLSTONES present, early interval cholecystectomy + IntraOpCholangiogram is required on SAME admission 3-5 days after
pancreatic inflammation has resolved (33% would otherwise recur w/ pancreatitis w/in 8 weeks). If Gallstone Pancreatitis (by U/S), may
require ERCP if bilary obstruction persists (monitor Bilirubin).

7
7.) Complications:
LOCAL:
hemorrhage: decreased HCT,
necrosis: ~3-4 days (does not enhance on contrast CT) PPX ABx may be indicated. Even if sterile necrosis, but clinically worsening,
Tx: surgical debridement and drain placed (D/D) (infected necrosis must be drained).
fluid collection: phlegmon: , pseudocyst: 1-4 weeks, NO FEVER OR WHC count (vs. abscess) encapsulated collection of pancreatic
fluid and necrotic tissue, may be palpable on exam. WALL is formed by inflammatory fibrosis and NOT epithelial cells. Usually resolve
over several weeks, occasional requires surgery. MCC = chronic alcoholic pancreatitis. Only 10% in alcoholic pancreatitis. Suspect
when patient w/ acute pancreatitis fails to resolve pain. EXAM: palpable epigastic mass. CT/US (fluid filled mass). DDx:
cystadenoma/cystadenocarcinoma. Complications = bleeding into it, infection, fistula, pancreatic ascites. Tx: observation (50% resolve)
or drainage (PCT or operative) of cyst (>5cm). (first wait 6 weeks for walls to mature).
infection = infected pancreatic necrosis: secondary infection from bowel derived organisms w/in a few weeks of onset. surgical
debridement usually indicated. Abscess: ~ 4-6 weeks days. secondary infection of pancreas and peripancreatic fluid collection
accumulation of thick, purulent fluid and infected debris. Fever, unresolving pancreatitis, epigastric mass. Tx: = ABDOM CT w/ needle
aspiration > Gram stain/Cx (bact = PEK and Staph A.) > ABx and may require surgical debridement + drain placed. Infected pancreatic
pseudocyst: a late process, several weeks/months later. Tx: PCT or operative drainage. Splenic vein thrombosis (can cause gastric
varices).
SYSTEMIC: hypocalcemia, ARDS, renal dysfunction, cardiac dysfunction. DIC
8.) Follow-up:
9.) Misc/PP: MCC of Acute panc = EtOH (50%) and GS (30%), Idiopathic (10%). Its a systemic inflammatory state. Amylase and
lipase level dont correlate w/ prognosis!
Causes: EtOH, GS, Hypercalcemia, high TGs, Trauma, ERCP, Drugs: HCTZ, steroids, Scorpion bite (from Pacific islands).
Mild/Self limited (85%) = edema
Severe/Complicated (15%) = necrosis followed by infection in 50%.

CHRONIC PANCREATITIS:
-Indications for surgery = intractable pain, bowel or biliary obstruction and persistent pseudocysts.
-MCC=alcohol (70%). Up to 1/3 get Type I DM, Steatorrhea (72 hour fecal fat analysis) (no lipase), and weight loss. Amylase and
lipase may be normal.

9.) Gallbladder disease (2)

1.) History: female, forty, fat, fertile. Biliary colic (temporary RUQ, referred epigastrium,or R subscapular region in back (Boas sign),
postprandial after fatty foods Sx last for hours therefore not TRUE colic). Cholecystits: unrelenting RUQ pain, fever, N/V. Chills?
Sign/Sxs of biliary obstruction: jaundice, pruritus, dark urine, clay-colored stools. Steatorrhea: ask if stools are greasy and/or float.
PMH: pancreatitis, hyperlipidemia, hemolytic dz (pigment stones), MEDS: OCPs, SH: Alcohol use
2.) Physical Examination: Vitals (Fever?)
As listed above: must do complete Physical examination including Cardiac and Lung exam > Focusing on Abdominal exam including
pelvic (if female)/genital exam and rectal exam. GENERAL appearance /Jaundice? = Fever? If yes, leads more to Cholecystitis,
or Cholangitis (Charcot = fever, RUQ pain, and jaundice > Reynolds pentad includeds Hypotension and Mental status changes).
If RUQ tenderness exists, more likely cholecystitis. With Cholelithiasis, there is pain without tenderness usually as there is no
inflammation. Cholecystitis: unrelenting RUQ pain/tenderness, positive Murphys sign. Painful palpable gallbladder.
3.) Laboratory / Other tests: CBC w/ diff (elevated WBC), C7, U/A, UPreg, LFTs (Alk phosphatase elevated w/ Choledocho and
Cholangitis) and Bilirubin. Amylase
4.) Imaging: AXR: to R/O free air from ruptured PUD. U/S (very sensitive for cholelithiasis not choledocholithiasis!!! (Cholecystitis:
PCFluid, thickened GB wall > 3mm, stones in GB, sonographic murphys, ANY CBD thickening?), HIDA radioisotope scan (if clinical
suspicion is high by U/S nondiagnostic = if stone is in cystic duct, no visualization of GB during scan), IOC (intraoperative
cholangiogram to R/O stone in CBD if ), ERCP (Tx for Cholangitis), IMAGING for Cholangitis: U/S AND contrast study (ie. ERCP)
after patient has cooled off w/ IV ABx. CBD Normal diameter rules for age >60= 6mm, >70=7mm, >100 y/o, >10mm=abnormal.
5.) Differential Diagnosis: BILIARY: cholelithiasis, choledocholithiasis, cholecystitis, cholangitis, cholangiocarcinoma, gallbladder
adenoCA (main 6 Biliary Dz), Hepatitis, NASH, Cirrhosis (R/O by Hx/Exam ie. EtOH, HepC, stigmata, jaundice, ascities,
gyncomastia, mildly elevated INR), RLL PNA, Fitz hugh curtis, Pancreatitis, PUD, perforated PUD,
6.) Treatment options both medical and surgical: Cholelithiasis: if symptomatic> cholecystectomy (lap or through standard Kocher
incision = right subcostal incision). Do IOC if jaundice, hyperbili direct, elevated alk phos. or choledoch on U/S. Cholecystitis: IVFs,
ABx (Unasyn- Amp and Sulbactam or Zosyn), and early cholecystectomy > send for Path to R/O Gallbladder cancer. If patient is
unstable, PCT cholecystostomy tube can be placed. Choledocholithiasis: ECRP w/ sphincterotomy w/ stone retrieval. Can also do
Lap or Open. Once cool off, do Cholecystectomy. Medical mgmt is not great: ie. ursodeoxycholic acid to dissolve a cholesterol stone.
Cholangitis: If non-suppurative (w/o sepsis) = IVF + ABx w/ ERCP later. If suppurative: IVF + ABx + decompression w/ ERCP w/
sphincterotomy
7.) Complications: of Cholelithiasis: Acute cholecytitis (abscess, perf), Gallstone Pancreatitis, Gallstone ileus (elderly women > 70),
Cholangitis of Lap CCectomy = CBD injury > Tx = Choledochojejunostomy. Can also injur Right hepatic duct/artery or Cystic duct
leak. of Choledocholithiasis: cholangitis
8.) Follow-up: N/A
9.) Misc/PP: triangle of Calot: Cystic duct, Cystic artery, Common hepatic duct. Bile: bile acids, bilirubin, cholesterol > emulsify fats.
Jaundice (1st under tongue, TBili> 2.5). 75% are cholesterol stones. 25% pigmented (calcium bilirubinate). Pathophys of acute
Cholecystitis = obstruction of cystic duct > inflammation > infection. 95% from calculi. Acalculous cholecystis: biliary stasis/sludge,
lack of CCK, risk factors=prolonged fasting, TPN, ICU, postop. U/S: shows sludge and HIDA shows nonfilling of GB. Cause of

8
Obstruction and Cholangitis: Choledocholithiasis (MCC), stricture (post-op), Neoplasm (ampullary carcinoma), Pancreatic
pseuodcyst/pancreatitis. Cholangitis organisms: PEK (proteus, ecoli, Klebsiella) + pseudomonas/enterococcus. Anaerobes less
common. Cholangiocarc RF: choledochal cysts, UC, PSC, chlonorchis, contrast (Thorotrast). Mirizzi syndrome: gallstone in cystic duct>
compresses common hepatic duct. Primary stones for in CBD. Secondary in GB. Sudden onset Jaundice > Think STONES. Rare to see
jaundice in Cholecystitis unless Maritzy syndrome. Painless jaundice > Think pancreatic CA (head), cholangiocarcinoma, duodenal
mass. New onset DM can be 2/2 pancreatic cancer but its still not a common cause of new onset DM in patient > 70 y/o. Pancreatic
CA> CA 19-9

10.) Hernia (1)

1.) History: HPI: OP (pain or heaviness more prominent w/ standing or physical activity) QRST, Assoc Sx: straining at defecation or
urination (If older man, ask BPH Sx, freq, hesitancy, nocturia, etc. last colonoscopy/rectal exam, hx. Constipation? Symptoms of bowel
obstruction=constipation, obstipation), N.B. Acute incarceration may be the initial presenting symptom. PMH: BPH?, COPD, SBO,
previous abdominal surgeries (incisional hernia)?, FH: colon cancer.
2.) Physical Examination: Vitals: fever? General, Then, complete Physical CP, focusing on Abdom exam including Inspection for
scars, Auscultation for BS, palpation for tenderness, distention, w/ groin exam, and rectal exam evaluating for BPH, rectal masses, stool
guaiac. Hernia exam: can examine standing up with index finger, bare down, reducible/complete or incomplete (defect present without
sac or contents protruding completely through it). Look for skin changes over the site. Reducable? In OR if strangulated, check for
viable looking bowel s/p reduction wait 15 minutes or so. Small bowel can always try primary anatomosis.
Testicular exam (scrotal swelling)/Labial swelling (indirect)
3.) Laboratory / Other tests: CBC (white count, anemia), C7 (lytes if obstruction), U/A?,
4.) Imaging: Dx. can be MADE from H&P, but if still clinical uncertainty, can do Ultrasound or CT to distinguish incarc hernia from
abscess, LNs, or hematoma. AXR? Look for dilated loops, air-fluid levels, free air.
5.) Differential Diagnosis: of groin pain/mass = lymphadenopathy, lymphoma, hematoma, muscle strain (acute onset) ie Pulled
groin this is what you think it is, must F/U in 2-4 weeks to confirm, abscess, varicocele, hydrocele, undescended testicle, femoral
artery aneurysm, testicular torsion, testicular tumor. Diastasis recti is NOT true hernia because no fascial break. (newborns and pregnant
women)- can R/O Ventra Hernia by U/S. Generally, no Tx necessary.
6.) Treatment options medical and/or surgical: Fitzigibbons, JAMA 2006, Watchful waiting is okay if minimal symptoms w/
inguinal hernia. Delaying surgery until symptoms increase is okay because acute hernia incarceration occur rarely If incarcerated, may
attempt to reduce it. If cant > surgery. To avoid complications of incarceration/strangulation > bowel necrosis / SBO. Layers: Skin,
SubQ fat, Scarpas Ext ob, Int ob, Tranversus abdominus, Transversalis fascia, preperitoneal fat, peritoneum.
Emergent Herniorrhaphy (following fluid/lytes resuscitation) is indicated if acute incarceration or strangulation is suspected.
Otherwise, elective Herniorrphaphy is indicated to prevent chance of incarc/strang and decrease symptoms. Can do laparoscopic or open.
If B/L laparoscopic is preferred. Mesh plug repair. Avoid mesh if bowel is compromised. Can use regional anesthetic with most elective
repairs. General anesthesia for Lap. = 1.) Reduce the hernia, 2.) obliterate opening, 3.) reinforce closure.
7.) Complications: of surgery: ilioinguinal nerve (medial thigh numbness 6 mo.) runs in spermatic cord in the inguinal canal.
8.) Follow-up:
9.) Misc/PP: hernia = rupture, protrusion of peritoneal sac through a fascial defect. 50% indirect, 20% direct, 5% femoral. Strangulation
= incarcerated hernia w/ compromised blood flow, ischemia and intestinal obstruction signs/sx or bowl necrosis sign/sx. >necrosis>perf.
Sliding: hernia sac partially formed by wall of a viscus (bladder/cecum/sigmoid), Littres: involving Meckels diverticulum. Richters:
incarcerated or strangulated hernia involving only ONE SIDEWALL OF THE BOWEL, which can spontaneously reduce, resulting in
gangrenous bowel and perf without signs of obstruction. Femoral: medial to femoral vessels under inguinal ligament (swelling below
inguinal ligament). Protrude through femoral canal = inguinal ligament superiorly, fem vein laterally, and pubic ramus medially. Highest
risk of strangulation. Assoc. w/ women, pregnancy. Direct: medial to inferior epigastric vessels, within floor of Hesselbachs triangle.
Does not traverse internal ring, directly through abdominal wall. Cause = acquired defect from mechanical breakdown over the years.
Indirect: MOST COMMON. through internal and external rings. If complete, may enter scrotum. Cause= patent processus vaginalis.
Higher risk of strangulation than direct. Cremaster derived from Internal Oblique muscle. Inguinal ligament (Pouparts) derived from
External oblique aponeurosis. In spermatic cord = Cremaster, Vas Def, Test art/venous plexus, Genital branch of GF nerve. Hernia sac
made of peritoneum or patent processus vaginalis. Two types of Esophageal Hiatal Hernias = Sliding (Type I, >90% of all Hiatal H, GE
junction slides up, GERD, 85% treated medically) and Paraesophageal. Obturator: mass in medial thigh, multiparous women w/ hx of
weight loss.

11.) Breast mass (2)

Name it, Stage it, Treat it
1.) History: HPI (Sx of cancer: None, mass, painless, nipple discharge, local edema, nipple retraction, nipple rash), trauma. PMH
(HRT), PREVIOUS Hx. Radiation/Connective Tissue Dz. Age,
-Previous Mammogram? Previous breast biopsy?
NAACP (Nulliparity, Age at menarche <13, Age at menopause > 55, Cancer of the breast in self/family, Pregnancy 1st > 30 y/o). Family
Hx Breast or Ovarian in 1st degree relatives. BRCA1 (B/O), BRCA2 (B).
2.) Physical Examination: Inspect (unequal height, [can look drawn up in lobular CA], visible mass, erythema, nipple
retraction/dimpling, pou dorange (inflammatory breast cancer = swollen dermis from tumor plugging dermal lymphatics), nipple
eczema (Pagets invasion of skin from underlying ductal carcinoma), edema. Palpate feeling for an edge and discrete dominant mass
(1 cm= smallest detected on exam), Axillary nodes / Supraclavicular nodes.
3.) Laboratory / Other tests:
4.a) Imaging: Mammography (bad = spiculated mass, microcalcifications, linear, pleomorhophic or new calcifications), U/S (<30 y/o),
MRI. With U/S, anechoic=cyst, iso/hypoechoic=solid mass, hyperechoic=fatcould be fatty lymph node.

9
4.b) Biopsy: FNA (cytology-NOT helpful for histology, okay for Lymph nodes cause all you care about is presence or absence of cancer
cells), core biopsy prefer U/S guided (+/- stereotactic or needle localization), open biopsy (incisional or excisional). Indications =
suspicious lesion by mammag/US/MRI, solid mass, bloody nipple discharge, bloody aspirate of cyst, ulcer/dermatitis of nipple,
persistent mass after aspiration, patients concern. Pathology: check ER, PR status.
5.) Differential Diagnosis: fibrocystic disease (breast pain varying w/ menstrual cycle; cysts and fibrous/nodular fullness, straw/green
colored D/C), fibroadenoma (MC tumor <30 y/o, solid, mobile, well-circumscribed round > can observe small ones), fat necrosis,
intraductal papilloma (MCC unprovoked bloody nipple D/C in young women), duct ectasia (inflammatory condition of ducts>Tx:
Debridement and ABx), mastitis, DCIS, atypical hyperplasia (RF for B.CA), abscess, simple cyst, cystosarcoma phyllodes
(mesenchymal benign tumor from breast lobular tissue, resembles Fibroadenoma on exam/imaging > if benign =WLE, if malig, simple
mastectomy), breast cancer (infiltrating ductal carcinoma (90%), Invasive lobular (10%), inflammatory (peau dorange chemotherapy
1st!>rads, mastectomy))
6.) Staging / Treatment options both medical and surgical:
If find breast CA, workup/staging must include: B/L mammogram!, CXR, LFTs, Calcium, Alk phos, > if + or bone pain> Bone scan.
Neuro sx. > head CT. > Staging by TNM:

ADAMs Basic Approach:

-palpable suspicious mass > Core Needle Bx
-Non-palp > Stereotactic or Needle localization Bx (if they ask, can say goal = excisional bx)
-Wait to hear back on Tissue Dx:
-If DCIS (hasnt left BM, therefore) 2 options (no survival difference)
1 = B.C.Tx= Segmental Mastectomy + Radiation (as long as no C/I to B.C.Tx.
2 = Total (Simple) Mastectomy
--- Really, no need to sample lymph nodes, however, some say with certain risk score (ie. VN), you can do SLN.
-Pending ER/PR status, can use TAMOXIFEN, but NEVER CHEMO!
-confirm negative margins if segmental (lumpectomy)

-If Infiltrating Ductal Carcinoma, 2 options

1.) B.C.Tx = Segmental Mastectomy + post op Radiation. w/ intraop SLN Bx. If SLN Bx comes back +, full axillary dissection.
2.) MRM= Remove entire breast, nipple, and axillary LN dissection.
-With invasive cancer, can offer CHEMO (ACT) (even if NODES are negative, unless tumor is <1cm) and Tamox (ER/PR), +/-
Herceptin.
-B.C.Tx: 1-2 cm neg. margins.

-If LCIS, 3 options

1.) Watch and wait w/ B/L mammograms, 2.) B/L simple mastectomies, 3.) Tamoxifen.

Treatment for invasive cancer:

-CONTRAINDICATION FOR BREAST CONSERVING THERAPY = 1. Previous Radiation, 2. CTDz, 3. Multicenter Dz, 4.Small
breasts.
A) Modified radical mastectomy (+ radiation if >4 LN plus chest wall invasion) = 1.) remove entire breast, 2.) nipple, and 3.)
sentinal/axillary nodes (level I & II) w/ drains placed (DO NOT REMOVE PECTORALIS Major or Minor).
B) Segmental mastectomy and radiation (Breast Conserving Tx) (Stage I/II tumor <5 cm) = 1.) remove part of breast and 2.)
sentinal/full axillary node dissection (if sentinel nodes are positive) + post-op radiation over several weeks C/I if: pregnancy, extensive
DCIS, positive margins, very small breasts).
**Both either w/ or w/o postop chemo = (ACT) Adriamycin, Cytoxan, Taxol (if node +) /tamoxifen (if ER+). ?neoadjuvent chemo. +/-
Herceptin (HER2-neu/erb-b2 blocker)
-Indication for Radiation w/ Modified Radical Mastectomy = tumor 5 cm, 5 positive nodes, invasion of chest wall/skin, or Inflammatory
CA. W/ Inflammatory CA > give CHEMO 1st, then Mod Radical following by radiation.
7.) Complications: during Axillary dissection: Long thoracic (Serratus anterior> winged scapula), thoracodorsal (latissimus dorsi) nerve
damage. InterCostoBrachial nerve (cutaneous). Post MRM: ipsi arm lymphedema, infection, lymphangiosarcoma. Side effects of
medicine: tamoxifen (endometrial cancer, DVT/PE, hot flashes). Aromotase inhibitor (anastrozole, exemestane) = can use ONLY in
POST-MENOPAUSAL women. Its not powerful enough to block estrogen from pre-menopausal ovaries. Side effects: risk of early
osteoporosis.
8.) Follow-up:
9.) Misc/PP: 12% lifetime risk for Breast Cancer. 75% without known RF. Screening recs: monthly self exams (1 wk. post menstrual
period), 20-40, breast exam Q2-3 yrs, >40 annual physician breast exam and mammogram. Basal mammogram 35-40 y/o. Can use
tamoxifen in prevention.
DCIS (intraductal: no invasion of BM, risk of infiltrating ductal in SAME breast, treatment: <1cm = Segmental mastectomy w/ 1 cm
margins +/- radiation. If > 1cm tumor SM + Rads OR can do Total (Simple) Mastectomy (includes nipple) [w/ Van Nyes score >
15 ie. comedonecrosis, etc.] without axillary dissection = ONLY TIME!!). Some do sentinel L.N. bx for high-grade DCIS and lesions
>5cm before Total Mastectomy. Can use Tamoxifen post-op. Decreases risk in ipsi and contralateral breast.
LCIS: found incidentally on bx. Increases risk equally for carcinoma (usually infiltrating ductal) in EITHER breast. Tx: close follow-up
or B/L simple mastectomy in high-risk patients.
-Spontaneous bloody nipple discharge = 10-15% chance of occult malignancy. Therefore, even if Mamm, U/S, MRI all negative> do
Ductography, and even it thats negative, must do surgical Ductal Bx.
-Only aspirate cyst for symptomatic relief

10
-fibrocystic change is camoflouge for more concerning lesions.

12.) Thyroid mass (3)

Name it, Stage it, Treat it
1.) History: HPI: painful/painless, dysphagia-esop, stridor (difficulty breathing)-trachea, hoarseness-larynx, rapid enlargement,
symptoms of Thyrotoxicosis ie. sweating, palpitations, afib, PMH: previous neck radiation, thyroid dz (ie. hashimotos for thyroid
lymphoma). FH: history of thyroid cancer, Adrenal cancer (MEN IIa/IIb) Lymphoma. SH: alcohol, tobacco. ROS: Signs of
HypoHyperT: heat/cold intolerance, weight loss, diaphorese, palpitations, lethargy.
2.) Physical Examination: Signs of Thyrotoxicosis (Inc. DTR, HTN, exophthalmos, pretibial myxedema), COMPLETE HEAD AND
NECK EXAM (ie. skin on scalp> SCC mets to neck) Evaluate oropharynx, Inspection (erythema-thyroiditis), palpation of mass,
complete neck exam (palpating for L/A), movement of mass on deglutition, tender, trachea midline, stridor.
3.) Laboratory / Other tests: CBC, C7, + TSH, T3/ free T4, Calcium, calcitonin, intact PTH. (5)
4.) Imaging: Fine Needle Aspirate (FNA): cytology (5% false neg). Go straight to FNA w/TSH if clinically euthyroid or hypothyroid
OR clinically hyperthyroid but TSH is NL or High . If clinically hyperthyroid and TSH is low, do I131 scan). 4 FNA results >
Benign (follow/up), Malignant (operate), Nondiag (if insufficient sample, repeat), Cellular (ie. Follicular > If TSH is low, do I131
(Hyperfxn = Follow up +/- Tx, if Hypofxn = Operate). If TSH is NL, High > Operate!>get tissue for Dx), U/S: solid/cystic. RAI uptake
(ie. I131 scitigraphy) scan: hot (hyperfunctioning, increased uptake of iodine) /cold nodule (nonfunctioning more likely cancer 25%
of colds in adults). (Do the scan if nodule w/ multiple nonDx FNA w/ LOW TSH. ?)
5.) Differential Diagnosis: multinodular goiter (MCC of rapid thyroid enlargement, do surgery for 1. Cosmesis, 2. Compressive Sx, 3.
Cant R/O cancer), adenoma (+/- hyperfunctioning), cyst (ie. thyroglossal duct), thyroid carcinoma (family hx, previous neck radiation,
young, male, cold, most euthyroid, single nodule, increased calcitonin, hard immobile nodule), lymphoma, thyroiditis, parathyroid
carcinoma, HNSCC, abscess, lymphadenopathy.
**5 Types of Thyroid Carcinoma: Papillary (80%, spread slowly via lymphatics> cervical L/A, 10-year survival is 95%, has positive
uptake for I131?), Follicular (10%, hematogenous like a sarcoma, more aggressive, cant make Dx by FNA> need tissue structure and
capsular or blood vessel invasion for Dx), Medullary (5%, calcitonin, amyloid on histology, ), Hurthle (4%, origin is follicular cells),
Anaplastic (1%).
**STAGING: prognostic factors = AGE, >50 as woman, >40 as man = worse prognosis for each given stage. AMES = Age, Mets
(distant), Extent of primary and Size (5 cm).
6.) Treatment options both medical and surgical:
-N.B. Dr. ROYE: if Sx/Signs of thyrotoxicosis and Biochemically positive, ie. Low TSH, High T3/4, DO RADIONUCLEIDE SCAN
BEFORE FNA Bx to avoid potential Thyroid storm.
Thyroid suppression = Dx and Tx: give Thyroid hormone, suppresses TSH, and up to 50% of benign thyroid nodules will disappear!
Papillary cancer: <1.5 cm w/o hx neck rads = Lobectomy + remove isthmus or total thyroidectomy. >1.5 cm, B/L+ cerv. Node mets
OR hx neck rads = Total thyroidectomy. W/ palpable lateral cervical nodes > Ipsi modified neck dissection. POSITIVE NODES do
NOT affect prognosis. Replace Synthroid. Post-op > I131 scan to ck. for residual tumor/distant mets > treat them with ablative doses of
I131.
N.B. if Bx = Papillary CA, always take at least a Lobe + Isthmus OR Total Thyroidectomy. Depends on size of tumor.
TREAT Papillary and Follicular cancer if total thyroidectomy s/p 16 weeks, w/ Radioactive Iodine therapy.
Papillary: <1cm = Lobectomy +isthmus, >1cm = thyroidectomy.
For Pap and Follicular> only do Ispi neck dissection if 1.) Clinically palpable LNs 2.) seen on ultrasound.
Medullary: Treatment = TOTAL Thyroidlectomy + Central Node dissection. (NO RAI Tx)
Hurthle: Total Thyroidectomy
-Dr. ROYE: if FNA > NL cells and it was good sample (ie. U/S guided and truly benign), then probably a goiter. MGMT= if affects
airway or cosmetic, can try TSH suppression for 3-6 months by giving synthroid to suppress axis and shrink it (T4 will decrease TSH).
Can follow lesion with U/S. Dr. ROYE part 2: If indeterminate comes back on FNA Bx: ask why? If quantity not sufficient> repeat
Bx, if because Follicular cells, then must do excision and Frozen section intraoperatively > w/ plan for resection if comes back Follic
CA.
7.) Complications: during surgery Recurrent laryngeal nerve damage: unilateral-hoarseness, B/L airway obstruction. Superior
laryngeal nerve: deeper voice, wont be able to hit higher pitches. Post-op: Follow Calcium, secondary to parathyroid damage/removal
(implantation in forearm/SCM), Dyspnea: neck hematoma, or B/L RLN damage. Hypothyroidism> synthroid.
8.) Follow-up: Dr. Roye: F/U for Mets w/ Radioscan, good post-op only for total thyroidectomy cause then, even if cancer is somewhat
cold, it will still light up. Can also track Thyroglobulin = serum marker to Follicular CA. Calcitonin = tumor marker to follow for
recurrence of medullary CA.
-Genetic counseling for Medullary CA if RET mutation positive!
9.) Misc/PP: synthroid=T4 (half life 7 days), parafollicular cells > calcitonin. 10% of thyroid nodules are malignant. MEN IIa
(Medullary, Pheo, parathyroid hyperplasia RET, AD), MEN IIb (Medullary, Pheo, Marfanoid habitus, mucosal neuromas). Lateral
aberrant thyroid rest = thyroid papillary cancer lymph node metastasis. > Therefore TX: Modified Neck Dissection + Total
Thyroidectomy. If concern for MEN IIa/IIb w/ medullary > can check for PHEO w/ 24 urine VMA/Metanephrines or serum
Metenephrines. If NO pheo > Total Thyroidectomy + SLN Bx. If positive PHEO> remove PHEO before thyroid. Titrate alpha1
blockade to NL blood pressure. If hypertensive in OR, STOP SURGERY> alpha block, THEN b-block.

13.) Malignant Melanoma (1)

1.) History: HPI: when did you first notice it, etc. ithchy? Bleeding? PMH: hx. Of blistering sunburns <18 y/o, skin cancer, giant
congenital nevi, multiple dysplastic nevi FM: skin cancer? Other cancers?

11
2.) Physical Examination: Vitals: Inspection of pigmented lesion - ABCDE: Asymmetry, Border irregularity, Color variation, Diameter
> 6mm, Evolution also check for ulceration, satellite lesions (full body skin exam w/ oral mucosal/rectal exam especially
MEN=back, WOMEN: extremities, back of legs) GOOD LYMPH NODE EXAM. RFs = white patient, blonde/red hair, fair skin,
freckling, blue/green eyes, actinic keratosis. MC site: SEA (Skin, Eyes, Anus), Palms of hands/soles of feet (esp. if AA acral
lentiginous). Anal sx = bleeding.
3.) Laboratory / Other tests: ALL suspicioius lesions = Diagnosis MADE by: A.) Excisional biopsy (<1cm) OR B.) Incisional biopsy
for very large lesions. SAFE TO SAY: Punch (Full thickness) Bx
***If comes back as Melanoma (histological classification and microstaging), then TREATMENT= Wide Local Excision w/ clear
margins to prevent LOCAL recurrence (0.5-2cm depending on depth of microstaging In-situ= 0.5 cm, <1mm=1cm, 1-4mm=2cm,
>4mm=2-3cm).
SAFE TO SAY: <1mm, = 1cm. >1mm, = 2cm.
Depending on depth of invasion, +/- sentinel LN Bx w/ radiolabeled blue dye later if >1mm in depth.
-Also can do SLNBx if histology has high grade features i.e. High mitotic rate, or gross signs of ulceration.
If positive, LN dissection (clinically positive LNs = lymphadenectomy). + pending microstaging, and LN involvement, evaluation of
localregional metastasis and distant metastasis.
4.) Imaging: if suspect metastasis, CXR (bone scan/CT/MRI reserved for Sx)
5.) Differential Diagnosis: dysplastic nevus, basal cell carcinoma, blue nevus, seborrheic keratosis, Types of Malignant Melanoma = 5
types, SS (75%), LM (10% elderly patients, head or neck, least aggressive, Hutchinson freckle if noninvasive) , AL (palms/soles,
subungual, MC melanoma in AA), Nodular (15%, vertical growth phase predominate, worst prognosis), and Amelanotic.
**STAGING: Microstaging: Clarks (anatomic) (I-Epidermis=5 yr. recurrence 0-5%, II-Pap dermis, III-Jxn. pap/retic dermis, IV-Retic
dermis, V-Subq fat=5 yr. recurrence 75%). Breslow (depth of lesion by measurement = better predictor of survival, less variability)
less than 0.75 mm thickness = > 90% cure w/ excision. Greater than 4.0 mm = 80% risk of local recurrence of metastasis in 5 years.
AJCC = TNM (M=distant mets and LDH): simplified (ulceration upstages! & is an independent prognostic factor) = I: <1.5mm depth,
II: >1.5mm depth, III: positive regional nodes, IV: metastasis (including NONregional nodal basin) = mets often to distant skin (many
without primary identified), BRAIN (Rads), adrenal/lung (surgical resection), bone, heart, SMALL BOWEL (bleeding/obstruction).
Metastatic workup: physical exam, LFTs, CXR (bone scan/CT/MRI reserved for symptoms)
6.) Treatment options both medical and surgical: See above regarding Excisional/Incisional Bx, if proves to be Melanoma, > Wide
Local Excision +/- Sentinel Node, and if SN = positive, Lymphadenectomy. SURGERY: Stage I and II, Adjuvent chemotherapy = Stage
III: Interferon-!-2B, Stage IV: Interleukin-2 (mortality=10-15%), Autologous Cell Transfer.
7.) Complications: of lymphadenectomy = lymphedema.
8.) Follow-up: monthly self skin exams. Yearly dermatologist appointment to evaluate mole mapping. median survival with distant
metastasis = ~ 6 months. Prevention, avoiding sun-exposure.
9.) Misc/PP: neural crest, S100 antigen positive. Horizontal/Radial growth phase (SS and LM) vs. Vertical growth phase (nodular)!
One of few cancers increasing in incidence. **Melanoma starts in the epidermis> if NO cells found in epidermis of a lesion, it may be a
METASTASIS.

14.) Abdominal trauma

Start: PENETRATING or BLUNT And IS THE PATIENT HD STABLE/Normal?
ATLS PROTOCOL
1. Primary survey / Resuscitation
2. Secondary survey
3. Definitive care
Primary Survey / Resuscitation (obtain History while completing primary survey >ie rescue squad, witnesses, and family members
= helpful also to get Allergies, Meds, brief PMH, last mean, and Events!) = ABCDEs + Life-threatening problems discovered during
primary survey are ALWAYS addressed before proceeding to next step
-Airway (and C-spine stabilization): GOALS: Secure airway and protect spinal cord.
listen to patient, ie. Speaking and conscious, then presume airway is adequate. If intubated on arrival, double check its in correct
position. DEFINITIVE/Surgical airway = Cricothyroidotomy. (between cricoid and thyroid cartilage). GCS < 8 buys you an
intubation or high obstructive risk (ie. Bad wheezing w/ Hx. of Anaphylactic risk). Stridor> lost 90% CSA of airway.
-Breathing: GOALS: securing oxygenation and ventilation. Treat life-threatening thoracic injuries. Inspection: RRate, JVD, accessory
muscles, trachea midline. Auscultation: Listen to patients breath sounds. Percussion: dullness, hyperresonance Palpation: subq
emphysema, flail segements. CANT MISS: Tension PTX, Open PTX, HemoTX (HTX) N.B.>Poor oxygenation = anxious (ie. think:
under water). Vs. CO2 retention > Obtunded.
-Circulation: GOALS: adequate tissue perfusion and treat external bleeding (by DIRECT pressure).
If palpable radial pulse, systolic > 60 mm Hg. Fem/Carotid, then >60mm Hg.
Vital signs (heart rate, tachycardia), UOP, Mental status. Exam (cool skin, or capillary refill > 2 seconds might be indication of shock.
Examine neck veins for JVD or muffled heart sounds > might indicate cardiac tamponade and require immediate treatment). N.B. Those
on BBlockers may not mount tachycardic response or very young may not get hypotensive until crashing. Ask what the Patients
BASELINE vitals are.
-TWO large bore IVs = 14-16G perip IVcathers w/ 2 liters LR (lactate > converted to bicarb, helps buffer hypovolemia-induced
metabolic acidosis) while waiting Type and Cross. Type O = universal blood dOnor. Type AB = universal PLASMA donor (plasma
lacks antibodies to A or B!) If use central line, must use CORDIS for fluids. Triple lumen is NOT big enough.
-Decompression post RECTAL exam: Gastric (NGT) and Bladder (Foley C/I if urethral injury high riding prostate on exam, blood in
external meatus> perfor RUGram if uncertain BEFORE Foley)
4 Classes of Hemorrhagic Shock: (assuming~5L = NL blood volume)
I: <750 cc lost (15% BV), no parameter changes except orthostatics

12
II: 750-1500 cc lost, (15-30%), increase HR (>100), thready, cap refill 3-5 sec, anxiety
III: 1500-2000 cc lost (30-40%), increase HR (>120 weak), SBP <80, confusion, cool skin. Oliguria.
IV: >2 liters cc lost, >40%, increase HR (>140) or Brady + Obtunded (mentally dulled/lethargic, unconscious), decreased UOP, SBP
<60, loss of carotid pulse. ANURIC.
-Give 2L Isotonic fluids as DIAGNOSTIC>?= III or IV? If no response to 2L, then = class IV. Note for Class III and IV > give
crystalloids followed by BLOOD. 3:1 rule w/ crystalloids.
-Types of Shock: Hemorrhagic, Cardiogenic, Neurogenic, Anaphylatic, Septic, Adrenal
-Disability: NEURO status. GCS (Eye Opening, Motor, Verbal>coma is 8 or less. Dead = 3). Pupils. Lateralization motor/sensory.
-Exposure and Environment: disrobe patient and warm room! To avoid coagulapathic, hypothermic and acidotic death triad.
Secondary Survey = thorough HEAD to TOE physical exam w/ inventory of all injuries and look in ALL ORIFICES > w/ CLOTHES
OFF. Dont forget to TURN patient over. If hypotensive, survey for all open wounds, and clothing for blood. ABDOMEN STARTS at
Nipple and below on full expiration.

-In this case, most important part = abdominal exam. Seatbelt sign (20% will have small bowel perf), rigidity, guarding, or significant
tenderness distant from stab wounds = indication for LAPAROTOMY (aka. Celiotomy). N.B. PE may not be reliable in intoxicated or
obtunded patients. RECTAL: check sphincter tone (indicator of spinal cord injury).
N.B. Whenever patient develops significant change in clinical condition, a thorough reevaluation with the ABCs should be performed
immediately. > UNSTABLE Trauma patients go straight to OR and OPEN abdomen.
TRAUMA LABS: Blood for CBC (crit wont be low acutely), C7, amylase, LFT, Lactate, PT/PTT, TYPE AND CROSSMATCH,
urine for U/A
Tension PTX: clinical Dx=JVD(?), unilateral decreased/absent breath sounds, tracheal shift AWAY, hyperressonance on affected side.
Tx: Immediate needle thoracostomy 2nd ICS midclavicular line > tube thoracostomy (anterior/midax line in 4th ICS)
-FLAIL CHEST: concern for underlying pulmonary contusion (=2 separate fractures in 3 or more consecutive ribs). Tx: intubation w/
PEEP
-Tamponade: Becks= muffled heart sounds, hypotension, JVD. Pulsus too. Dx: echo, Tx: IVF bolus and pericardiocenteis w/
subsequent surgical exploration!
-Massive HTX: clinical> hypotension, unilaterally decreased or absent breath sounds w/ DULLNESS to percussion. CXR appearance.
May not be obvious cause diaphragm can hide 500cc. Tx: IVF and Tube thoracostomy.
-Thoracic aorta injury: CXR> gold standard aortogram. MC site of tear= distal to take off of LEFT subclavian artery.

PENETRATING:
1.) History: HPI: penetrating or blunt? Witness? How long ago?
2.) Physical Examination: VITALS: temp (fever, hypothermic? Tachy? Hypotensive?), GENREAL: cold, clammy? PE:
3.) Laboratory / Other tests:
4.) Imaging: If patient is HD stable > upright CXR to assess PTX, HemoTX, widened mediastinum and free intra-abdominal air. >If
CXR = Normal can repeat in 4-6 hours to R/O delayed PTX. > FAST to R/O pericardial effusion (cardiac injury) Incredibly sensitive
to R/O hemopericardium, but only 50% sensitive in detetecting abdominal injury. > Diagnostic Laparoscopy to determine if peritoneal
penetration of stab wound or if there is diaphragm injury. Any suspicion of a hollow viscus injury during laparoscopy >
LAPAROTOMY.

-If exam is not alarming w/ penetrating abdominal trauma, and patient HD stable, can consider ADMISSION to hospital for serial
abdominal exams (peritoneal findings/HD instability? Minimum 24-48 hrs), local wound exploration (done w/ local anesthesia check
for fascial penetration?), followed by Diagnostic Peritoneal Lavage (DPL) > FAST, and abdominal CT > or exploratory laparscopy.
Ballistic injuryHoles+Bullets = even number
-Gunshot wound to abdomen requires Ex Laparotomy!!!
-Stab wound to belly: if peritoneal signs, heavy bleeding, shock, unstable, > DO EX Laparotomy! Otherwise, observe asymptomatic
stab wound patient closely > use local wound exploration to R/O fascial penetration or use DPL.

UNSTABLE Vitals in BLUNT trauma:

DPL (post NGT and Foley): bedside, during secondary survey in unstable patients > sample intra-abdominal contents for blood, WBC or
fecal matter. Catheter over guidewire (Seldinger technique), > aspirate, gross blood (>10cc)/fecal contents? If negative, add 1 Liter of
warmed NS and remove w/ gravity. POSITIVE DPL w/ BLUNT trauma= gross aspiration of 10cc blood, fecal contents, or
>100,000/mm3 RBCs, or >500/mm3 WBCs in lavage fluid. Sensitive but NOT specific. If Postive> LAPARTOMY.
BAD for Retroperitoneal injuries.

FAST: quick U/S exam during Secondary Survey in unstable patients: FOUR views: subxiphoid, right and left Upper quadrants and
pelvic. Identifies intraperitoneal fluid and pericardial fluid.
---
STABLE Vitals:
CT: get ONLY if STABLE > NEVER GO TO RADIOLOGY IF PATIENT UNSTABLE > can use ORAL/IV/RECTAL contrast.
Positive if free intraperitoneal fluid or air, extravasation of contrast, or injury to intraabdominal organ.
BAD for IMAGING: DIAPHRAGM and SMALL BOWEL injuries. Good for identifying SOLID ORGAN injuries, or retroperitoneal
injuries or peritoneal fluid. Indication = stable patient w/ abdominal pain/tenderness.
LAPAROSCOPY: NOT SENSITIVE in detecting hollow viscus injury. BUT, GOOD for DIAPHRAGM injuries. Can be Dx and Tx. IF
ANY EXAM FINDINGS (ie. peritoneal signs and trajectory of stab wound tract) suggestive of hollow viscus injury > LAPAROTOMY.

13
BLUNT TRAUMA FINDINGS indicating LAPAROTOMY =
1. peritoneal signs (rebound, guarding) 2. Free air on CXR/CT 3. Unstable patient w/ POSITIVE FAST or DPL.
-EMERGENT ORTHO: 1. Hip dislocation (reduce immediately) 2. Exsanguinating pelvic fracture (external fixator).
-MOTOR VEHICLE ACCIDENT:
-treat Pneothorax w/ Chest tube.
-Causes of tachycardia, hypotension and unresponsiveness here included 1. Hemorrhagic shock 2. tension PTX (based on exam) 3.
Neurogenic shock (cervical/upper thoracic spinal cord injuries disrupt sympathetic fxn plain xrays of spine can R/O boney
fractures/dislocations) 4. Primary cardiac dysfunction (occasionally 2/2 blunt trauma, ECHO or elevated CVP) 5. Closed head injury.
-PRIORITIZE injuries if multiple.
-FIRST learn details of collision from patient, eyewitnesses, or paramedics to gain insight into injury MECHANISM and SEVERITY.
-GCSif low, EARLY AIRWAY control = essential for oxygeneation, ventilation, and minimizing risk of secondary brain injury.
-Tension PTX: suspect if chest wall crepitation, decreased breath sounds, and hypotension > BASED ON CLINICAL EXAM, place
CHEST TUBE BEFORE CXR. Confirm later.
-If suspect hemorrhage as source of hypotension, do INTRAVASCULAR resus while trying to identify source of blood loss.
-HYPOTENSION in polytrauma patient should be presumed to be result of hemorrhage until bleed from all possible sources can be
RULED OUT. Ie. External (ie. scalp lac), pleural space (HTX- B/L chest tubes can help localize pleural blood loss), intraperitoneal
(FAST or DPL during secondary survey of unstable patients), retroperitoneal, pelvic (Pelvic XRAY can identify fractures/dislocations),
soft tissue.
-FAST= Focused Assessment with Sonography for Trauma: peritoneal cavity fluid/blood: hepatorenal recess, bladder, spleen,
pericardial sac. Replacing DPL for BLUNT trauma in UNSTABLE patient.
MISCELLANEOUS:
-3:1 or 4:1 rule. 3L LR for every 1L blood loss.
-Minimal trauma adult UOP = 50 cc /hr
-Neck zone II can do surgical or selective exploration. (selective uses studies, ie. angiogram)
-Closed femur fracture can lose up to 3L of blood! (>50% patients blood volume).
-Seatbelt sign: Small bowel injuries, T12-L2 fracture, cardiac contusion (monitor for any dysrhythmia) and pancreatic injury.
-Penetrating colon injury = if unstable, resection and colostomy. If stable, primary anastomosis/repair +/- resection.
-Small bowel injury: primary closure or resection and primary anastomosis.
-MC injured abdominal organ in blunt trauma = spleen
-Minor pancreatic injuries = JP drain
-DAMAGE control surgery = stop major bleed and GI soilage > Pack and get out of OR to ICU to warm, correct coags and resuscitate.
Back to OR when warm, stable and not acidotic.

15.) Abdominal Aortic Aneurysm (1)

1.) History: HPI: most are ASYMPTOMATIC - PCP. Can see vague epigastric pain and abdominal/back pain. Male (6:1), Caucasian,
>60 y/o (5%), PMH: CAD (MI/Angina), CVD, PVD, HTN, connective tissue disease FH: CAD SH: Smoking
2.) Physical Examination: Vitals: Blood pressure. Hypertension is a RF for rupture. Hypotension may be a sign of rupture. Complete
Cardiopulmonary exam, evaluating for bruits (carotid, AAA, renal, femoral), assessing extremities for signs of PVD). Focusing on
Abdominal exam> pulsatile mass (above the umbilicus)?
3.) Laboratory / Other tests:
4.) Imaging: U/S to follow clinically. Contrast CT (can use if patient has known AAA w/new onset pain but no hypotension > if leak, go
to OR, if no leak, next elective), Aortogram (assesses lumen patency and iliac/renal involvement) (AXR not great, but can see eggshell
calcifcations in aneurysm wall sometimes. NO ROLE FOR IMAGING IF RUPTURED AAA IS SUSPECTED> straight to OR for
laparotomy.
4.b) PRE-OP Evaluation: cardiopulmonary risks. Careful discussion of risks and benefits with patient and informed consent.
5.) Differential Diagnosis: acute pancreatitis, aortic dissection, mesenteric ischemia, MI, perforate ulcer, diverticulitis, renal colic.
6.) Treatment options both medical and surgical: INDICATIONS: AAA> 5cm diameter = surgical repair pending risk factor
assessment. Also, rupture and any size with rapid growth/Sxs/plaque embolization. Surgery = 1. Prosthetic graft placement. 2.
Endovascular (femoral catheter placed stents) = for high risk / poor operative candidates (CAD, COPD) requires follow-up q3-6
months. Long-term data pendind. Also requires infrarenal AAA.
7.) Complications: Only 50% of ruptured AAA reach hospital alive. Of those who arrive alive, only 50% survive emergency surgery.
Elective surgery mortality = < 4 %. Leading cause of Post-op death in elective = MI. Other comps of surgery = atheroembolism, acute
renal failure, colonic ischemia w/in first week (IMA sacrificed heme+ stool, BRBPR, diarrhea, abdom pain = study of choice is
COLONSCOPY, Tx: resection of necrotic colon, Hartmann and end colostomy), Aortoenteric fistula (Long term complication, UGI &
LGI ie. w/ duodenum resect graft and perform extra-anatomic bypass ie. Ax-Fem bypass/Fem-Fem), Anterior spinal syndrome (artery
of Adamkiewicz - loss of pain/temp B/L below, paraplegia, loss of bowel/bladder, SPARES proprioception), Graft infection (Staph A/E
8.) Follow-up:
9.) Misc/PP: Pathophys: true aneurysm (all 3 layers) > 1.5-2X normal). Atherosclerosis (95%), Infrarenal (95%). Classic triad of rupture
AAA= Abdom/Back pain, Pulsatile abdom.. mass, hypotension. Larger ones grow fasterLaplaces law (wall tension = pressure X
diameter). Less than 5 cm (4% /yr), 5-7 = 7%/yr. >7cm= 20%/yr. Mean NL AA = 2 cm.

16.) Carotid Bruit (2)

1.) History: HPI: episodic >TIA (ie. aphasia, hand weakness, amaurosis fugax (transient - <24hrs, monocular blindness),) CVA/stroke
(permanent brain damage) try to localize symptoms ie. Right hand is left carotid. Ipsilateral AFugax. C/L motor Sx. N.B. dizziness,
syncope, and confusion are almost never caused by carotid artery stenosss. With B/L high grade disease, just tilting head back can

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produce symptoms. May just report whooshing sound in the ear without other symptoms. PMH: HTN, CAD, DM, MEDS: on
aspirin/plavix? FH: stroke? SH: Smoking?
2.) Physical Examination: Complete Physical w/ cardiopulmonary exam and abdominal exam listening for bruits and feeling for
peripheral pulses, focusing on neck exam > Carotid bruits? B/L?
3.) Laboratory / Other tests:
4.a) Imaging: Carotid ultrasound/Duplex give general location/anatomy (b-mode) and degree of stenosis. Evaluate both sides.
Should be done by a major center lab which is accredited for quality in duplex ultrasound. With equivocal duplex results ie. 50-75%
stenosis > can do MR angiogram or CT recon angio. Gold standard = Carotid Angiogram. Before CEA, head CT
4.b) PRE-OP Evaluation: cardiopulmonary risks. Careful discussion of risks and benefits with patient and informed consent. ECG.
5.) Differential Diagnosis: TIA, Migraine, focal seizure (Todds paralysis), Vasculitides (ie. temporal arteritis), hypoglycemia.
Subclavian steal physiology (most=asymptomatic) vs. subclavia steal syndrome.
6.) Treatment options both medical and surgical: Conservative mgmt: Aspirin/Clopidogrel. Give aspirin regardless. Surgical: 4-6
weeks post stroke, if one occurred.> carotid endarterectomy (CEA) +/- EEG, can use intraluminal shunt, EEG, and patch angioplasty to
decrease risks remove diseased intima and media. INDICATIONS: Ipsi Symptomatic (TIA, CVA) - NASCET: > 70% stenosis. 5 yr.
stroke rate > 7 vs. 24%. (>50% marginal benefit) Asymptomatic CA stenosis ACAS > 60% as 5.5% w/ CEA 5 yr. stroke vs. 11.1%
(greatest benefit probably w/ >80%). If high-grade B/L stenosis, exists, do symptomatic side first, if asymp, do left side first to protect
language centers. N.B. These recommendations only uphold if an institutions surgeons have safety record equal to or better than the
perioperative complication rates observed during the trials. Carotid Angioplasty/Stenting: jury not out yet. Long term data not good, but
may be better for higher risk candidates and those with recurrent stenosis.
7.) Complications: of CEA: STROKE (1% asymp, 5% symp), MI (MCC of early postop death), hematoma, wound infection, vagal
nerve injury (change in voice), hypoglossal never injury (tongue deviates towards lesion), intracranial hemorrhage. 1% mortality.
8.) Follow-up:
9.) Misc/PP: atherosclerosis w/ embolization. Plaque at carotid bifurcation (branch point) Carotid sheath: carotid artery, internal jugular
vein, Vagus nerve. Symptomatic>plaque ruptures. Asymptomatic > subintimal plaque.

17.) Peripheral Vascular Disease (4)

1.) History: HPI: intermittent claudication (usually the calf muscle, REPRODUCIBLE after walking a certain distance resolves with
stopping for a specific amount of time), rest pain (classically at night in feet, waking patient resolves w/ hanging foot over side of bed
or standing), ED, sensorimotor impairments, tissue loss. Progressive? PMH: Cardiac disease, HTN, DM (can confound an impression of
ischemic rest pain! And increase risk for infection/tissue loss), AAA? Carotid Dz. SH: Tobacco.
2.) Physical Examination: Complete physical focusing on Cardiovascul and Abdominal. Great pulse exam (femoral>absent femoral
pulses may signal Aortoiliac occlusion, Popliteal, DP, PT) > Do DOPPLER to check pulses if necessary. Bruits (carotid, AAA, femoral),
muscular atrophy, decreased hair, thick toenails, tissue necrosis/ulcers (toes/foot vs. venous stasis ulcer is medial malleolus)/infection.
DRY gangrene=dry necrosis w/o signs of infection (mummified). WET = moist, necrotic tissue with signs of infection. TISSUE LOSS
requires intervention! (ie. revascularization).
3.) Laboratory / Other tests: Ankle to Brachial Index (ABI) ratio systolic BPs w/ Doppler. 1.0-1.3 = NL, <0.7 Claudication, <0.4
Rest pain. >1.3 Calcific dz. (DM false positive). Pulse Volume Recordings (PVR): large wave form means good flow uses pressue
cuffs.
4.) Imaging: prior to surgery> Arteriogram (x-ray w/ dye in vessel) > maps disease and decides for best treatment option (angioplasty
vs. surgical bypss)
5.) Differential Diagnosis: arterial insufficiency (ischemia 2/2 arterial stenosis 2/2 atherosclerosis), neurogenic claudication (nerve
entrapment, spinal stenosis, disc), arthritis, diabetic neuropathic pain, chronic compartment syndrome, venous ulcers (medial
maleolus)N.B. with Spinal Stenosis, even standing still doesnt stop the pain, but they generally have to SIT down. N.B. L5-S1, cant
plantar flex foot cant step on the gas or stand on toeS! +St. leg raise test. L4-L5= cant dorsiflex foot.
6.) Treatment options both medical and surgical: MEDICAL: Most patients can be managed w/ conservative mgmt: BEST
INITIAL TREATMENT = LIFESTYLE modifications: (PACE) Pentoxifylline (increases RBC flexibility), Aspirin, Cessation of
smoking, Exercise, treatment of HTN, diet, bedside sheep skin, foot cradle, skin lotion. HbA1c<7, LDL<100, BP<130/80
-Follow up in 3 months time. If progresses, check CT-ANGIOGRAPHY (check Creatinine first!)
Indications for surgery = STIR: Severe claudication refractory to conservative treatment which affects quality of life/livelihood. Ie.
Mailman. Tissue necrosis, Infection, Rest pain. SEVERE PVD: 1) surgical graft bypass (gortex/autologous vein saphenous vein has
better patency) 2.) angioplasty 3.) endarterectomy (remove diseased intima/media). Indications for amputation=irreversible tissue
ischemia, sever infection, no bypassable vessels. FOR SUCCESSFUL arterial bypass, you need: 1.) Inflow (ie. patent aorta), 2.) Outflow
(ie. open distal popliteal artery) 3.) Run off (patent trifurcation vessels down to the foot). Major principle of vascular surgery = get
Proximal and Distal control of the vessel to be worked on! Treatment for most extreme disease = AMPUTATION. POST OP
ANGIOGRAM, OR DOPPLER.
7.) Complications: 20% have AAA, and MI is most common cause of post-op death. Carotid disease also probable.
8.) Follow-up:
9.) Misc/PP: Pathophys: atherosclerosis. MCommon site: SFA in Hunters canal.
-smokers>SFA, DM> Tibial claudication. Claudication often in muscle group ONE distal to the disease. Ie. Calf pain> SFA, Thigh pain
> ileofemoral, Buttock>Aorto-Iliac
Claudication, 5% limb loss at 5 years. Rest pain> 50% at some point. Leriches syndrome: CIA = Claudication (buttock), Impotence,
Atrophy > from occlusive disease of iliacs/distal aorta. ** When tissue loss is noted, multilevel disease is likely. If Diabetic
Osteomyelitis+/-ascending cellulitis: if can probe to bone w/ open DM ulcer, very like Osteo. Admit> need IV ABx for good
penetration to poorly vascularized tissue. Gram Stain/Cx (Gram +, staph/strep, polymicrobial, anaerobes, pseudomonas) > Zosyn will
cover pseudomonas and anaerobes. Add Vancomycin if recent hospitalization. Give fluids, I and D w/ debridgment!! DM dont tolerate
undrained PUS!. Aggressive draining.

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**Related topic > Acute Arterial Occlusion or Cold Foot
-2/2 embolization (85% heart AFib, previous MI, endocarditis, myxoma). Also, acute thrombosis of atheromatous lesion, vascular
trauma. History of thrombophilia?
-History: classic = acute onset, patients know when/where it happened. How long has it been since it started?
signs/sx: 6 Ps: Pain, Paralysis, Pallor, Paresthesia, Poikilothermia, Pulselessness
-Most common site of embolic occlusion = CFA. Most common site from athero = SFA
-Diagnostic tests: Arteriogram, EKG (AFib, MI), +/- Echo (clot, valve vegetation)
-Treatment:
-Immediate pre-op mgmt = anticoagulation w/ Heparin (80 U/kg bolus + 18 U/kg drip) and Arteriogram.
-surgical thrombectomy/embolectomy via cutdown and Fogarty balloon catheter. Feel for pulses at end!
-Post-op/Complications: Compartment syndrome following reperfusion if >4-6 hours since ischemia started> Also, hyperkalemia,
myoglobinuria and renal failure. Compartment syndrome = tissue swelling from reperfussion, resisted by very unyielding fascia,
increased intracompartmental pressure, decrease capillary flow, ischemia, and myonecrosis. SIGNS: pain w/ passive flex/extension,
paresthesias, paralysis, pallow, PRESENT PULSES, > Treatment = fasciotomies of all 4 calf compartments. Leave open. Continue to
monitor for reperfusion syndrome and check creatinine, K/Phosp (myoglobin damage), check Urine pigment (want it to be clean) and >
2cc/kg/hr and put on Telemetry.

18.) Hyperparathyroidism (2) (hypercalcemia)

1.) History: HPI: symptoms = less common today, but many complain of weakness, fatigue, constipation and hx of kidney stones.
Classically, Bones (pathologic fractures, bone pain, osteoporosis, subperiosteal resorption), Stones (polyuria, polydipsia, renal colic,
hematuria), Moans (abdominal pain, constipation, N/V, PUD, pancreatitis), Groans (malaise, fatigue, muscle weakness, gout), Psychic
overtones (lethargy, depression, hallucinations, pyschosis). N.B. also, CVascular complications such as HTN, LVH, calcification of
aortic and mitral valves (increases risk of death ~10% if untreated) PMH: neck irradiation, MEDS: thiazide, Vit. D, Vit. A. FH: MEN I
(ParaT hyperplasia), MEN IIA (ParaT hyperplasia)
2.) Physical Examination: Complete physical exam, including thorough neck exam. If palpable neck mass, hypercalcemia, and elevated
intact PTH, likely PT carcinoma. Other forms of PHPT are NOT palpable.
3.) Laboratory / Other tests: today, most diagnosed as incidental finding of high calcium on routine blood testing as outpatient (NL =
8.5-10.5), low phosphate (2.5-4.5). Serum intact PTH levels will be elevated in Primary HyperPT as will Chloride to Phosphate > 33:1
, increased chloride, and mild metabolic acidosis. PTH blocks phosphorus and bicarb reabsorption, therefore Chloride increases to
maintain EN w/ Na. 24 hour urine calcium to look for hypercalciuria for PHPT. Can get HCG if suspicion of PT Carcinoma.
4.) Imaging: Plain X-ray (subperiosteal bone resorption in hand digits said to be pathognomonic for HPTH), Ultrasound,
Sestamibi scan
5.) Differential Diagnosis: essentially for hypercalcemia Primary HPT (MCC=PT adenoma, usally single > 85%, hyperplasia 10%,
carcinoma 1%) and malignancy > 90%. Ambulatory setting, PHPT is most common (50-60%). Tertiary HPT (renal failure), Malignancy
MCC in hospital setting = (PTHrp RCC/ SCC of lung, lymphoma/myeloma, metastasis), Hyperthyroidism, Granulomatous Dz
(Sarcoid, TB), Exogenous (Vit. D tox, Thiazides), Pagets, Familial Hypocalciuric Hypercalcemia (AD, low calcium in urine,
asymptomatic, NO SURGERY). Aside from FHH and PHPT, all other causes of hypercalcemia will have suppressed PTH levels.
6.) Treatment options both medical and surgical: initial medical mgmt for PHPT for treatment of hypercalcemia = IVFluids and
Furosemide. Definitive treatment for PHPT = parathyroidectomy + frozen section (+/- bx of all abnormally sized glands).
INDICATIONS: all symptomatic patients, asymp <50 y/o WITH at least one of: Calcium > 11.5, 24 hour urine Calcium > 400 mg,
Creatnine clearance reducded >30% for age group without other cause, or BMD greater than 2 SD below NL for matched controls. Do
intraoperative PTH levels post resection of adenoma. Should drop by 50% in 5 minutes. For hyperplasia, remove all 4 parathyroid
glands w/ 30 microg autotransplant into non dominant forearm/SCM. And R/O MEN I and IIA. If carcinoma, remove carcinoma, ipsi
thyroid lobe, and all enlarged LNs.
7.) Complications: recurrent laryngeal nerve injury (U/L voice change, B/L airway obstruction), superior laryngeal nerve injury, neck
hematoma (open at bedside if breathing compromised), wound infection, Hypocalcemia will need calcium and vitamin D supplements.
Signs of tetany include perioral tingling, Chvostek, Trousseau, stridor. Hungry bone syndrome severely deprived/ eaten away of its
calcium, will see aggressive reabsorption and thus hypocalcemia.
8.) Follow-up:
9.) Misc/PP: DiGeorge = absence of thymus and paraTs, Inferior thyroid artery is main blood supply. Chief cells make PTH. PTH
increases Calcium from Bone, GI (via Vit D production 2/2 1-alpha OHase synthesis in Kidney, increases absorption from kidney),
promotes renal excretion of Phosphate. Vit D increases intestinal (Duo/prox Jej) absorption of Ca and P and mineralizes the organic
(Type 1 collagenous part) of bone. PTH hooks into Osteoblast, induces IL-1, activates Osteoclast to increase Ca resorption from bone.
Vit D plugs into osteoblast and induces Alk Phosphatase secretion. Secondary HPT is from low calcium, ie. Renal failure, induces
increased PTH secretion. N.B. Low calcium or HIGH phosphate induces PTH secretion.

19.) Soft Tissue Sarcoma (1)

1.) History: HPI: increasing in size?, swelling in thigh noticed from incidental trauma. Painful? Event notable to account for hematoma?
Wt loss, anorexia, F/C/S, PMH: previous radiation, lymphedema, chemotherapy. FH: Li-Fraumeni, NF-1, Retinoblastoma,, Gardners
2.) Physical Examination: Vitals: General: PE: inspection=inflammatory/infectious signs? Dolor/Calor/Rubor/Tumor firm, nontender
(occasionally painful rapid tumor growth and partial necrosis) mass. > 5cm? (more likely STS). Musculoskeletal exam. plus Neuro
exam. (sensorimotor deficits?) Good lymph node exam.
3.) Laboratory / Other tests: LFTs,
4.a) Imaging: X-ray (no boney abnormalities), CXR, For DEEP tumors, MRI/CT pre-op can help. CT of lung if large, or high grade.
4.b) DIAGNOSE: Mass <3cm = excisional biopsy. >3cm = core needle biopsy (obtain tissue for early dx/tx)

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PATH: if large size, or high grade (poor differentiation, high mitotic index), increased risk for Pulmonary metastasis.
4.c) STAGE: Size, Grade, Depth. LN or Mets = Stage IV.
5.) Differential Diagnosis: hematoma, bruised muscle, abscess, benign lipoma (more common than STS)
6.) Treatment options: surgical WIDE LOCAL Excision w/ 2 cm gross margins and negative microscopic margins. For high-
grade/larger STS, pre/postop chemotherapy and radiation may be indicated. Can sometimes resect Pulmonary mets. STAGE 2/3 consider
RADIATION to reduce risk of LOCAL recurrence. If tumors are involving important structures, may require PREOP CHEMO/RADS to
shrink before surgery.
7.) Complications:
8.) Follow-up: low risk of recurrence: 2x / yr PE, and yearly CXR. High risk, examine Q3 months and CXR 3-6 months indefinitely.
9.) Misc/PP: types: extremity (50%, 3.5x more likely in LOWER ext. ie. Thigh), truncal, and retroperitoneal (most likely to recur
locally, MC=liposarcoma) . Type = malignant fibrous histiocytoma 25% (myofibroblast), liposarcoma (20%), leiomyosarcoma (15%),
fibrosarcoma. KIDS: 50%=rhabdomyosarcoma
More common spread = hematogenous to LUNGS. Mesoderm origin. Sarcoma in greek=fish flesh. Median age = 55. Invade locally
along anatomic planes ie. fascia/vessels.

20.) Carcinoid (1)

1.) History: HPI: most asymptomatic! Episodic: Syndrome (requires hepatic metastasis if GI and since appendix tumors are small, rare
to have appendix tumor Syndrome. Therefore ILEUM = most common GI site liver metastasis and for syndrome) Flushing (transient
warmth, redness of skin), Diarrhea, Wheezing, abdominal pain? Sx: Derm Dementia Diarrhea. PMH: Meds? False 5HIAA can be
seen w/ Tylenol, caffeine, bananas, pineapples, eggplant, walnut).
2.) Physical Examination: Vitals: hypotension? General: appear flushed? PE: Focus on Cardio (murmur, signs of HF- Right side
endocarditis (TI, PS) signs of R sided heart failure> JVD, pitting edema) - pulmonary exam (wheezing?), GI examabdomen, liver,
rectal, etc. 3.) Laboratory / Other tests: CBC, C7, 24 hour urine 5-hydroxyindoleacetic acid (5-HIAA). Increased urine and blood 5-HT
levels. Pentagastrin stimulation test can increase seratonin levels.
4.) Imaging: CXR, Radiolocalization tests: Octreotide scan and MIBG scan (less sensitive). Barium enema, UGI/SBFT, colonscopy,
abdominal CT (usually not helpful-cause tumors are small/slow growing), Broncoscopy. PET (w/ tryptophan tracer)
5.) Differential Diagnosis: idiopathic flushing, anaphylaxis, pellagra, angioedema, other causes of diarrhea, ie. IBS.
6.) Treatment options both medical and surgical: Syndrome = Octreotide IV (reduces diarrhea and flushing >85%, may shrink
tumor in 15%). Diarrhea = Odansetron (zofran) = seratonin antagonist (5HT-3). Anti-Sertatonin drug= Cyproheptadine. Surgical
treatment = excision of primary and single/feasible liver metastasis (or RFA). If appendiceal, >2cm = right hemicolectomy. <2cm,
appendectomy. Chemotherapy for advanced disease.
7.) Complications:
8.) Follow-up: PROGNOSIS: 66% alive at 5 years. (less if liver metastasis)
9.) Misc/PP: MC GI site = appendix. Then, Ileum, rectum. Bronchus. Neuroendocrine, APUDoma, Kulchitski cells > Seratonin and
vasoactive peptides. oid like carcinoma but clinically/histologically less aggressive than most GI carcinomas. 25% of small bowel
tumors. Some may get Pellagra from Niacin > 5HT. (Derm, Diarrhea, Dementia). Carcinoid syndrome (10% of those w/ tumor). Tumors
>2cm increase chances of being malignant (ie. metastasis). Tryptophan = precursor for both niacin and seratonin (5-HT> Melatonin).

17