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Surgery Clerkship > Hepatopancreaticobiliary > Flashcards

Hepatopancreaticobiliary Flashcards

1
Q

Why is biliary colic a misnomer? What is a better term?

A

Colicky pain waxes and wanes, but gallstone pain is constant, lasting from min to hours before dissipating.
Symptomatic cholelithiasis is better

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2
Q

What are the main risk factors for developing cholesterol gallstones?

A

Female
Fat
Forty
Fertile

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3
Q

Why is it important to distinguish between symptomatic cholelithiasis and acute cholecystitis?

A

Management: symptomatic cholelithiasis is managed as an OP with elective lap chole. Acute cholecystitis requires hospital admission, IV AB and urgent cholecystectomy

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4
Q

What are key differences in history between symptomatic cholelithiasis and acute cholecystitis?

A

SC: RUQ pain that resolves min to 3-4 hours
AC: Unremitting RUQ pain > 6 hours, N/V

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5
Q

What are key differences in PE between symptomatic cholelithiasis and acute cholecystitis?

A

SC: Mild RUQ tenderness to palpation
AC: Murphy’s sign

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6
Q

What are key differences in vitals between symptomatic cholelithiasis and acute cholecystitis?

A

SC: normal
AC: Fever, tachycardia

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7
Q

What are key differences in labs between symptomatic cholelithiasis and acute cholecystitis?

A

SC: normal WBC
AC: Elevated WBC with left shift

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8
Q

What are key differences in US findings between symptomatic cholelithiasis and acute cholecystitis?

A

SC: Gallstones
AC: Gallstones, GB wall thickening > 4mm, pericholecystic fluid, sonographic Murphy’s sign

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9
Q

What is the significance of RUQ pain + scapular pain in GB disease?

A

GB and scapula share same cutaneous dermatome: scapula receives cutaneous innervation from supraclavicular nerves: same STT pathways activated!

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10
Q

What is Murphy’s sign?

A

When RUQ palpated, patient ceases inspiration

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11
Q

What is significance of Murphy’s sign?

A

Specific to acute cholecystitis: represents focal peritonitis of anterior abdominal wall parietal peritoneum due to inflammation of adjacent gallbladder

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12
Q

Characterize somatic and visceral pain?

A

Somatic: well localized, secondary to peritoneal irritation
Visceral: difficult to localize: due to mechanical stretching of visceral organs

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13
Q

What is chronic cholecystitis?

A

Recurrent bouts of symptomatic cholelithiasis: cause chronic inflammation of GB with fibrotic changes on history consistent with “chronic cholecystitis”
* Biliary colic, symptomatic cholelithiasis and chronic cholecystitis are interchangeable terms

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14
Q

What exactly causes acute cholecystitis?

A

Sustained obstruction o the cystic duct (by a gallstone usually). This leads to inflammation and edema of the GB wall and eventually bacterial overgrowth and invasion of GB wall. Can lead to ischemia, necrosis and rarely GB perforation

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15
Q

What are typical organisms in bile in acute cholecystitis?

A

E. coli, Bacterioides, Klebsiella, Enterobacter, Enterococcus, Pseudomonas

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16
Q

What are the 3 components of bile?

A

Bile salts
cholesterol
Lecitihin

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17
Q

How to cholesterol gallstones form?

A

Concentration of cholesterol in bile exceeds its solubility: causes precipitation of cholesterol crystals. (Due to low concentration of bile salts or lecithin, or higher levels of cholesterol)

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18
Q

What is the dark color in pigmented stones comprised of?

A

Calcium bilirubinate

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19
Q

What are black pigmented gallstones associated with? What is the black pigment composed of, and where are they found?

A

Hemolytic disease: hereditary spherocytosis or sickle cell.

Composed of unconjugated bilirubin in the GB

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20
Q

What are brown pigmented gallstones associated with? Where are they found?

A

Associated with bacterial infection and parasites.

Found in the bile ducts where they form, more common in Asian countries.

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21
Q

What is choledocolithiasis?

A

Obstruction of CBD

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22
Q

What is cholangitis?

A

Obstruction of common bile duct
bacterial overgrowth
infection of the entire biliary tree which ascends into liver

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23
Q

What is acute gallstone pancreatitis?

A

Obstruction of the common bile duct and pancreatic duct causing pancreatic enzyme release

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24
Q

What is Mirizzi’s syndrome?

A

Large gallstone impacted in the cystic duct, compressing the common hepatic duct

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25
Q

What is the next step in the work-up for suspected acute cholecystitis?

A
  1. RUQ US to look for:
    gallstones
    GB thickness (>4mm)
    Pericholecystic fluid
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26
Q

What is sonographic Murphy’s sign?

A

Direct pressure to RUQ by US probe when patient inspires, and pain causes cessation of inspiration. More specific!

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27
Q

What is a normal CBD diameter? Dilated?

A

Normal 4-5mm

CBD > 6mm considered abnormally dilated

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28
Q

How accurate is US to detect gallstones in GB vs. CBD?

A

GB: > 95% sensitive and 97% specific
CBD: Sensitivity of only 50% since bowel gas interferes

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29
Q

What if US shows gas bubbles in GB wall?

A

Concern for emphysematous cholecystitis: GB infected with gas forming organisms causing a necrotizing soft-tissue-like infection

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30
Q

Who get emphysematous cholecystitis?

A

Older men with diabetes mellitus

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31
Q

What labs should be sent in presence of RUQ and epigastric pain? Why?

A 
Total/direct bili
AST
ALT
Alk phos
GGT
To rule out other conditions like hepatic disease, pancreatitis
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32
Q

What are the proper tests for synthetic liver function?

A

Serum albumin
PT
INR

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33
Q

What if acute cholecystitis is suspected but US does not demonstrate gallstones?

A
  • False negative US with very small stones or very few

- Acalculous cholecystitis in critically ill patients

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34
Q

What causes acalculous cholecystitis?

A
  • Biliary stasis + GB ischemia with severe illness

- TPN associated with it

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35
Q

What is the next step if gallstones aren’t seen on US but biliary disease is suspected?

A

HIDA scan

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36
Q

How do we treat acalculous cholecystitis?

A

Emergent cholecystectomy or cholecystostomy tube to decompress GB

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37
Q

With a patient with clinically confirmed acute cholecystitis, how to manage?

A
  1. Admit
  2. NPO
  3. IV fluids and IV antibiotics for gram negative and anaerobic coverage
  4. Lap chole w/in 48 hours
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38
Q

What are best antibiotics for acute cholecystitis?

A
  • 2nd gen
  • cephalosporins
    broad spectrum penicillin/beta lactamase inhibitors
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39
Q

Do incidental gallstones require surgery?

A

No

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40
Q

What is major complication of lap chole that is most common in setting of acute cholecystitis?

A

CBD injury: higher risk in men and during surgery for acute cholecystitis

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41
Q

How to manage injury to the CBD during GB surgery?

A

<50% injury: primary via stent
>50% injury: loop of jejunum brought up to anastomose to proximal end of bile duct. Don’t attempt primary repair: could form ischemic stricture

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42
Q

How does CBD injury manifest when it isn’t recognized until late?

A

ab pain, bloating, anorexia and elevated LFTs

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43
Q

How do we work up suspected delayed CBD injury?

A
  1. US and/or CT
  2. Sepsis?
  3. If no: HIDA scan
  4. If bile leak or no flow to duodenum: ERCP
    (See flow chart page 162)
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44
Q

What is differential if lap chole patient develops RUQ pain several weeks after operation?

A 
Post-cholecystectomy syndrome:
1 residual stone in CBD
2 gallstone in cystic duct stump
3 dysfunction of biliary tree
4 Gastritis, PUD
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45
Q

What is the work-up for RUQ pain several weeks after lap chole?

A

CBC
Liver function tests
RUQ US
ERCP if needed

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46
Q

What is ideal timing for cholecystectomy for patient with acute cholecystitis?

A

< 48 hours

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47
Q

When should acute cholecystitis be managed non operatively?

A

Critically ill patients may have too much operative risk

- if patient doesn’t improve with AB alone, place a percutaneous cholecystectomy tube

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48
Q

When to suspect gangrenous cholecystitis?

A 
Severe, unrelenting abdominal pain
High fever
Persistent tachycardia
Markedly elevated WBC
Hyponatremia
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49
Q

What are the key symptoms associated with cholangitis?

A

Charcot’s triad: RUQ pain, jaundice, fever

Reynolds pentad: plus AMS and hypotension

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50
Q

What is the treatment for cholangitis?

A

Immediate decompression of biliary tract (ERCP)

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51
Q

What is the definition of SIRS?

A

2+ of the following:

  1. T > 100.4 or < 98.6
  2. HR >90
  3. RR > 20 / PaCO2 < 32 or mechanically vent
  4. WBC > 12 or < 4 or > 10% band forms
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52
Q

When does SIRS become sepsis?

A

When there is an identifiable source of infection

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53
Q

What are the diagnostic criteria for cholangitis?

A

Tokyo guidlines:

  1. Evidence of systemic inflammation (fever/leukocytosis)
  2. Cholestasis (jaundice and/or abnl liver enzymes)
  3. Biliary obstruction (dilated bile ducts on US)
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54
Q

What are the causes of obstructive jaundice that lead to cholangitis?

A 
MC: gallstones
Bile duct strictures
Parasites (Ascaris, Clonorchis sinensis)
Instrumentation of biliary tract (ERCP)
Indwelling biliary stents
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55
Q

When do we expect pale stools?

A

Prolonged biliary obstruction (NOT with gallstone cholangitis: too short)

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56
Q

At what level of bilirubin will jaundice first be visible? What is normal?

A

> 2.5 mg/dL

Normal up to 1.0 mg/dL

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57
Q

Where is jaundice first visible, and where does it progress?

A

First: sclerae of eyes and under tongue because BV more superficial!
Then: chest, abdomen, legs

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58
Q

What is Charcot’s triad? What is it classically associated with?

A

Fever
RUQ
jaundice
Cholangitis!

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59
Q

What percent of patients with cholangitis present with Charcot’s triad?

A

40-50%

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60
Q

What is Reynolds pentad? What percent of cholangitis patients have it?

A

Charcot’s triad + hypotension + AMS.

Only 5%

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61
Q

How can elderly patients present with cholangitis?

A

Asymptomatically until in septic shock

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62
Q

What is the mortality associated with cholangitis? Who dies?

A

5%: hepatic abscesses or if original biliary obstruction secondary to malignancy

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63
Q

Why are gallstones MCC of obstructive jaundice with cholangitis?

A

Need biliary obstruction + bacteria in bile. Gallstones MC because perfect vehicles to harbor bacteria in biliary tree! As the stone passes from GB: get trapped in distal CBD to harbor infection

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64
Q

What are potential consequences of unrecognized acute cholangitis?

A

Severe sepsis
Hepatic micro abscess
death

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65
Q

What are key differences in labs between hepatic and post hepatic jaundice?

A

Hepatic: Disproportionate rise in ALT/AST
Posthepatic: disproportionate rise in alk pos and GGT (confirm liver, not bone!)

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66
Q

What is imaging test for cholangitis?

A

RUQ US to look for dilation of CBD

*But - it is bad at seeing stones in CBD!

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67
Q

What is normal CBD diameter?

A

<4mm until age 40, then 1mm for every 10 years over 40

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68
Q

What are the 3 most important management steps after identifying SIRS?

A
  1. Aggressive fluid resuscitation
  2. Obtain blood cultures
  3. Broad spectrum antibiotics w/in 1 hour (cover enteric organisms)
  4. Coagulation studies due to increased risk of bleeding
69
Q

Where to admit patient with cholangitis?

A

ICU: hemodynamic monitoring/vasopressors if need hemodynamic support

70
Q

Once patient is stabilized, what intervention is recommended for cholangitis?

A

Drain infected bile by biliary decompression: in order of preference:

  • ERCP
  • percutaneous trans hepatic drainage
  • T-tube drain into CBD
71
Q

What is definitive management for cholangitis after biliary decompression?

A

Lap chole to prevent future episodes

72
Q

Why do cholangitis patients not get surgery immediately?

A

High morbidity/mortality bc septic patient subjected to general anesthesia / open procedure

73
Q

In an elderly patient with AMS or hypothermia alone, what should we always look for?

A

Send LFTs since cholangitis can easily be missed

74
Q

What to consider in a patient with bloody diarrhea and cholangitis?

A

UC with primary sclerosing cholangitis: inflammation and fibrosis of intrahepatic and extra hepatic bile ducts

75
Q

What does ERCP show in a patient with primary sclerosis cholangitis?

A

beaded appearance of pearls on a string

76
Q

Why can acute cholangitis be missed in elderly and immunosuppressed?

A
  • No fever or pain
77
Q

What is the differential for epigastric abdominal pain?

A 
Gastroenteritis
Acute gastritis
Acute cholecystitis
PUD
Perforated ulcer
Pancreatitis
Appendicitis
SBO
Mesenteric ischemia
Ruptured AAA
MI referred pain
78
Q

How to diagnose acute pancreatitis?

A

Clinically: 2/3:

  1. Sudden, severe persistent epigastric pain radiating to back
  2. Elevated lipase or amylase to 3x normal
  3. Characteristic imaging: enlarged pancreas, sentinel loops, colon cutoff sign
79
Q

What non surgical conditions can mimic an acute abdomen?

A 
Gastroenteritis
Acute adrenal insufficiency
sickle cell crisis
DKA
Acute porphyria
PID
Nephrolithiasis
Pyelonephritis
80
Q

What is Grey Turner’s sign and what does it indicate?

A

Blue-black discoloration in flanks: retroperitoneal hemorrhage due to acute pancreatitis

81
Q

What is Cullen’s sign and what does it indicate?

A

Blue-red discoloration at the umbilicus: digested blood products in retroperitoneum forming methemalbumin that then travel to anterior abdominal walls

82
Q

What is first step in evaluation for gallstones?

A

abdominal US

83
Q

What are the signs and symptoms of acute pancreatitis?

A

Epigastric pain radiating to the back (worsened with food)
N/V
Anorexia / decreased oral intake
PE: fever, tachycardia, epigastric tenderness w/ localized guarding, hypoactive bowel sounds

84
Q

What are the structures in the retroperitoneum?

A 
SAD PUCKER:
Suprarenal (adrenals)
Aorta
Duodenum (2/3)
Pancreas
Ureter
Colon (asc/desc)
Kidneys
Esophagus
Rectum
85
Q

What is the pathophysiology of pancreatitis?

A

Inappropriate activation of pancreatic enzymes leading to peripancreatic inflammation. Enzymes primarily damage peripancreatic tissues and vasculature: inflammatory response is out of proportion to insult, with time: damage leads to fluid sequestration, fat necrosis, vasculitis and hemorrhage

86
Q

What are etiologies for pancreatitis?

A 
GET SMASHED:
Gallstones (40%)
Ethanol (30%)
Tumors
Scorpion stings
Mycoplasma/mumps
Autoimmune (SLE)
Surgery / trauma
Hyper lipidemia/calcemia
Embolic / ischemic
Drugs / toxins
87
Q

What meds can cause pancreatitis?

A 
furosemide, thiazides
Sulfasalazine, ASA
Azathioprine
Valproate
Exenatide
Didanosine, pentamidine
88
Q

How do gallstones cause acute pancreatitis?

A

Gallstone passes into CBD and has transient impaction at ampulla: increases pancreatic duct pressure and causes reflux of duodenal juices and bile into the pancreatic duct

89
Q

In gallstone pancreatitis, how often does the gallstone remain impacted in distal CBD?

A

Not often: usually passes into duodenum shortly after impaction: ERCP not needed!

90
Q

How does alcohol cause acute pancreatitis?

A
  • Usually only after many years of abuse: intra-acinar activation of proteolytic enzymes necessary.
  • Ethanol metabolism byproducts: pancreatic hypoxia and oxidative damage
  • Excessive increase in Ca ion ccn in pancreatic cells
  • Overtime: sensitizes cells to respond to CCK prematurely: leading to inappropriate activation of zymogens in cells
91
Q

What are the key labs in acute vs. chronic pancreatitis?

A

Acute: high amylase and lipase
Chronic: low fecal elastase levels

92
Q

What are the key radiologic findings in acute vs. chronic pancreatitis?

A

Acute: dilated loops of bowel near pancreas (sentinel loops) on plain films
Chronic: pancreatic calcifications on plain films

93
Q

How many phases are there in acute pancreatitis?

A

3:
1 Premature activation of trypsin within pancreatic acing cells
2 Intrapancreatic inflammation
3 Extrapancreatic inflammation (affects multiple organ systems)

94
Q

How do we classify pancreatitis severity?

A

Mild: resolves 2-5 days
Severe: development of complications

95
Q

How do we define organ failure?

A

1 Shock < 90 systolic
2 PaO2 < 60
3 Creatinine > 2 after rehydration
4 GI bleeding > 500cc after 24 hours

96
Q

What is the mechanism for hypotension in pancreatitis?

A

Inflammation causes endothelial injury –>
1 increased permeability in peripancreatic vasculature–> fluid leaks into retroperitoneal space
2 Vasodilation –> hypotension

97
Q

What are pulmonary complications of acute pancreatitis?

A

Pleural effusions

ARDS

98
Q

How does pancreatitis cause pleural effusion?

A

Inflammation can obstruct lymph drainage around diaphragm: collection of lymph fluid travels across the diaphragm pores and into ipsilateral base on lung

99
Q

How does pancreatitis cause ARDS?

A

Severe inflammation can contribute to fistula formation between pancreatitis and thoracic cavity: free flow of pancreatic enzymes into the lungs

100
Q

What is the predominant histopathologic type of pancreatitis?

A

enlargement of pancreas due to inflammatory edema: no destruction of pancreatic cells or inflammation

101
Q

What is necrotizing pancreatitis? What is the mortality?

A

Necrotic pancreatic parenchyma: can lead to sepsis in over half of cases
17% mortality

102
Q

What are the Ranson criteria used for in acute pancreatitis?

A

Predict severity based on parameters at admission and 48 hours later

103
Q

Do amylase and lipase elevation correlate with the severity of acute pancreatitis?

104
Q

What is the main drawback of the Ranson criteria?

A

By 48 hours, most patients have declared themselves as to whether their course will be mild or severe

105
Q

Why does hypocalcemia occur in setting of pancreatitis?

A

FFA generated by pancreatic lipase: chelate calcium salts in the pancreas, leading to saponification (deposition of Ca soaps in retroperitoneum)

106
Q

What is the natural disease course of acute pancreatitis?

A

Recover in < 5 days

107
Q

What is most common cause of mortality in first week of acute pancreatitis?

A

1st week: multi organ failure due to severe systemic inflammatory response

108
Q

What is most common cause of mortality after the first week of pancreatitis?

A

Sepsis due to pancreatic necrosis of peripancreatic abscess. MUST drain abscess to reduce mortality!

109
Q

What are key labs to order when suspecting acute pancreatitis?

A 
Amylase/lipase
LFTs
Electrolytes
CBC
Lipid panel - rule out hyperlipidemia as cause
110
Q

In patients with hemorrhagic pancreatitis, what is an important marker that can be falsely reassuring?

A

Hematocrit: can take 1-2 days to equilibrate. plus dehydration can hemoconcentration: falsely elevated or nl!

111
Q

What is the diagnostic imaging of choice for acute pancreatitis?

A

RUQ US bc gallstones are MCC

112
Q

What else can cause high amylase, besides pancreatic disease?

A 
Salivary disease (parotitis)
GI disease 
Gyn disease
Neoplasms
Renal failure: amylase really cleared
113
Q

What are classic abdominal XR findings in acute pancreatitis?

A
  1. Sentinel loop: dilated loops of small bowel in LUQ near pancreas
  2. Colon cutoff sign: distended proximal colon w/ abrupt collapse in LUQ at splenic flexure
    + Due to local ileus from pancreatic inflammation
114
Q

What is classic CXR finding in acute pancreatitis?

A

Pleural effusion: Left side

Strongly assoc w severe pancreatitis (85% patients have it)

115
Q

What is role of CT scan in evaluation of acute pancreatitis?

A

None - only use when diagnosis is in doubt

116
Q

When do we use CT for pancreatitis?

A

If patient is not clinically improving after several days of conservative management

117
Q

When is ERCP used in gallstone pancreatitis?

A

Only if suspected concomitant acute cholangitis

118
Q

What is initial management for acute pancreatitis?

A

Supportive: IVF, NPO, analgesics, NGT if vomiting

119
Q

Why do some clinicians prefer meperidine vs. morphine for pain control in acute pancreatitis?

A

Meperidine does not contract sphincter of Oddi (morphine does)
BUT: it also increases risk of seizures

120
Q

What is subsequent management of pancreatitis after supportive care?

A

If gallstones: cholecystectomy to reduce recurrence

If alcohol: counsel on cessation

121
Q

How does severity of pancreatitis affect management?

A
  1. Location of bed in hospital
  2. If severe: raises awareness for close monitoring
  3. Gallstone: assist in timing of cholecystectomy
122
Q

What to suspect: severe acute pancreatitis patient develops fever + leukocytosis 3 weeks into hospitalization?

A

Pancreatic abscess

123
Q

What to suspect: recently pancreatitis patient comes in 4 weeks later with persistent abdominal pain, palpable epigastric mass and persistently elevated amylase? How do we test for it?

A

Pancreatic pseudocyst: test with CT scan.

124
Q

What is management for pancreatic pseudocyst?

A

Most resolve w/in 6 weeks with supportive treatment.

  • Intervene if > 6cm or persists > 6 weeks or symptomatic
  • Do internal drainage: connect cyst and adjacent intestine
125
Q

What is timing of cholecystectomy in mild vs. severe gallstone pancreatitis?

A

Mild: w/in 48-72 hours
Severe: weeks later

126
Q

What are the complications of chronic pancreatitis?

A

1 Diabetes: destruction of beta-islet insulin-producing cells
2 Steatorrhea
3 Chronic pain

127
Q

What is the most common indication for surgical management in chronic pancreatitis? What is done?

A

Severe and persistent pain: place stent in pancreatic duct to improve pancreatic juice flow

128
Q

Should prophylactic antibiotics be administered for sever acute pancreatitis?

A

No: inflammation, not infection

129
Q

In a patient with HTN on HCTZ, what to consider as cause for pancreatitis?

A

Hypercalcemia: can cause secretory block in pancreatic duct. Patient may be normocalcemic since pancreatitis causes hypocalcemia.

130
Q

What are the complications of pancreatitis: early and late?

A

1st week: Development of systemic complications (organ failure)
3 weeks plus: pancreatic complications (pseudocyst, abscess, necrosis

131
Q

If a pancreatitis patient does not clinically improve within 3 days of conservative management, what is the next step?

A

Get CT scan with contrast to look for underlying complications

132
Q

In patients with prolonged NPO status due to acute pancreatitis or their condition is severe, what should be done about nutrition?

A

Begin enteral nutrition

133
Q

What is the differential diagnosis of jaundice in terms of location?

A

Preheptic/hemolytic
Intrahepatic/hepatocellular
Posthepatic

134
Q

What is in the differential for prehepatic jaundice?

A

Hemolytic anemia

Gilbert’s

135
Q

What is in the differential for hepatic jaundice?

A 
Ischemic liver injury
Viral
Toxic ingestion
Primary biliary cirrhosis
Primary sclerosing cholangitis
Wilson's disease
136
Q

What is in the differential for posthepatic jaundice?

A 
Choledocholithiasis
Acute cholangitis
Chronic pancreatitis
Mirizzi syndrome
Pancreatic carcinoma
Ampullary carcinoma
Cholangiocarcinoma
137
Q

What is Courvoisier’s sign?

A

palpable RUQ mass = non tender, enlarged GB which signifies obstruction of CBD. Associated with malignancy

138
Q

What is the implication of painful vs. painless jaundice?

A

Painful: gallstone obstruction
Painless: insidious obstruction, associated with malignancy

139
Q

What are the risk factors for pancreatic cancer?

A 
Chronic pancreatitis
Tobacco
High fat diet
Male gender
Family history
Recent onset DM
140
Q

What are the risk factors for cholangiocarcinoma?

A

UC/primary sclerosis cholangitis

141
Q

What are the risk factors for adenocarcinoma of the GB?

A

Long standing gallstone disease

142
Q

Where is jaundice best detected?

A

Mucous membranes of mouth
Palms/soles
Sclerae
* places not exposed to sunlight: more bilirubin due to lack of photodegeneration

143
Q

What is a sister Mary Joseph nodule?

A

Periumbilical mass: possible metastatic abdominal or pelvic malignancy (usually stomach, pancreatic)

144
Q

What is Blumer’s shelf?

A

Step-off felt during rectal exam: suggests metastatic disease to pouch of Douglas. Usually mets from lung, pancreas, stomach cancer

145
Q

What is the mechanism behind “clay colored stools”?

A

Biliary obstruction decreases bilirubin in intestines: decreasing stercobilin and causing clay-colored stools

146
Q

In a patient with obstructive jaundice, what labs are characteristic?

A

Elevated T bili

Elevated alk phos

147
Q

What initial imaging for painful jaundice?

148
Q

What is the imaging recommendation for painless jaundice?

A

triple phase abdominal CT: contrast during:

  1. Arterial phase
  2. Early venous phase
  3. Late venous phase
    * Detect pancreatic and periampullary masses to provide information about its respectability
149
Q

What is the role of MRCP and ECRP in evaluation for jaundice?

A

Only if no mass is seen and cause of biliary obstruction is unclear!

150
Q

What is the role of CA 19-9 and CEA in pancreatic cancer?

A

Not for screening: can use for monitoring or prognostication if malignancy is suspected.
CA 19-9: pancreatic
CEA: colorectal cancer

151
Q

What makes pancreatic cancer unresectable?

A

1 Tumor invasion into SMA, celiac or hepatic arteries

2 Metastatic disease

152
Q

Do we biopsy a resectable pancreatic mass?

A

No: just resect!

153
Q

What is the the role of preoperative stunting in presence of pancreatic mass with obstructive jaundice?

A

No benefit

154
Q

What is the role of neoadjuvant therapy for pancreatic adenocarcinoma?

A

Only to shrink “borderline resectable” tumors to make them resectable

155
Q

What is the surgical management of pancreatic or periampullary cancer?

A

Whipple procedure: pancreaticoduodenectomy. If it is resectable!

156
Q

What other conditions besides pancreatic cancer is a Whipple performed?

A

Cancer of duodenum, cholangiocarcinoma and ampullary carcinoma

157
Q

In non-resectable pancreatic tumors, what conditions warrant palliative procedures?

A

Chronic abdominal pain
Gastric outlet obstruction
Symptomatic biliary obstruction

158
Q

What is the most common complication from a Whipple?

A

Gastroparesis: treat with metoclopramide

159
Q

Is there a high risk of diabetes after a Whipple?

A

Only if patient had elevated glucose before the procedure

160
Q

When to suspect a pancreatic or biliary leak after a Whipple?

A

Look at drain:

  • Sanguinous drainage: hemorrhage
  • green drainage: biliary leak
  • Milky-gray white fluid with a sheen on bulb: pancreatic leak (will have high amylase)
161
Q

What is a non-specific clinical sign of post-operative (Whipple) leak?

A

tachycardia

162
Q

How can pancreatic cancer cause increased INR?

A

Need bile for vitamin K absorption

163
Q

How to treat increased INR from biliary tract obstruction/pancreatic cancer?

A

Parenteral vitamin K

FFP

164
Q

If a stricture is seen in the biliary tree without a mass, what diagnostic step should follow?

A

FNA or biopsy

165
Q

If a periampullary mass is unresectable, what are the next treatment options?

A

Biliary stent
Palliative chemotherapy
Surgical bypass (biliary and intestinal)

166
Q

How do we treat a borderline resectable periampullary mass?

A
  • Consider neoadjuvant chemotherapy

- Repeat imaging to assess for surgical intervention

167
Q

What labs for suspected periampullary / pancreatic mass?

A

LFTs: Bili, AST, ALT, ALP

Amylase/Lipase to rule out pancreatitic

168
Q

What are the 3 most common causes of malignant biliary obstruction?

A

Pancreatic cancer
Cholangiocarcinoma
Ampullary carcinoma

Surgery Clerkship (16 decks)

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