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Oral Exam Review Samir Trehan

Topic, Page Number

General Format 2
1. Appendicitis 2
2. Colon Cancer 4
3. Diverticulitis 6
4. Melanoma 7
5. Peripheral Vascular Disease 8
6. Bowel Ischemia 10
7. Inflammatory Bowel Disease 11
8. Gallbladder Disease 13
9. Carotid Bruit 17
10. Trauma 18
11. Bowel Obstruction 22
12. Pancreatitis 24
13. Hemorrhoids/ Perianal Pain 27
14. Upper GI Bleed 29
15. Lower GI Bleed 32
16. Hernia 33
17. Abdominal Aortic Aneurysm 36
18. Neck Mass 37
19. Breast Mass - 41

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General Format
State presentation and differential

History
-Symptoms
-Risk factors

Physical exam
-VS
-General
-Heart
-Lungs
-Abdomen
-Extremities

Labs/Imaging

Treatment



1. Appendicitis
1) History
a. Periumbilical pain ! nausea/vomiting ! anorexia ! RLQ pain (within 24 hours)
i. Periumbilical pain = referred pain
ii. RLQ pain = peritoneal irritation
b. Vs. gastroenteritis (in which vomiting precedes pain)
c. Pregnant women may have RUQ pain
2) Physical exam
a. Peritoneal irritation ! guarding, rebound, low-grade fever (high-grade with perforation)
b. Obturator sign (pelvic appendicitis) internal rotation of leg with hip/knee flexed
c. Psoas sign (retrocecal appendicitis) (15% retrocecal) hip flexion against resistance
d. McBurneys point 1/3 from ASIS to umbilicus
e. Rovsings sign LLQ pressure ! RLQ pain
3) Differential diagnosis
a. Everyone
i. Meckels
ii. Crohns
iii. Perforated ulcer (Valentinos sign)
iv. Pancreatitis
v. Volvulus
vi. Pyelonephritis
vii. Diverticulitis
viii. Mesenteric adenitis (yersinia enterolytica)
b. Females
i. Ovarian cyst
ii. Ovarian torsion
iii. Tuboovarian abscess
iv. Mittelschmerz
v. PID
vi. Ectopic pregnancy
4) Labs/imaging
a. CBC (WBC >10K with left shift in 90%)
b. UA (rule out pyelonephritis and renal calculus)
i. Mild hematuria/pyuria can occur with appendicitis (pelvic ! ureter inflammation)
c. CXR (rule out pneumonia; evaluate for free air)
d. AXR
i. Calcified fecalith (5%)
ii. Scoliosis away from right
iii. Loss of psoas shadow and pre-peritoneal fat stripe
e. CT
i. Appendix diameter >6cm
ii. Periappendiceal fat stranding and fluid
iii. Fecalith
f. Ultrasound
i. Non-compressible tube
ii. Useful for pelvic pathology and young children
5) Treatment
a. Pre-op: IV fluids (LR) and antibiotics (anerobic coverage)
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b. Perforated vs. non-perforated
i. Perforated
1. Appendectomy ! wound left open after closing fascia (heal by secondary intention) ! 3-
7 days of antibiotics (triple antibiotics (Amp/Cipro/Clinda OR Zosyn)
2. Continue antibiotics until normal WBC, afebrile, diet and exercise
ii. Non-perforated
1. Appendectomy ! 24 hours of antibiotics (Unasyn, Flagyl or Cipro) ! discharge home on
POD1
c. Appendectomy
i. Lap
1. Lap vs. open? Women (visualize adnexa), obese, quick return to activity
a. If normal appendix, explore terminal ileum (Crohns, Meckels), ovaries, groin
(hernia, rectus sheath hematoma)
2. Steps: ID appendix ! staple/coagulate mesoappendix ! transect at base ! remove
from abdomen ! irrigate until clear
ii. Open
1. McBurneys incision (angled down) vs. Rocky-Davis (transverse)
2. Finger sweep lateral ! medial (to avoid tearing mesoappendix)
iii. Complications
1. Wound infection (most common), SBO, ECF, infertility, right inguinal hernia, stump
abscess
2. Electrocauterize stump to kill mucosal cells (to avoid mucocele)
d. Abscess
i. Percutaneous drainage ! antibiotics ! elective appendectomy 6 weeks later
6) Miscellaneous
a. Pathophysiology
i. Obstruction (fecalith, lymphoid hyperplasia, tumor) ! inflammation ! necrosis ! perforation
ii. Perforation risk = 25% (24 hours), 50% (36 hours), 75% (48 hours)
iii. Complications of appendicitis = pelvic abscess, liver abscess, portal pyelothrombophlebitis
iv. Causes of visceral abdominal pain = stretch, hypoxia and acidity
1. Push on belly ! decreased stretch ! decreased pain (thus, rebound)
v. Location of visceral abdominal pain = epigastric (celiac), periumbilical (SMA) and hypogastric
(IMA)
vi. Reflex of visceral abdominal pain = n/v/c/d
vii. Reflex of somatic pain = involuntary guarding (lateralized via reflex)
b. Anatomy
i. SMA ! ileocolic ! appendiceal artery (contained within mesoappendix)
ii. Abdominal wall layers = skin, subcutaneous fascia (Campas), Scarpas fascia, external oblique,
internal oblique, transverses abdominus, transversalis fascia, preperitoneal fat, peritoneum
iii. Appendix arises from cecal diverticulum and rotates from posterior location to iliac fossa
c. Epidemiology
i. Lifetime incidence = 7%
ii. 20% negative appendectomies acceptable
d. First appendectomy by Hancock (1848)
e. First lap appy by Semm (1983)
f. Laparoscopy surgery basics
i. Contraindications
1. Absolute: hypovolemic shock, severe cardiac decompensation
a. CO2 depresses cardiac function
2. Relative: extensive adhesions, diaphragmatic hernia, COPD
ii. CO2 used (better solubility; less risk of gas embolism; not combustible)
1. Pneumoperitoneum ! increased afterload and decreased preload (but CVP and PCWP
are elevated!)
iii. Hasson technique = no Veress needle (i.e. cut down/place trocar under direct visualization)
iv. Complications
1. CO2 embolus
2. Pneumothorax
3. Post-laparoscopic shoulder pain from diaphragm stretch


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2. Colon cancer
1) History
a. Bleeding, change in bowel habits, anemia (can cause angina), perforation (can cause peritonitis)
b. Left-sided tumors ! obstruction, change in bowel habits, BRBPR (hematochezia)
c. Right sided tumors ! microcytic anemia, occult blood (melena), fatigue
d. Rectal tumors ! hematochezia, tenesmus
2) Physical exam
a. 10% colorectal cancer palpable on rectal exam
3) Differential diagnosis
a. Adenocarcinoma, carcinoid tumor, lipoma, liposarcoma, leiomyoma, lymphoma
b. Diverticular disease
c. IBD
d. Polyps
4) Staging
a. TMN
i. T: 1 (into submucosa), 2 (into muscularis propria), 3 (thru muscularis propria), 4 (perforation into
visceral peritoneum)
ii. N: 1 (1-3 regional nodes), 2 (>4 regional nodes), 3 (nodes along major vessel)
b. Astler-Coller modification of Duke classification
c. Metastatic workup
i. CXR (lung) (via lumbar/vertebral veins)
ii. LFTs (liver) (via portal circulation)
1. 20% liver mets at diagnosis
iii. CT abdomen/pelvis (liver) (direct invasion of other abdominoperineal organs)
iv. For rectal carcinoma, endorectal ultrasound to assess tumor invasion depth and perirectal lymph
nodes
5) Labs/imaging
a. See metastatic workup
b. CEA (useful for recurrence surveillance)
c. Pre-op: CBC, chem10, type/cross, UA
6) Treatment
a. Colon surgery
i. Bowel preparation
1. GoLYTELY (polyethylene glycol) or Fleets Phospho-Soda
2. Broad-spectrum antibiotics to decrease colonic bacterial count
a. PO: 1gm neomycin + 1gm erythromycin (3 doses)
b. IV: Unasyn (24 hrs) (Cipro or Flagyl, if allergic)
ii. Colon resection
1. Depends on blood supply and lymphatic drainage
2. Stapled vs. hand-sewn anastamosis = similar outcomes
3. 2-5cm margins
4. 12 lymph nodes required
iii. 10% unresectable at diagnosis
b. Rectal surgery
i. Rectal carcinoma (distal 15cm) accounts for 30% of colorectal carcinoma
ii. Abdominoperineal resection (APR) = resection of anal canal/sphincter complex with permanent
colostomy
1. Indicated for cancers near anal sphincter complex
iii. Low anterior resection (LAR) = resection of rectum to level of levator ani muscles (leaving anal
canal/sphincter complex intact)
1. Indicated for cancers above anal sphincter complex
iv. 2cm margins
v. All rectal cancer operations include mesorectal excision (with lymph nodes)
c. Stage III (positive nodes) / IV (distant mets) colorectal cancer benefit from adjuvant chemotherapy =
FOLFOX4 = 5-FU, leucovorin, oxaliplatin
d. T3/T4 rectal cancer benefit from neoadjuvant radiation therapy and 5-FU (radiosensitizer)
e. If feasible, can resect liver mets with 1cm margin + chemotherapy
7) Surveillance
a. Post-op colonoscopy every 6 months (for 1 year), yearly (for 2 years) and then 3 years
b. CEA, LFTs, CXR, CT
c. 90% recurrences within first 3 years
8) 5YS by stage = I (90%), II (75%), III (50%), IV (5%)
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9) Screening
a. Colonoscopy every 10 years beginning at 50
b. If adenomatous polyp found, repeat colonoscopy every 3 years; once clear, every 5 years
c. Polypectomy curative if polyp has not penetrated submucosa
10) Miscellaneous
a. Pathophysiology
i. 70% arise from adenomatous polyps
ii. Risks increase with larger polyps (1.3% <1cm, 9.5% 1-2cm, 46% >2cm)
iii. Neoplastic polyps: villous (sessile; broccoli) (40%) > tubulovillous (20%) > tubular
(pedunculated) (5%) adenomas
iv. Most polyps found in rectosigmoid region (30%)
v. Mucin-producing tumors and lymphovascular invasion = poor prognosticators
b. Anatomy
i. Arterial supply to colon
1. SMA ! ileocolic, right colic and middle colic arteries
a. Middle colic ! marginal artery of Drummond and meandering artery of Gonzalez
2. IMA ! left colic and sigmoidal arteries
a. Sigmoidal ! superior rectal artery
3. Internal iliac (hypogastric) ! middle rectal and pudendal (!inferior rectal) arteries
ii. Venous drainage of rectum
1. Proximal rectum ! IMV ! splenic vein ! portal vein
2. Middle/distal rectum ! iliac vein ! IVC
iii. White lines of Toldt = lateral peritoneal reflections of ascending/descending colon
iv. Bowel wall layers
1. No serosa in esophagus and middle/distal rectum
2. Mucosa ! submucosa ! muscularis mucosa ! muscularis propria ! serosa !
mesentery (contains lymph nodes and blood vessels)
c. Epidemiology
i. Lifetime risk = 6%
ii. Risk factors = dietary (low fiber, high fat), genetic, IBD
d. At risk groups
i. Familial adenomatous polyposis (FAP) (APC gene; AD)
1. 100s adenomatous polyps at puberty; CRC by 40-50 in 100%
2. Flex sigmoidoscopy every 1-2 years beginning at 10-12
3. Upper endoscopy at 20 or age of prophylactic colectomy (duodenal)
4. Treatment: total proctocolectomy + ileostomy or ileoanal anastamosis
ii. Gardners syndrome (AD)
1. Neoplastic polyps of small bowel and colon
2. CRC by 40 in 100%
3. SOD = sebaceous cysts, osteoma (skull), desmoid tumor (abdomen)
a. Desmoid tumor treated by wide local excision
b. Desmoid tumor growth slowed by tamoxifen, sulindac, steroids
4. Treatment: total proctocolectomy + ileostomy or ileoanal anastamosis
iii. Peutz-Jeghers syndrome (AD)
1. Hamartomas throughout GI tract (increased cancer risk from polyps)
2. Ovarian cancer
3. Melanotic pigmentation of buccal mucosa
4. Treatment: removal of symptomatic polyps
iv. Cronkhite-Canada syndrome
1. Diffuse GI hamartoma polyps ! malabsorption, weight loss, diarrhea, loss of
protein/electrolytes, nail atrophy, alopecia
v. Turcots syndrome
1. Colon polyps with malignant CNS tumors (GBM)
2. Head CT surveillance
vi. Hereditary nonpolyposis colorectal cancer (HNPCC) (Lynchs syndrome) (mismatch repair genes;
AD)
1. Colonoscopy every 3 years beginning at 25
vii. Ulcerative colitis
1. Colonoscopy/biopsy every 1-2 years beginning 7-8 years after diagnosis
viii. Strong family history
1. Colonoscopy at 40 (or 10 years before diagnosis of 1
st
degree relative)

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3. Diverticulitis
1) History/physical
a. Symptoms of diverticulosis = bleeding and diverticulitis
i. Risk factors: low fiber diet, chronic constipation, family history
ii. Treat diverticulosis with high-fiber diet
b. Symptoms of diverticulitis = LLQ pain, diarrhea, fever, chills, anorexia, LLQ mass, nausea, vomiting,
dysuria, tachycardia
i. Complications: colovesical fistula (air/feces in urine; frequent UTIs)
ii. Diverticulitis = most common cause of GI tract fistulas
iii. Massive lower GI bleeding is seen with diverticulosis, NOT diverticulitis
2) Differential diagnosis for LLQ pain
a. Sigmoid volvulus
i. Omega / bent inner tube signs on AXR
ii. Birds beak on gastrografin enema
iii. If there is no strangulation (i.e. discolored/hemorrhagic mucosa), sigmoidoscopic reduction
successful in 85%
iv. 50% recurrence rate after non-operative reduction
b. GI: SBO, IBD, colon cancer
c. GU: pyelonephritis, UTI
d. Gyn: ectopic pregnancy, PID, mittelschmerz, ovarian cyst, ovarian torsion
e. Referred hip pain
3) Labs/imaging
a. Bleeding (suspect diverticulosis) ! colonoscopy
b. Diverticulitis (i.e. pain/inflammation)
i. Abdominal/pelvic CT (edematous bowel wall, abscess, mesenteric fat stranding)
ii. Elevated WBC
iii. AXR (ileus, air-fluid levels, free air with perforation)
iv. Only safe to get colonoscopy/barium enema (to rule out cancer) 6 weeks after inflammation
resolves due to risk of perforation
4) Treatment
a. IV fluids
b. NPO
c. Broad-spectrum antibiotics with anaerobic coverage
d. NGT (as needed for emesis/ileus)
e. Surgery
i. Indications for immediate surgery: complications (fistula, obstruction, stricture, diffuse peritonitis),
recurrence, hemorrhage, suspected cancer, abscess not drainable percutaneously, sepsis
1. Hartmanns procedure = resection of involved segment with end colostomy and stapled
rectal stump ! 2-3 months ! reanastamosis
2. Small abscess usually resolve with antibiotic therapy alone (if not improved within 72
hours, take to OR)
3. For fistula ! sigmoid colon resection, excision of fistula tract and repair of involved organ
(e.g. bladder, vagina, skin)
4. For partial bowel obstruction ! bowel preparation ! resection
5. For complete bowel obstruction ! surgical exploration
ii. Indications for elective surgery: two episodes or 1
st
episode in young (<40), diabetic or
immunosuppressed
1. Elective surgery = resection of involved segment with primary anastamosis
f. After resolution of diverticulitis, patients >50 and not immunocompromised require no further treatment
5) Miscellaneous
a. Pathophysiology
i. Diverticulosis = diverticula (false; only mucosa/submucosa herniate) in colon
1. Sigmoid colon (Western) vs. right-sided colon (Asian)
2. 50-60% by age 60 (80-90% asymptomatic)
3. Bowel wall weakness at points where blood vessels enter between antimesenteric and
mesenteric teania
ii. Diverticulitis caused by obstruction (fecalith)
b. Lifelong recurrence after 1
st
episode = 33%; after 2
nd
episode = 50%


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4. Melanoma
1) History/physical
a. Risk factors: prior history of melanoma, family history, easily burned skin, white, >20 nevi, blond/red hair,
freckles, male, many sunburns (especially before 18), actinic keratosis, giant congenital nevi, multiple
dysplastic nevi, UVB exposure
b. Most common sites: skin, eyes, anus
i. Palms/soles in blacks
ii. Trunk (back) in men
iii. Extremities (legs) in women
iv. ABCDE (diameter > 6mm)
2) Staging work-up: LFT, CXR, PET, LDH, sentinel node biopsy, diagnostic biopsy
3) Staging
a. Clark classification
i. Stage I epidermis (0-5% recurrence at 5 years)
ii. Stage II papillary dermis (5% recurrence at 5 years)
iii. Stage III junction of papillary/reticular dermis (33% recurrence at 5 years)
iv. Stage IV reticular dermis (66% recurrence at 5 years)
v. Stage V subcutaneous fat (75% recurrence at 5 years)
b. Breslow classification
i. Depth of invasion (more objective and accurate)
ii. <0.76mm ! >90% cure with excision
iii. >4mm ! >80% recurrence or metastases in 5 years after excision
c. AJCC staging
i. Stage I = <1.5mm
ii. Stage II = >1.5mm
iii. Stage III = positive nodes
1. Satellite/in-transit metastases considered stage III
iv. Stage IV = distant metastases (including non-regional lymph node basin)
d. Sites of distant metastases = skin, lung, liver, bone, heart, brain, small bowel
i. Spread via lymphatic and hematogenous routes
4) Treatment
a. Sentinel node biopsy
i. Indication = >1mm thickness
ii. Inject lymphazurin blue dye or colloid with radiolabel ! identify sentinel lymph node ! send to
pathology
iii. If positive ! lymph node dissection
b. Wide local excision
i. Melanoma in situ ! 0.5mm margin
ii. <1mm thick ! 1mm margin
iii. 1-4mm thick ! 2mm margin
iv. >4mm thick ! 2-3mm margin
c. Treatment of digital melanoma = amputation
d. Treatment of intestinal metastases = resection (to prevent bleeding/obstruction)
e. Treatment of isolated adrenal or lung metastases = resection
f. Adjuvant therapy with IFN-alfa-2B for stages III/IV
g. Adjuvant therapy with IL-2 for stage IV
5) Miscellaneous
a. Pathophysiology
i. Melanocytes (neural crest derivative)
ii. Types
1. Superficial spreading (75%)
2. Lentigo maligna melanoma (<10%) Hutchinsons freckle (radial growth phase only),
least aggressive, elderly, head/neck
3. Acral lentiginous melanoma )5%) palms/soles/subungal
4. Nodular melanoma (15%) most aggressive
5. Amelanotic melanoma
b. Prognosis best correlates with depth of invasion and metastases
i. Median survival with distant metastases = 6 months


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5. Peripheral Vascular Disease
1) History/physical
a. Chronic
i. Claudication reproducible onset with walking / relief with rest
1. SFA ! calf
2. External iliac ! thigh
3. Common iliac ! buttock
ii. Rest pain (metatarsalgia) foot (distal metatarsals); at night; resolves with hanging foot over bed
iii. Erectile dysfunction
iv. Tissue loss/ulcer
1. Dry gangrene vs. wet gangrene (moist, necrotic tissue with infection)
2. Non-healing ulcer suggests critical limb ischemia / multi-vessel disease
v. Sensorimotor impairment
vi. Findings: decreased distal pulses, decreased hair, muscle atrophy, thick toe nails
b. Acute (6 Ps)
i. Pain, paralysis, pallor, polar, paresthesia, pulseless
c. Risk factors: HTN, DM, smoking, age, male, high cholesterol, family history
2) Differential diagnosis
a. Neurogenic nerve entrapment, spinal stenosis
b. Arthritis
c. Popliteal artery syndrome
d. Compartment syndrome
e. Neuropathy
f. Coarctation of aorta
3) Labs/imaging
a. CBC, chem7, homocysteine, fasting lipid panel
b. EKG
c. ABI (higher of systolic PT/DP divided by higher of arm systolic pressures)
i. >0.9 = normal
ii. <0.6 = intermittent claudication
1. Stage 2 ! potential intervention
iii. <0.4 = rest pain (critical limb ischemia)
1. Stage 3 ! + probably bypass
iv. <0.2 = ulceration (stage 4), minor gangrene (stage 5), major gangrene (stage 6)
d. PVR (pulse volume recording): large wave form = good collateral flow
e. Angiogram (CTA, MRA, fluoro)
f. Echo (for acute embolus ! looking for source)
4) Treatment for chronic limb ischemia
a. Risk factor reduction
b. Wound care: sheepskin, foot cradle, lotion
c. Medical: aspirin, Trental (pentoxifylline ! increased RBC deformity/flexibility), Pletal (cilostazol ! PDE
inhibitor)
i. Most patients with intermittent claudication can be managed conservatively
d. Surgery
i. Indications: refractory claudication, infection, tissue necrosis, rest pain
ii. Open
1. Bypass
a. Fem-pop (AK or BK) vs. fem-distal
b. Vein vs. prosthetic
i. Always use ipsilateral vein for bypass (unless trauma)
2. Endarterectomy for common femoral occlusion
iii. Endovascular
1. Balloon angioplasty best for proximal vessels with short, focal, concentric, noncalcified
atherosclerotic stenosis
2. Stent residual gradient or dissection following angioplasty
3. Other options: cryoplasty, arthrectomy
4. Reduce risk of kidney injury by contrast with fluids, NAC, bicarbonate (3 mg/kg for first 8
hours ! 1 mg/kg next 16 hours)
iv. Patency for SFA occlusion repair at 5 years = 70% (bypass) vs. 35% (endo)
v. Amputation
1. Indications: irreversible ischemia, necrosis, severe infection
2.
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e. Post-op: MI
i. Endovascular can cause atheroemboli
ii. 20% PVD patients also have AAA
5) Treatment for acute limb ischemia
a. Anticoagulation: IV heparin (bolus ! infusion)
b. Arteriogram with embolectomy (Fogarty balloon; inflate with saline)
i. French / pi = mm
c. Open bypass reserved for embolectomy failure
d. Post-op: MI, hyperkalemia, renal failure (myoglobinuria), compartment syndrome
6) Miscellaneous
a. Pathophysiology of chronic limb ischemia
i. Most common site of occlusion = SFA (Hunters canal)
ii. Risk of limb loss = 5% (5 years) and 10% (10 years)
iii. Risk of limb loss with rest pain = 50% (eventually)
b. Pathophysiology of acute limb ischemia
i. Most common site of occlusion = common femoral artery
ii. Common sources of emboli = afib, MI, endocarditis, myxoma, aneurysm, plaque
c. Anatomy
i.
d. Blue toe syndrome = intermittent, painful blue toes due to microemboli from proximal arterial plaque
e. Leriches syndrome = impotence, butt claudication and leg muscle atrophy from occlusion of iliac arteries
and distal aorta
f. Compartment syndrome
i. Reperfusion ! tissue swelling ! ischemia and myonecrosis (starting at 30mmHg) ! pain (with
passive flexion/extension), paralysis, paresthesia, pallor
ii. Pulses may be present in compartment
iii. Treatment = fasciotomy x4


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6. Bowel ischemia
1) History/physical
a. Bowel ischemia
i. BRBPR, diarrhea, abdominal pain, hypotension, shock
ii. 1 week post-op AAA repair
b. Acute mesenteric ischemia
i. Pain out of proportion, diarrhea, vomiting
ii. OB+ stool
iii. No peritoneal signs unless bowel necrosis
iv. History of afib, MI, cardiomyopathy, endocarditis
v. History of digitalis use
c. Chronic mesenteric ischemia
i. Weight loss secondary to food fear (intestinal angina)
ii. Abdominal bruit
iii. +/- OB+ stool, diarrhea, vomiting
2) Differential diagnosis
a. Lower GI bleed causes
b. Abdominal compartment syndrome
3) Labs/imaging
a. CBC, chem7
b. Pneumatosis on AXR?
c. Bowel ischemia ! colonoscopy (i.e. visualize colon)
d. Mesenteric ischemia ! arteriogram (gold standard; usually multi-vessel disease), duplex ultrasound,
MRA
i. Perform ultrasound before/after food challenge
ii. Echo to find emboli source
e. Must rely on clinical judgment in diagnosis of acute mesenteric ischemia since arteriography can delay
diagnosis/treatment
4) Treatment
a. Bowel ischemia: resection ! Hartmans ! end colostomy
b. Acute mesenteric ischemia
i. Embolus: Fogarty catheter embolectomy, resect necrotic intestine and leave marginal bowel !
secondary laparotomy 24-72 hours later
1. If absolutely no evidence of bowel ischemia, can proceed carefully with trial of catheter-
directed thrombolytic therapy
ii. Thrombus: papaverine vasodilator (opium alkaloid; PDE inhibitor) via arteriogram catheter ! OR
! supraceliac aorta graft to involved intestinal artery or endarterectomy
c. Chronic mesenteric ischemia
i. Definitive treatment = antegrade aortomesenteric bypass or perivisceral aortic endarterectomy
ii. Other options
1. Angioplasty can be useful in select, high-risk patients
2. Retrograde bypass from iliac can be useful in setting of aortic disease
5) Miscellaneous
a. Mesenteric ischemia
i. Acute: emboli (most commonly, distal main trunk of SMA) or thrombosis
1. With embolus, proximal jejunum spared by collaterals
ii. Chronic: atherosclerosis
b. Anatomy of celiac, SMA and IMA systems


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7. Inflammatory Bowel Disease

1) Crohns disease (regional enteritis)
a. History/physical
i. Female, bimodal age distribution
ii. Abdominal pain, diarrhea, fever, weight loss, anal disease
b. Pathophysiology
i. Mouth ! anus; skip lesions
1. Anal involvement common; rectal involvement rare
2. 20% small bowel alone; 30% colon alone; 40% small bowel and colon
ii. Mucosal findings: aphtoid ulcers, granulomas, linear ulcers, transverse fissures, swollen
thickness, transmural inflammation
c. Labs/imaging
i. Colonoscopy with biopsy (observe cobblestoning)
ii. Barium enema
iii. UGI with small bowel follow-through
d. Complications
i. Fistula (anal, colovesical, enterovaginal)
ii. Abscess
iii. Stricture/obstruction
iv. Toxic megacolon (5%)
1. Acutely/massively distended colon (>6cm); cecum most frequent site
2. Fever, sepsis and abdominal pain
3. Treatment: fluids, broad-spectrum antibiotics ! 1/3 fail medical management and require
colectomy
v. Cancer (1/2 risk of UC)
e. Treatment
i. Medical
1. Nutritional
a. Bowel rest with TPN
b. Elemental feedings
c. Omega-3 supplementation
2. 5-ASA derivatives (sulfasalazine, mesalamine, Pentasa) ! maintenance
a. Sulfasalazine active metabolite = 5-ASA (released in colon)
b. Side effects: sperm abnormalities, folate malabsorption
3. Metronidazole ! treatment of choice for perianal Crohns; maintenance
a. Side effects: peripheral neuropathy, disulfaram-like reaction
4. Steroids ! induce remission during acute flares
a. Side effects: immunosuppression, osteoporosis, hirsutism, aseptic necrosis,
glucose intolerance, muscle atrophy
b. Budesonide has fewer systemic side effects than prednisone
5. Azathioprine, 6-MP (and MTX) ! maintain remission after acute flare
6. Infliximab (chimeric monoclonal anti-TNF) ! refractory patients; first-line in fistulizing
perianal disease
ii. Surgery
1. Indications: stricture/obstruction (most common), fistula, perforation, refractory abscess,
refractory toxic megacolon, dysplasia
2. Intra-operative findings: mesenteric fat creeping onto anti-mesenteric border, thick
bowel wall, fistula, abscess
3. Surgical options
a. Stricturoplasty
i. Similar to Heineke-Mikulicz pyloroplasty (i.e. open longitudinally ! sew
close transversely)
ii. Preserves bowel length/function
b. Bowel resection with gross margins
i. 30% require another operation within 5 years
ii. Repeated bowel resections ! short bowel syndrome
c. Note: fibrotic strictures cannot be treated conservatively
4. Remove appendix if cecum not involved with active Crohns
f. Crohns recurrences linked to NSAID use and smoking


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2) Ulcerative colitis
a. History/physical
i. Male, bimodal age distribution, family history (20%)
ii. Bloody diarrhea, fever, weight loss
b. Pathophysiology
i. Rectum ! proximal spread (may cause backwash ileitis)
1. Anal involvement uncommon; always rectal involvement
ii. Mucosal findings: mucosa/submucosa inflammation, crypt abscesses
c. Labs/imaging
i. Colonoscopy with biopsy (observe pseudopolyps = hypertrophied mucosa surrounded by
mucosal atrophy)
ii. Barium enema (chronic UC ! lead pipe appearance)
iii. UGI with small bowel follow-through (to rule out Crohns disease)
d. Complications
i. Cancer (5% at 10 years; 20% at 20 years; 30% at 30 years)
ii. Toxic megacolon (10%)
iii. Hemorrhage
iv. Perforation
e. Treatment
i. Medical
1. See Crohns
2. Steroid and 5-ASA enema
ii. Surgery
1. Indications: refractory toxic megacolon, cancer prophylaxis, intractable disease, failure of
child to mature due to steroid therapy
a. 40% with high-grade dysplasia have synchronous cancer
b. 20% with low-grade dysplasia have synchronous cancer
2. Surgical options
a. Total proctocolectomy, distal rectal mucosectomy and ileoanal pull through ! all
colorectal disease removed (e.g. intractability/cancer) with symptom resolution
and maintenance of transanal incontinence
i. Pouchitis = inflammation of pouch (bacterial overgrowth is contributory
factor; thus, treat with metronidazole)
ii. 4-12 BM/day
b. Total proctocolectomy and Brooke ileostomy ! less morbidity under urgent
setting (e.g. acute toxic colitis)
i. Rectal cancer risk 15-20% at 30 years
c. Note: total proctocolectomy and ileal pouch-anal reconstruction contraindicated
in Crohns disease
3. Surgery can cure GI symptoms and cancer risk of UC
3) Extraintestinal manifestations of IBD: ankylosing spondylitis, aphthous (oral) ulcers, iritis, pyoderma
gangrenosum, erythema nodosum, clubbing, sclerosing cholangitis, arthritis, nephritic syndrome, amyloid
deposits in kidney


!"#$ &'#( )*+,*-. /!#

8. Gallbladder disease
1) History/physical
a. Obstructive jaundice ! jaundice, dark urine, acholic (clay-colored) stool, pruritis, anorexia, nausea
i. Pruritis caused by bile salts in dermis
b. Cholelithiasis ! biliary colic, cholangitis, choledocholithiasis, pancreatitis
i. 10% population; 80% asymptomatic
ii. Risk factors: female, fertile, forty, fat, OCP, chronic hemolysis, cirrhosis, rapid weight loss (e.g.
bariatric surgery), IBD, TPN, vagotomy, hyperlipidemia, somatostatin therapy
iii. Biliary colic = pain (minutes to hours; after food) from gallstones at cystic duct
1. RUQ, epigastric or right subscapular (Boas sign)
2. Biliary colic = temporary vs. acute cholecystitis = constant
c. Acute cholecystitis ! unrelenting RUQ pain, fever, n/v, tender/palpable gallbladder (33%), Murphys
signright subscapular pain (referred), epigastric discomfort (referred)
d. Acalculous cholecystitis
i. Risk factors: prolonged fasting, TPN, transfusion, prolonged post-op/ICU
e. Cholangitis ! Charcots triad (fever, RUQ pain, jaundice), Reynolds pentad (+ MS changes and shock)
i. Causes (see pathophys) which can be obtained via history: post-op stricture, pancreatitis, past
PTC/ERCP/biliary stent
f. Gallstone ileus ! RUQ pain + SBO symptoms (distention, vomiting, hypovolemia)
i. Risk factors = women older than 70
g. Sclerosing cholangitis ! same symptoms as obstructive jaundice
i. Risk factors: IBD (especially UC) (<5% IBD patients)
h. Cholangiocarcinoma ! same symptoms as obstructive jaundice
i. Risk factors: UC, Thorotrast contrast dye, sclerosing cholangitis, liver flukes (clonorchiasis),
Agent Orange, choledochal cysts
i. Carcinoma of gallbladder ! biliary colic, weight loss, anorexia, jaundice, palp. gallbladder (advanced dz)
i. Often asymptomatic until late (cholecystitis)
ii. Risk factors: female (4x), gallstones, porcelain gallbladder (50%), cholecystenteric fistula
2) Differential diagnosis
a. Proximal obstruction: cholangiocarcinoma, LAD, scler. cholangitis, gallstone, hepatoma, stricture, parasite
b. Distal obstruction: choledocholithiasis, pancreatic cancer, pancreatitis, Ampulla of Vater stricture,
sphincter of Oddi dysfunction, LAD, lymphoma, parasite
c. Gallstone ileus differential = SBO differential
3) Labs/imaging
a. Ultrasound
i. Cholelithiasis: test of choice (98% specificity)
ii. Choledocholithiasis: 33% specificity
iii. Acalculous cholecystitis: test of choice
b. ERCP (endoscopic retrograde cholangiopancreatography)
i. Can perform spincterotomy (at sphincter of Oddi) to allow passage of stone from common bile
duct
ii. Complication: pancreatitis
c. PTC (percutaneous transhepatic cholangiogram)
d. HIDA scan: radioisotope concentrated in liver and secreted into bile ! can show cholecystitis (non-
opacification of gallbladder), bile leak or common bile duct obstruction
e. XR detects gallstones in 10-15%
f. Obstructive jaundice ! !AP, !bili +/- !LFT
i. Ultrasound
g. Choledocholithiasis ! common bile duct diameter >5mm in presence of !LFT
h. Cholecystitis ! !WBC, slightly ! AP/LFT/amylase/bili
i. Ultrasound ! thickened gallbladder wall (>3mm), pericholecystic fluid, distended gallbladder,
gallstone, sonographic Murphys sign
i. Cholangitis !!WBC, !AP, !bili, +blood culture
i. Ultrasound
ii. Contrast study, once patient has cooled down (IV antibiotics) ERCP or IOC
j. Gallstone ileus
i. AXR (test of choice) ! air in biliary tract, SBdistention, air-fluid levels, gallstone in ileocecal valve
ii. UGI ! visualize cholecystenteric fistula and obstruction
k. Sclerosing cholangitis ! !AP
i. ERCP or PTC ! beads on a string
l. Cholangiocarcinoma ! ultrasound, CT, ERCP/PTC with biopsy/brushings
m. Carcinoma of gallbladder ! ultrasound, abdominal CT and ERCP
!"#$ &'#( )*+,*-. /!$

4) Treatment
a. Actigall (chenodeoxycholic acid, ursodeoxycholic acid) ! dissolves cholesterol gallstone, but when
stopped, gallstones recur
b. Choledocholithiasis management
i. Admit for observation (risk of cholangitis) and early ERCP/cholecystectomy
c. Acute cholecystitis management: IVF, antibiotic, cholecystectomy
d. Acute acalculous cholecystitis management: cholecystectomy or (if patient is unstable) cholecystostomy
e. Cholangitis management
i. Non-suppurative: IVF, antibiotics and definitive treatment later (i.e. lap chole +/- ERCP)
ii. Suppurative: IVF, antibiotics and decompression (i.e. ERCP with sphincterotomy, PTC with
catheter drainage or laparotomy with T-tube placement)
f. Gallstone ileus management
i. Enterotomy with removal of stone +/- interval cholecystectomy
g. Sclerosing cholangitis management
i. For extrahepatic duct disease ! hepatoenteric anastomosis with resection of extraheptic ducts
(due to cholangiocarcinoma risk)
ii. For intrahepatic duct disease ! transplant
iii. Endoscopic balloon dilation
h. Cholangiocarcinoma management
i. Proximal: resection with Roux-en-Y hepaticojejunostomy +/- hepatic lobectomy
1. Two upper limbs of Y = proximal small bowel and the distal small bowel it joins with
(which is often a blind end)
2. Lower part of the Y = distal small bowel (beyond the anastomosis)
ii. Distal: Whipple (pancreaticoduodenectomy)
a. Cholecystectomy
b. Truncal vagotomy
c. Antrectomy
d. Pancreaticoduodenectomy (head of pancreas/duodenum removed)
i. Duodenum must be removed with pancreas head since share same
blood supply
e. Choledochojejunostomy (CBD/jejunum anastomosis)
f. Pancreaticojejuostomy (distal pancreas/jejunum anastomosis)
g. Gastrojejunostomy (stomach/jejunu anastomosis)
2. Pylorus-preserving Whipple ! no antrectomy; thus, anastomose duodenum to jejunum
3. 25% complication rate
a. Delayed gastric emptying, anastomotic leak (from bile duct or pancreatic
anastomosis), pancreatic/biliary fistula, sepsis, pancreatitis, death (3%)
i. Carcinoma of gallbladder management
i. Mucosa only ! cholecystectomy (open!)
ii. Mucosa/muscularis/serosa ! radical cholecystectomy (i.e. wedge resection of overlying liver and
lymph node dissection) +/- chemo/XRT
iii. Complication of lap chole = trocar site tumor implants
j. Gallstone pancreatitis requires cholecystectomy (once pancreatitis has resolved) since up to 30%
patients have recurrent pancreatitis within 6 weeks
k. Surgical
i. Cholecystectomy
1. Indications
a. Asymptomatic: sickle cell, calcified (porcelain)gallbladder, child
2. Lap
a. Preferred treatment
b. Steps: dissect peritoneum overlying cystic duct and artery ! clip cystic duct and
artery and transect between clips ! dissect gallbladder from liver bed !
cauterize/irrigate/suction to achieve hemostasis of liver bed ! remove
gallbladder through umbilical trocar site
3. Open (right subcostal (Kocher) incision)
4. Complications
a. Right hepatic duct/artery injury
b. Biloma (intraperitoneal bile accumulation)
i. Treat by percutaneous drainage or ERCP with stent placement past leak
c. Cystic duct leak
d. Common bile duct injury
i. Major injury treated by choledochojejunostomy
!"#$ &'#( )*+,*-. /!%

e. Injury to hepatic flexure (colon) or duodenum
f. Must retrieve spilled gallstones since can be infection nidus
5. Gallbladder specimen should be opened in OR to look for cancer
ii. IOC (intraoperative cholangiogram)
1. Indications: jaundice, hyperbilirubinemia, gallstone pancreatitis, elevated AP,
choledocholithiasis, define anatomy
2. Steps: place clip on cystic duct/gallbladder junction ! cut small hole in distal cystic duct
! cannulate ! inject 50% strength contrast ! fluoro
iii. Choledochojejunostomy = anastamosis between common bile duct and jejunum
iv. Hepaticojejunostomy = anastamosis between common hepatic duct and jejunum
v. Choledocholithiasis surgical options
1. ERCP with sphincterotomy and basket/balloon retrieval of stones
2. Laparoscopic trans-cystic or common bile duct retrieval of stones
3. Open common bile duct exploration

5) Miscellaneous
a. Pathophysiology
i. Bile = cholesterol, lecithin (phospholipid), bile acids and bilirubin
ii. Gallbladder emptying increased by CCK and vagus
iii. AP source = bile duct epithelium
iv. CCK source = duodenal mucosal cells
1. Release stimulated by fat, AA, HCl
2. Release inhibited by trypsin and chymotrypsin
3. Function = empty gallbladder, open Ampulla of Vater, decrease gastric emptying,
increase pancreatic acinar growth
v. Jaundice observed when total bilirubin > 2.5 (first seen under tongue)
vi. Cholelithiasis
1. Cholesterol (75%) stones = 2/2 bile supersaturated with cholesterol
2. Pigment (25%) stones = black (calcium bilirubinate) (caused by cirrhosis, hemolysis) or
brown (caused by biliary tract infection)
3. Complications = acute cholecystitis, choledocolithiasis, gallstone pacreatitis, gallstone
ileus, cholangitis
vii. Acute cholecystitis
1. 95% from calculi
2. 5% from acalculous obstruction
3. Causative bacteria via lymphatics: E. Coli, Klebsiella, Proteus, S. faecalis
4. Complications = abscess, perforation, choledocholithiasis, cholecystenteric fistula,
gallstone ileus
viii. Acalculous cholecystitis
1. Gallbladder disuse ! biliary stasis ! sludge
ix. Cholangitis
1. Biliary tract bacterial infection secondary to obstruction; can be lethal
2. Causes = choledocholithiasis, stricture (post-op), neoplasm (ampullary), extrinsic
compression (pancreatic pseudocyst, pancreatitis), ERCP, PTC, biliary stent
3. Causative organisms: GN (most common), enterococci
x. Gallstone ileus
1. SBO from >2.5cm gallstone which has eroded through gallbladder wall and obstructed
ileocecal valve
xi. Sclerosing cholangitis
1. Fibrous thickening of bile duct walls ! strictures ! progressive obstruction ! liver failure
/ cirrhosis
a. 10% develop cholangiocarcinoma
2. Complications = cirrhosis, cholangiocarcinoma, cholangitis
xii. Cholangiocarcinoma = primary bile duct cancer (adenocarcinoma), most commonly at proximal
bile duct
1. Klatskins tumor = tumor at junction of right/left hepatic ducts
xiii. Carcinoma of gallbladder
1. Adenocarcinoma (90%)
2. 60% in fundus
3. 1% of all gallbladder specimens
4. Most common spread = contiguous spread to liver
!"#$ &'#( )*+,*-. /!&

xiv. Hydrops of gallbladder = cystic duct obstruction by gallstone ! mucosa fluid (not bile) fills
gallbladder
xv. Gilbert syndrome = hyperbilirubinemia due to error in bilirubin uptake and glucuronyl transferase
xvi. Courvoisiers gallbladder
xvii. Mirizzis syndrome = common hepatic duct obstruction due to extrinsic obstruction from gallstone
impacted in cystic duct
b. Anatomy
i. Proximal bile ducts = close to liver
ii. Ducts of Luschka: small bile ducts draining directly into gallbladder from liver
iii. Calots triangle borders = cystic duct, common hepatic duct, cystic artery
1. Contains Calots node
2. 10% patients have accessory cystic artery
iv. Gallbladder: fundus, infundibulum (Hartmans pouch) and spiral valves of Heister


!"#$ &'#( )*+,*-. /!'

9. Carotid Bruit
1) History/physical
a. TIA (<24 hours)
i. Unilateral neurologic deficits
1. Amaurosis fugax = temporary monocular blindness (retinal microemboli)
2. Hollenhorst plaque = microemboli to retinal arterials = bright defects
ii. Speech impairment
b. Dizziness, syncope and confusion are almost never caused by carotid artery stenosis
c. Risk factors: HTN, DM, smoking, age, male, high cholesterol, family history
2) Labs/imaging
a. Carotid ultrasround/Doppler
b. Arteriogram (gold standard)
c. Head CT in symptomatic patients
3) Treatment
a. Medical (aspirin, Aggrenox or Plavix)
b. Surgery
i. CEA = removal of diseased intima/media
1. Indication: symptomatic >50% stenosis
a. NASCET trial showed 26% stroke at 2 years with BMT vs. 9% stroke with CEA !
19% absolute risk reduction
2. Indication: symptomatic >60% stenosis
a. ACAS trial showed 11% stroke at 5 years with BMT (aspirin) vs. 5.5% stroke with
CEA ! 6% absolute risk reduction
i. Men benefit at 2 years
ii. Women benefit at 3 years
b. Greatest benefit in patients with >80% stenosis
3. Steps: dissect platysma ! retract SCM posteriorly ! dissect carotid sheath ! ligate
facial vein (branching from internal jugular) ! identify carotid bifurcation ! clamp CCA,
ECA, ICA ! endarterectomy ! patch closure ! unclamp ECA, ICA then CCA
4. Shunt vs. EEG monitoring vs. intra-operative neurologic observation
5. Primary closure vs. patch
6. Complications: stroke (<3% in asymptomatic and <5% in symptomatic patients), MI (most
common cause of death early post-op), hematoma, wound infection, vagus nerve injury
(hoarse), hypoglossal nerve injury (tongue deviation), death (1%)
ii. Post-op f/u at 2 weeks and then every 6 months
iii. Stent only considered for symptomatic >70% stenosis (EVA3S and SPACE trials), recurrent
stenosis or history of neck radiation
iv. If bilateral stenosis, perform CEA first on either symptomatic side or, if both asymptomatic,
dominant hemisphere
4) Miscellaneous
a. Risk of CVA in patients with TIA = 10%/year
b. Anatomy
i. Carotid triangle = SCM (posterior) (CN XI), superior belly of omohyoid (inferior) (ansa cervicalis
C1-C3) and posterior belly of digastric (superior) (CN VII) (anterior belly CN V3)
ii. Carotid sheath contains carotid artery, internal jugular vein, vagus (98% posterior), deep cervical
lymph nodes


!"#$ &'#( )*+,*-. /!(

10. Trauma
1) Primary survey (ABCDE)
a. Airway and C-spine stabilization
i. If patient can speak ! airway intact
ii. Establish airway
1. Chin lift + jaw thrust ! endotracheal intubation (oral if patient not breathing with C-spine
traction) ! cricothyroidotomy (between cricoid inferiorly and thyroid superiorly)
a. Nasotracheal intubation contraindicated with maxillofacial fracture or apnea
b. In children <12, perform needle cricothyroidotomy
2. Patients should be ventilated with 100% O2 using bag/mask before any attempts at
establishing airway
iii. Immobilize spine via full backboard and rigid cervical collar
b. Breathing
i. Inspection (cyanosis, tracheal shift, JVD, accessory muscles), auscultation, percussion, palpation
(flail segments, subcutaneous emphysema)
ii. Chest tube indications = diminished breath sounds, chest wall tenderness and left-sided soft
tissue crepitation
1. If lungs fail to re-expand after chest tube placement ! consider major tracheobronchial
injury
iii. Life-threatening diagnoses = tension pneumothorax, open pneumothorax, massive hemothorax
c. Circulation
i. If palpable radial pulse ! systolic pressure >80
ii. If palpable femoral/carotid pulse ! systolic pressure >60
iii. HR, BP, peripheral pulses, UOP, MS, capillary refill (normal <2 seconds), skin
1. Young patients can be hypovolemic with normal BP (i.e. autonomic tone maintains BP
until CV collapse imminent)
2. Athletes, beta-blockers and spinal cord injury patients can be hypovolemic with normal
HR
3. Treat external bleeding with pressure +/- tourniquet
iv. IV access: 2 large bore IVs in upper extremities
v. Fluids: LR (isotonic; buffers against hypovolemia-induced metabolic acidosis)
1. Ideal urine output = 0.5mg/kg/hr in adults (1 in children)
vi. Gastric decompression with NGT or OGT
1. NGT contraindication: maxillofacial fracture (may perforate cribiform plate into brain)
vii. Bladder decompression with Foley (after ruling out urethral injury)
1. Foley contraindications: pelvic fracture in men, bloody urethral meatus, high-
riding/ballotable prostate, scrotal/peineal ecchymosis
2. If urethral injury suspected, obtain retrograde urethrogram (RUG) checking for dye
extravasation
viii. Shock = inadequate tissue perfusion
1. Symptoms: pallor, "capillary refill, anxiety ! confusion ! obtundation, oliguria ! anuria
2. Class I = 15% blood loss (750cc)
3. Class II = 20-25% blood loss (1.25L) ! !HR, anxious
4. Class III = 30-35% blood loss (1.5L) ! "SBP, "UOP, cool extremities
5. Class IV = >45% blood loss (>2L) ! HR>140, SBP<60, anuria
d. Disability
i. Determine neurological injury
ii. Mental status (GCS)
1. Eye opening (4) (4 eyes)
a. 4 = opens spontaneously
b. 3 = opens to voice
c. 2 = opens to pain
d. 1 = does not open
2. Motor response (6) (6 cylinder motor)
a. 6 = obeys commands
b. 5 = localizes pain
c. 4 = withdraws from pain
d. 3 = decorticate
e. 2 = decerebrate
f. 1 = no movement
3. Verbal response (5)
a. 5 = alert, oriented
!"#$ &'#( )*+,*-. /!)

b. 4 = confused
c. 3 = inappropriate words
d. 2 = incomprehensible wounds
e. 1 = no sounds
4. =< 8 ! coma
5. If intubated, highest score is 11T
iii. Blown pupil ! ipsilateral brain mass ! herniation ! CN III compression
e. Exposure and environment
i. Warm environment since hypothermic patients can become coagulopathic
2) Secondary survey (AMPLE history / physical exam)
a. Signs of thoracic trauma on neck exam = crepitus/subcutaneous emphysema (tracheobronchial
disruption, pneumothorax), tracheal deviation, JVD, carotid bruit (seatbelt neck injury ! carotid artery
injury)
b. Signs of broken ribs/sternum = pain on lateral and A/P thorax compression
c. Signs of great vessel injury = none
d. Must consider abdominal injury up to nipples
e. Seatbelt sign = ecchymosis on lower abdomen
i. 10% have small bowel perforation
ii. Also associated with L2 fracture and pancreas injury
f. Signs of pelvic fracture = pain on lateral compression of iliac crests/great trochanters or A/P compression
of symphysis pubis
g. Progressive decline in mental status ! consider epidural/subdural hematoma, cerebral edema, hypoxia
and hypotension
3) Trauma studies
a. Blunt trauma ! CXR and pelvis XR
i. Femur XR if fracture suspected
ii. Normal initial CXR should be repeated in 4-6 hours (for delayed pneumothorax)
b. Labs: CBC, chem7, amylase, LFT, lactic acid, coags, type/cross, UA
i. LFT useful to asses abdominal injury in children
c. C-spine evaluation/clearance
i. Exam: no neck tenderness, FROM, GCS 15, no alcohol/drugs/narcotics, no distracting injury
ii. CT: rule out bony fracture
iii. MRI and flexion/extension XR: rule out ligament injury
d. Evaluation of intra-abdominal injury
i. FAST (focused assessment with sonography for trauma)
1. Test of choice in unstable patient with blunt abdominal trauma
2. Checks blood in peritoneal cavity (Morisons pouch, bladder, spleen) and pericardial sac
ii. DPL (diagnostic peritoneal lavage)
1. Steps: catheter below umbilicus into peritoneal cavity ! aspirate for blood ! if less than
10cc aspirated, infuse 1L NS ! drain by gravity
a. Place catheter above umbilicus in patients with pelvic fracture (to avoid false
positive from blood in pelvis)
b. NGT and Foley must be placed beforehand
2. Positive DPL! laparotomy
a. >10cc blood or enteric contents on initial aspiration
b. RBC>100K, WBC>500, lavage fluid (NS) drained from chest tube/Foley/NGT,
bile, bacteria, feces, elevated amylase
3. DPL misses retroperitoneal injuries
iii. CT indicated for patients with normal vital signs with abdominal tenderness
1. Oral, IV and rectal contrast
2. CT misses small bowel and diaphragm injuries
3. Look for wall thickening, free fluid and stranding
iv. Diagnostic laparoscopy useful to detect peritoneal penetration, solid organ injury and diaphragm
injury
1. Not sensitive in detecting hollow viscus injury
2. 50% stable, abdominal stab wound patients go on to need laparotomy
4) 3-for-1 rule ! 3L LR for every 1L blood loss in patients with hypovolemic shock
a. Minimal UOP for adult trauma patient = 50cc/hr
b. 1.5L can be lost in thigh secondary to femur fracture
5) Laparotomy indications in blunt trauma = peritoneal signs, free air on CXR, unstable patient with positive FAST or
DPL
6) Penetrating trauma
!"#$ &'#( )*+,*-. /"*

a. Gunshot/stabwound to chest
i. CXR
ii. FAST, chest tube
iii. +/- OR for sub-xiphoid window ! if positive for blood ! sternotomy to assess cardiac injury
b. Gunshot wound to belly ! exploratory laparotomy
c. Stab wound to belly
i. Asymptomatic ! observation (24-48 hours), local wound exploration (rule out fascial
penetration), DPL
ii. Peritoneal signs, significant tenderness distant from stab wound site or unstable vital signs !
exploratory laparotomy
d. Rectal injury
i. Treatment: diverting proximal colostomy, closure of perforation and pre-sacral drainage
e. Colon injury
i. Treatment: resection/primary anastomosis (if stable) or resection/colostomy (if in shock)
f. Small bowel injury
i. Most commonly injured abdominal organ with penetrating trauma
ii. Treatment: resection/primary anastomosis
7) Tension pneumothorax
a. H/P: dyspnea, PVD, tachycardia, pleuritic chest pain, unilateral decreased breath sounds, tracheal shift
away from affected side, hyperresonance on affected side
b. Treatment: immediate needle thoracostomy (2
nd
ICS, mid-clavicular line) ! tube thoracostomy (4
th
ICS,
mid-axillary line)
8) Open pneumothorax
a. H/P: sucking chest wound
b. Risk: opening >2/3 trachea diameter ! resistance to airflow less through defect than trachea !
preventing effective ventilation
c. Labs: CXR (pneumothorax)
d. Treatment: intubation with PPV, tube thoracostomy and occlusive dressing over defect (taped on 3 sides
to create one-way flap valve)
9) Flail chest
a. Two separate fractures in 3+ consecutive ribs
b. H/P: paradoxical chest wall movement with breathing (i.e. sucks in with inspiration and pushes out with
expiration)
c. Major cause of respiratory compromise = underlying pulmonary contusion
i. Pulmonary contusions result from hemorrhage into alveolar and interstitial spaces ! may result
in significant shunting and hypoxia
d. Treatment: intubation with PPV and PEEP PRN; pain control for rib fractures to prevent hypoventilation,
atelectasis and pneumonia
10) Blunt cardiac injury ! 40% arrhythmia, 45% cardiogenic shock, 15% anatomic defects (latter die before reaching
hospital)
11) Cardiac tamponade
a. H/P: tachycardia/shock, Becks triad, Kussmauls sign, pulsus paradoxus
i. Becks triad = hypotension, muffled heart sounds, JVD
ii. Kussmauls sign = JVD with inspiration
iii. Pulsus paradoxus = weakening of pulse with inspiration (exaggeration of normal)
b. Labs: ultrasound (echo)
c. Treatment: IVF (bolus), pericardiocentesis ! surgical exploration
12) Massive hemothorax
a. H/P: hypotension, unilateral decreased breath sounds, dullness to percussion
b. Labs: CXR, CT
c. Treatment: IVF, tube thoracostomy, cell saver
i. Chest tube confirms diagnosis (i.e. blood output) and helps appose parietal/visceral pleura
d. Indications for emergent thoracotomy: >1500cc blood on initial chest tube placement or >200cc/hour
blood x4 hours
13) Basilar skull fracture
a. H/P: Raccoon eyes, Battles sign, clear otorrhea/rhinorrhea (halo sign), hemotympanum
14) Traumatic hyphema = blood in anterior chamber of eye
15) Nasal septal hematoma
a. Treatment: immediate evacuation
b. Complication: pressure necrosis of septum
16) Mandibular fracture
a. H/P: dental malocclusion (ask patient to bite down)
!"#$ &'#( )*+,*-. /"!

17) Thoracic aortic injury
a. Traumatic tear most commonly distal to take off of left subclavian artery
b. H/P: high speed blunt trauma, 1
st
/2
nd
rib fracture, scapula fracture
c. CXR: widened mediastinum, apical pleural capping, loss of aortic knob, left bronchus depression, right
bronchus elevation, tracheal/NGT deviation
d. CTA, TEE and thoracic arch aortogram (gold standard) better tests
18) Emergent orthopedic injuries = hip dislocation and exsanguinating pelvic fracture
a. Pelvic fracture treatment = IVF, blood, pelvic binder (until external fixator placed), +/- arterigram to
embolize bleeding pelvic vessels
b. Pelvic fracture bleeding = 90% venous
19) Bladder rupture
a. Minor/extraperitoneal ! Foley drainage and observation
b. Major/intraperitoneal ! operative closure
20) Pancreas injury
a. Minor pancreatic injury ! drainage (JP)
b. Massive tail injury ! distal pancreatectomy (usually with splenectomy)
c. Massive head injury ! trauma Whipple
21) Liver = most commonly injured abdominal organ with blunt trauma
22) Spleen injury
a. Grade I = <10% subcapsular hematoma; <1cm capsular tear
b. Grade II = 10-50% surface area, non-expanding subcapsular hematoma; 1-3cm parenchymal depth
c. Grade III = >50% surface area subcapsular hematoma OR ruptured subcapsular hematoma; >3cm
parenchymal depth OR involvement of trabecular vessels
d. Grade IV = actively bleeding, ruptured intraparenchymal hematoma; >25% devascularized
e. Grade V = completely shattered/devascularized
23) Duodenal injury
a. Treatment: close duodenal injury, staple off pylorus, gastro jejunostomy
24) Diaphragm rupture
a. CXR: NGT in chest and stomach in pleural cavity
25) Chance fracture
a. MOA: acute hyperflexion ! T12/L1/L2 fracture ! pancreatic/duodenal injury


!"#$ &'#( )*+,*-. /""

11. Bowel obstruction
1) History/physical
a. HPI: Abdominal cramping, nausea, distention, emesis
i. Bowel strangulation ! fever, severe/constant pain, shock, gas in bowel wall, free air, peritoneal
signs, acidosis, tachycardia
ii. Proximal bowel obstruction ! more vomiting
iii. Distal bowel obstruction ! more distension
b. Surgical history, gallstones, weight loss, Coumadin, diverticulitis, Crohns, radiation
c. PE: high-pitched bowel sounds, surgical scars, hernia, DRE
2) Differential diagnosis
a. Post-op ileus usually resolves within 3-5 days
i. Order of recovery after surgery = small intestine ! stomach ! colon
ii. Patient can be fed via J-tube 12-24 hours post-op (i.e. small intestine OK)
b. Hypokalemia
c. Medications narcotics, anticholinergic
d. Sepsis
e. Spinal cord injury
f. Retroperitoneal hemorrhage
3) Labs/imaging
a. Chem7, CBC, type/screen, UA, amylase, ABG, lactate
i. Classic finding = hypovolemic hypochloremic hypokalemia alkalosis
ii. Note: patients may be dehydrated at presentation (thus, slight elevations in counts may resolve
with resuscitation)
b. AXR: distended loops of small bowel; air-fluid levels on upright film
i. Paralytic ileus reveals gas distension throughout bowel (including colon)
c. CT with oral contrast and small bowel follow-through helpful for obscure diagnoses
i. Thickened bowel wall, mesenteric edema, free fluid
ii. Can differentiate between complete and partial SBO
iii. Can identify transition point
iv. Can identify carcinomatosis, small bowel tumor, Crohns, gallstone ileus, hernia
v. Note: contrast may aggravate vomiting
4) Treatment
a. NPO, NGT, IVF, Foley
i. Must replete fluids prior to OR to prevent profound hypotension with anesthesia
1. Adult UOP = 0.5cc/mg/kg is adequate
ii. NGT for decompression and prevention of further vomting/aspiration
b. Partial SBO with history of abdominal surgery and no palpable hernia (i.e. likely adhesions) !
conservative treatment with close observation
i. 80% improvement within 6 to 24 hours
ii. If incarcerated hernia present, but can be reduced ! close observation and repair following
resolution of obstructive signs to prevent recurrence
iii. If not definitive improvement in 24-48 hours, take to OR
c. Complete SBO ! laparotomy and LOA
i. Identify transition point
ii. Close mesenteric defect after small bowel resection to prevent internal hernia
1. OK to anastomose small bowel primarily
iii. 25% mortality in patients with strangulation
d. Indications for OR
i. Absolute = peritoneal signs, free air
ii. Relative = !WBC, fever, tachycardia, abdominal pain
e. Pre-op antibiotics to cover CNR and anaerobes
f. If concern of bowel viability ! 2
nd
look operation indicated in 24 hours
g. Sodium hyaluronate and carboxymethylcellulose effective in decreasing adhesions post-laparotomy; but
no proven decrease in recurrent SBO
5) Miscellaneous
a. Pathophysiology
i. Most common cause of large bowel obstruction = cancer
ii. Most common causes of SBO (adult) = adhesion, hernia (incarcerated), cancer
1. Other: gallstone ileus, intussusceptions, volvulus, external compression, SMA syndrome,
bowel wall hematoma, abscess, diverticulitis, Crohns, radiation enteritis, annular
pancreas, Meckels diverticulum, mesenteric fibrosis, cancer
2. SMA syndrome: SMA compresses duodenum (e.g. weight loss)
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3. Carcinoid tumor ! mesenteric fibrosis
4. Most common small bowel tumor = adenocarcinoma, carcinoid, lymphoma, sarcoma
5. Meckels diverticulum: remant of omphalomesenteric duct / vitelline duct
a. 2 feet from ileocecal valve on antimesenteric bowel border
b. 2 inches long; true diverticulum
c. 2% incidence; men (2x)
d. Symptom onset within first 2 years
e. Complications: painless hemorrhage (50%), obstruction (e.g. volvulus and
intussusceptions) (25%), inflammation (20%)
i. Bleeding due to ectopic gastric mucosa secreting acid
f. Diagnosis with Meckels scan (technectium pertechnetate IV)
iii. Most common causes of SBO (child) = hernia, malrotation, meconium ileus, Meckels,
intussusception
iv. Complete SBO ! no colon gas
1. Patients with complete SBO can have bowel movements and flatus (via clearance of
bowel distal to obstruction)
v. Partial SBO ! some colon gas
vi. Complications: strangulation, necrosis, sepsis
1. Intravascular fluid loss ! ARF
b. Anatomy
i. Small bowel = 20 feet long; site of digestion/absorption; supplied by SMA; plicae circulars (a.k.a.
valvulae conniventes)
1. Duodenum = 1 foot
2. Jejunum = long vasa rectae, large plicae, thick wall
3. Ileum = short vasa rectae, small plicae, thin wall


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12. Pancreatitis
1) History/physical
a. Acute pancreatitis
i. H/P: epigastric pain radiating to back, n/v, decreased bowel sounds, fever, dehydration/shock
b. Chronic pancreatitis
i. H/P: unrelenting epigastric/back pain, weight loss/malnutrition, steatorrhea (25%), type I diabetes
(33%)
c. Hemorrhagic pancreatitis
i. H/P: abdominal pain, shock, ARDS, Cullens sign, Grey Turners sign, Foxs sign
1. Cullens sign = bluish discoloration of periumbilical area
2. Grey Turners sign = ecchymosis of flank
3. Foxs sign = ecchymosis of inguinal ligament
d. Pancreatic abscess
i. H/P: fever, unresolving pancreatitis, epigastric mass
e. Pancreatic pseudocyst
i. H/P: epigastric pain/mass, emesis, mild fever, weight loss, ileus
2) Differential diagnosis
a. Acute pancreatitis: PUD, acute cholecystitis, SBO, mesenteric ischemia, ruptured AAA, biliary colic,
inferior MI
b. Chronic pancreatitis: PUD, biliary tract disease, AAA, pancreatic cancer, angina
c. Pseudocyst: cystadenocarcinoma, cystadenoma
3) Labs/imaging
a. Acute pancreatitis: CBC, chem7, LFT, amylase, lipase, type/cross, ABG, calcium, chemistry, coags,
serum lipids
i. !amylase, lipase, WBC
ii. AXR: sentinel loop, colon cutoff, gallstone
iii. U/S: phlegmon, cholelithiasis
iv. CT: phlegmon, pancreatic necrosis, edema
b. Chronic pancreatitis: amylase, lipase, 72-hour fecal fat analysis, GTT
i. Amylase/lipase may be normal due to tissue loss
ii. CT: greatest sensitivity
iii. AXR: calcification
iv. ERCP: duct irregularities with dilation/stenosis (chain of lakes), pseudocyts
c. Gallstone pancreatitis: RUQ U/S and CT
d. Hemorrhagic pancreatitis
i. !amylase/lipase, "Hct, "Ca
ii. CT with IV contrast
e. Pancreatic necrosis
i. CT with IV contrast (dead tissue does not take up IV contast)
f. Pancreatic pseudocyst: amylase/lipase, bilirubin, CBC
i. !amylase/lipase, !bilirubin (if obstruction present), !WBC
ii. U/S or CT: fluid-filled mass
iii. ERCP: contrast fills cyst if there is communicating pseudocyst (i.e. communicates with pancreatic
duct)
4) Treatment
a. Acute pancreatitis
i. NPO, IVF, NGT (if n/v), adequate oxygenation/ventilation
ii. Nutrition TPN vs. post-pyloric tube feeds
1. TPN with lipids OK, as long as patient does not have hyperlipidemia
iii. H2 blockers/PPI
iv. Analgesia Demerol causes decreased sphincter of Oddi spasm
v. Correction of coags/electrolytes
vi. Alcohol withdrawal prophylaxis
vii. 85% improve within first 3-5 days with conservative measures only
1. If no improvement or severe disease based on Ranson criteria ! contrast CT for
pancreatic necrosis ! if present, prophylactic antibiotics (imipenem/cilastatin good
pancreatic penetration)
a. Cilastatin: dehydropeptidase inhibitor ("imipenem breakdown)
2. Patients with sterile necrosis usually improve with non-operative therapy, but surgical
exploration indicated with clinical deterioration
b. Chronic pancreatitis
i. Discontinue alcohol use
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1. Reduce attacks, but parenchymal damage continues due to ductal fibrosis and
obstruction
ii. Pancreatic enzyme replacement
iii. Narcotics for pain
iv. Surgery (indicated for severe, refractory pain)
1. Puestow = longitudinal pancreaticojejunostomy
a. Longitudinal filleting of pancreas/pancreatic duct with side-to-side anastomosis
with small bowel (jejunum)
2. Duval = distal pancreaticojejunostomy
3. Frey procedure = longitudinal pancreaticojejunostomy with core resection of pancreatic
head
4. Near-total pancreatectomy
c. Gallstone pancreatitis
i. Conservative management and interval cholecystectomy with IOC (3-5 days after pancreatitis
resolution)
1. If total bilirubin does not decrease with non-operative management in acute setting,
ERCP should be conducted to clear duct of stones and prevent biliary complications
ii. 33% patients have recurrent pancreatitis within 8 weeks, if untreated
d. Pancreatic abscess
i. Antibiotics
ii. Abdominal CT with needle aspiration ! send for Gram stain/culture
1. Most common = GN (E. Coli, Klebsiella, Pseudomonas), GP (S. aureus)
iii. Operative debridement with drain placement
e. Pancreatic necrosis
i. Surgical debridement/drainage indications = severely ill, infected necrosis, refractory to medical
management
ii. Prophylactic antibiotics (imipenem/cilastatin)
f. Pancreatic pseudocyst
i. Observation for 6 weeks
1. Wall matures/becomes firm to handle sutures
2. 50% resolve spontaneously
ii. Infected pseudocyst ! percutaneous drainage and IV antibiotics
iii. Hemorrhage into cyst ! arteriogram and embolization
iv. Cysts >5cm, calcified wall, thick wall ! drainage
v. Surgical options
1. Pseudocyst adherent to stomach ! cystogastrostomy
2. Pseudocyst adherent to duodenum ! cystoduodenostomy
3. Pseudocyst not adherent to stomach/duodenum ! Roux-en-Y cystojejunostomy
(draining into Roux limb of jejunum)
4. Pseudocyst in pancreas tail ! resection of tail with pseudocyst
vi. Biopsy cyst wall to rule out cystadenocarcinoma to surgical drainage

5) Miscellaneous
a. Ransons criteria
i. At presentation = GA LAW
1. Glucose > 200
2. AST > 250
3. LDH > 350
4. Age > 55
5. WBC > 16K
ii. Over 48 hours = C HOBBS
1. Ca < 8
2. Hct decrease > 10%
3. O2 < 60
4. BUN increase > 5
5. Base deficit > 4
iii. Mortality
1. 0-2 ! <5%
2. 3-4 ! 15%
3. 5-6 ! 40%
4. 7-8 ! 100%

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b. Pathophysiology
i. Acute pancreatitis
1. Etiologies (most common): alcohol abuse (50%), gallstones (30%), idiopathic (10%)
a. I GET SMASHED = Idiopathic, Gallstones, Ethanol, Trauma, Scorpion Bite,
Mumps, Autoimmune, Steroids, Hyperlipidemia, ERCP, Drugs
2. Complications: pseudocyst, abscess, necrosis, splenic/mesenteric/portal vessel
thrombosis, pancreatic ascites, ARDS, sepsis, DIC, severe hypocalcemia,
encephalopathy
a. Hypocalcemia secondary to fat saponification (i.e. fat necrosis binds Ca)
b. Splenic vein thrombosis ! gastric varices (treat with splenectomy)
3. 85% mild/self-limited
4. 15% severe ! infection (50%), increased microvascular permeability ! intravascular
volume loss
ii. Chronic pancreatitis
1. Chronic inflammation ! destruction of parenchyma, fibrosis and calcification !
endocrine/exocrine insufficiency
a. Subtypes: chronic calcific and chronic obstructive (5%)
2. Etiologies: alcohol abuse (75%), idiopathic (15%), hypercalcemia (hyperparathyroidism),
hyperlipidemia, familial, trauma
3. Complications: pancreatic cancer (2%), biliary obstruction, pseudocyst, abscess,
pancreatic ascites, splenic vein thrombosis, gastric varices
iii. Gallstone pancreatitis = gallstone in ampulla of Vater
iv. Hemorrhagic pancreatitis = bleeding into parenchyma and retroperitoneum with pancreatic
necrosis
v. Pancreatic abscess = infected peripancreatic purulent fluid collection
vi. Pancreatic necrosis = dead pancreatic tissue (after acute pancreatitis)
vii. Pancreatic pseudocyst = encapsulated collection of pancreatic fluid
1. Wall = inflammatory fibrosis (not epithelium)
2. 10% incidence following alcoholic pancreatitis; late complication
a. Most common cause = chronic alcoholic pancreatitis
3. Complications: infection, hemorrhage into cyst (most common cause of death), fistula,
gastric outlet obstruction, SBO, biliary obstruction
viii. Lipase has longer half life ! amylase may normalize while lipase stays elevated
c. Anatomy
i. Pancreatic ducts = Wirsung (main) and Santorini
ii. Blood supply to pancreas
1. Celiac trunk ! gastroduodenal ! anterior/posterior superior pancreaticoduodenal
arteries
2. SMA ! anterior/posterior inferior pancreaticoduodenal arteries
3. Splenic artery ! dorsal pancreatic artery
iii. Duodenum must be removed with head of pancreas since both receive arterial supply from
gastroduodenal artery
iv. Kocher maneuver = separation of lateral duodenal attachments ! examine posterior pancreas
and posterior duodenum


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13. Hemorrhoids / Perianal pain
1) Hemorrhoids
a. H/P: anal mass/prolapsed, bleeding, itching, pain (minor compared to abscess)
i. Excruciating anal pain + hemorrhoid history = thrombosed external hemorrhoid (treat by excision)
ii. Risk factors: constipation/straining, portal HTN, pregnancy, obesity
iii. DRE: enlarged soft mass
b. Labs/imaging
i. Rule out colon/anal cancer with colonoscopy/proctoscopy
c. Treatment
i. Treatment by classification
1. 1
st
degree ! conservative management
2. 2
nd
degree ! conservative, rubber band ligation, infrared coagulation
3. 3
rd
degree ! rubber band ligation, hemorrhoidectomy
4. 4
th
degree ! hemorrhoidectomy
ii. High-fiber diet, anal hygiene, topical steroids, Sitz baths
iii. Surgical resection of large, refractory hemorrhoids
1. Complication: exsanguination (blood may pool proximally without external evidence),
pelvic infection (can be lethal), incontinence (injury to sphincter muscle), anal stricture
2. Contraindication: Crohns
d. Pathophysiology
i. Healthy hemorrhoid tissue involved with fluid/air continence
ii. Engorgement of venous plexi of rectum/anus ! mucosa/anal margin protrusion
iii. External hemorrhoid (below dentate line) = painful (vs. internal)
iv. Three quadrants = left lateral, right posterior, right anterior
v. Classification
1. First degree = hemorrhoid does not prolapsed
2. Second degree = prolapses with defecation, but turns spontaneously
3. Third degree = prolapses with any Valsalva and requires active reduction
4. Fourth degree = prolapsed hemorrhoid which cannot be reduced
2) Anal cancer
a. H/P
i. Risk factors: HPV, herpes, chronic inflammation (fistula, Crohns), STD, smoking
ii. Symptoms: bleeding (most common), mass, mucus per rectum, pruritis
1. 25% asymptomatic
iii. DRE
b. Labs/imaging
i. Proctoscopic exam and colonoscopy with biopsy
ii. Transanal U/S
iii. Abdominal/pelvic CT, CXR, LFTs
c. Treatment
i. NIGRO protocol: chemotherapy (5-FU, mitomycin C), radiation and post-radiation scar biopsy (6-
8 weeks)
1. 90% complete response ! 85% 5YS
2. Local recurrence after NIGRO ! repeat chemo/XRT or salvage APR
d. Pathophysiology
i. Most common carcinoma of anus = squamous cell (80%)
ii. Margin cancer = anal verge out 5cm ! perianal skin
1. Small (<5cm) treated with surgical excision with 1cm margins
2. Large (>5cm) treated with chemo/XRT
iii. Canal cancer = proximal to anal verge up ! internal sphincter
iv. Metastasize to lymph nodes, liver, bone, lung
1. Lymphatic drainage below dentate line ! inguinal lymph nodes
2. Lymphatic drainage above dentate line ! pelvic chain
v. Anal melanoma
1. Treated with wide excision or APR (if large)
2. 33% amelanomtic tumors (thus often need pathology for diagnosis)
3. <5% 5YS
3) Anal fistula
a. H/P
i. Symptoms: perianal drainage/abscess, itching, diaper rash
1. 50% perirectal abscess develop fistula after drainage (weeks to months)
ii. Crohns disease
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b. Diagnosis via DRE and proctoscope
c. Treatment
i. Marsupialization of fistula tract (i.e. fillet tract open)
1. Define anatomy via H2O2/methylene blue injection into external opening
ii. Wound care with routine Sitz baths (TID) and dressing changes
iii. Seton placement if fistula is through sphincter muscle (weeks to months)
1. Allows slow transaction of sphincter muscle with scar tissue formation ! continence
retained after transection
d. Pathophysiology
i. Anal fistula from rectum to perianal skin
ii. Caused by anal crypt/gland infection
iii. Goodsalls rule (straight nose; curved tail)
1. Anterior fistulas have linear tract toward dentate line
2. Posterior fistulas have curved tract
iv. Intersphincteric = between internal/external sphincters
v. Transsphincteric = across both internal/external sphincters
vi. Suprasphincteric = above sphincter complex (originate at dentate line)
vii. Extrasphincteric = above sphincter complex (originate in rectum)
4) Perirectal abscess
a. H/P: rectal pain, pus drainage, fever, mass
b. Treatment
i. Drainage, Sitz bath, anal hygiene, stool softeners
ii. Post-op IV antibiotic indications: cellulitis, immunosuppression, diabetes, heart valve abnormality
c. Pathophysiology: crypt abscess in dentate line
5) Anal fissure
a. H/P: anal pain, painful BM, rectal bleeding, painful rectal exam, sentinel tag/pile, fissure
i. Chronic fissure triad = fissure, sentinel pile and hypertrophied anal papilla
ii. Constipation secondary to refusal to defecate
iii. DRE: increased spincter tone, hypertrophic anal papilla
b. Differential diagnosis: Crohns, anal cancer, STD, UC, AIDS
i. Non-healing anal fissue or fissure located anwhyere other than posterior area of anus ! worry
about Crohns or malignancy
c. Labs/imaging: anoscopy and proctoscopy
d. Treatment
i. Conservative: Sitz baths, stool softeners, high fiber diet, topical nifedipine, Botox, topical
nitroglycerin
ii. Surgery
1. Indications: chronic fissure refractory to conservative management (10%)
2. Lateral internal sphincterotomy ! release from spasm (90% successful) ! reduce
resting sphincter tone
a. Complication: incontinence (35%)
e. Pathophysiology: tear in anal epithelium
i. Posterior midline = most common site (due to low blood flow) (90%)
ii. Caused by constipation, hyperactive sphincter, Crohns
iii. Sentinel pile = thickened mucosa/skin at distal end of anal fissure (often confused with small
hemorrhoid)


!"#$ &'#( )*+,*-. /")

14. Upper GI Bleed
1) History/physical
a. Vital signs stable vs. unstable
b. Coffee-ground emesis, melena (>50cc), shock, epigastric, hypovolemia, orthostatics
i. Blood = cathartic ! vigorous rate can ! hematochezia
c. Relationship to food intake
d. Risk factors: alcohol, burn/trauma, NSAID, vomiting, PUD, portal HTN, splenic vein thrombosis, AAA
i. 10% patients taking daily NSAID develop acute ulcer
2) Differential diagnosis
a. Common causes: PUD (50%) (duodenal>gastric), acute gastritis, esophageal varices, Mallory-Weiss tear
b. Uncommon causes: gastric cancer, gastric volvulus, Boerhaaves syndrome, AEF, paraesophageal hiatal
hernia, Dieulafoys ulcer, angiodysplasia
3) Labs/imaging
a. Chem7, bilirubin, LFTs, CBC, type/cross, PT/PTT, amylase
i. !BUN because of absorption of blood by GI tract
b. NGT aspirate
c. AXR
d. EGD (>95% diagnosis)
4) 80-85% spontaneously stop bleeding
5) 10% mortality; risk factors for death are age>60, shock, >5U PRBC
6) Treatment
a. ABC
b. IVF (2 peripheral IVs) / Foley
i. Resuscitation response determines whether bleeding is active
c. NPO
d. H2/PPI; discontinue NSAIDs (or if not possible, misoprostol or COX-2)
e. NGT suction and water lavage (to remove blood clot / expose mucosa)
f. EGD coagulation and epinephrine (for non-variceal bleeding); sclerosing agents and variceal
ligation/banding (for variceal bleeding)
g. Mesenteric arteriography/embolization for massive UGIB with failed EGD diagnosis
h. Surgery
i. Indications: refractory/recurrent bleeding at known site, >3U PRBC to stabilize, >6U PRBC
overall; required in 10% patients with UGIB
7) PUD
a. 10% prevalence; 20% bleed
b. Associated with H. pylori infection
c. Duodenal ulcers
i. Age 40-65; men (3x)
ii. Epigastric/back pain relieved by food; n/v; anorexia
1. Perforation may initially be painless since fluid can be sterile
iii. Most located in duodenal bulb (within 2cm of pylorus)
1. Caused by increased gastric acid production
iv. Differential: ZE syndrome, pancreatitis, cholecystitis, MI, GERD
v. Diagnosis: EGD, UGI series (if patient not actively bleeding)
vi. Treatment
1. Medical: PPI and H. pylori antibiotic therapy ! most heal in 4-6 weeks
a. Antibiotics x2 weeks = MOC (metronidazole, omeprazole, clarithromycin) or ACO
(ampicillin, clarithromycin, omeprazole)
2. Surgery
a. Indications (IHOP): intractability, hemorrhage, obstruction (gastric outlet),
perforation
i. Giant ulcers (>3cm)
b. Options
i. Oversew bleeding vessel
ii. Truncal vagotomy with pyloroplasty incorporating ulcer
1. Truncal vagotomy = resection of 1-2cm of each vagal trunk as it
enters abdomen on distal esophagus ! decreased gastric acid
secretion
2. Drainage procedure required with truncal vagotomy (e.g.
pyloroplasty, antrectomy, gastrojejunostomy)
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iii. Proximal gastric vagotomy (PGV) (highly selective vagotomy) ! lowest
mortality; no drainage procedure needed since vagal fibers to pylorus
preserved; low rate of dumping syndrome
iv. Graham patch (omentum closure) for duodenal perforation in poor
operative candidates (e.g. shock)
v. Truncal vagotomy with antrectomy ! higher mortality, higher rate of
dumping syndrome, but lower recurrence
3. Complications
a. Posterior duodenal perforation ! gastroduodenal artery bleeding and
pancreatitis
b. Anterior duodenal perforation (more common) ! free air
c. Kissing ulcers ! hemorrhage and free air
d. Diagnosis: free air on AXR or LLD XR, leukocytosis, !amylase
d. Gastric ulcers
i. Age 40-70; men
ii. Epigastric pain increased by food
iii. Most located on lesser curvature (70%); 5% on greater curvature
1. Pain caused by decreased cytoprotection (mucus/bicarbonate)
iv. Diagnosis: EGD with multiple biopsies
v. Treatment
1. Medical: PPI and H. pylori antibiotic therapy ! most heal in 4-6 weeks
a. Antibiotics x2 weeks = MOC (metronidazole, omeprazole, clarithromycin) or ACO
(ampicillin, clarithromycin, omeprazole)
2. If ulcer does not heal within 6 weeks of treatment, re-biopsy
3. Surgery
a. Indications (ICHOP) = IHOP + cancer
b. Distal gastrectomy with excision of ulcer for hemorrhage, obstruction and
perforation
i. No vagotomy unless duodenal involved
c. Resection, truncal vagotomy with Billroth I/II reconstruction for concomitant
duodenal and gastric ulcers
d. Antrectomy, truncal vagotomy with Billroth I/II reconstruction for pyloric gastric
ulcer
e. Graham patch for poor operative candidate with perforated gastric ulcer
4. Note: Billroth I contraindicated for gastric cancer
e. Complications: pain, hemorrhage, perforation, obstruction
i. Valentinos sign = RLQ pain/peritonitis secondary to success collection from perforated peptic
ulcer
f. Cushings ulcer, Curlings ulcer, marginal ulcer (at margin of GI anastomosis), Dieulafoys ulcer (pinpoint
mucosal defect bleeding from underlying vascular malformation)
8) Stress gastritis
a. Risk factors: sepsis, trauma, intubation, shock, burn, brain injury
b. Symptoms: NGT blood, painless
c. Prophylactic treatment: H2 blockers, antacids, sucralfate
d. Diagnosed via EGD if bleeding is significant
e. Treatment: lavage out blood clots ! maximum PPI dose via IV drip x24 hours
9) Mallory-Weiss syndrome
a. Post-vomiting longitudinal tear (submucosa/mucosa) of stomach near GE junction !
thoracic/substernal/epigastric pain, hematemesis (85%)
b. Risk factors: hiatal hernia (50%), alcoholic (50%)
c. Treatment: RT water lavage (90% success) ! electrocautery, arterial embolization
i. Surgery indicated when endoscopic treatment fails (>6U PRBC)
ii. Sengstaken-Blakemore tamponade worsens bleeding
10) Esophageal varices
a. 66% portal HTN ! esophageal varices; 66% esophageal varices ! bleed
b. Treatment
i. Medical: vasopressin, somatostatin (octreotidE)
1. Give nitroglycerin to patients with CAD to prevent coronary artery vasoconstriction
ii. Endoscopic therapy: sclerotherapy, band ligation, Sengstaken-Blakemore balloon tamponade
iii. Surgical therapy: TIPS (decreases portal pressure, but increases encephalopathy), liver
transplant

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11) Boerhaaves syndrome
a. Acute chest pain after vomiting
i. Esophagus more susceptible to perforation and more likely to break down anastomosis due to
lack of serosa
ii. Perforation most commonly in posterolateral esophagus, 3-5cm above GEJ
iii. 50% have GERD
b. Signs: chest pain (immediate) ! subcutaneous/mediastinal emphysema (1 hour after perforation; most
commonly with iatrogenic cervical perforation) ! pleural effusion (immediate or late), fever/leukocytosis
(>4 hours)
i. Signs of infection by 24 hours
ii. Pleural effusion caused by disruption of mediastinal pleura
1. Contamination of mediastinum ! mediastinitis and chest pain
iii. Hammans sign = mediastinal crunch/clicking
iv. Macklers triad = emesis, lower chest pain, cervical emphysema
c. Diagnosis: esophagram (gastrografin) with water-soluble contrast in RLD position
i. CXR: left pneumothorax, left pleural effusion, widened mediastinum
d. Treatment
i. IVF and IV antibiotics
ii. Tube thoracostomy
iii. Right posterolateral chest thoracotomy
1. <24 hours ! expose, debride and primarily close tear; reinforce with intercostal or pleural
flap; drain area
2. >24 hours ! if not repairable, gain proximal control and perform gastrostomy or
jejunostomy via laparatomy
e. Prognosis 15% mortality if surgery <24hrs vs. 33% if surgery>24hrs\
12) Rebleeding rate
a. Esophageal varices = 60%
b. Gastric cancer = 50%
c. Gastric ulcer = 28%
d. Duodenal ulcer = 24%
e. Gastritis = 15%
f. Mallory-Weiss tear = 7%


!"#$ &'#( )*+,*-. /#"

15. Lower GI Bleed
1) Distal to Ligament of Trietz
2) Symptoms: BRBPR, melena, anorexia, syncope, SOB, shock, abdominal pain, orthostatics
a. Melena does not always signify active LGIB (could be stored several days)
b. Melena requires >50cc blood and storage in GI tract for >14 hours
3) Medications: aspirin, warfarin, clopidogrel
4) Differential: diverticulosis (right-sided), angiodysplasia, colon cancer, IBD, Meckels, AEF, infracted bowel, anal
fissure, volvulus, intussusceptions, hemorrhoids
a. Adults (most common) = diverticulosis, angiodysplasia, colon cancer
b. Children (most common) = Meckels, IBD, polyps
c. Angiodysplasia = small, dilated thin-walled veins in mucosa (cecum); 50% have associated cardiac
disease; 25% have AS
5) Labs: CBC, chem7, PT/PTT, type/cross, Fe
6) Algorithm
a. NGT !
i. Blood ! work up potential UGIB with endoscopy
1. Negative ! anoscopy/proctoscopy#
ii. Bile, no blood ! UGIB ruled out ! anoscopy/proctoscopy !
1. Positive ! treat
2. Negative !
a. Significant bleed ! tagged RBC scan (Tc-99m) !
i. Positive ! mesenteric arteriogram ! if positive, surgery
ii. Negative ! colonscopy ! if positive, surgery
b. Slow bleed ! colonscopy ! treat problem (+) or tagged RBC study (Tc-99m) (-)
iii. Clear ! work up potential UGIB with endoscopy
1. Negative ! anoscopy/proctoscopy#
b. Tagged RBC scan more sensitive (>0.5mL/min) than arteriography (>1.0mL/min)
c. Colonoscopy
i. Provides option of therapy (e.g. epinephrine, coagulation)
ii. Preferably in hemodynamically stable patients
iii. Highest specificity in identifying source of LGIB
d. Arteriogram provides option of therapy (e.g. vasopressin or embolization ! control bleeding in 75%)
7) Treatment
a. IVF (LR, PRBC), IVx2, Foley, NGT
b. Discontinue aspirin
c. Bleeding angiodysplasia or polyp ! electrocoagulation or local epinephrine injection
d. Known site with massive or recurrent bleeding ! bowel resection
e. Unknown site with massive bleeding ! exploratory laparotomy and total abdominal colectomy with
primary anastomosis of ileum to rectum (last resort)
8) 80-90% stop bleeding spontaneously
9) 10% require emergent surgery


!"#$ &'#( )*+,*-. /##

16. Hernia
1) Pathophysiology
a. Definition: protrusion of peritoneal sax through musculoaponeurotic barrier; fascial defect
b. Repair to prevent complications of incarceration/strangulation, necrosis, SBO, pain
2) Hernia types
a. Complete hernia = hernia sac/contents protrude all the way through defect
b. Incomplete hernia = defect present without sac or contents protruding all the way through
c. Sliding hernia = hernia sac partially formed by wall of viscus (e.g. bladder, cecum, sigmoid colon)
d. Littres hernia = hernia with Meckels
e. Spigelian hernia = hernia through linea semilunaris
f. Internal hernia = hernia into/involving intra-abdominal structure
g. Obturator hernia = hernia through obturator canal
i. Multiparous women with recent history of weight loss
ii. Howship-Romberg sign = medial thigh mass (particularly with hip flexed, externally rotated and
abducted); pain attributed to obturator nerve compression
h. Lumbar hernia
i. Petits hernia through inferior lumbar triangle
ii. Grynfeltts hernia through superior lumbar triangle
i. Pantaloon hernia = hernia sac exists as both indirect and direct (i.e. straddles inferior epigastric vessels;
protruding through floor of canal and internal ring)
j. Incisional hernia = commonly caused by wound infection
i. Ventral hernia = incisional hernia in anterior abdominal wall
k. Parastomal hernia = hernia adjacent to ostomy
l. Sciatic hernia = hernia through sciatic foramen
m. Richters hernia = incarcerated/strangulated hernia involving only one sidewall of bowel through anterior
abdominal wall defect
i. Thus, can have perforation/necrosis without obstruction
n. Epigastric hernia = hernia through linea alba above umbilicus
o. Umbilical hernia = hernia through umbilical ring
i. Associated with ascites, pregnancy and obesity in adults
ii. 80% pediatric umbilical hernias close by 2 years of age
p. Intraparietal hernia = hernia between layers of abdominal wall
q. Femoral hernia = hernia medial to femoral vessels (under inguinal ligament)
r. Hesselbachs hernia = hernia lateral to femoral vessels (under inguinal ligament)
s. Bochdaleks hernia = hernia through posterior diaphragm (usually on left)
t. Morgagnis hernia = anterior parasternal diaphragmatic hernia (usually on right)
u. Properitoneal hernia = intraparietal hernia between peritoneum and transversalis fascia
v. Coopers hernia = hernia through femoral canal and tracking into scrotum or labia majus
w. Indirect inguinal hernia = hernia lateral to Hasselbachs triangle
x. Direct inguinal hernia = hernia within Hasselbachs triangle
y. Hiatal hernia = hernia through esophageal hiatus
i. Sliding esophageal hiatal hernia associated with GERD
z. Amyands hernia = hernia containing ruptured appendix
3) Anatomy
a. Hesselbachs triangle = inferior epigastric vessels (superolateral), inguinal ligament (inferolateral), lateral
border of rectus sheath (medial); floor composed of internal oblique and transverses abdominus muscles
i. In this triangle, peritoneum and transversalis fascia are only components of anterior abdominal
wall
b. Layers of abdominal wall = skin, subcutaneous fat (Campas fascia), Scarpas fascia, external oblique,
internal oblique, transverses abdominus, transversalis fascia, preperitoneal fat, peritoneum
i. Three muscle aponeuroses form anterior rectus sheath
ii. Posterior rectus sheath deficient below arcuate line
c. Spermatic cord contents
i. Cremaster muscle (derived from internal oblique)
ii. Vas deferens
iii. Testicular artery
iv. Testicular pampiniform venous plexus
v. Genital branch of genitofemoral nerve
d. Ilioinguinal nerve runs on top of spermatic cord in inguinal canal
e. Iliohypgastric lies just under external oblique fascia
f. In women, round ligament lies in inguinal canal (vs. vas deferens)
g. Hernia sac lies anteromedially in inguinal canal (vs. other structures)
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h. Inguinal ligament derived from external oblique aponeurosis
i. Testicle attached to scrotum via gubernaculums
j. Cord lipoma = preperitoneal fat on cord structures ! remove surgically
k. Testicular appendage = outpouching of testicular tissue off testicle ! electocauterize
l. Conjoint tendon = aponeurotic attachments of conjoining of internal oblique and transverses abdominus
to pubic tubercle
m. Boundaries of femoral canal = Coopers ligament (posterior), inguinal ligament (anterior), femoral vein
(lateral), lacunar ligament/piriformis/pubic ramus (medial)
n. Cooper (pectineal) ligament extends from public tubercle laterally and passes posteriorly to femoral
vessels
4) History/physical
a. Usually long history of groin pain/heaviness that increases with standing/activity
i. Increased intra-abdominal pressure = precipitating factor ! constipation, BPH, obesity,
pregnancy, ascites, COPD
b. Sudden development of painful groin mass suggests incarceration
c. Attempt to reduce incarcerated hernia
i. Apply ice ! sedate ! Trendelenburg position for inguinal hernias ! steady, gentle manual
pressure ! admit/observe ! herniorrhaphy ASAP
d. Silk-glove sign = inguinal hernia sac in infant/toddler
5) Ultrasound or CT helpful to differentiate incarcerated hernia from LN, hematoma or abscess
6) Inguinal hernia
a. Direct
i. Caused by acquired defect from mechanical breakdown with aging
ii. Hernia sac = peritoneum
iii. 1% men
b. Indirect
i. Hernia through internal ring ! inguinal canal ! may exit external ring into scrotum (if complete)
ii. Caused by patent processus vaginalis; hernia sac = patent processus vaginalis
iii. 5% men; most common hernia in both men and women
c. Most common organ in inguinal hernia sac (men) = small intestine
d. Most common organ in inguinal hernia sac (women) = ovary/fallopian tube
e. Differential diagnosis of groin mass: LAD, hematoma, seroma, abscess, hydrocele, femoral artery
aneurysm, undescended testicle, sarcoma, testicular torsion
f. Treatment
i. Strangulation or acute incarceration ! emergent herniorrhaphy
1. Correct volume depletion and electrolyte abnormalities before operative intervention
ideally
2. Urgent repair requires incision over incarcerated hernia ! close inspection ! tension-
free reapproximation
ii. For inguinal hernias, transverses abdominus is sutured to either Cooper ligament (McVay) or
shelving edge of inguinal ligament (Bassini)
1. Bassini: sutures approximate reflection of inguinal ligament to transverses abdominis
aponeurosis/conjoint tendon
2. McVay: Coopers ligament sutured to transverses abdominis aponeurosis/cnjoint tendon
iii. With compromised bowel, avoid prosthetic mesh due to infection risk
iv. Other options:
1. Lichtenstein: tension-free repair using mesh
2. High ligation: ligation/transaction of indirect hernia sac without repair of inguinal floor
a. Used only in children (rarely necessary to repair inguinal floor)
v. Laparoscopic repair
1. Indications: bilateral, recurrent, need to resume full activity ASAP
vi. Open vs. lap for unilateral groin hernias
1. Equal recurrence rates, disability times and costs
2. Lap may have less post-op pain and sooner return to work
vii. Complications
1. Operative mortality increases 9-10x in emergent vs. elective cases
viii. Relaxing incision = incision in rectus sheath to relax conjoint tendon to approximate reflection of
inguinal ligament without tension
ix. Final result ! internal inguinal ring should allow Kelly clamp tip and external inguinal ring should
allow finger
1. External oblique aponeurosis does not contribute to inguinal floor repair strength
x. Before leaving OR, make sure to pull testicle down to scrotum
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g. Surgical complications
i. 6-13% chronic pain
ii. Deliberate ligation of superficial epigastric vein
iii. Deliberate cutting of ilioinguinal nerve (! numbness inner thich/lateral scrotum; usually resolves
within 6 months) to remove risk of entrapment/post-op pain
7) Femoral hernia
a. Hernia beneath inguinal ligament, within femoral canal, medial to femoral vessels
b. Associated with female (85%), pregnancy and exertion
c. 33% incarcerate
d. Treatment
i. McVay (i.e. Coopers ligament sutured to transverses abdominis aponeurosis/conjoint tendon)
ii. Mesh plug repair
8) Risk of strangulation: femoral > indirect inguinal > direct inguinal
9) 5-10% lifetime incidence
a. 50% indirect inguinal
b. 25% direct inguinal
c. 5% femoral


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17. Abdominal Aortic Aneurysm
1) History/physical
a. Risk factors: atherosclerosis, HTN, smoking, male, CTD, COPD
b. Most asymptomatic; may have vague epigastric/back discomfort
i. Symptoms of rupture = abdominal pain, pulsatile mass, hypotension
ii. Testicular pain + AAA ! retroperitoneal rupture with ureter stretch (referred pain to testicle)
2) Labs/imaging
a. Ultrasound, contrast CT
b. Arteriogram can assess lumen patency and iliac/renal involvement, but limited in determining diameter
due to potential presence of mural thrombi
c. AXR: eggshell calcification
d. If rupture suspected, proceed to immediate exploratory laparotomy
3) Treatment
a. Indications for repair: AAA>5.5cm, rupture, >1cm/year expansion, symptoms, emboli
b. Endovascular
i. Risk of post-op rupture = 0.7-1% per year ! requires 3-6 month monitoring
ii. Anatomic requirements
1. Proximal landing zone (distal to renal arteries) at least 1.5 cm without significant
calcification or thrombus
2. Distal landing zone at least 2.5 cm
3. Proximal neck angulation less than 45 degrees
4. Access vessels at least 6-8 mm luminal diameter (without extreme tortuosity)
iii. Endoleak (14% incidence)
1. Type I: anastomotic at the attachment sites
2. Type II: collateral back bleeding into the aneurysm sac
3. Type III: modular disassociation
4. Type IV : graft material porosity
c. Prosthetic graft placement
i. Rewrap with native aneurysm adventitia ! reduce risk of AEF
d. Aortobifemoral graft
i. Indicated with AAA and severe bilateral iliac occlusion
e. Complications
i. Death = 4% (elective) vs. 50% (ruptured)
ii. MI, declamping hypotension, embolism, ARF, ureter injury, colonic ischemia, AEF (duodenum),
erectile dysfunction, retrograde ejaculation, AVF (IVC), graft infection (S. aureus, S. epidermidis),
anterior spinal syndrome (artery of Adamkiewicz) (paraplegia, loss of bowel/bladder control, low
of pain/temp inferiorly, proprioception spared)
iii. Graft infection and AEF treatment require extra-anatomic bypass (e.g. axillofemoral + fem-fem
bypass) with resection of graft
4) Pathophysiology
a. True aneurysm; >1.5-2x normal diameter (2cm)
i. Grow 3mm/year
ii. Larger AAA rupture more often and grow faster due to LaPlaces law (wall tension proportional to
radius squared and inverse of wall thickness)
iii. Annual risk of rupture = 4% (<5cm), 7% (5-7cm) and 20% (>7cm)
b. 95% atherosclerotic etiology; other causes = mycotic (bacteria) and inflammatory (CTD)
c. 95% infrarenal (due to bifurcation and increased MMP-9)
5) Anatomy
a. Left renal vein crosses AAA neck proximally
b. IMV runs to left of AAA
c. Left common iliac vein runs behind right common iliac artery
6) Epidemiology
a. Male (6x), white
b. Incidence among >60yo = 5%
c. 20% AAA have peripheral artery aneurysm


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18. Neck mass
1) Signs/symptoms/history suggestive of cancer
a. History: neck radiation, family history, young age, male, hypo/hyperthyroid symptoms
b. Signs: single nodule, cold nodule, increased calcitonin, LAD, hard/immobile nodule
c. Symptoms: voice change, dysphagia, discomfort, rapid enlargement
2) Labs/imaging
a. TSH, Ca, CXR, FNA, U/S +/- I123 scintiscan
i. FNA false negative rate = 5%
ii. Benign FNAB followed with yearly PE and TSH (thyroidectomy reserved for progressive
enlargement or compressive symptoms)
iii. 25% cold nodules = malignant (vs. 1% hot nodules)
b. Solitary nodule with history of neck radiation ! 40% cancer risk
c. Solitary hypofunctioning nodule with cellular FNAB ! 25% cancer risk
d. Pentagastrin stimulation test (medullary)
e. Diagnostic algorithm
i. Clinically hyperthyroid !
1. Low TSH ! I123 scan
2. Normal/high TSH ! FNAB#
ii. Clinically euthyroid/hypothyroid !
1. Serum TSH and FNAB !
a. Benign ! yearly follow up with PE/TSH
b. Nondiagnostic ! repeat ! persistently nondiagnostic ! review TSH level !
normal/high (! operate) vs. low (! I123 scan ! hypofunctioning (operate) vs.
hyperfunctioning (follow up))
c. Cellular ! review TSH level ! normal/high (! operate) vs. low (! I123 scan !
hypofunctioning (operate) vs. hyperfunctioning (follow up))
d. Malignant ! surgery
3) Differential diagnosis of thyroid nodule: multinodular goiter, adenoma, hyperfunctioning adenoma, cyst, thyroiditis,
carcinoma, parathyroid carcinoma
a. 50% population have thyroid nodule
b. Non-thyroid neck mass: abscess, LAD, thyroglossal duct cyst, branchial cleft cyst, lymphoma, metases,
scrofula
4) Treatment
a. Synthroid (T4); half-life = 7 days
b. Thyroid hormones ! suppresses TSH ! half of benign nodules disappear
c. Papillary carcinoma
i. <1.5cm and no history of neck radiation ! thyroid lobectomy/isthmectomy, near-total
thyroidectomy, total thyroidectomy
ii. >1.5cm, bilateral, positive cervical node metastases or history of radiation exposure ! total
thyoidectomy
iii. Lateral palpable cervical lymph nodes ! modified neck dissection (ipsilateral)
iv. Central palpable cervical lymph nodes ! central neck dissection
1. Positive cervical nodes do not affect prognosis
v. Post-op therapy
1. Synthroid
2. I123 scan to locate residual tumor or distant metastases that can be treated with ablative
doses of I123
vi. 95% 10YS
d. Follicular carcinoma
i. Total thyroidectomy
ii. Post-op I123 scan for diagnosis/treatment
iii. 85% 10YS
e. Hurthle cell cancer
i. Total thyroidectomy
f. Medullary cancrer
i. Total thyroidectomy and median lymph node dissection
1. Modified neck dissection if lateral nodes are positive
ii. 50% 10YS; 95% cure rate in MEN family members when screened for calcitonin
g. Anaplastic cancer
i. Small tumors ! total thyroidectomy +/- external beam radiation
ii. Airway compromise ! debulking surgery and tracheostomy
iii. 3% 5YS
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h. Post-op follow Ca, neck hematoma, airway compromise
5) Pathophysiology
a. TRH (hypothalamus) ! TSH (anterior pituitary) ! T3/T4
i. T4 ! T3 conversion peripherally
b. Ras and RET oncogenes associated with thyroid cancer
c. Papillary carcinoma (80%)
i. Associated with Gardners syndrome and neck irradiation
ii. Psammoma bodies
iii. Lymphatic spread
iv. Good I123 uptake
d. Follicular carcinoma (10%)
i. Female (3x)
ii. Hematogenous spread (most commonly to bone)
iii. Cannot make diagnosis by FNA (require histologic finding of capsular/vessel invasion)
iv. Good I123 uptake
e. Medullary carcinoma (5%)
i. Associated with MEN type II
ii. Derived from parafollicular cells (secrete calcitonin)
1. Calcitonin secretion increased by pentagastrin stimulation test
iii. Amyloid on histology
iv. Hematogenous and lymphatic spread
v. Poor I123 uptake
f. Hurthle cell carcinoma (4%)
i. Lymphatic > hematogenous spread
ii. Derived from follicular cells; cannot make diagnosis by FNA (require histologic finding of
capsular/vessel invasion)
iii. No I123 uptake
g. Anaplasic (undifferentiated) carcinoma (1%)
i. Associated with female
ii. Arising in 75% of previously differentiated thyroid cancers (most commonly, follicular)
iii. Histology: giant cells, spindle cells
iv. Very poor I123 uptake
v. Major differential = thyroid lymphoma (much better prognosis)
6) Anatomy
a. Arterial supply to thyroid = superior thyroid artery (ECA) and inferior thyroid artery (thyrocervical trunk off
subclavian artery)
i. IMA = small inferior artery to thyroid from aorta or brachiocephalic
b. Venous return from thyroid = superior, middle and inferior thyroid veins
c. 50% patients have pyramidal lobe; surrounded by Delphian lymph nodes
d. Ligament of Berry connects thyroid to trachea
e. Tubercle of Zuckerkandl = most posterior extension of lateral thyroid lobes
f. Recurrent laryngeal nerve runs in TE groove; innervates laryngeal abductors
i. Injury ! hoarseness (unilateral) and airway obstruction (bilateral)
g. Superior laryngeal nerve injury ! deeper/quieter voice
7) Graves disease
a. Female (6x)
b. Antibodies stimulating TSH receptors on follicular cells ! diffuse goiter ! hyperthyroid (most common
cause) ! exophthalmos and pretibial myxedema
c. Treatment
i. Medical blockade: iodide, propranolol, PTU, methimazole, KI (Lugols)
1. PTU blocks iodine incorporation into T4/T3 (i.e. peroxidase oxidation of iodide to iodine)
and inhibits peripheral conversion of T4!T3
2. Methimazole blocks only iodine incorporation into T4/T3
ii. Radioiodide ablation
iii. Surgical resection (bilateral, subtotal thyroidectomy)
1. Indications: suspicious nodule, refractory, pregnant, child, refuse radioactive iodide
therapy
8) Toxic multinodular goiter (Plummers disease)
a. Most common cause of thyroid enlargement
b. Hyperfunctioning thyroid (nodules localized by I123 scan)
c. Pembertons sign = plethora of head with raising of both arms
d. Treatment: lobectomy or near total thyroidectomy
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i. IIndicated for cosmetic deformity, compressive symptoms or inability ot rule out cancer (1%
multinodular masses = malignant)
9) Thyroiditis
a. Acute thyroiditis
i. Painful, swollen thyroid; fever; overlying skin erythema; dysphagia
ii. Strep or Staph infection of thyroglossal fistula
iii. Treat with antibiotics, drainage/culture and surgery to remove fistula
b. Subacute thyroiditis (DeQuervains)
i. Swelling, tenderness, elevated ESR; often follows URI
ii. Treat with NSAID +/- steroids
c. Chronic thyroiditis
i. Hasimotos
1. 95% women
2. Firm/rubbery gland; lymphocyte invasion
3. Most common cause of hypothyroidism
4. Anti-thyroglobulin and microsomal antibodies
ii. Riedels
10) Parathyroid
a. Pathophysiology/anatomy
i. Superior/inferior parathyroids derived from 4
th
/3
rd
pharyngeal pouches, respectively
ii. Blood supply = inferior thyroid artery
iii. Chief cells produce PTH ! increase Ca and decrease P
1. Vitamin D increases intestinal absorption of Ca and P
2. Ca absorbed in duodenum and proximal jejunum
b. Hyperparathyroidism
i. Primary = increased secretion by parathyroid gland
1. 85% adenoma, 10% hyperplasia, 1% carcinoma
a. Carcinoma marker = hCG
2. Risk factors: family history, MEN I/IIA, neck radiation
3. Symptoms: stones, bones, groans, psychiatric overtones, HTN
a. Subperiosteal bone resorption
b. 33:1 rule = ratio of serum Cl to P
4. Treatment
a. Medical: IVF, furosemide
b. Hyperplasia ! surgery to remove all parathyroid glands and implant >30mg in
forearm
c. Adenoma ! surgery to remove adenoma and biopsy other abnormal looking
glands
d. Carcinoma ! surgery to remove carcinoma, ipsilateral thyroid lobe and all
enlarged lymph nodes
5. Post-op complications
a. Hungry bone syndrome = severe hypocalcemia (i.e. chronically Ca-deprived
bone aggressively absorbs Ca)
b. Hypocalcemia (Chvosteks, Trousseaus, tetany, perioral tingling, paresthesia)
i. Acute treatment: IV Ca
ii. Chronic treatment: PO Ca and vitamin D
ii. Secondary = increased secretion secondary to Ca wasting from renal failure or decreased GI
calcium absorption
c. Imaging
i. Ultrasound
ii. Thallium subtraction scan
iii. Sestamibi scan
iv. Indication for localizing pre-op study = reoperation for recurrent hyperPTH
11) Familial hypocalciuric hypercalcemia (AD) = asymptomatic hypercalcemia with/without !PTH
12) Hypercalcemia differential (CHIMPANZEES)
a. Ca overdose
b. HyperPTH
c. Immobility / iatrogenic (thiazide)
d. Metastases (breast) / milk alkali syndrome
e. Pagets disease
f. Addisons disease / acromegaly
g. ZE syndrome
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h. Excess vitamin D
i. Excess vitamin A
j. Sarcoidosis
13) MEN syndromes
a. AD inheritance
b. All family members should be screened)
c. I (Wermers)
i. Chromosome 11
ii. Parathyroid hyperplasia (90%)
iii. Pancreatic islet cell tumor (66%) (gastrinoma (ZE), insulinoma)
1. 25% ZE patients have MEN I
iv. Pituitary tumor (50%)
d. IIA (Sipples)
i. RET oncogene
ii. Medullary thyroid cancer (100%)
iii. Pheochromocytoma (33%)
iv. Hyperparathyroidism (50%)
e. IIB
i. Mucosal neuroma (100%)
ii. Medullary thyroid cancer (bilateral) (85%)
iii. Pheochromocytoma (bilateral) (50%)
iv. Marfanoid body habitus, flatfoot, constipation


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19. Breast mass
1) History/physical
a. Risk factors: female (100x), white, nulliparity, menarche < 13, menopause > 55, 1
st
degree relative
(1!2x; 2!5x), 1
st
pregnancy > 30, HRT (1-1.5x), prior chest radiation
b. Risk factors: hyperplasia (2x), atypical hyperplasia (4x), DCIS, LCIS, BRCA (1!85% lifetime risk;
2!75%), papilloma (1.5x), sclerosing adenosis (1.5x)
c. Symptoms: breast mass (>1cm), pain (most cancers painless), nipple discharge, edema, nipple
retraction, dimple, rash
i. Often asymptomatic and discovered on screening
ii. 50% in UO quadrant
iii. Peau dorange (due to dermal edema) inflammatory carcinoma
2) Differential: fibrocystic, fibroadenoma, intraductal papilloma, fat necrosis, abscess
3) Labs/imaging
a. Mammography
i. Suspicious: spiculated mass, clustered microcalcifications
ii. Bilateral (3% synchronous contralateral cancer)
iii. False negative rate = 10%
b. Ultrasound
i. Women younger than 30 (denser breasts)
ii. Improves specificity and sensitivity of mammogram
c. MRI
i. Screening in younger women with BRCA
ii. Assess chest wall involvement
d. Breast imaging reporting and data system (BIRADS) ! 1-5 radiology scale correlating to probability of
malignancy
e. Biopsy
i. Indications: suspicious lesion on screening, bloody nipple discharge, ulcer/dermatitis of nipple,
solid mass, persistent mass after aspiration, blood in cyst aspirate, patient concern
ii. Steterotactic or needle localization core biopsy (mammogram) painful
iii. Open biopsy of breast cyst indications: recurrence, bloody fluid, palpable mass after aspiration
iv. Send biopsy to pathology; check ER, PR and HER2 status
f. If BIRADS 5 ! ultrasound ipsilateral axilla ! FNA nodes
g. Pre-op metastatic work-up
i. CXR
ii. LFTs
iii. Serum Ca and alkaline phosphatase (! bone scan)
iv. Head CT, if symptomatic
4) Staging
a. T: 1 (<2), 2 (2-5), 3 (>5), 4 (extension into chest wall or skin)
b. N: 1 (1-3), 2 (4-9), 3 (>10 or supraclavicular)
c. Inflammatory breast cancer, chest wall invasion, internal mammary nodes ! stage IIIB
d. Distant metastases (including supraclavicular nodes) ! stage IV
5) Treatment
a. Chemotherapy
i. Neoadjuvant chemotherapy indicated for inflammatory cancer
ii. Tamoxifen
1. Reduces breast cancer risk by 50% after 5 years
2. Side effects: endometrial cancer (2.5x), DVT, cataracts, hot flashes
iii. CMF (cyclophosphamide, methotrexate, 5-FU)
iv. CAF (cyclophosphamide, adriamycin, 5-FU)
v. Chemotherapy indications: positive lymph nodes, >2cm, lymphatic/vascular invasion, high
nuclear grade, S phase, ER negative
b. Radiation
i. Radiation always given after lumpectomy (6 weeks)
ii. Indications for post-MRM radiation: >4 lymph nodes, chest wall invasion, inflammatory cancer
c. Surgery
i. Lumpectomy/XRT
1. Indications: stage I/II (tumors < 5cm); low tumor/breast ratio
2. Neoadjuvant chemotherapy may be helpful in shrinking tumor
3. Contraindications: pregnancy, multicentric disease, prior XRT, positive margins, SLE,
extensive DCIS (diffuse microcalcification)
ii. MRM
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1. Removal of entire breast, pectoralis fascia and axillary lymph nodes (I/II)
2. Preserve pec major/minor (Auchincloss modification
3. Place drains in axilla ! remove when <30cc/day or POD14
iii. Axillary dissection
1. Level I/II/III = lateral/deep/medial to pec minor
a. Rotters nodes = between pec minor and major
2. Anatomical borders: axillary vein (superior), long thoracic nerve/subscapularis/teres
minor (posterior), latissimus dorsi (lateral), pec minor muscle (medial)
3. Nerves to identify/avoid during dissection: long thoracic, thoracodorsal, medial/lateral
pectoral, intercostobrachial
4. Do not paralyze patient during axillary dissection ! identify nerves via muscle
contraction
iv. Sentinel node biopsy
1. Inject technetium-labeled sulfur colloid or blue dye
v. Breast reconstruction
1. TRAM (transverse rectus abdominus myocutaneous) flap, latissimus dorsi flap, implant
6) Pathophysiology
a. Lymphatic drainage of breast = axillary (lateral) or parastenal (runs with IMA) (medial)
b. Suspensory breast ligaments = Coopers ligament
c. Tail of Spence = breast tissue tapering into axilla
d. DCIS
i. Usually no symptoms
ii. Microcalcifications on mammogram ! diagnose via core or open biopsy
iii. Comedo = most aggressive histologic type
iv. Risk of developing of invasive ductal carcinoma in same breast
v. Risk of lymph node metastasis (<2%)
vi. Surgical therapy
1. <1cm ! remove with 1cm margin
2. >1cm ! lumpectomy with 1cm margin + radiation OR simple mastectomy (i.e. no axillary
dissection)
vii. Adjuvant therapy: tamoxifen
e. LCIS
i. No symptoms or mammogram findings (found incidentally on biopsy)
ii. Risk of developing carcinoma in either breast (30% at 20 years)
iii. Treatment = close follow-up or bilateral simple mastectomy in high-risk
f. Most common cause of bloody nipple discharge = intraductal papilloma
i. Abnormal ductogram ! surgical biopsy
ii. 6-12% patients with nipple discharge have carcinoma
g. Most common breast tumor in patients younger than 30 = fibroadenoma
i. Histology: stromal overgrowth, collagen arranged in swirls
ii. Core biopsy (no fluid to aspirate)
iii. Surgical resection for large or growing tumors
h. Fibrocystic disease
i. Varies with menstrual cycle
ii. Aspirate fluid (straw-colored or green)
iii. Treatment: stop caffeine, NSAID, vitamin E, evening primrose oil
i. Pagets disease = scaling rash/dermatitis of nipple caused by invasion of skin by cells from ductal
carcinoma
j. Mondors disease = thrombophlebitis of superficial breast veins
k. Invasive ductal (90%)
l. Invasive lobular (10%)
m. Inflammatory
7) Screening
a. Self exams monthly
b. Annual breast exam and mammography after 40
i. Self breast exam ideally 1 week after menstrual period
8) Epidemiology
a. Lifetime incidence of breast cancer in females = 12%
i. 75% patients have no known risk factors
ii. 2% patients younger than 30
iii. 33% patients older than 75
9) Prognosis correlates best with axillary lymph node involvement, tumor size and ER status