Orals

Question 1

What is the differential diagnosis of post-op fever? After abdominal surgery, how does an intra-abdominal abscess present? How do you diagnose and treat it?

Answer 1

5 Ws: wind, water, wound, walking and wonder drugs o 1: wind (pulmonary complications)
Atelectasis: tx c cough, deep breathing, ambulation, IS, nasotracheal suction or bronchoscopy (for collapsed segments/lobe)
Pneumonia: can occur if atelectasis not tx adequately
Pulmonary problems: pre-existing pulm dysfunction coupled c incisional pain, respiration/cough depression 2/2 narcotics, abdominal distention
o 3: water (UTI)
After bladder catherization
Positive leukocyte esterase (bac UTI),
positive nitrite test (gram – UTI except S.
saprophyticus)
Catheter-associated: yeast, E. Coli, GNR, S.
epidermidis, S. aureus, enterococci
Dx: UA, C&S
Tx: FQ, TMP-SMX
o 5-7: wound
Streptococcal and clostridial
o 9: Walking (venous complications)
DVT or phlebitis usually starts LE (can
happen any time postop)
PE
IV catheter infections and thrombosis
o 10: Wonder drugs (technically any time drug
administered)
direct cause (lamictal, progesterone, chemotherapeutics),
side effects (cocaine, MDMA, meth)
adverse reaction (antibiotics, sulfa)
withdrawal (heroin, fentanyl)
neuroleptic malignant syndrome (antidopaminergics i.e. antipsychotics)
serotonin syndrome (antidepressants, triptans)

Question 2

Persistent abdominal pain, focal tenderness, spiking fever, persistent tachycardia, prolonged ileus, leukocytosis, intermittent polymicrobial bacteremia, mild liver dysfunction, GI dysfunction

Answer 2

intra-abdominal abscess
Complications: intra-abdominal sepsis
o Volume depletion, catabolic state, high cardiac output, tachycardia, low urine output, low peripheral oxygen extraction C. Diagnosis and Treatment
Diagnosis
o Hematologic studies: CBC
Leukocytosis, anemia, abnormal plt, abnormal liver function test o Blood culture
Polymicrobial bacteremia highly suggests intraabdominal abscess
90% abdominal abscesses contain anaerobic organisms, B. fragilus (highly suggestive of intra-abdominal
abscess)
o Radiography: KUB – rarely diagnostic but indicate further investigation
Subphrenic or subhepatic abscess: pleural effusion, elevated diaphragm, basilar infiltrates, atelectasis o U/S: accuracy rate >90% for dx of abdominal abscesses in experienced hands
o CT with oral/IV contrast: best diagnostic imaging method for abdominal abscess, >95% accuracy
Not recommended for use in dx of abscess until POD 7, by which postoperative tissue edema and nonsuppurative fluids are reduced and reabsorbed
o Radioisotope Scanning: WBC tagged scan can localize to area of inflammation
Substantial false positive rate, no pertinent information that is not found on CT
Limited use to cases in which intra-abd abscess is strongly suspected but not shown on U/S or CT
Treatment
o Antibiotic therapy against aerobic and anaerobic organisms: initiated before abscess drainage and condluded when signs of
sepsis resolved
o Percutaneous abscess drainage: standard treatment for single unilocular abscess with no enteral communication
o Laparoscopic or open abscess drainage: complex abscesses with multiple loculations, interloop abscesses a/w enteric
fistulas, tenacious contents: infected hematoma, infected pancreatic necrosis, fungal abscess

Question 3

2. What is the cause an enterocutaneous fistula (ECF)? How do you make the diagnosis? What is the initial treatment?
   Why wouldn’t an ECF close?

Answer 3

ECF causes
Postoperative: Anastomotic leak, inadvertent enterotomy, inadvertent small bowel injury Trauma: iatrogenic or recreational injury to bowel/colon
Spontaneous: abscess, inflammation, infection, Crohn’s, Diverticulitis

Question 4

Diagnosis? Imaging and Labs

Answer 4

Fistulography: water-soluble contrast is injected into fistulous tract performed 7-10 days after presentation
o Gives length of tract
o Extent of bowel wall disruption o Location of the fistula
o Presence of distal obstruction
Water soluble contrast enema
o I = simple, short blind ending 2cm o III = continuous complex, multiple linear
CT to rule out abscess or inflammatory process
Oral administration of markers (charcoal, Congo red, methylene blue): confirm presence of ECF Lab studies: CBC, CMP, protein/albumin/globulin, transferrin, CRP
o Leukocytosis, electrolyte abnormalities due to fluid and electrolyte loss, malnutrition-associated anemia/hypoalbuminemia, serum transferrin

Question 5

TMT

Answer 5

Conservative (few weeks to months): rehydration, antibiotics, anemia correction, electrolyte repletion, drainage of obvious abscess, nutritional support, control of fistula drainage, skin protection
o Drainage control: octreotide reportedly diminishes fistula output
o Fluid/electrolytes: correct dehydration, hyponatremia, hypokalemia, metabolic acidosis
o Nutrition: parenteral nutrition in proximal small bowel ECF, enteral nutrition in distal ECF
o Skin management: pouch system for high output fistula, skin barrier with dressing for low output
o Pouches: ostomy bags
Skin barriers: powder, paste, wafers, spray, creams
Surgical intervention: should be undertaken after a 4-6 week trial of conservative therapy
o Abscess drainage, stoma to exterioze bowel, create controlled fistulas, resection of fistulous site, anastomosis of remaining bowel

Question 6

failure to close

Answer 6

Failure to close: HIS FRIENDS High output (>500 cc/day)
Intestinal destruction (>50% of circumference) Short segment fistula (

Question 7

17 y/o m POD #5 s/p ex lap for GSWs, small bowel resection c primary anastomosis now c red painful wound and upon opening it up you get pus and Cx sent and wound is packed. Next day nurse calls you bc wound drainage is bilious.
What’s your DDx? And F/U

Answer 7

eaking anastamosis, fistula, abscess, unrecognized injury (of GB, biliary tree or small bowel) bc GSW so now leaking through wound.
W/u via upper GI c small bowel follow through (XRAY), CT, fistulogram (if think fistula).

Question 8

Define Fistula

Answer 8

Definition of fistula from NMS and FA: “Abnormal communication between two or more hollow organs
or between one hollow organ and skin.” “Communication between two epithelialized cavities.”
Trauma injury or anastomotic breakdown can produce fistulization (colocutaneous fistula from anastomotic leak)
Fluid and electrolyte imbalances frequent complications of fistulas especially if it involves proximal bowel or pancreas (electrolyte losses from drainage).

Question 9

Imagine

Answer 9

Radiographic studies- fistulogram or sinogram (contrast administered directly in fistula). U/s, upper GI c small bowel follow through, CT and MRI locate undrained collection (abscess) associated c fistula and could be source infxn, lab tests (CBC, renal panel, cx; observe electrolyte losses and cx)

Question 10

TMT

Answer 10

Hydration and correction electrolyte disturbances, correction of
infxn
Low output fistula: Conservative management (Bowel rest,
TPN, IVF)
Spontaneous closure will occur in most c conservative
therapy to minimize drainage and c appropriate
nutrition.
Closure c conservative measures takes 2-8 weeks
Surgery indicated if failed medical management, if converts to high output fistula, or when is becomes infected. Operative repair required if any of the following present:
“FRIENDS” cause persistent fistulas (foreign body, radiation, inflammation, epithelialization of fistula tract, neoplasia at fistula, distal obstruction beyond fistula)

Question 11

What are the signs and symptoms of wound infection? How do you classify wounds according to risk of infection? What are the measures to prevent wound infection?

Answer 11

Wound infection: Signs and symptoms
Classic signs: Calor (heat, warmth), Rubor (redness), Tumor (swelling), Dolor (pain), induration, frank purulent discharge
Severe signs: fever (after POD #3), chills, rigors of surgical wounds
Classification
Clean
Wound created in sterile, nontraumatic fashion in area with no inflammation Respiratory, alimentary, genital, urinary tract NOT entered
Aseptic technique maintained
Risk of infection: 1.5%
Clean-contaminated
o Respiratory, alimentary, genital, or urinary tract entered – no significant spillage of contents, no established
local infection
o Minor break in aseptic technique
o Risk of infection: 3% (By age: 15-24 yo = 4-5%, > 65 yo = 10%)
Contaminated
o Gross spillage from GI tract
o GU and biliary tracts entered in presence of local infection (ie cholangitis) o Wound was the result of recent rauma
o Major break in aseptic technique
o Risk of infection: 10%
Dirty/Infected
o Wound was the result of remote trauma and contains devitalized tissue o Established infection or perforated viscera prior to procedure
o Risk of infection: 30-35%
C. Prevention
Antimicrobial prophylaxis: efficacy is determined by appropriate coverage against most probable contaminating organisms, optimal concentration in serum and tissues at time of incision, maintained in therapeutic levels throughout
o Gram positive cocci: 1st and 2nd generation cephalosporin
o Gram negative rods: 3rd generation cephalosporins, aminoglycosides o Anaerobes: clindamycin, metronidazole
o MRSA: vancomycin

Question 12

46 y/o f hx of non-insulin dependent DM, severe steroid-dependent emphysema and s/p ex lap for perf diverticulitis, underwent sigmoid resection c end colostomy and on POD #6 dev postop wound infxn, what are the sources of the infxn?

Answer 12

Since pt has DM and taking steroids-immunologic incompetence
Bacteria from bowel- colon flora (Bacteroides fragilis, E. Coli), skin (Staphylococcus epidermidis), break
in technique

Question 13

Treat wound?

Answer 13

Open it up, drain and pack it and give abx

Question 14

Types of surgical wounds infection rate

Answer 14

Clean (infxn rate 1.5%)
Wound created in sterile and nontraumatic way in area c
no preexisting inflammation
Pulm, GI, GU tracts not entered.
All participating individuals maintained strict aseptic
technique.
Clean contaminated (infxn rate 3%)
Pulm, GI, GU tracts entered but no significant spillage of contents and no local infxn.
Minor break sterile tech. Contaminated (infxn 10%)
Gross spillage of GI tract. GU and biliary tracts entered c local infxn present.
Wound due to trauma
Major break sterile technique Dirty (infxn 30-35%)
Wound due to distant trauma. With dead tissue.
Infxn or perf viscera before procedure.

Question 15

Prof Abx

Answer 15

Given perioperative period to combat bacterial contamination of tissues that occur during operative period
Operation must carry significant risk postoperative infxn Clean-contaminated procedure where nonsterile area entered Contaminated procedures
Implantation of prosthesis
Given 1-2 hours before surgery and only 6-24 hours after surgery (prevent superinfection)

Question 16

4. How does a post-op PE present? What is in the differential? What are the appropriate prophylaxis for DVT and PE? What is the treatment algorithm for PE? What predisposes to DVT and PE?

Answer 16

A. PE: Clinical presentation
PULM: SOB, tachypnea, cough, hemoptysis with pulmonary infarct, pleuritic chest pain CV: hypotension, tachycardia, loud pulmonic component of S2
HEME/ID: Fever, occasionally
NEURO: syncope seen in large PE
Note:
Think MI in patient with CV risk factors who develops CP/SOB in POD 1-2 Think PE in patient who develops CP/SOB in POD 5
B. Differentials
Cardiac ischemia, MI, pericarditis, aortic dissection Respiratory infection ie. PNA, pleuritis
Acute lung injury ie. pneumothorax
C. DVT/PE prophylaxis
Low molecular weight heparin (Lovenox) 40 mg SQ QD or 30 mg SQ BID Heparin SQ q 8 hr (started pre-op)
Sequential compression devices, SCD, (started in OR)
Early ambulation
D. Treatment algorithm
Supplemental oxygen to correct hypoxia
Start anticoagulation therapy (unfractionated or LMWH) immediately on basis of clinical suspicion
o Give one bolus followed by continuous infusion 5-10 days
o Goal: aPTT = 1.5-2.5 times normal Long term treatment: warfarin
o Therapeutic INR 2-3
o Continue treatment for 3-6 mo.
IVC filters for patients who develop recurrent PE, complications, or have contraindications to anticoagulation Stable patient: anticoagulation (heparin followed by warfarin 3-6 mo.)
Unstable patient: consider thrombolytic therapy (streptokinase, TPA), trendelenburg operation (pulmonary artery embolectomy), catheter suction embolectomy
E. Predisposition
Injury: postoperative status, multiple trauma, paralysis, immobility
Comorbidities: CHF, MI, Cancer
Hematology: Polycythemia, HIT syndrome, Hypercoagulable state (protein C/S deficiency) Demographic/lifestyle: Obesity, birth control pills/tamoxifen, advanced age

Question 17

How to assess someone’s cardiac risk before a major operation? What can you do to minimize risks?

Answer 17

1) urgent
2) coronary revasc in past 5 yrs
3) cardiac eval in past 2 yrs?
4) unstable coronary syndromes?
5) intermediate predictor of risk
6) intermediate with high or moderate fxn–> ok; low to moderate fun could need noninvasive testing
7) intervention usually occurs if mortality is less than planned surgery

Question 18

How do you make a diagnosis of cardiogenic vs. hypovolemic shock post-op, and what are the treatments?

Answer 18

Hypovolemic shock –
o Cause: Hemorrhage, burn, SBO
o Most common sign: Thachycardia
o Other signs: hypoten, diaphoresis, vasoconst
o Tx:
IVF 2L of LR: Responders, transient responders (slow bleed), non-responders (bleeding out)
Stop bleeding if needed (L,R chest, abdo, pevis, multiple long bone, from external wounds)
NOT from cranial hemorrhage
Cardiogenic Shock – LV failure in most cases
o Cause: MI, CHF, tamponade, Tension PT, valve failure
o sign: inc CVP/PCWP, dec CO, dec UOP, tachy
o Tx: diuretics +/- pressers

Question 19

6. What are the signs and symptoms of SBO? What are the typical x-rays findings? What are the initial treatments? What would prompt you to operate? How do you assess small bowel viability at laparotomy (or laparoscopy)?

Answer 19

3 major cause: Adhesion (most common, prior Sx), Cancer/tumor, Hernia
Signs/symp: abdo discomfort/pain, n/v, +/- flatus/BM (distal to obstruction can still produce flatus/BM), high-pitch BS KUB: distended loops proximal to obstruction, air-fluid levels.
Initial Tx: NPO, NGT, IVF, Foley
o Emergent Sx: Complete obstruction, ischemia (acidosis), perforation (free air in KUB, peritoneal signs); more emergent if inc WBC, fever, pain, tachy, shock
Viability assessment: Doppler c ultrasonic flow (good), clinical judgment (better), Fluorescien fluorescence (best)

Question 20

60 y/o m 3 d hx n/v and abd distention. No bm or flatus during this period. Additional Hx and Ddx.

Answer 20

Additional hx you want: prior surg, poss malig (changes bowel habits, blood in stool, change in stool, abd pain, weight loss, prior episodes, hernias)
Thinking ileus vs bowel obstruction

Question 21

SBO: During procedure see adhesive band incarcerating loop of small intestine, you lyse adhesions and
there’s 4cm small bowel that appears mildly purple and swollen- how to proceed?

Answer 21

Viable or nonviable bowel? Peristalsis, palpate mesentery and see if good blood flow, doppler mesentery, fluorescein and woodslamp in OR (IV medication- bowel under woodslamp will light up green if viable and not viable then that part of bowel won’t pick it up and rest of bowel will). If not viable, resect and do primary anastamosis (always for small bowel, worry about for colon; small bowel bac content a lot smaller).

Question 22

What is the differential diagnosis of RLQ pain in a young woman? How do you diagnose acute appendicitis by CT scan? What do you do if the appendix is normal at laparoscopy? What if there is a large periappendiceal abscess?

Answer 22

DDx: Appendicitis (most common for M & F), mittelschmerz, pregnancy, mesenteric LAD, cecal/Meckel’s diverticulitis, ectopic preg, ovarian cyst, PID, TOA, ovarian torsion, CA, nephrolithiasis, bowel ischemia
CT findings: Periappendiceal fat stranding and fluid, diameter >6mm, fecalith.
If normal in OR – still take it out
Steps of LAP APPY (3rd year level)
1. ID appendix
2. Staple/coag mesoappendix
3. Staple and transect appendix at the base (or use Endoloop® and cut between)
4. Remove appendix from abdomen
5. Irrigate and aspirate till clear
Periappendiceal abcess Tx: Percutaneous image-guided drainage, IV Abx, elective appy 6-8 wks later.

Question 23

Signs of appendicitis

Answer 23

Guarding, rebound, tenderness beginning at the umbilicus and localizing at McBurney’s point (one-third of the distance from ASIS and umbilicus, + iliopsoas sign (flex hip and leg raise against pressure), +obturator sign (flex leg at hip and rotate leg laterally and medially), +Rovsing (pain in RLQ intensified by palpating LLQ), +Aarons sign (cardiothoracic pain when McBurney’s point is palpated)

Question 24

8. What are the signs and symptoms of diverticulitis? What are the findings on labs and CT scans? When do you treat it non-operatively? What are the indications for surgical intervention? What is the common surgical procedure for acute perforated diverticulitis?

Answer 24

Signs/symp: LLQ pain, Δ BM (DIARRHEA), f/c, n/v, dysuria, anorexia
Lab/CT: inc WBC, swollen edematous bowel wall, NO ENEMA OR COLONOSCOPY
Non-operative Tx: IVF, NPO, broad-spectrum Abx (anaerobic coverage) NGT,
Indication for Sx: obstruction, fistulas, perforation, sepsis, refractory to medical treatment, inaccessible abscess for percutaneous drainage
o Hartman’s procedure:
Resection of involved segment endcolostomy and rectal stump Subsequent reanastomosis of colon if possible in 2-3 months

Question 25

59 y/o m LLQ pain, f, diarrhea, happened before and hosp c antibiotics

Answer 25

DDx: diverticulitis
Imaging: CT, KUB
Labs: CBC, Renal, UA
Primary tx for noncomplicated: conservative management (IVF, abx)
Tx for complicated c intraabdominal abscess: Percutaneous drain and resect when infxn clears Complications of diverticulitis: Perf, fistulas or obstruction
To OR immediately if perf- signs of sepsis/hypotension, obstruction
Surgery for perf diverticulitis c significant spillage: Resection and Hartman’s (no anastomosis), or
primary anastamosis and divert with a loop (resect bowel, give them loop ileostomy)

Question 26

9. What is your differential for large bowel obstruction? What is the initial treatment? How do make a diagnosis? What is the right operation?

Answer 26

Background
- Large bowel obstruction classified as mechanical or pseudo-obstruction
o Mechanical causes:
Colorectal CA most common cause
Inflammation
Diverticulitis, Crohn’s
Adhesions (most common cause for small bowel obstruction, but rarely causes large bowel
obstruction)
Hernias
Volvulus o Pseudo-obstruction
Primary–motilitydisorder
Secondary–associatedwithneurolepticdrugs,opiates,metabolicillnesses,diabetes,
hyperparathyroidism, lupus, scleroderma, Parkinson’s
- Clinical presentation:
o Abdominal distention, cramping abdominal pain, nausea and vomiting, obstipation
b. Large bowel obstruction DDx
- abdominal hernia
- diverticulitis
- colonic polyps
- pseudomembranous colitis
- toxic megacolon
- small bowel obstruction
- colon cancer
- ileus
c. Initial treatment
- All patients should be treated with IV fluids, nasogastric suction, continuous observation until diagnosis is
established
- for pseudo-obstruction:
o nasogastric decompression
o fluids
o correction of electrolyte abnormalities
o discontinue all medications that inhibit bowel motility such as opiates
d. Diagnosing large bowel obstruction
- History and physical examination provide important clues. Abdomen should be palpated for masses, groins
inspected for hernias, and a digital rectal exam performed to exclude rectal cancer.
o Physical exam usually shows abdominal distention, tympany, high-pitched metallic rushes, and gurgles.
Palpation may reveal localized, tender, palpable mass that may indicate a strangulated closed loop or an
area of inflamed diverticular disease.
- Plain films of abdomen provide considerable information concerning location of obstruction.
- Barium enema confirms diagnosis of colonic obstruction and identifies exact location
o If plain film shows the obstruction, barium enema is not necessary
o Barium should never be given orally in the presence of suspected colonic obstruction because it may
accumulate proximal to the obstruction and cause a barium impaction - If pseudo-obstruction is suspected, colonoscopic exam may be used.
e. Operation
- patients with complete (rather than partial) bowel obstruction should undergo emergent operation
- emergency laparotomy is undertaken for acute large bowel obstruction with cecal distention beyond 12cm, severe
tenderness, peritonitis, or generalized sepsis

Question 27

Consider post-op complications after colon resection: How does wound dehiscence present? Why would someone have profuse diarrhea after colectomy? How do you stage colon cancer?

Answer 27

if cause of obstruction is cancer of distal or mid-rectum:
o loop colostomy and then neoadjuvant chemoradiation, with plan to resect the primary lesion at a later time
- if obstructing cancer is in sigmoid colon, options are:
o Hartmann’s operation (sigmoidectomy with descending colostomy and closure of rectal stump) o Sigmoidectomy with primary colorectal anastomosis
o Abdominal colectomy with ileorectal anastomosis
- for pseudo-obstruction: fiberoptic colonoscopy with decompression and placement of rectal decompression tube
- right-sided colonic obstruction, whether caused by cancer or volvulus, is generally treated by resection and
primary anastomosis of ileum and transverse colon
f. Post-op complications
- Wound infection
- Small bowel obstruction
- Diarrhea
- incontinence
- post-op ileus (due to leakage from anastomosis) or mechanical obstruction (due to adhesions, internal hernia, or
obstructed anastomosis)
o This causes failure to propel food and secretions distally, leading to bacterial overgrowth in the stomach
and proximal small bowel feculent vomiting - Anastomotic leak
o May cause post-op ileus
o May also cause wound infection that spontaneously drains to the skin - Obstruction of anastomosis
o Causes fistula formation - Abscess
g. Dehiscence presentation
- In 25% of patients, dehiscence is preceded by a sudden, dramatic drainage of a relatively large volume of clear,
salmon-colored fluid
- Ripping sensation
h. Profuse diarrhea after colectomy
- Normally, 1 to 1.5L or fluid enters the colon from the small intestine. It takes time for small intestine to adapt
after resecting colon. Adaptation eventually results in decrease in flow from the small intestine. i. Staging of colon CA
- Staging of colon CA is based on depth of invasion of the primary lesion, presence of regional lymph nodes, and distant metastasis. The TNM system of staging is as follows:
o Stage 0 = Tis, N0, M0
Tumorislimitedtomucosa(insitu)
o StageI = T1/T2,N0,M0
Tumor is limited to mucosa and submucosa (T1) OR deeper into, but not beyond, the
muscularis propria (T2)
Noregionallymphnodeinvolvement
Nometastasis
>90%5-yearsurvival
o StageII= T3/T4,N0,M0
Tumor extends through the full thickness of the bowel wall (T3) OR into adjacent structures
(T4)
Noregionallymphnodeinvolvement
Nometastasis
60-80%5-yearsurvival
o StageIII=AnyT,N1/N2/N3,M0
Tumor has metastasized to regional lymph nodes at various levels 20-50%5-yearsurvival
o StageIV=AnyT,AnyN,M1
Presenceofliverorotherdistantmetastasis

Question 28

75 y/o f presents c 3 day hx diffuse abd pain and constipation. 3-way of abd show air-fluid levels.

Answer 28

Hx: Change in bm, hx hysterectomy, bloody stools, last colonoscopy, pain hx, past surgeries DDx: SBO (2/2 adhesions, volvulus, hernias), ileus, cancer, diverticulitis
Labs: CBC, renal, CEA, CA19-9, UA, LFTs

Question 29

CT shows mass in descending colon causing obstruction c no liver mets. Plan?

Answer 29

Colonoscopy, bx If colon cancer
IVF, NGT, plan for OR resection
POD #3 develops rush of serous fluid- likely cause and tx:
Dehiscence, go back to OR
POD #7 spikes f c diarrhea- what tests: CBC, C diff, CT abd
(look for abscess)
CT shows multiple intraloop abscesses- need to go OR for
washout (if only 1 can drain it, if multiple can’t perc drain it)

Question 30

10. What is the presentation for colonic volvulus? How do you make the diagnosis? What are the initial treatments? What is the definitive treatment?

Answer 30

Clinical presentation of colonic volvulus
- Abdominal distention, vomiting, abdominal pain, obstipation, tachypnea
- Physical exam shows distention, tympany, high-pitched tinkling sounds and rushes
- patients confined to mental institutions or nursing homes have increased risk
b. Diagnosing volvulus
- abdominal radiographs show a massively dilated cecum or sigmoid without haustra that often assumes a kidney
bean appearance
- barium enema shows exact site of obstruction, with a characteristic funnel-like narrowing often resembling a
bird’s beak
c. Initial treatment
- hydration is necessary
- electrolytes, CBC, abdominal obstructive radiographic series needed to rule out obstruction or other abdominal
pathology
- In stable patients, it is often possible to “detorse” the sigmoid colon by rigid proctosigmoidoscopy and placement
of a rectal tube.
o If endoscopic management is unsuccessful, urgent laparatomy is required. Recurrence rate is
approximately 30%. d. Definitive treatment
- Definitive treatment is either sigmoid colectomy with diverting colostomy OR resection with primary anastomosis – depending on the preoperative condition of the patient
- For cecal volvulus: cecopexy (suturing the cecum to the parietal peritoneum) or right hemicolectomy with ileotransverse colostomy

Question 31

85 y/o f debilitated in nursing home dev abd distention c constipation, n/v

Answer 31

DDx: obstruction, volvulus, colon cancer, diverticulitis, SBO, perf viscus
Labs: CBC, comprehensive metabolic panel, CEA, lactic acid (if dead bowel)
Imaging: CT, plain film
If sigmoid volvulus if can’t do CT- do barium enema
If no signs ischemic bowel at presentation before OR- tx: undo sigmoid volvulus by barium enema (not
so much for adults as for children), do sigmoidoscopy (colonic decompression c sigmoidscope c
rectal tube). Definitive tx for volvulus is sigmoid resection.
If presents c intrabdominal abscess at time of operation, the operation you will perform is
sigmoidectomy c Hartmann’s pouch.
If pt stable and in OR see viable sigmoid after undoing volvulus, do sigmoid resection c primary
anastomosis (don’t have to divert bc not perf; trauma literature states that can do primary anatasmosis on colon inj if

Question 32

11. What is the initial treatment for GERD? If refractory, how do you work up the patient for possible surgery? What is the standard operation? What are the complications of GERD? What alternative operation is appropriate if there is also an esophageal motility disorder?

Answer 32

Initial treatment for GERD - double dose of PPI
o this also serves as a diagnostic tool: more extensive evaluation necessary if symptoms persist after a trial of medical therapy
- other medications available include:
o antacids, motility agents, H2 blockers,
b. Refractory GERD workup
- pH monitoring (24-hour pH test) – gold standard for diagnosing and quantifying acid reflux
- endoscopy
- manometry – rules out primary motility disorders such as achalasia
- esophagography
c. Standard operation
- Total fundoplication (360-degree wrap)
o gastric fundus is wrapped around the lower end of the esophagus and then sutured to reinforce the function of the lower esophageal sphincter
o whenever stomach contracts, it also closes off the esophagus instead of squeezing gastric acids into it.
d. GERD complications
- Barrett’s esophagus (esophageal mucosa changes from squamous epithelium to columnar)
- Shortened esophagus as a result of repeated injury
- Extraesophageal symptoms: hoarseness, laryngitis, cough, wheezing, aspiration
e. Alternative operation if there is esophageal motility disorder
- partial fundoplication

Question 33

12. What is the initial treatment for lower GI bleed? What is your differential? How do you localize the bleed and make a diagnosis? What is the indication for surgery? What is the extent of standard colon resections?

Answer 33

Initial treatment for lower GI bleed
- Resuscitation first (e.g. transfusion)
- Endoscopic control (e.g. endoscopic clip placement, cautery)
- Angiographic control (e.g. intra-arterial injection with vasoconstrictors)
b. DDx
- hemorrhoids
- colonic polyps
colon cancer
- rectal cancer
- bowel obstruction
- inflammatory bowel disease (Crohn’s, Ulcerative colitis)
- diverticulitis
- AV malformation (angiodysplasia)
- Mesenteric ischemia
- Meckel’s diverticulum
- trauma
c. Localizing bleed
- Colonoscopy is mainstay
- Adjuncts to colonoscopy:
o tagged RBC scan – most sensitive but least accurate o angiography
o push enteroscopy
d. Diagnosis
- rule out upper GI bleed by NGT aspirate or EGD
- colonoscopy for minor bleeding
- for major bleeding:
o if stable: tagged RBC scan
o if unstable:
e. Indications for surgery
- hymodynamic instability despite vigorous resuscitation (>6 units transfusion)
- failure of endoscopic techniques to arrest hemorrhage
- recent hemorrhage after initial stabilization (with up to 2 attempts at obtaining endoscopic hemostasis)
- shock associated with recurrent hemorrhage
- continued slow bleeding with a transfusion requirement >3U/day
f. Extent of standard colon resections
o for cancer: need histologically cancer-free margin at the distal extent of the resection. Minimum of
10cm of grossly normal bowel on both sides of the tumor is required to keep the risk
o for inflammatory bowel disease: need to evaluate the extent of pericolic inflammation first

Question 34

13. How do you approach a baby with non-bilious vomiting? What is the likely diagnosis? What is the likely acid/base electrolyte abnormality? What renal compensatory mechanism takes place if the vomiting is more than a week?

Answer 34

Hypertrophic Pyloric Stenosis
- Common between ages 2 and 8 weeks
- Boys affected 4x as often than girls, 1st born male highest risk
- Hypertrophy of the circular muscle of the pylorus results in constriction and obstruction of the gastric outlet, leading to
nonbilious, projectile emesis, loss of hydrochloric acid with the onset of hypokalemic hypochloremic metabolic
alkalosis, and dehydration.
- Clinical Presentation: progressively worsening nonbilious emesis and with time, emesis becomes more frequent,
forceful, and projectile in nature.
- Diagnosis: Palpation of the pyloric tumor (olive-shaped) in the epigastrium or right upper quadrant is pathognomonic
o A plain abdominal radiograph shows an upper abdominal gas bubble in the stomach
o When the olive is nonpalpable, the diagnosis of HPS can be made by ultrasound. A persistent pyloric muscle
thickness more than 3 to 4 mm or a pyloric length more than 15 to 18 mm in the presence of functional
gastric outlet obstruction is generally considered diagnostic
o With equivocal clinical history, an upper GI contrast study is useful to evaluate for other causes of vomiting.
- Renal compensatory mechanism:
o Vomiting/loss of gastric acid hypochloremia impairs kidneys’ ability to excrete bicarbonate. o Hypovolemia hyperaldosteronism retention of Na and excretion of increased amounts of K
hypochloremic, hypokalemic metabolic alkalosis.
o Body compensates to metabolic alkalosis by hypoventilation resulting in elevated PaCO2
- Tx: Pyloromyotomy

Question 35

What is the differential diagnosis of bilious vomiting in a new born?

Answer 35

Bilious Vomiting in a Newborn DDx:
- Duodenal Atresia
o Associated with Down Syndrome
o Presents a few hours after birth
o Findings: Abdominal film, “double bubble” sign - Malrotation with V olvulus
o Incomplete bowel rotation during 7th -12th weeks of gestation
o Presents at 3-7 days, rapid deterioration with volvulus
o Findings: UGI spiral sign on ultrasound; abnormal location of superior mesenteric vessels
- Jejunoileal Atresia
o Mesenteric vascular accident during fetal life o Presents within 24 hours of birth
o Findings: Air fluid levels on abdominal film
- Meconium Ileus
o Genetic, 15% of newborns with cystic fibrosis
o Presents immediately after birth
o Findings: abdominal film; distension, air-fluid levels, sweat test, “ground glass” sign
- Necrotizing Ileus
o Presents 10-12 days after birth
o Findings: Abdominal film; distension, pneumatosis, air in the aortal vein

Question 36

14. What is the differential diagnosis of acute epigastric pain? What are the findings of perforate duodenal ulcer? What is your therapy? In a stable patient with chronic DU, what are the indications for ulcer surgery, and what operations are available?

Answer 36

Differential Dx of Acute Epigastric Pain
- Cardiac: MI, pericarditis, myocarditis
- Gastric: esophagitis, GERD, gastritis, peptic ulcer
- Biliary: cholecystitis, cholelithiasis, cholangitis
- Pancreatic: mass, pancreatitis
- V ascular: aortic dissection, mesenteric ischemia
Perforated Duodenal Ulcer
- Sudden onset, frequently severe epigastric pain; localized peritoneal signs
- Free air in CXR
- Usually in 1st portion of duodenum
- Tx: Emergent surgical intervention
o If smaller than 1cm: close primarily and buttressed with well-vascularized omentum
o Larger perf: Graham patch repair with a tongue of healthy omentum
o Very large perf greater than 3 cm: close with application of healthy tissue like omentum or jejunal serosa,
with placement of a duodenostomy tube and wide drainage Or antrectomy and Bilroth II reconstruction
- Stable patient with chronic DU indications for ulcer surgery:
o Elective operative intervention has become rare as medical therapy has become more effective. o Indications for ulcer surgery:
Intolerant of medications or do not comply with medication regime
High risk of complications (ex: transplant recipients, pt dependent on steroids or NSAIDs)
H.pyloricannotbeeradicated
Pt with large ulcers that fail to heal with adequate treatment
o Options:
Truncal V agotomy
TruncalVagotomyandAntrectomywithgastroduodenostomy(BilrothI)orgastrojejunostomy (Bilroth II)
SelectiveVagotomy:preservingthehepaticandceliacbranchesofthevagus
Highly selective vagotomy: division of only the gastric branches of the vagus, preserving Latarjet’s
nerve to the pylorus
Partialgastrectomy

Question 37

15. What are the initial treatments for exacerbation of ulcerative colitis? How is UC different from Crohn’s? What is the long term complication of UC and what do you recommend? With what other pathologic entities do you recommend prophylactic colectomy?

Answer 37

Ulcerative Colitis
- Initial Treatments:
o Aminosalicylates
Most common therapy for mild to moderate UC
Sulfasalazine,5-ASA,Mesalamine o Corticosteroids
ForactiveUC
o Immunomodulatory medication
ForlongtermmanagementofUC
6-Mercaptopurine,Azathioprine,Cyclosporine,Infliximab
See UC Vs Crohn’s comparison chart
UC Long term complications:
o Fulminant colitis and toxic megacolon o Massive bleeding
o Dysplasia or Carcinoma
- UC Recommendation
o Prophylactic colectomy
Total proctocolectomy with ileostomy; Segmental colectomy has been shown to be inadequate for controlling disease, Recommended in:
Inflammatory Bowel Disease Polyposis syndromes
Lynch syndrome
High risk for development of CRC

Question 38

16. What are the common presentations of an inguinal hernia? What is the anatomy of this region? What are the complications of inguinal hernia repair?

Answer 38

Common presentations of Inguinal Hernia
- Aching in groin, may radiate to area of hernia
- Pain in medial thigh (femoral hernia)
- If strangulated/ incarcerated:
o Increased pain
o Increased size
o No reduction in size with recumbency o Fever
o N/V
o Severe constipation
- Palpable and/or visible lump in groin
- Lump decreases in size with recumbency, increases in size with standing and with increased intra-abdominal pressure
(ex: Valsalva)
- If strangulated/ incarcerated:
o Irreducible
o Tenderness
o Abd distention
o Tympany
o Hyperperistalsis early but with advancing peritonitis BS may be absent o Erythema of skin overlying it
Inguinal Canal
- Oblique space, 4 cm in length
- Lies above medial half of the inguinal ligament
- Beneath EO aponeurosis, between:
o External/ Superficial Inguinal Ring
MedialopeninginEOapnoneurosis
Liesaboveandlateraltothepubiccrest
o Internal/ Deep Inguinal Ring Lateralend
Opening within the transversalis fascia lateral to inferior epigastrics
- Males:
o spermatic cord
o Cremasteric muscle fibers
o Testicular artery and veins
o Genital branch of genitofemoral nerve o Vas deferens
o Cremasteric vessels
o Lymphatics
o Processus vaginalis
- Females:
o round ligament of the uterus
- Boundaries
o Anterior/superficial:
EO fascia with contribution of IO fascia in lateral 1/3 o Posterior:
fusion of the transversalis fascia and transversus abdominis fascia o Inferior/ floor:
inguinalligament o Superior/ roof:
arch formed by IO and transversus abdominis (Conjoint Tendon) o Think of it as a cylinder!
- Hesselback’s Triangle – margins of the floor of the IC
Superolateral: inferior epigastrics o Medial: rectus sheath
o Inferior: Inguinal ligament
Complications of Hernia Repair
- Infection
- Recurrence 1.7-10%
o Tension free repairs have a lower rate of recurrence than tissure repairs o 50% of recurrences are found within 3 years after primary repair

Question 39

17. How do you work up a patient with a bleeding problem? What are some common coagulation factor disorders and platelet disorders? How do you make a diagnosis of ITP? What are the initial treatments, and when is surgery indicated? What are the complications of splenectomy?

Answer 39

Bleeding Disorders and ITP
Approach to patient with bleeding diathesis-
History- bleeding disorders- menorrhagia, epistaxis, bleeding after dental procedures, family history of abnormal bleeding, medication use.
Physical- pallor and additional signs of anemia, petechiae, ecchymosis
Laboratory Evaluation- platelet count (quantitative not qualitative), bleeding time (measures platelet function), coagulation studies- PT (extrinsic pathway), PTT (intrinsic pathway), INR, factor deficiency tests (vwd, hemophilia), fibrinolysis tests, fibrinogen levels, ristocetin aggregation studies (causes vwf to bind to gp1b- fixed with addition of vwf with VWD, not with Bernard Soulier)
Common Bleeding Disorders- refer to page 387 of FA2012
21
ITP
Coagulation disorders (macrohemorrhages, hemarthrosis, easy bruising, elecated PTT, PT)- Hemophilia A, B (Christmas Disease), Vitamin K Deficiency
Platelet Disorders (microhemorrhage- mucous membrane bleedin, epistaxis, petechiae, purpura, increased bleeding time and decreased platelet count)- Bernard-Soulier (GP1b defect- defect in platelet to collagen adhesion), Glanzmann’s thrombasthenia (GP2b3a defect- defect in platelet to platelet aggregation- low clumping on blood smear), ITP (discussed below), TTP (deficiency of ADAMTS13- a vwf metalloproteinase causing a decreased degradation of VWF multimers- get increased platelet aggregation and thrombosis- see schistocytes (MAHA) and increased LDH- pentad of symptoms- neurological deficits fever, hemolytic anemia, thrombocytopenia, renal symtpoms)
Decreased platelet survival due to premature destruction by antibodies (often against GPIIB/IIIa). Labs show increased megakaryocytes.
Initial treatment with glucocorticoids – dexamethasone, methylprednisone
Treatment with IV immunoglobulin (IVIG) which blocks macrophage Fc receptors
Second line- Splenectomy if medical management fails (unresponsive to steroids or requiring chronic treatment- over 1 year). Complications include: overwhelming sepsis from encapsulated bacterial infection (must be immunized for S. pneumo, H. influenza, and N. meningitides), arterial and venous thrombosis, increased risk of cardiac events, increased risk of pulmonary hypertension
Rituximab (anti-CD20) is another second line therapy

Question 40

18. What do you look for in someone with a necrotizing soft tissue infection? What are the initial treatments? What antibiotics? Likely organisms?

Answer 40

Etiology
A spectrum of infections diseases result in necrosis of skin and soft tissue. These NI include clostridial infections, which are rare, or necrotizing soft tissue infections of various types, which are more common. The broad categories within the latter group include necrotizing fasciitis, bacterial synergistic gangrene, and streptococcal gangrene.
The bacteriology of the various disease processes included in the infectious gangrenes is complex. The majority of NIs resulting in necrotizing fasciitis consist of a mixture of β-hemolytic streptococci (90%), anaerobic Gram-positive cocci, aerobic Gram-negative bacilli, and Bacteroides species. A single organism, with the unusual exception of Group A β- hemolytic streptococci (GAS), rarely causes an infection resulting in necrotizing fasciitis.
Bacterial synergistic gangrene is primarily a subcutaneous gangrenous infection caused by the same organisms as those that cause necrotizing fasciitis, but there is no involvement of any fascial tissue. Classically, cultures yield the combination of a microaerophilic nonhemolytic streptococcus in the spreading periphery of the lesion and Staphylococcus aureus found in the zone of gangrene. Streptococci can be accompanied by a variety of other organisms, such as Proteus, Enterobacter, Pseudomonas, and Clostridium species. Streptolysin S-producing strain of Group G hemolytic streptococci recently was reported to produce NI.
Clostridial and mycotic infections must be considered in any initial evaluation of skin and soft tissue NIs, despite their relatively rare occurrence. Clostridial infections should be suspected when necrotic muscle is found during debridement of an infectious gangrene with severe systemic toxicity associated with clinical central nervous system manifestations. Patients with malignancies are particularly prone to NIs caused by Clostridium septicum
Predisposing events include: mild trauma, insect bites, drug reactions, illicit drug injections, perirectal abscesses, major traumas, and surgical procedures. Some may occur without an inciting event or portal of entry.
The frequent association of soft tissue NIs with underlying chronic diseases such as diabetes mellitus, hypertension, congestive heart failure, obesity, renal insufficiency, cancer, malnutrition, arteriosclerosis, alcoholism, autoimmune disease, acquired immunodeficiency syndrome, and immunosuppression, as well as with patients older than 60 years of age, is diagnostically helpful.
Signs: elevated WBC, hypoNa, inc BUN, hypoCa,prot, alb
elevated glucose
Diagnosis
Often presents as mild cellulitis or ulcer. Spontaneous gangrenous infection often on perineum but most often occurs on the extremities. Neither clostridial nor nonclostridial infections initially demonstrate prominent external evidence of skin death.
Severe pain and systemic symptoms that occur out of proportion to the local infection characterize clostridial infections. As the clostridial infection progresses, the skin may develop a bronze color, followed by hemorrhagic bullae, then dermal gangrene, and finally crepitus. Clostridial exotoxins produce extensive tissue necrosis, with minimal hyperemia, fibrin formation, or neutrophil infiltration seen within the affected tissue.
Nonclostridial infections are most likely to be associated with erythema, pain, and swelling but frequently are initially identical to simple cellulitis. Failure to respond to antibiotics, rapid progression, or evolving systemic signs of infection are significant clues that NI may be present.
The patient generally appears ill and has a rapid pulse and significant temperature elevation. An occasional unique finding of necrotizing fasciitis is numbness of the involved area. Skin anesthesia probably is due to infarction of the cutaneous nerves located in necrotic subcutaneous fascia and soft tissue. Some patients with necrotizing fasciitis may present with localized pain of the involved site, and the overlying skin is erythematous, hot, and edematous.
TMT: H&P, WBC Ca lytes, XR
consult with ID and surg
Gram’s stain
central line and foley
fluids, cardio, preop check
IV Abx, tetanus
Surgical debridement –> amputation
post op nutrition and physical therapy

Question 41

Abe for clostridium nec fasc

Answer 41

Penicillin or ampicillin for clostridia, streptococci, and Peptostreptococcus.
Clindamycin or metronidazolefor anaerobes, Bacteroides fragilis, Fusobacterium, and Peptostreptococcus. Clindamycin may be useful for treating GAS in patients with the toxic
streptococcus syndrome because it inhibits toxin production.
Gentamicinor another aminoglycoside for Enterobacteriaceae (ie, Gram-negative organisms).
Gentamicin has a synergistic effect with penicillin against streptococci.
Imipenem and meropenem by virtue of their high β-lactamase resistance, wide-spectrum efficacy, and inhibition of endotoxin release from aerobic (ie, Gram-negative) bacilli, may be the initial agents of choice for treatment of the frequent polymicrobial infections that result in necrosis or skin and soft tissue. Postoperative antibiotic coverage is adjusted on the basis of microbiologic testing results from cultures of tissue and blood

Question 42

45 y/o m intense pain medial thigh over past 24 hrs.

Answer 42

Hx: OLD CARTS for pain, trauma, exposure/break in skin, drug use, DM, HIV status
DDx: Infxn- cellulitis, necrotizing fasciitis, compartment syndrome
PE: VS (can be septic shock bc of infxn- need to know if hypotensive or tachycardic). If soft tissue infxn
look for erythema, induration, fluctuance, edema. ROM. Sensation. Neurovascular.
Dx tests: Blood cx, CBC, renal panel, CT or plain film (look for air)
Tx: For necrotizing skin infxn- IVF, resus, abx, foley.
Likely microbes for necrotizing soft tissue infxn: polymicrobial (GPC, GNB, anaerobes- staph, strep,
Clostridium, Pasturella, Sporothrix)
Discuss role of hyperbaric oxygen in recovery after debridement
Wounds that fail to heal are usually hypoxic. Wound healing process affected by O2 concentration/gradients. Angiogenesis occurs in response to high O2. Fibroblast proliferation and collagen synthesis are O2 dependent (collagen is the foundational matrix for angiogenesis). HBOT also likely stimulates growth factors in angiogenesis. HBOT also shown to have antimicrobial activity (increases intracellular leukocyte killing).
Options to close wounds after recovery
Primary intention
Clean and clean-contaminated All layers closed
Secondary intention Infected wounds
Deep layers closed, subcutaneous and skin left open Wound care consists multiple dressing changes per day c
wound irrigation, packing and sterile dressings Open portion granulates and re-epithelializes
Delayed primary Contaminated
Deep layers closed while subcutaneous and skin open and packed
Skin graft Block coverage

Question 43

19. How do you work up someone with a suspicious skin lesion? What features of the lesion would make you suspect a malignancy? How do you classify a cutaneous melanoma? What is the surgical treatment? How do you deal with lymph nodes and metastasis?

Answer 43

Presentation
History- family history of skin cancer, personal history, sun exposure, irregular moles
Whole body physical, exam nevi for ABCDEs. Asymmetry, irregular Borders, Color change (to dark black or blue), Diameter greater than 6mm, Evolution. Also do a lymph node examination
DDX- BCC, SCC, dysplastic nevus, pigmented actinic keratosis, metastatic tumors to the skin, histiocytoid hemangioma, spindle and epithelioid nevus, etc
Workup for malignant melanoma
CMP- AST, ALT (liver mets), ALP (bone or liver mets), creatinine (baseline before chemo which is often nephrotoxic), total protein and albumin (measure of overall health and nutrition)
LDH (measure of distant metastases, part of staging, poor prognosis)
CXR/CT of lungs for metastasis
MRI of brain in patients with evidence of distant metastases (esp if on IL-2 therapy)
PET Scans (not indicated for stages I and II)- good for patients with known nodal involvement or satellite migration Biopsy of suggested lesion- excisional, with 1-2cm margins.
Surgical excision or re-excision after biopsy- (if not done, associated with a 40% chance of local recurrence)- based on thickness. Less than 1mm, 1cm margins, 1-4mm, 2cm margins, greater than 4mm- greater than 2cm (usually 3cm). Elective lymph node dissection (ELND)- found only to be useful in patients with thickness 1.2-2mm
Sentinel lymph node dissection- currently recommended for those patients with intermediate Breslow thickness (1- 4mm). Complete lymph node dissection (CLND) is recommended for all patients with positive SLND
Histologic findings of melanoma: cellular atypia, pleomorphic nuclei, enlarged nucleoli, pagetoid upward growth of melanocytes no longer confined to the basal layer, positive stains for S-100 (highly sensitive, not specific) and HMB45 (higher specificity).
Classification
Superficial spreading (most common type, prolonged radial growth phase)
Nodular sclerosis (second mot common, aggressive vertical growth phase, poorer prognosis)
Lentigo maligna- long radial growth phase and good prognosis
Acral lentigious melanoma (common in African Americans, Asians, and Hispanics) and appears primarily on palms and soles. Aggressive vertical growth phase, poor prognosis.
Treatment
Surgical excision and lymph node dissection as discussed above
Pharmacologic treatment includes interferon 2a for stage III disease and IL-2 for metastatic melanoma (stage IV) CTLA4 blocker Iplimumab for stage IV

Question 44

What are the stages of skin cancer?

Answer 44

1A: ≤0.1 mm no ulceration, no node, no mets
1B: ≤0.1 mm w/ ulceration, 1-2 mm no ulceration, no node no mets
2A: 1-2 mm with ulceration, 2-4 mm w/o ulceration, no mets, no node
2B: 2-4 mm w/ ulceration, >4mm w/o ulceration, no node, no mets
2C: >4 mm w/ ulceration, no node, no mets
3A: any thickness, 1-3 + nodes, micromets
3B: any thickness 1-3 +nodes, macromets,
3C: any thickness 1-3 + nodes + ulceration, macromets
4: distant mets

Question 45

65 y/o m black skin lesion upper back

Answer 45

HPI: How long, changing (size, color, shape), sun exposure, presence other nevi, FHx Detailed description of lesion: ABCDE, look at LNs and other part of body
Do not observe this lesion- excisional unless huge then do incisional bx
Know Clark and Breslow
Clark
Based on level of invasion of dermal layers
Breslow
Based on depth of invasion, which is vertical height of
melanoma from granular layer to area of deepest
penetration
Histological types matter- explain
Superficial spreading Most common
Long radial growth phase, delayed vertical growth phase
Favorable prognosis Nodular sclerosis
Second most common
No radial, aggressive vertical, spreads quickly Poorer prognosis
Lentigo maligna Long radial
Good prognosis Acral lentiginous
Palms and soles hands and feet, nail beds
Very aggressive vertical and poor prognosis
Mets w/u for melanoma: PET scan
Role sentinel LN dissection (bx?) in melanoma (for certain ones only- thin, intermediate questionable,
deep don’t do it- do PET and if + do complete LN dissection): staging Investigative tx for met dz: IFN and surg resection

Question 46

20. How do you work up someone with an enlarged lymph node in the neck? What are some benign and malignant etiologies? How do you make a diagnosis? If it turns out to be lymphoma, what is the primary therapy, and when is splenectomy indicated?

Answer 46

Workup
History- duration, associated symptoms (especially constitutional), recent illnesses, infection, local trauma, bites, exposure to drugs or antibiotics, travel, vaccination status, social (including sexual contact)
Physical exam- characteristics of the lymph node (soft/indurated, compressible/not, mobile/fixed, tender/nontender), accompanying cellulitis or inflammation
Acutely infected nodes tend to be large, warm, tender with surrounding erythema and edema. Causative organisms usually S. aureus or group B strep
Chronically infected nodes tend to have discrete margins, few signs of inflammation, and be adherent to underlying tissues
Nodes associated with malignancy- firm, rubbery, discrete, fixed, tend to be larger than 2cm
Lab studies- CBC, LDH (rapid turnover for lymphoma and leukemia), tuberculin skin tests, titers for EBV, CMV, catscratch disease, toxoplasmosis (in general indices of inflammation such as ESR and CRP are non-specific and noncontributory to making the diagnosis)
CXR (for hilar adenopathy and to r/o tuberculosis, pneumonia, etc)
U/S can help distinguish a node that is difficult to palpate and can distinguish the mass from other anatomic abnormalities (thyroglossal duct cyst, branchial cleft cyst, dermoid cysts). Can also describe as solid, liquid gas, heterogenous, homogenous
CT scanning can help assess deep lymph nodes in abdominal and thoracic cavity- can look for other causes of malignancy such as Burkitt’s, neuroblastoma, rhabdosarcoma,
18FDG-PET scanning for Hodgkins and NHL
FNA for biopsy, or core needle with CT or U/S guidance
Etiologies
Immune response to infective agents (bacterial- including mycobacteria, viral, fungal)
Inflammatory cells in infections involving the lymph node
Collections of neoplastic cells carried to node by lymphatics or blood vessels (distant metastasis) Neoplastic proliferation of lymphocytes or macrophages (leukemia or lymphoma-HL, NHL, Burkitts) Collections of macrophages filled with metabolite deposits (storage diseases, granulomas)
Kawasaki disease, Langerhans cells histiocytosis, SLE
Treatment of lymphoma
HL- MOPP (mechlorethamine (nitrogen mustard), vincristine (oncovarin), procarbazine, and prednisolone) or ABVD (Adriamycin, bleomycin, vinblastine, dacarbazine). ABVD causes less infertility than MOPP, but bleomycin can cause fatal pulmonary toxicity. For advanced stages use chemotherapy in conjunction with radiation
NHL- CHOP- (cyclophosphamide, hydroxydaunorubicin, vincristine, and prednisolone. May use radioimmunotherapy using anti-CD20.
Aggressive B cell lymphomas (DLBCL, burkitts, mantle cell lymphoma, lymphoblastic lymphoma/ALL)- systemic chemotherapy followed by radiotherapy.
Rituximab may be added for NHL (anti-CD20)
Surgery is very rarely indicated for the treatment of lymphoma due to its systemic nature.

Question 47

40 y/o m presents L neck c mass.

Answer 47

Hx: OLD CARTS, recent illness (f/c), thyroid (radiation exposure, prior cancer, sweats, malaise, weight loss, FHx), trauma
PE
Know size, location, characteristic of mass
Examine thyroid, examine oral and nasal areas Endoscopy- laryngoscopy and exam oro- naso- pharynx
Know LN anatomy of neck- all the diff levels Know DDx of both benign and neoplastic
Benign: thyroglossal duct cyst, brachial cleft cyst, thyroid nodule, abscess
Neoplastic: thyroid cancer, lymphoma, lipoma
Workup and staging for lymphoma
PE: Most are firm and rubbery, non-hodgkin’s in upper cervical nodes, hodgkin’s in nodes throughout chain
Studies
Most common sites extranodal involvement in Non-Hodgkin’s in
head and neck (Waldeyer’s tonsillar ring, nasal cavity,
paranasal sinuses, orbit and salivary glands) Endoscopy to r/o primary epithelial tumor
Biopsy of lymph nodes (tissue dx via bx- FN, core, open
excisional) and CT
Once dx, chest radiograph, CT abd, bone marrow bx
Staging
I: Single LN region or single extralymphatic site
II: 2+ LN regions same side diaphragm or local involvement
extranodal site and 1+ LN regions same side diaphragm III: LN regions or extranodal sites both sides diaphragm IV: Diffuse or disseminated involvement of 1+ distant
extranodal organs
Indications for splenectomy in lymphoma:
Symptomatic splenomegaly
Pain from recurrent splenic infarctions Hematologic depression from hypersplenism

Question 48

21. What is the differential of a breast mass? Cystic vs. solid? What imaging modalities? How do you make a diagnosis? What are the surgical options for breast cancer? What is the significance of receptor status? What are the adjuvant therapies?

Answer 48

Malignancy / DCIS Fibroadenoma Fibrocystic change Cyst
Cystic vs. solid?
Cyst: cyst, fibrocystic change
Solid: fibroadenoma, malignancy / DCIS What imaging modalities?
Ultrasound- ddx solid vs cystic mass
Mammogram- Used for screening or evaluation of palpable mass. Detects 85% of breast cancers. CT- Used for guiding biopsy.
MRI- Detects cancers that mammography misses.
How do you make a diagnosis?
Core biopsy – for readily palpable masses
Excisional biopsy – for masses likely to be cancer
Stereotactic biopsy – for non-palpable masses or suspicious microcalcifications
What are the surgical options for breast cancer?
Lumpectomy with sentinel node biopsy- Contraindicated in multi-centric disease. Radical mastectomy
Modified radical mastectomy
What is the significance of receptor status?
Effects treatment options. Only hormone receptor positive cancers are eligible for treatment with hormonal agents.
What are the adjuvant therapies? Hormonal
o Tamoxifen – benefit restricted to ER or PR positive tumors
o Aromatase inhibitors – used in metastatic hormone receptor positive disease or in combination with
tamoxifen for early disease. Radiation
o Indicated post lumpectomy
o Indicated in patients with 4 or more positive lymph nodes Chemotherapy
o Trastuzumab for the treatment of ERBB2 positive breast cancer as part of a regimen with dozorubicin, cyclophosphamide, and paclitaxel

Question 49

40 y/o presents c lump upper outer quadrant L breast.

Answer 49

How long been there, growing/changing, asymmetry, painful, nipple discharge, skin changes/rashes
Breast hx: Age of menarche, age of first child, age of menopause, birth control, estrogen, FHx,
Fibrocystic changes, fibroadenoma (Phalloydes tumor similar),
DCIS, cyst (tender, well-circumscribed), breast cancer
Dx of cyst via u/s, tx by aspiration
PE findings that suggest breast cancer: non-mobile, hard, unilateral, skin changes, nipple discharge,
adenopathy
Diagnostic tests for suspected breast cancer- mammography, u/s, bx
If breast cancer confirmed, surg tx- lumpectomy, sentinel LN bx, radiation, chemotherapy
If considering hormonal tx, what are the considerations- est or prog +, pre- or post- menopausal
Pre- or post- menopausal imp bc Tamoxifen can be used in both groups and aromatase inhibitors can only be used in post. Both take away estrogen but aromatase inhibitors don’t work in pre.
Chemo for breast cancer pts, what are your considerations?
Chemo given when + LNs, mets, if ER PR – (chemo only option), menopausal status, size of tumor

Question 50

22. What are the findings of acute pancreatitis? What prognostic criteria are helpful? What is the initial therapy? What are the indications for surgery?
    What are the findings of acute pancreatitis?

Answer 50

LUQ or epigastric pain that may radiate to back. May improve by leaning forward. n/v
low grade fever
tachypnea
Abdomen is tender with guarding but no rebound.
Retroperitoneal fluid
Cullen (periumbical ecchymosis) and Grey-Turner (flank ecchymosis) signs are indicative of sever hemorrhagic pancreatitis.
Elevated amylase – not seen in chronic pancreatitis
Elevated lipase
AXR – sentinel loop sign ( distention and/or air fluid levels near a site of abdominal distention. In pancreatitis it is secondary to pancreatitis associated ileus)
What prognostic criteria are helpful?
Ranson’s Criteria – predicts risk of mortality
o On admission
Age>55
Bloodsugar>200
WBC >16,000
Serum glutamic oxaloacetic transaminase (SGOT) > 250
LDH>700
o After 48 hours
DropinHct>10%
IncreaseinBUN>5 Ca4
Fluiddeficit>6
o # of risk factors above predict mortality
6 risk factors 70-100% What is the initial therapy?
Hydration
Electrolyte monitoring
NG Tube for severe disease with vomiting NPO
Abx if infection is identified
What are the indications for surgery? Secondary infected necrosis
Correction of associated biliary tract disease Progressive deterioration despite medical care

Question 51

62 y/o m hx HTN, takes Hydrochlorothiazide, comes in complaining 0f severe epigastric pain. Associated c n/v and radiating to back. WBC 17, bili 1.7, lipase 4,000.

Answer 51

DDx: acute pancreatitis, pancreatic cancer, cholangitis Etiology for acute pancreatitis
“ I GET SMASHED”
Idiopathic, gallstones, ethanol, trauma, steroids, mumps,
autoimmune, scorpion, hypertriglyceridemia, ERCP, drugs
Know Ranson’s criteria
At dx
Age > 55
WBC > 16000 Glucose > 200 AST > 250 LDH > 350
At 48 hours Calcium 10% Hypoxemia with PO2 5 mg/dl
Base deficit > 4 Sequestration of fluids > 6L
Tx for pancreatitis: conservative management (NPO/bowel rest/IVF, NGT, foley)
Indications for surgery for pancreatitis: necrosis, infxn, hemorrhagic, biliary pancreatitis (so can take
gallstones out that are causing the problems)`

Question 52

23. How do you work up painless jaundice or bilary obstruction? How do you diagnose and treat a pancreatic mass? How do you do a Whipple resection? What makes a periampullary cancer unresectable? What palliative procedures can you perform? How do you treat gallbladder cancer?

Answer 52

How do you work up painless jaundice or bilary obstruction?
1. HPI: Weight loss, diarrhea, recent onset of diabetes may indicate cancer. History of hemolytic anemia or blood transfusion may cause non-obstructive painless jaundice.
2. PE:. Courviosier’s sign in chronic progressive biliary obstruction rather than acute choledocolithiasis.
3. LFT: Alk phos elevation indicates biliary tract inflammation. Elevated direct bilirubin in obstructive jaundice. Elevated
indirect bilirubin in non-obstructive jaundice.
4. US and CT
5. ERCP: If tumor is visualized, it can be biopsied. Can also perform a sphincterotomy to relieve obstruction at the ampulla of vater.
How do you diagnose and treat a pancreatic mass? Dx
o ERCP can diagnose peri-ampullary lesions and treat biliary obstruction.
o CT can localize lesion for biopsy. Tx
o Resectable tumors: Whipple with adjuvant chemoradiation
o Unresectable (180 abutment of SMA, abutment of celiac axis, occlusion of portal vein or SMV): Palliative treatment of biliary obstruction, duodenal obstruction or chemical splanchiectomy. How do you do a Whipple resection? Remove gallbladder, CBD, antrum of stomach, duodenum, proximal jejunum and hed of pancreas. See Mingle for technical details. What makes a periampullary cancer unresectable? 180 abutment of SMA, abutment of celiac axis, occlusion of portal vein or SMV What palliative procedures can you perform?
Treatment of biliary obstruction, duodenal obstruction or chemical splanchiectomy for pain control. How do you treat gallbladder cancer?
Tumor confined to gallbladder mucosa: Cholecystectomy
Tumor involving muscularis or serosa: radical cholecystectomy, wedge resection of overlying liver, and lymph node dissection
Tumor involving liver: palliative measures such as decompression of proximal biliary tree or a bypass procedure of the obstructed duodenum

Question 53

55 y/o m c new onset jaundice. Asymp except for weight loss of 20 lbs. Amylase and lipase nl, bili 16.

Answer 53

DDx: pancreatic cancer, hepatocellular carcinoma, cholangiocarcinoma, hepatitis, choledocolithiasis (benign ones down on list)
W/u: CT, ERCP, u/s
Tx pancreatic cancer: Whipple, if unresectable palliation, bypass, ERCP c stent
Tx GB cancer: cholecystectomy (if just mucosa), cholecystectomy c wedge resection of liver, too (if
invades submucosa, too)

Question 54

24. What is the differential diagnosis of an anterior neck mass? If this is a thyroid mass, how do you work it up? What are the different types of thyroid cancer? What treatment do you recommend for papillary cancer? What are the complications of thyroid surgery?

Answer 54

What is the differential diagnosis of an anterior neck mass?
Thyroglossal duct cyst, thyroid carcinoma, thyroid nodule, thyroiditis, goiter, laryngeal carcinoma, lymphoma,
infection of the anterior neck space.
If this is a thyroid mass, how do you work it up?
US: cystic vs solid
FNA: differentiate between cancer and benign nodule What are the different types of thyroid cancer?
Papillary Follicular Medullary anaplastic
What treatment do you recommend for papillary cancer? Total thyroidectomy – most patients
Lobectomy with isthmusectomy – only for low risk patients with tumor

Question 55

36 y/o f comes in for neck mass

Answer 55

DDx: LN, thyroid, congenital cysts, soft tissue masses
Upon PE: 3 cm firm nodule appears to involve L lobe thyroid
Know risks for malignancy: cold nodule, radiation hx, family hx (MENs syndromes, LAD, fixation of mass, hoarseness)
Know at least 2 studies useful for isolated thyroid nodules and know value of abnormal
Know serum thyroid levels, u/s (looks for isolated vs multiple, looks for LNs, too), radioactive scans (hot vs cold), CT scan, FNA
Know 3 most common types of thyroid cancer and typical pathways of spread: Papillary, follicular, medullary
Papillary – associated w/prior exposure to ionizing radiation, well behaved tumors that spread to cervical lymph nodes but have a good prognosis; appear as cold masses on scintiscans and demonstrate Orphan Annie cells on FNA
Follicular – associated w/dietary iodine deficiencies, likes to metastasize hematogenously and prognosis is dependent on extent of invasion; appears as cold mass on scintiscan and demonstrates follicular cells on FNA
Medullary – associated w/MEN 2A or 2B syndrome, comes from parafollicular C-cells and secretes calcitonin; those associated w/congenital syndromes metastasize wider and earlier; appears as a cold mass on scintiscan and amyloid is
present on FNA
What are the important adjacent structures to avoid in
thyroidectomy: recurrent laryngeal, superior laryngeal,
parathyroids, trachea
When do you do a complete thyroidectomy for pt c unilateral cancer?
No clean margins, MEN syndrome, multifocal, large tumor
Benefit of complete thyroidectomy: recurrence lower, can also
tx c radioactive iodine
Drawbacks of complete thyroidectomy: life time hormonal
replacement, life time trach (injury to both laryngeal nerves)

Question 56

25. In a cirrhotic patient with a liver mass, what are you most concerned about? How do you make the diagnosis? How do you assess his perioperative risk? When do you recommend resection vs. transplantation? What other less invasive modalities are available to treat a hepatoma?

Answer 56

In a cirrhotic patient with a liver mass, what are you most concerned about?
Hepatocellular carcinoma
How do you make the diagnosis?
Symptoms:
o RUQ pain
o Weight loss
o May be associated with malaise, anorexia, abdominal pain Signs:
o Hepatomegaly
o Ascites,
o Periumbilical ecchymosis (Cullen’s sign) o Flank ecchymosis (Turner’s sign)
Labs:
o Alpha fetoprotein o LFTs
o Alpha-1 antitrypsin
Imaging:
o Ultrasound
o MRI
o CT Biopsy
o Fine needle aspiration How do you assess his perioperative risk?
Standard for assessing perioperative morbidity and mortality in patients with cirrhosis has been the Child-Turcotte- Pugh (CTP) scoring system, which is based on the patient’s serum bilirubin and albumin levels, prothrombin time, and severity of encephalopathy and ascites
Child Class A: 5 to 6 points
o Life expectancy: 15 to 20 years
o Abdominal surgery peri-operative mortality: 10%
Child Class B: 7 to 9 points
o Indicated for liver transplantation evaluation
o Abdominal surgery peri-operative mortality: 30%
Child Class C: 10 to 15 points
o Life expectancy: 1 to 3 years
o Abdominal surgery peri-operative mortality: 82%
When do you recommend resection vs. transplantation?
Hepatic resection beneficial with small solitary lesion with good liver function
Liver transplantation if advanced liver dysfunction, solitary tumor

Question 57

What is the breakdown of a CTP?

Answer 57

Encephalopathy, ascites, bili (2-3), albumin (3.5-2.8), PT (4-6)

Question 58

62 y/o m hx HTN, RUQ pain 4 mos. Not assoc c eating. Loss of appetite, 20 lbs weight loss. Has EtOH abuse hx and documented cirrhosis. Mild pain upon palp RUQ, bili 2.1 (nl total bili 0.2-1.0 mg/dL). Other lab nl.

Answer 58

HPI
DDx: hepatocellular carcinoma, hepatitis, worsening of cirrhosis
Also hepatic adenoma
Mets
W/u: CBC, renal panel, LFTs, lipase, amylase, UA, AFP (Alpha-fetoprotein dx for hepatocellular carcinoma, will be off charts- 20,000-25,000), CEA, CA19-9, u/s, abd + pelv CT,
If mass on u/s or CT, bx
Pts c cirrhosis- for surg risk know Child classification (need to know
nutritional assessment to calc score)
According to NMS, Child’s classification determines operative
risk of a shunting procedure in pt c portal HTN. Categories
include bili, albumin, ascites, encephalopathy, nutrition Operative mortality rate
A (5-6): 2%
B (7-9): 10%
C (10-15): 50%
Pt receives points depending on values of 5 categories- albumin, bilirubin, PT, ascites, encephalopathy
Depending on score, pt placed in class A-C, which predicts prognosis of pt
Tx hepatocellular CA: resection, transplantation (for bridging to get them to transplant for liver failure- tx c chemo- intraarterial embolization- cryoablation, radio frequency ablation of alcohol injection)
Hepatocellular CA
Most common primary malignant liver tumor. Solitary or multiple, local invasion (diaphragm) as well as distant mets (lung)
Incidence: M:F 2:1, 50 y/o
Associations: HBC, HCV, cirrhosis, hemochromatosis, parasites,
carcinogens Clinical presentation:
HPI: Small- asymp, larger- RUQ pain, jaundice, malaise, f
PE: hepatomegaly, weight loss, cirrhosis findings, hemorrhage,
paraneoplastic (Cushing’s)
Dx: LFTs, AFP, CT and MRI c IV contrast, u/s > 2cm Tx:
Surgery- resect, transplantation
Chemo- administration of drugs into hepatic artery Combination therapy- chemoembolization (embolizing
arterial supply tumor c chemotherapeutic agents mixed c thrombus), local ablation (instillation absolute ethanol into lesion or insertion of probe and delivery of radio frequency energy into lesion) may be palliative for unresectable lesions. Both cause local necrosis of tumor and combo may improve survival.

Question 59

26. What is the differential diagnosis for RUQ pain? How do you diagnose biliary colic? What is the surgical anatomy of the gallbladder? What is biliary dyskinesia?

Answer 59

Biliary colic Cholecystitis Choledocholithiasis Cholangitis Gastritis
Peptic ulcer
Hepatitis
Pancreatitis
Pyelonephritis
Pancreatic CA/hepatic CA/gastric CA/cholangio CA Gastroenteritis
MI
Pneumonia (right lower lobe)
How do you diagnose biliary colic?
Symptoms:
o Severe right upper quadrant or epigastric pain that can radiate to the back, right scapula or shoulder o Pain waxes and wanes in intensity
o May be associated with fever, nausea, vomiting, fatty meals
Labs:
o CBC, LFTs, amylase and lipase
Imaging:
o Ultrasound
o HIDA o ERCP o CT
What is biliary dyskinesia?
Biliary dyskinesia is a motility disorder that affects the gallbladder and sphincter of Oddi. Patients with this condition present with biliary-type pain, and investigations show no evidence of gallstones.

Question 60

45 y/o f c intermittent RUQ pain for 1 yr. Associated c eating fatty foods- 30-40 min after eating. Assoc c n/v. Goes away couple hrs. Labs nl except alk phos 180 (nl ~100).

Answer 60

HPI
PE (remember vitals)
DDx: Biliary colic (gallstones) bc lab nl, symptomatic cholelithiasis, cholangiocarcinoma, biliary
dyskinesia
W/u: CBC, renal panel, LFTs, amylase, lipase, UA, pregnancy, u/s (r/o cholecystitis), CT abd, HIDA scan
(to see that GB functioning properly)
Know anatomy of GB- arterial supply off aorta c variations.
Extrahepatic biliary tree Ducts of Luschka
R and L hepatic ducts common hepatic duct Cystic duct
Variations consists of abnormal connections c common hepatic duct and accessory hepatic ducts
CBD
CBD and pancreatic duct enter duodenum/ampulla of Vater in 3
configurations
GB: Fundus (ant), body (storage), infundibulum (post), neck Arterial supply
Cystic artery
95% time branch of R hepatic artery that passes behind
cystic duct
Can arise from R hepatic artery outside Calot’s triangle Can arise from L hepatic artery
Can arise from proper hepatic artery
Can arise from gastroduodenal artery
Can arise from celiac trunk
Can arise from abnormal R hepatic (from SMA)
Can have double (both from R hepatic, one from R
hepatic other from gastroduodenal, both from
abnormal R hepatic from SMA)
Triangle of Calot: cystic duct, common hepatic duct and inferior border of liver c cystic artery within the triangle
Biliary dyskinesia: Abnl contraction of GB. Dx via HIDA EF

Question 61

27. How do make the diagnosis of acute cholecystitis?

Answer 61

Symptoms:
o RUQ or epigastric pain lasting more than 6 hours o Fever and chills
o Nausea and vomiting
o Jaundice
Signs:
o Murphy Sign
Labs:
o CBC, LFTs, amylase and lipase, CRP
Imaging:
o Ultrasound
o CT
o HIDA o ERCP o MRI

Question 62

What are the common laboratory and imaging findings?

Answer 62

Leukocytosis present in more than 70% of patients
CRP frequently elevated
Liver function tests (serum bilirubin, serum alkaline phosphatase, ALT, AST) may be mildly elevated Ultrasound
o Thickened gallbladder
o Enlarged gallbladder
o Pericholecystic fluid collection o Incarcerated gallstone
HIDA
o Nonvisualized gallbladder with normal uptake and excretion of radioactivity o Rim sign (augmentation of radioactivity around gallbladder fossa)
MRI
o Pericholecystic high signal o Enlarged gallbladder
o Thickened gallbladder wall
CT
o thickened gallbladder wall
o pericholecystic fluid collection
o enlarged gallbladder
o linear high-density areas in pericholecystic fat tissue

Question 63

What antibiotics do you recommend?

Answer 63

for mild cholecystitis, recommended antimicrobials include
o oral fluoroquinolones such as levofloxacin or ciprofloxacin
o oral cephalosporins such as cefotiam or cefcapene
o first-generation cephalosporin such cefazolin
o broad-spectrum penicillin/beta-lactamase inhibitor such as ampicillin-sulbactam
for moderate cholecystitis, first-line antimicrobials
o broad-spectrum penicillin/beta-lactamase inhibitor such as piperacillin-tazobactam or ampicillin-sulbactam o second-generation cephalosporin such as cefmetazole, cefotiam, oxacephem, flomoxef
for severe cholecystitis,
initial antibiotic options: third/fourth-generation cephalosporins such as cefoperazone/sulbactam, ceftriaxone, ceftazidime, cefepime, cefozopran OR aztreonam + metronidazole when anaerobic bacteria are detected or expected to coexist
secondary options: fluoroquinolones such as ciprofloxacin, levofloxacin, pazufloxacin, and metronidazole (when anaerobic bacteria are detected or expected to coexist) OR carbapenems such as meropenem, imipenem-cilastatin, panipenem/betamipron

Question 64

45 y/o f RUQ pain 4 hrs c n/v. Multiple similar episodes past 6 mos.

Answer 64

Chronic cholecystitis Cholelithiasis (biliary colic)
HPI:
Risks- fat, female, forty, fertile
Usually asymp. If symp- RUQ pain worse after eating
(especially fatty food). Studies
U/s (acoustic shadow- headlight, gravity-dependent movement gallstones), plain film
Tx
Asymp: surgery usually not indication (exceptions) Symp: lap chole, medical
Acute calculous cholecystitis
Inflammation GB usually 2/2 obstruction cystic duct by
gallstones
HPI: Pain > 3 hrs, f, n/v, anorexia PE: Murphy’s, sonographic Murphy’s Dx:
Labs: CBC, LFTs, amylase, lipase, UA
Imaging: U/s (inflammation wall > 4mm, pericholecystic
fluid, stones in GB, dilation CBD if stone passed), HIDA (radionucleotide scan c Technetium-99m labeled iminodiacetic acid injected IV into hepatocytes. Nl GB visualized w/in hour)
Tx:
NPO, IVF, IV abx, IV analgesia, chole w/in 24-48 hrs (lap
or open) Acalculous cholecystitis
Biliary stasis. No stones.
10% cases of acute cholecystitis ICU pts, TPN
Choledocolithiasis
Studies: ERCP, endoscopic u/s, transabdominal u/s Tx: ERCP or CBD open surgically
Ascending cholangitis
HPI: f/c, n/v, jaundice, altered mental status, septic shock Dx
CBC, LFTs
U/s (dilation CBD and intrahepatic bile ducts) Tx
If stable- conservative (NPO, IVF, abx) c definitive tx later
If in shock- ERCP/percutaneous transhepatic cholangiography (PTC). If unsuccessful, intraop decompression c T-tube placement
Sclerosing cholangitis Gallstone pancreatitis Hepatitis
HPI: Illicit drug use, sexual practices, blood, travel
Studies: LFTs, serology HCC
Acute pancreatitis
HPI: EtOH, gallstones, pain radiating to back Studies: Lipase, amylase
Gastroenteritis
HPI: Diet, anorexia
Appendix
Studies: CBC, CT
Pyelonephritis
HPI: Kidney stones, kidney surgery, catherization, DM,
pregnancy. F/c, flank pain, CVA tenderness, hematuria Studies: UA
Leukocyte esterase, WBC casts, nitrite
UTI
Nephrolithiasis
Lower lobe pneumonia
HPI: cough, sputum, fever, SOB, hx of pulm conditions, smoking
PE: Breath sounds
Studies: CBC, CXR Angina
HPI: Cardiac hx, chest pain, SOB upon exertion PE: Heart sounds
Studies: Cardiac enzymes, EKG and CXR
Ulcers
HPI: Pre- vs post- prandial pain and relief EUrease breath test, serology, endoscopy c bx

Question 65

How to narrow differential?

Answer 65

Pertinent hx to narrow DDx
Association c food
Worse or better, f/c, bm, recurrent, etc.
Physical findings
Murphy’s: Stop of insp upon palp RUQ Jaundice
Rebound, guarding
Breath sounds for pneumonia
Kidney symptoms, appendicitis
Labs and dx studies and why
Lipase (pancreatitis) CBC (infxn)
LFTs
CXR
UA
U/s
Sources of alk phos and how to determine source if elevated
Bone, bilary GGT Fractionation
Upon heating, isozymes diff levels of activity
Pathophysiology of gallstone formation
Supersaturation of bile c cholesterol or bilirubin salts predisposes stone formation, which can be made of cholesterol monohydrate stone (crystallizes when bile supersaturated) or bilirubin calcium salt
Cholesterol
Supersaturation, nucleation, stasis and mucus trapping
Types of gallstones and risk factors each type
Cholesterol
Risks: Native American, industrialized societies, age, fat,
fertile, forty, female, estrogens, pregnancy, rapid weight
loss, hyperlipidemia syndromes Pigmented
Risks: Asians, chronic hemolytic syndromes, biliary tract infections (bacterial microbial beta-glucuronidases that hydrolyze bilirubin glucuronides), ileal dz, CF c panc insufficiency
Significance of inc bili and/or dilation intra- and extra- hepatic bile ducts and how to approach
DDx: choledocolithiasis, cancer or stricture (from pancreatitis) ERCP see stone or strictures (can remove stone)

Question 66

28. In a non-cirrhotic woman with a liver mass, what is differential diagnosis? How do you work it up? What are the different histologic findings between adenoma and FNH? What is the treatment for adenoma? What is the segmental anatomy of the liver?

Answer 66

In a non-cirrhotic woman with a liver mass, what is differential diagnosis?
Liver hemangioma
Focal nodular hyperplasia Hepatic adenoma
How do you work it up?
History Physical Labs Imaging Biopsy
Liver hemangioma
o Most are asymptomatic, may present with pain
o Usually a normal physical exam and found on imaging only
o Usually appears as a solitary lesion
o Ultrasound: usually shows well-defined, homogenous, hyperechoic lesions
o CT: usually shows well-defined, homogenous hypodense lesions
o Biopsy: histology characterized by vascular blood-filled spaces line by endothelium and separated by fibrous
septa
Focal nodular hyperplasia
o Usually asymptomatic, rarely abdominal pain
o Rarely palpable abdominal mass, non-tender
o LFTs are usually normal
o CT shows well-circumscribed mass of low density o Arteriogram shows hypervascular mass
o Normal uptake on liver nuclear scan
o Biopsy: single or multiple lesions with nodular appearance, central scar with radiating septa on cut section,
hyperplastic hepatocytes with inflammatory cells, bile duct epithelium prominent
Hepatic adenoma
o Usually asymptomatic, RUQ fullness, 25% palpable mass or abdominal pain o Abdominal tenderness if there is hemorrhaging
o Associated with oral contraceptives and anabolic steroids
o Normal AFP
o Normal LFT
o CT hepatic mass, liver scan cold spot, ultrasound, angiography
o Biopsy with fine needle aspiration
o Soft, sharply circumcised edges, no true capsule
What are the different histologic findings between adenoma and FNH?
Hepatic adenoma
o Sheets of normal to slightly atypical hepatocytes which are frequently vacuolated. Only an occasional fibrous
septum traverses lesion. No bile ducts or Kupffer cells. FNH
o Single or multiple lesions with nodular appearance, central scar with radiating septa on cut section, hyperplastic hepatocytes with inflammatory cells, bile duct epithelium prominent
What is the treatment for adenoma?
Stop oral contraceptives and anabolic steroids Surgical removal to prevent rupture
o if large and superficial or pregnancy anticipated
If spontaneous rupture with hemorrhage
o surgery when stable
o hepatic artery ligation - if liver not cirrhotic
o hepatic resection - high mortality when acute, elective resection later
o if very unstable - open packing or angiographic embolization of hepatic artery may control hemorrhage

Question 67

What is the segmental anatomy of the liver?

Answer 67

The liver is divided into three functional lobes: the right lobe, the left lobe, and the caudate lobe. The right and left lobes are further divided into 2 segments each: The anterior and posterior segments of the right lobe. The medial and lateral segments of the left lobe.
Look at photo.

Question 68

29. How do you work up someone with suspected cholangitis? What are the laboratory and imaging findings? What are the options to relieve cholangitis due to choledocholithiasis?

Answer 68

Work-up: CBC, Complete Metabolic Panel, Lactate Dehydrogenase, ultrasound
Lab and imaging findings: leukocytosis, increased bilirubin, AST, ALT, Alk Phos, BUN, Creatinine, Glucose, LDH
Options to relieve: if stable make NPO, IVF and antibiotics with definitive treatment later. If in shock: ERCP or percutaneous transhepatic cholangiography. If unsuccessful, intraoperative decompression with T-tube placement

Question 69

30. When would you recommend post-op nutritional support? How do you calculate nutritional requirement? What are the pros and cons of enteral vs. parenteral nutrition? What is refeeding syndrome?

Answer 69

If the patient will be NPO for more than 7 days.
Patients with severe illness who will be unable to eat for approximately more than 7 days should receive nutritional support earlier because it takes several days for nutritional support to take effect, it is more effective to begin such support if there is any question of nutritional deficit rather than to wait until there is a severe deficit to correct.
If there are increased risk of complications of the planned surgery, if intervention will help (i.e. 7-10 days of nutritional support may decrease post-op complications and infections).
Also, patients with enterocutaneous fistulas, short bowel syndrome or prolonged ileus
Nutritional requirement calculations:
Total Energy Requirement is the BEE x Activity Factor x Stress Factor where BEE can be calculated using the Harris-Benedict Equation or the estimated BEE shown below.
-Harris-Benedict Equation: IDEAL body weight is in kg, height in cm, age
-Male: 66 + (13.7 x W) + (5 x H) – (6.8 x A)
- Female: 655 + (9.6 x W) + (1.8 x H) – (4.7 x A) PLUS: 0.8 to 1 gram protein/kg/day
-Estimated BEE: 30 cal/kg/day in adults PLUS 0.8 to 1 gram protein/kg/day

Question 70

Enteral vs parenteral

Answer 70

Enteral: less defined, more difficult to maintain, less expensive, less infection and complication

Parenteral: well-defined, easy to initiate, assured delivery, costly, unused gut SEs

Question 71

Define referring syndrome

Answer 71

In starvation the secretion of insulin is decreased in response to a reduced intake of carbohydrates. Instead
fat and protein stores are catabolised to produce energy. This results in an intracellular loss of electrolytes, in particular phosphate.
Malnourished patients’ intracellular phosphate stores can be depleted despite normal serum phosphate concentrations. When they
start to feed a sudden shift from fat to carbohydrate metabolism occurs and secretion of insulin increases. This stimulates cellularuptake of phosphate, which can lead to profound hypophosphataemia.This phenomenon usually occurs within four days of
starting to feed again. Serum phosphate concentrations of less than 0.50 mmol/l (normal range 0.85-1.40 mmol/l) can produce the
clinical features of refeeding syndrome, which include rhabdomyolysis, leucocyte dysfunction, respiratory failure, cardiac failure,
hypotension, arrhythmias, seizures, coma, and sudden death

Question 72

35 y/o pt undergoes ex lap found to have pancreatic inj c multiple small bowel endarterotomies, leave drain near panc, resect 1 ft of bowel and do primary anastomosis, what is the nl caloric need in healthy person and how does this change for this pt?

Answer 72

Nl: 20-25 kcal/kg/day non-protein calories (protein cals 1 g/kg/day) Trauma pts: 20-40%
Postop feeding options for this pts: J tube c tube feeds, TPN
Complications of TPN (sepsis, acalculous cholecystitis, fatty liver)
Pt c pancreatic leak, what are your options: Conservative manangement (NPO, TPN), somatostatin Define refeeding syndrome and how to prevent it
Starvation leads to decreased insulin secretion as body utilizes fats and protein instead of carbs, resulting in intracellular loss of electrolytes, particularly phosphate. When nutrition resumed, there’s a sudden shift to carb metabolism and a rush of insulin stimulates cellular uptake of phosphate, leading to symptoms of hypophosphatemia (rhabdo, leukocyte dysfunction, resp failure, cardiac failure, hypotension, arrhythmias, seizures, coma and sudden death).
Prevent this by using a low caloric diet initially and correcting electrolyte imbalances slowly
How do you determine nutritional optimization
Albumin Pre-albumin Nitrogen balance
What if pt on vent- metabolic cart

Question 73

80 y/o cachectic m dx c colon cancer requiring bowel resection, how to determine preop nutritional
status?

Answer 73

Nl albumin > 4 and prealbumin > 16
How to optimize status preop? Inc protein (protein shakes), vitamins,
supplements, nutritional consults, calorie count
Complication if fail to optimize them? Poor wound healing, dehiscence,
break down of anastomosis

Question 74

31. In a cachectic patient about to undergo a large operation, how do you assess nutritional need pre-operatively? What routes do you recommend if he needs supplementation? Exactly what is in a bag of TPN? What contents are important for wound healing?

Answer 74

Assessment: albumin levels (which helps you evaluate nutrition in the past few months), prealbumin (helps evaluate nutrition in the past 1-2 weeks) and C-reactive protein (helpful to assess inflammatory state)
Also look at history and PE findings: >15% weight loss, anorexia, organ failure, cancer, HIV, sepsis. Temporal wasting, tricep skin fold, enlarged liver, ascites, ileostomy, prior bowel resection.
Routes of supplementation for cachectic patients: enteral or parenteral
TPN: Na (40-50 mEq/L), K (40 mEq/L), Cl (50 mEq/L), Mg (4-6 mEq/L), Ca (2.5-5.0 mEq/L), HPO (20-25 mmol/L), and acetate (40 to 60 mEq/L), and other additives including P, Folic Acid, Vitamin B, C, D, K, micronutrients, amino acids, lipids. Contents important for wound healing: vitamin C, micronutrients (zinc, copper, chromium, selenium, manganese), amino acids.

Question 75

32. How to manage someone in a motor vehicle crash? What are the ABC’s? What if someone does not respond to initial resuscitation? What are the common places of hemorrhage and how do you make the diagnosis? If intra-abdominal bleeding is suspected, what are the common sources?

Answer 75

Do an initial assessment for trauma: Mechanism of injury- C-spine, and then ABCDE
A: airway: make sure patent
B: breathing: B/L breath sounds
C: circulation: pulses
If patient doesn’t respond to initial resuscitation (i.e. 2 L crystalloids) start blood
Places of hemorrhage: chest, abdomen, pelvis, thigh and external. Use vitals, FAST, CXR, labs and CT to determine whether bleeding is occurring and where.
Common sourves of intraabodominal bleeding are the spleen and liver.

Question 76

34. What injuries do you suspect with a rapid accel-decel mechanism? How do you diagnose and treat them? What are signs of vascular injury? How do you diagnose lower extremity compartment syndrome?

Answer 76

Possible injuries
- Traumatic brain injury, diffuse axonal injury o Brain MRI (CT less sensitive)
o Tx – controlling ICP - Vascular injury
o Kidney/spleen/small & large intestines – sheering of points of attachment to the retroperitneum and of pedicle vasculature.
o Thoracic aorta injury – from compression onto bony structures and torsion; usually fatal
o Superior mesenteric artery – intestinal loops that stretch may tear the mesenteric attachments injuring the
SMA Diagnoses and Treatment
- Diagnoses – history, clinically, FAST, DPL, exploratory lapraotomy
- Treatment – resuscitation followed by lapraotomy and repair of damage vessel Signs of vascular injury
- Pain
- Paralysis
- Pallor
- Paresthesia
- Poikilothermia – cold
- Pulselessness
Diagnoses
- Clinically – the 6P’s although pain and paresthesia are the two most reliable indicators. Pulselessness is rarely present.
Paresthesia and paralysis are late symptoms. May have tense/swollen shiny skin with bruising.
- Direct compartment pressure measurement – transducer with catheter introduced into the compartment to be measured.
Most accurate method of measuring compartment pressure and diagnosising compartment syndrome.

Question 77

Pt doesn’t respond to 2L crystalloids, what should you do next?

Answer 77

Start blood.

Question 78

33. How do you manage penetrating trauma in the thoraco-abdominal region? What are the immediately life threatening injuries and how do you treat them? What is the indication for ED thoracotomy and what are the steps?

Answer 78

Management of thoraco-abdominal penetrating injuries.
1) ABCs
o Airway
100%oxygenbag+mask
IntubationGCS
Breathing
circulation: Hemodynamics
Pulses,capillaryrefills,coldextremities
Fluid resuscitation with LR or crystalloids infused through two large bore IVs
Foley for measuring UOP .
Cricothyroidotomy if intubation not feasible because of C-spine injury or laryngeal obstruction.
2) CXR – signs of pneumothorax/effusion; widening mediastinum
3) FAST – pericardial/intraperitoneal bleeding
4) Exploratory lapraotomy/thoracotomy – hemodynamically unstable despite resuscitation, signs of peritonitis,
tamponade, hemothorax
Life threatening injuries and treatments
- Pneumothorax/Tension pneumothorax
o Needle thoracostomy
o Tube thoracostomy - Hemothorax
o Tube thoracostomy - Cardiac tomaponade
o Pericardiocentesis or pericardial window to drain and assess for presence of blood
o Median sternotomy to treat cardiac injury - Splenic injury
o Stable patient – nonoperative managmenet
o Unstable patient – splenectomy or splenorrhapy - Large vessel injury
o Emergent thoracotomy with cross clamping of vessels (e.g cross clamp descending aorta in patients with intra-abdominal bleeds and cannot maintain BP; cross clamping aorta in patient with subclavian arterial injury).
o Internal cardiac massage in absence of pulse or cardiac activity. - Small/Large bowel/mesentary
o Laparotomy
Indications for ED thoracotomy
- Penetrating traumatic cardiac arrest
o Persistent BP

Question 79

35. How do you manage a burn patient? What if there is also airway injury? How do you treat significant, circumferential burns? What are the long term complications of burn wounds?

Answer 79

Management
- Airway
o Inhalation injury – requires intubation (can cause laryngeal edema); look for signs of inhalation injury (red
oropharynx, facial/upper torso burns)
o CO poisoning – assess COhgb (>30% may indicate significant CNS dysfunction, >60% may cause
coma/death).
o Smoke inhalation – can cause chemical injury to alveolar basement, pulmonary edema; can also lead to
secondary infection (bronchopneumonia)
- Resuscitation
o Patients with 80% TBSA, or pediatric burns usually require larger fluid requirements than calculated
o Urinary output
Assessadequacyoffluidresuscitation
UOPshouldnotbeinexcessunlesstotreatmyoglobinuria
- Calculate burn area
o Rule of nines
Adults–9%head,18%frontoftorso,18%backoftorso,9%eacharm,9%eachleg.
Keep in mind, only applies to 2nd, 3rd, and 4th degree burns. 1st degree burns are not counted. So if
patient has 10% first degree burns, 15% second, 15% third, the TBSA is only 30%.
- Wound coverings
o Antimicrobial topical
Silver sulfadizine – does not penetrate eschar so not helpful in already infected burn; more preventative; side effect is leukopenia
Sulfamylon – penetrates eschar and useful for full-=thickenes infected burns - side effect is carbonic anhydrase inhibitor causing metabolic acidosis, painful application
Acticoat–broadspectrumanti-microbialdressing
Pigskin–coverflatcleanwounds
o Grafts – autograft, allograft, exnograft, artificial, cultured.
- Skin debridement
o Allows for quicker healing
o Decreases infection
Treating circumferential burns
- Escharotomy to prevent compartment syndrome
Complications of burn wounds
- Renal failure for hypovolemia
- Gi bleed for curlings ulcer
- Burn wound sepsis (give a tetanus shot)
- Progressive pulmonary insufficiency
- Burn scar
o Avoid exposure to sunlight
o Contractures/hypertrophic scar formation
o Marjolin’s ulcer (ulcerating squamous cell carcinoma)
o Destruction of skin appendages requires creams/lotions to prevent drying/racking.

Question 80

signs of airway burn

Answer 80

singed hair, carbonaceous sputum, altered mental status, ABG c carboxyhemoglobin

Question 81

36. How do manage an electrical burn? What organs might be involved? What complication might be encountered if there is significant muscle injury and how do you treat it?

Answer 81

Management – mostly same as in question 36 except with some special types of injury. Usually mandates more fluid resuscitation than calculated.
- Types of injuries
o Current injury
Due to heat generated as it flows through tissues
Moresevereintissuewithhighresistance(bone>fat>tendon>skin>muscle>vessel>nerves). o Vascular injury - thrombosis
o Cardiac injury
Atrial/ventricular arrhythmias
ImmediatelygetanEKG o Renal injury
Due to hemoglobin/myoglobin deposits in renal tubules.
Alkalinze urine to keep hemoglobin and myoglobin in more soluble state.
o Fractures
Tetanic muscle contraction cause bone fractures especially in spine o Neuro/Spinal cord injury
Demyelination
Cancauseseizures
Canbesecondaryfromfracture
- Factors to consider
o Type of circuit
o V oltage of circuit
o Resistance offered by body
o Amperage of current flowing through tissue o Pathway of current through body
o Duration of contact.
Significant muscular injury
- Excessive myoglobinuria can lead to renal failure. Treat with HCO3 to alkalinze urine and solubilize myoglobin.

Question 82

Medication to stabilize heart?

Answer 82

Ca+

Question 83

How are kidney usually damaged in this setting?

Answer 83

Myoglobinuria

Question 84

What preventative medications should this pt receive?

Answer 84

Ulcer prophylaxis, DVT prophylaxis, fluid,

tetanus (burns and trauma)

Question 85

Pt develops rhabdo, elevated CPK and u/o dec, what can be done to tx this?

Answer 85

Alkalinize urine, fluid resus, mannitol (to push kidney).

Question 86

37. What are the findings of claudication?
    What is involved in the initial work up, and what treatments do you recommend? When is surgery indicated? What additional studies might be required?

Answer 86

Pain, impaired ambulation, tiredness, cramping, most commonly in the calves which occurs after physical exertion of the affected muscles over an extended period of time. Pain is relieved by resting the effected muscles. Can also get hair loss, exertion dependant rubor, loss of sensation, shiny skin if it is chronic.

Ankle brachial index first, Doppler. Normal abi is more than 1.0. Mild claudication 0.6-0.8. Initial treatment for mild claudication is exercise, which develops collateral circulation. Smoking cessation and statins helpful. If worsens revascularization via av graft or amputation may be necessary depending on the degree of ischemia. If there is absence of a femoral pulse, aortoiliac disease. This is typically more progressive, and will require balloon dilation, stent placement, av graft. If pt. returns after initial workup with ulceration, must determine if there is sufficient flow to heal ulcer. In diabetics, get toe bp. Repeat abi. Arteriogram to assess location and formulate revascularization plan. If ulcer is unable to be reperfused, amputation likely necessary. Tx for specific levels of occlusion- superficial femoral artery: saphenous vein graft, iliac artery: balloon dilation/stent placement, superficial femoral and/or popliteal: femoropopliteal bypass.

Question 87

38. In a patient with acute lower extremity ischemia (non-trauma), what are the common etiologies?

Answer 87

Embolus (usually concurrent with pvd), compartment syndrome,

Question 88

What is your initial treatment and work up? What treatment options do you have?

Answer 88

Severe ischemia is almost always an embolic event. Time is critical. Revascularization after more than 6 hrs can result in permanent impairment. Initiate heparin therapy immediately, and proceed with urgent operative therapy. Thrombolysis, preoperative angiogram will delay the tx without modifying its need, and should not be performed in most cases. Thrombolysis with tpa or ultrasound are other options that can be considered in certain cases where the ischemia is not severe enough to threaten function. Compartment syndrome will have sensory and motor deficits, and present with an inciting event such as trauma or ischemic injury. Tx is fasciotomy. 6 ps of arterial occlusion: pain, pulselessness, paralysis, pallor, paresthesia, poikilothermia.

Question 89

UGI bleed- initial work up and treatment

Answer 89

Scenarios: Ulcer in critical care setting w/coag blood in ng-initiate ppis and/or h2 blockade, scope not necessary. Bright red blood in ng tube- resuscitation w/ 2l ns, cross and match. Scope is necessary here.
Duodenal Ulcer c fresh clot: all ulcers maintain ph above 5. Endoscopic hemostasis.
Ulcer c white base: no recent bleed, observe for changes.
Duodenal ulcer c visible artery at base: or for operative therapy.
Ulcer c acute renal failure: platelet dyfn or uremia. Dialysis c mentioned therapies.
Gastric varices: cyanoacrylate glue, tips, splenectomy if there is splenic vein thrombosis. Less amenable to tx than esophageal varices.Esophageal varices c cirrhosis: vit k and ffp. Vasopressin or octreatide to lower portal pressure. Endoscopic sclerotherapy.
Acute bleeding of varices: 1. Band the bleeding vessels 2. Correct coagulopathy ffp and platelets. 3. Iv octreotide or vasopressin. 4. Repeat endoscopy. 5. Tips if amenable. High morbidity. Can proceed with balloon tamponade alternatively. In all cases- give beta block.

Question 90

Symptoms of carotid artery disease

Answer 90

TIA, amaurosis fugax: ophthalmic artery first branch of internal carotid, aphasia, stroke, bruit -procede with carotid Doppler. 70 percent or more stenosis with sx should have endarterectomy. Cardiac evaluation should be performed as well. Risk of perioperative stroke 1-3 percent.

Question 91

Treatment of lung cancer – small cell vs. non-small cell

Answer 91

Small cell lung cancer:
o Central location
o Sensitive to chemotherapy
o Surgery is not indicated.
o Poor prognosis (2 to 4 months from diagnosis to death)
Non–small cell lung cancer:
o Includes squamous, large cell, and adenocarcinoma o Poor response to chemotherapy
o Treated with surgery (debulking)
o Prognosis varies with stage

Question 92

Effects of pulmonary functions from: anesthesia, sepsis (ARDS)

Answer 92

ANESTHESIA: The primary functions of the respiratory system are:
1. Ventilation; the movement of air into and out of the lungs.
2. Gas exchange; the transfer of oxygen into the blood and the removal of carbon dioxide.
General anesthesia has a number of effects on both of these key functions. The passage of gas into the lungs may be impaired by obstruction of the airway; the drive to ventilation may be reduced or cease altogether; the distribution of gas within the lungs may change and the transfer of oxygen (and anesthetic gases) into the blood may be impaired. Most of these adverse effects can be seen during anesthesia and in many patients these extend into the post-operative period.
SEPSIS (ARDS): Acute lung injury caused by inflammatory process in both lungs causing increased permeability of the capillaries and severe V/Q mismatch. These patients are tachypneic and hypoxic and have bilateral crackles on lung exam.
The diagnostic criteria are: 1. Bilateral, fluffy infiltrates on chest x-ray; 2. Refractory hypoxemia; 3. No evidence of heart failure (PCWP ≤ 18 mm Hg). The diagnosis requires all three criteria.
CAUSES
There is a wide variety of causes of ARDS. The most common are: Sepsis (most common), Infectious pneumonia, Blood products, Aspiration, Severe trauma, burns
MANAGEMENT
It is often necessary to intubate because of hypoxemia. Treat underlying cause.
PEEP is often used

Question 93

Malignant hyperthermia

Answer 93

DEFINITION: Autosomal dominant inherited hypermetabolic syndrome occurring after exposure to an anesthetic agent (very rare, but life threatening).
ETIOLOGY: Impaired reuptake of calcium by sarcoplasmic reticulum in muscles.
SIGNS AND SYMPTOMS: Tachycardia, Hyperthermia, Hypercarbia, Hypoxemia, Acidosis, Muscle rigidity, Ventricular dysrhythmias
TREATMENT: Discontinue anesthetics, Benzodiazepines (work fastest to control hypermetabolic state). Dantrolene (considered more definitive treatment, but onset of action takes about 30 minutes).

Question 94

Dysphagia (esophageal disorders)

Answer 94

DEFINITIONS
-Dysphagia: Difficulty swallowing, occurs when there is obstruction to the passage of food from the mouth to the stomach.
Odynophagia: Pain on swallowing. May or may not accompany dysphagia.
TYPES
-Mechanical: Patient typically reports difficulty swallowing solids more than liquids. -Neuromuscular: Patient typically reports difficulty swallowing both solids and liquids. CAUSES
Mechanical
-Foreign body
-Inflammation (infectious esophagitis, caustic exposure)
-Strictures (inflammatory, post-irradiation)
-Neoplasms
-Extrinsic compression (aortic aneurysm, retropharyngeal abscess, thyromegaly, etc.) Neuromuscular
-Tongue paralysis
-Lesions of cranial nerves IX and/or X
-Disorders of the neuromuscular junction (NMJ) (e.g., myasthenia gravis)
-Primary disorders of muscle (e.g., polymyositis, dermatomyositis)
-Disorder of esophageal smooth muscle (scleroderma, achalasia, diffuse esohageal spasm)

Question 95

DDX for hematuria

Answer 95

The source of RBCs in the urine can be anywhere from the kidney glomerulus to the urethral meatus. Causes of hematuria may be generally grouped into the site of origin: glomerular and non-glomerular. Non-glomerular can be subdivided by whether the process is located in the upper urinary tract (kidney and ureter) or the lower urinary tract (bladder and urethra).
Glomerular:
IgA nephropathy (Berger’s), glomerulonephritis (ie: poststreptococcal, diffuse proliferative, hereditary), RPGN, Alport syndrome
Non-glomerular:
Upper tract: Urolithiasis, pyelonephritis, renal cell cancer, transitional cell carcinoma, urinary obstruction, benign hematuria
Lower tract: Bacterial cystitis, BPH, strenuous exercise, transitional cell carcinoma, spurious hematuria (ie: menses), instrumentation, benign hematuria.

Question 96

Diagnosis of neurogenic shock

Answer 96

Neurogenic shock refers to diminished tissue perfusion as a result of loss of vasomotor tone to peripheral arterial beds. Loss
of vasoconstrictor impulses results in increased vascular capacitance, decreased venous return, and decreased cardiac output.
Neurogenic shock is usually due to injuries to the spinal cord from fractures of the cervical or high thoracic vertebrae that
disrupt sympathetic regulation of peripheral vascular tone. Occasionally, an injury such as an epidural hematoma impinging on
the spinal cord can produce neurogenic shock without an associated vertebral fracture. Penetrating wounds to the spinal cord can
produce neurogenic shock as well.
The classic findings of neurogenic shock consist of decreased blood pressure associated with bradycardia (absence of reflexive
tachycardia due to disrupted sympathetic discharge), warm extremities (loss of peripheral vasoconstriction), motor and sensory
deficits indicative of an injury to the spinal cord, and radiographic evidence of a fracture in the vertebral column