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CHAPTER 33
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Pancreas
1. From which vessel does the most common anatomic
variant of the right (replaced) hepatic artery arise from?
A. Left gastric artery
B. Aorta
C. Superior mesenteric artery
D. Gastroduodenal artery
2. According to Ranson’s criteria a 67-year-old female
patient suspected of acute pancreatitis presenting to
the operating room (OR) with sudden onset of severe
abdominal pain, a serum aspartate aminotransferase
(AST) > 250 U/dL, a WBC > 16,000/mm3, and a blood
glucose > 200 mg/dL would receive a disease classification of:
A. Severe.
B. Mild, uncomplicated.
Answer: C
In 15% to 20% of patients, the right hepatic artery will arise
from the superior mesenteric artery and travel upward
toward the liver along the posterior aspect of the head of the
pancreas (referred to as a replaced right hepatic artery). It is
important to look for this variation on preoperative computed
tomographic (CT) scans and in the operating room so the
replaced hepatic artery is recognized and injury is avoided.
(See Schwartz 11th ed., p. 1433.)
Answer: A
See Table 33-1. (See Schwartz 11th ed., p. 1445, Table 33-7.)
TABLE 33-1 Ranson’s prognostic signs of pancreatitis
Criteria for acute pancreatitis not due to gallstones
At admission During the initial 48 h
Age > 55 y Hematocrit fall > 10 points
WBC > 16,000/mm
Blood glucose > 200 mg/dL Serum calcium < 8 mg/dL
Serum LDH > 350 IU/L Arterial PO2 < 60 mmHg
Serum AST > 250 U/dL Base deficit > 4 mEq/L
Criteria for acute gallstone pancreatitis
At admission During the initial 48 h
Age > 70 y Hematocrit fall > 10 points
WBC > 18,000/mm
Blood glucose > 220 mg/dL Serum calcium < 8 mg/dL
Serum LDH > 400 IU/L Base deficit > 5 mEq/L
Serum AST > 250 U/dL Estimated fluid sequestration > 4 L
Note: Fewer than three positive criteria predict mild, uncomplicated disease, whereas
more than six positive criteria predict severe disease with a mortality risk of 50%.
Abbreviations: AST = aspartate transaminase; BUN = blood urea nitrogen; LDH = lactate
dehydrogenase; PO2 = partial pressure of oxygen; WBC = white blood cell count.
Data from Ranson JHC. Etiological and prognostic factors in human acute pancreatitis:
a review. Am J Gastroenterol. 1982;77:633 and from Ranson JH, Rifkind KM, Roses DF,
et al. Prognostic signs and the role of operative management in acute pancreatitis.
Surg Gynecol Obstet. 1974;139:69.
3
3
BUN elevation > 5 mg/dL
Estimated fluid sequestration > 6 L
BUN elevation > 2 mg/dL
289
290
Very heavy drinking (15%)
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3. In the setting of acute pancreatitis, following aggressive
fluid resuscitation, what is the most ideal nutritional
approach?
A. Patient should undergo strict bowel rest until resolu-
tion of inflammation.
B. Enteral feeding can be started as early as 24 hours fol-
lowing stabilization.
C. Parenteral nutrition is preferred, to be started early
CHAPTER 33
after stabilization.
D. Tube feeding is inferior to parenteral nutrition dur-
ing inflammation.
4. What is the most common cause of chronic pancreatitis?
Pancreas
A. Hyperparathyroidism
B. Alcohol abuse
C. Idiopathic
D. Genetic
Answer: B
In contrast to analgesia and fluid therapy, there is a sound evidence base for nutritional support in acute pancreatitis. It is
no longer acceptable to “rest the pancreas” by avoiding enteral
nutrition, now the mainstay of nutritional support. Parenteral nutrition is now known to be more expensive, riskier,
and not more effective than enteral nutrition and should only
be offered if the patient’s calculated nutritional requirements
cannot be achieved by the enteral route. Early initiation of
enteral nutrition (within the first 24 hours of admission) is
not superior to delaying an oral diet until 72 hours. If this is
not tolerated over 48 to 72 hours, then nasogastric tube feedings can be started and increased in step-wise fashion over 2
to 3 days. (See Schwartz 11th ed., p. 1446.)
Answer: C
There are a variety of chronic pancreatitis etiologies, the most
common of which are idiopathic, genetic, heavy drinking,
obstructive, hyperlipidemia, hyperparathyroidism, etc. Idiopathic and genetic predispositions together comprise of more
than half of the root causes of chronic pancreatitis. A variety
of genes have been identified to play a role in chronic pancreatitis, with the cystic fibrosis transmembrane conductance
regulator (CFTR) gene being the most prevalent influencer
(Fig. 33-1). (See Schwartz 11th ed., p. 1452, Figure 33-17.)
5. In patients undergoing endoscopic retrograde cholangiopancreatography (ERCP) for diagnosis and staging
of chronic pancreatitis, the population most at risk of
developing procedure-induced pancreatitis are those
with:
A. Calculus disease.
B. Intraductal lesions.
C. Sphincter of Oddi dysfunction.
D. High percentage of parenchymal calcification.
Alcohol + genetic (3%)
Idiopathic
(42%)
Gallstone /
severe AP
(3%)
FIG. 33-1. Etiologies of chronic pancreatitis. (Reproduced with
permission from Whitcomb DC: Going MAD: development of a “matrix
academic division” to facilitate translating research to personalized
medicine, Acad Med. 2011;86(11):1353–1359.)
Genetic
(24%)
Obstructive
(9%)
Hyperlipidemia,
Autoimmune,
Other (4%)
CFTR
(14%)
CFTR +
SPINK1
(3%)
SPINK1
(4%)
PRSS1
(3%)
Answer: C
For the diagnosis and staging of chronic pancreatitis, ERCP
is considered to be the gold standard. It also serves as a
vehicle that enables other diagnostic and therapeutic maneuvers, such as biopsy or brushing for cytology, or the use of
stents to relieve obstruction or drain a pseudocyst. Unfortunately, ERCP also carries a risk of procedure-induced pancreatitis that occurs in approximately 5% of patients. Patients
at increased risk include those with sphincter of Oddi
6. Pain from chronic pancreatitis can be caused by:
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A. Ductal hypertension.
B. Parenchymal disease.
C. Obstructive pancreatopathy.
D. All of the above.
dysfunction and those with a previous history of post-ERCP
pancreatitis. Post-ERCP pancreatitis occurs after uncomplicated procedures, as well as after those that require prolonged
manipulation. Severe pancreatitis and deaths have occurred
after ERCP. It should be reserved for patients in whom the
diagnosis is unclear despite the use of other imaging methods, or in whom a diagnostic or therapeutic maneuver is specifically indicated. (See Schwartz 11th ed., pp. 1459–1560.)
Answer: D
Pain from chronic pancreatitis has been ascribed to three
possible etiologies. Ductal hypertension, due to strictures or
stones, may predispose to pain that is initiated or exacerbated
by eating. Chronic pain without exacerbation may be related
to parenchymal disease or retroperitoneal inflammation with
persistent neural involvement. Acute exacerbations of pain in
the setting of chronic pain may be due to acute increases in duct
pressure or recurrent episodes of acute inflammation in the setting of chronic parenchymal disease. Nealon and Matin have
described these various pain syndromes as being predictive of
the response to various surgical procedures. Pain that is found
in association with ductal hypertension is most readily relieved
by pancreatic duct decompression, through endoscopic stenting or surgical decompression. (See Schwartz 11th ed., p. 1460.)
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CHAPTER 33
Pancreas
7. What is the most ideal modality for evaluation of chronic
pancreatitis?
A. Computed tomography (CT) abdomen pelvis
B. Magnetic resonance cholengiopancreatography
(MRCP)
C. Endoscopic retrograde cholangiopancreatography
(ERCP)
D. Endoscopic ultrasonography (EUS)
Answer: D
EUS has heavily impacted the evaluation and management of
patients with chronic pancreatitis. Although it is more operator-dependent than transabdominal ultrasonography, EUS
provides not only imaging capability but also adds the capacity to obtain cytologic and chemical samples of tissue and fluid
aspirated with linear array monitoring (Fig. 33-2). EUS images
obtained through a high-frequency (7.5- to 12.5-mHz) transducer are able to evaluate subtle changes in 2- to 3-mm structures within the pancreas and can detect indolent neoplasms in
the setting of chronic inflammation. Small intraductal lesions,
intraductal mucus, cystic lesions, and subtle ductular abnormalities are recognizable by EUS (Table 33-2). This allows ERCP to
be reserved for these patients who require therapeutic maneuvers, or for the evaluation of more complex problems. EUS is
comparable to ERCP in the detection of advanced changes in
chronic pancreatitis and may be more sensitive than ERCP in
the detection of mild disease. (See Schwartz 11th ed., p. 1457.)
FIG. 33-2. Endoscopic ultrasound of
chronic pancreatitis. The endoscopic
ultrasound appearance of the
parenchyma is heterogeneous, and
dilated ducts are seen, indicating early
obstructive pancreatopathy. (Reproduced
with permission from Mark Topazian,
Division of Digestive Diseases, Department
of Medicine, Mayo Clinic.)
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CHAPTER 33
Pancreas
TABLE 33-2 Endoscopic ultrasound features of chronic pancreatitis
Endoscopic Ultrasound Feature Implication
Ductal changes
Duct size > 3 mm Ductal dilation
Tortuous pancreatic duct Ductal irregularity
Intraductal echogenic foci Stones or calcification
Echogenic duct wall Ductal fibrosis
Side-branch ectasia Periductal fibrosis
Parenchymal changes
Inhomogeneous echo pattern Edema
Reduced echogenic foci (1–3 mm) Edema
Enhanced echogenic foci Calcifications
Prominent interlobular septae Fibrosis
Lobular outer gland margin Fibrosis, glandular atrophy
Large, echo-poor cavities (>5 mm) Pseudocyst
Reproduced with permission from Catalano MF, Lahoti S, Geenen JE, et al.: Prospective evaluation of
endoscopic ultrasonography, endoscopic retrograde pancreatography, and secretin test in the diagnosis of
chronic pancreatitis, Gastrointest Endosc. 1998;48(1):11-17.
8. Which component of the pancreas is associated with the
long-term inflammatory process in chronic pancreatitis,
subsequently addressed in surgical resection?
A. The head
B. The body
C. The neck
D. The tail
9. Which of the following is the imaging modality of choice
for initial diagnosis of exocrine tumors?
A. Computed tomography (CT) with oral and intrave-
nous (IV) contrast
B. Positron emission tomography-CT (PET-CT)
C. CT with four-phase contrast
D. Magnetic resonance imaging (MRI)
Answer: A
The common element of these variations on the theme of
LR-LPJ remains the excavation or “coring out” of the central
portion of the pancreatic head. It remains uncertain, however, whether and to what degree the dichotomy needs to be
extended into the body and tail. The logical conclusion of all
of these efforts is that the head of the pancreas is the nidus of
the chronic inflammatory process in chronic pancreatitis and
that removal of the central portion of the head of the gland is
the key to the successful resolution of pain in the long term.
(See Schwartz 11th ed., p. 1478.)
Answer: C
As with pancreatic exocrine tumors, the initial diagnostic
imaging test of choice for pancreatic endocrine tumors is a
multidetector CT scan with four phases of contrast and fine
cuts through the pancreas and liver. Neuroendocrine tumors
of the pancreas often enhance with contrast. EUS can be
superior to CT in localizing these tumors, which can produce
dramatic symptoms despite their small (<1 cm) size. In contrast to pancreatic exocrine tumors, many of the endocrine
tumors have somatostatin receptors (SSTRs) that allow them
to be detected by a radiolabeled octreotide scan. A radioactive
somatostatin analogue is injected intravenously, followed by
whole-body radionuclide scanning (Fig. 33-3). The success of
this modality in localizing tumors and detecting metastases
has decreased the use of older techniques such as angiography and selective venous sampling. (See Schwartz 11th ed.,
p. 1480.)
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CHAPTER 33
Pancreas
10. Which of the following is the most common presenting
symptom in patients with a somatostatinoma?
A. Cholelithiasis
B. Constipation
C. Hypoglycemia
D. Hypocalcemia
FIG. 33-3. Radioactive octreotide scan
demonstrating pancreatic endocrine
tumor in the body of the pancreas
(arrow).
Answer: A
Because somatostatin inhibits pancreatic and biliary secretions, patients with a somatostatinoma present with gallstones due to bile stasis, diabetes due to inhibition of insulin
secretion, and steatorrhea due to inhibition of pancreatic
exocrine secretion and bile secretion. Most somatostatinomas originate in the proximal pancreas or the pancreatoduodenal groove, with the ampulla and periampullary area
as the most common site (60%). The most common presentations are abdominal pain (25%), jaundice (25%), and
cholelithiasis (19%). This rare type of pancreatic endocrine
tumor is diagnosed by confirming elevated serum somatostatin levels, which are usually above 10 ng/mL. Although
most reported cases of somatostatinoma involve metastatic
disease, an attempt at complete excision of the tumor and
cholecystectomy is warranted in fit patients. (See Schwartz
11th ed., p. 1483.)
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11. Treatment of a 1 cm gastrinoma in the wall of the duodenum is best accomplished by:
A. Enucleation.
B. Full-thickness resection.
C. Duodenectomy.
D. Whipple procedure.
CHAPTER 33
Pancreas
Answer: B
Fifty percent of gastrinomas metastasize to lymph nodes or
the liver, and are therefore considered malignant. Patients who
meet criteria for operability should undergo exploration for
possible removal of the tumor. Although the tumors are submucosal, a full-thickness excision of the duodenal wall is performed if a duodenal gastrinoma is found. All lymph nodes in
Passaro triangle are excised for pathologic analysis. If the gastrinoma is found in the pancreas and does not involve the main
pancreatic duct, it is enucleated. Pancreatic resection is justified
for solitary gastrinomas with no metastases. A highly selective
vagotomy can be performed if unresectable disease is identified
or if the gastrinoma cannot be localized. This may reduce the
amount of expensive proton pump inhibitors required. In cases
in which hepatic metastases are identified, resection is justified
if the primary gastrinoma is controlled and the metastases can
be safely and completely removed. Debulking or incomplete
removal of multiple hepatic metastases is probably not helpful, especially in the setting of MEN1. The application of new
modalities such as radiofrequency ablation seems reasonable,
but data to support this approach are limited. Postoperatively,
patients are followed with fasting serum gastrin levels, secretin
stimulation tests, octreotide scans, and CT scans. In patients
found to have inoperable disease, chemotherapy with streptozocin, doxorubicin, and 5-fluorouracil (5-FU) is used. Other
approaches such as somatostatin analogues, interferon, and
chemoembolization also have been used in gastrinoma with
some success. (See Schwartz 11th ed., p. 1482.)
12. Which of the pancreatic endocrine tumors are associated
with diabetes and dermatitis?
A. Glucagonoma
B. Somatostatinoma
C. Insulinoma
D. VIPoma
13. Which of the following have been proven to significantly reduce the rate of pancreatic leak following
pancreaticoduodenectomy?
A. Stent
B. Glue
C. Octreotide
D. None of the above
Answer: A
Diabetes in association with dermatitis should raise the suspicion of a glucagonoma. The diabetes usually is mild. The
classic necrolytic migratory erythema manifests as cyclic
migrations of lesions with spreading margins and healing
centers typically on the lower abdomen, perineum, perioral
area, and feet. Patients also complain of an enlarged, sensitive tongue. The diagnosis is confirmed by measuring serum
glucagon levels, which are usually >500 pg/mL. Glucagon is
a catabolic hormone, and most patients present with malnutrition. The rash associated with glucagonoma is thought to
be caused by low levels of amino acids. Preoperative treatment usually includes control of the diabetes, parenteral
nutrition, and octreotide. Like VIPomas, glucagonomas are
more often in the body and tail of the pancreas and tend to
be large tumors with metastases. Again, debulking operations
are recommended in good operative candidates to relieve
symptoms. (See Schwartz 11th ed., p. 1483.)
Answer: D
Considerable attention has been focused on the prevention
of pancreatic leak after pancreas resection. Modifications of
the anastomotic technique (end-to-side or end-to-end, ductto-mucosa, or invaginated), the use of jejunum or the stomach for drainage, the use of pancreatic duct stents, the use of
octreotide, and various sealants have all been evaluated.
Long-acting synthetic analogues of somatostatin have been
evaluated as a pharmacologic therapy to reduce pancreatic
secretion and the rate of pancreatic fistula after pancreatic
resection. Some European studies supported benefit particularly in selected higher risk patients, while previous North
14. A pancreatic cystic neoplasms that is <3 cm has atypical
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cells present and has a solid component requires:
A. A repeat computed tomography (CT) scan in 3 to 6
months.
B. A repeat CT scan in 1 year.
C. Continued observation.
D. Resection.
Are any of the following high-risk stigmata of malignancy present?
(i) obstructive jaundice in a patient with cystic lesion of the head of the pancreas,
(ii) enhancing solid component within cyst, (iii) main pancreatic duct ≥10 mm in size
Yes
Imaging: (i) cyst ≥3 cm, (ii) thickened/enhancing cyst walls, (iii) main duct size 5–9 mm, (iii) nonenhancing
Consider
surgery,
if clinically
appropriate
mural nodule, (iv) abrupt change in caliber of pancreatic duct with distal pancreatic atrophy.
If yes, perform endoscopic ultrasound
American trials concluded there was no benefit. A recent
single-center, randomized trial with Pasireotide (a newer
analog) suggested potential benefit.
Use of a pancreatic duct stent across the anastomosis has
been suggested as a means of preventing a pancreatic leak and
as an aid in technical precision. Both internal stenting as well
as external stenting have been practiced. A recent Cochrane
analysis of eight randomized, controlled trials failed to identify any convincing evidence of benefit with internal or external pancreatic duct stents. Some previous studies indicated
that stents might be harmful. A recent multicenter randomized trial comparing external to internal pancreatic duct
stents during pancreaticoduodenectomy showed a lower rate
of pancreatic fistula with internal stents, so this controversy is
likely to continue. (See Schwartz 11th ed., p. 1497.)
Answer: D
See Fig. 33-4. (See Schwartz 11th ed., p. 1501, Figure 33-78.)
No
Are any of the following worrisome features present?
Clinical: Pancreatitis
a
No
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CHAPTER 33
Pancreas
Yes
<1 cm
CT/MRI
in 2–3 years
a. Pancreatitis may be an indication for surgery for relief of symptoms.
b. Differential diagnosis includes mucin. Mucin can move with change in patient position, may be dislodged on
cyst lavage and does not have Doppler ow. Features of true tumor nodule include lack of mobility, presence of
Doppler ow and FNA of nodule showing tumor tissue.
c. Presence of any one of thickened walls, intraductal mucin or mural nodules is suggestive of main duct
involvement. In their absence main duct involvement is inconclusive.
d. Studies from Japan suggest that on follow-up of subjects with suspected BD-IPMN there is increased incidence
of pancreatic ductal adenocarcinoma unrelated to malignant transformation of the BD-IPMN(s) being followed.
However, it is unclear if imaging surveillance can detect early ductal adenocarcinoma, and, if so, at what interval
surveillance imaging should be performed.
d
Are any of the following features present?
(ii) Main duct features suspicious for involvement
(iii) Cytology: suspicious or positive for malignancy
(i) Denite mural nodule(s)
1–2 cm
CT/MRI
yearly × 2 years,
then lengthen
interval
if no change
d
b
2–3 cm >3 cm
EUS in 3–6 months, then
lengthen interval alternating MRI
with EUS as appropriate.
Consider surgery in young,
t patients with need for
prolonged surveillance
c
No
What is the size of largest cyst?
Inconclusive
d
MRI with EUS every 3–6 months.
Strongly consider surgery in young,
Close surveillance alternating
t patients
FIG. 33-4. Algorithm for management of pancreatic cystic neoplasms. CEA = carcinoembryonic antigen;
CT = computed tomography; ERCP = endoscopic retrograde cholangiopancreatography; EUS = endoscopic
ultrasound; FNA = fine-needle aspiration; Hx = history; IPMN = intraductal papillary mucinous neoplasm of the
pancreas; MCN = mucinous cystic neoplasm; MRCP = magnetic resonance cholangiopancreatography. (Reproduced
with permission from Tanaka M, Adsay V, Chari S, et al. International consensus guidelines 2012 for the management of
IPMN and MCN of the pancreas, Pancreatology. 2012;12(3):183–197.)
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15. The endoscopic retrograde cholangiopancreatography
(ERCP) finding that is virtually diagnostic of intraductal
papillary mucinous neoplasms (IPMNs) is:
A. A fish-eye lesion.
B. Calcification.
C. Beaded or chain-of-lakes appearance of the duct.
D. Cysts that resemble serous cystadenomas.
CHAPTER 33
Pancreas
Answer: A
IPMNs usually occur within the head of the pancreas and
arise within the pancreatic ducts. The ductal epithelium
forms a papillary projection into the duct, and mucin production causes intraluminal cystic dilation of the pancreatic
ducts (Fig. 33-5). Imaging studies demonstrate diffuse dilation of the pancreatic duct, and the pancreatic parenchyma
is often atrophic due to chronic duct obstruction. However,
classic features of chronic pancreatitis, such as calcification and a beaded appearance of the duct, are not present.
At ERCP, mucin can be seen extruding from the ampulla of
Vater, a so-called fish-eye lesion, that is virtually diagnostic of
IPMN. (See Schwartz 11th ed., p. 1502.)
FIG. 33-5. Intraductal papillary mucinous neoplasm histology.
Papillary projections of ductal epithelium resemble villous
morphology and contain mucin-filled vesicles. (Reproduced with
permission from Asiyanbola B, Andersen DK. IPMN. Editorial Update.
accesssurgery.com McGraw Hill; 2008.)
CHAPTER 34
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The Spleen
1. A patient with which of the following diseases would
most benefit from splenectomy?
A. Acute myeloid leukemia with neutropenia
B. Chronic lymphocytic leukemia with thrombocyto-
penia
C. Hairy cell leukemia with abnormal lymphocytes
D. Hodgkin lymphoma with lymphocytopenia
2. You are seeing a 13-year-old girl in clinic for a painless
lump in the left upper abdominal quadrant. Her father
reports she had jaundice as a newborn and on occasion,
she becomes pale. The father also says multiple relatives
have had their spleen removed for hemolytic anemia.
You order a complete blood count. Which of the following findings would identify the most likely etiology for
this presentation?
A. Anemia and thrombocytopenia
B. Thrombocytopenia and leukocytosis
C. Elevated mean corpuscular hemoglobin and elevated
red cell distribution width
D. Lymphocytosis and monocytosis
Answer: B
Chronic lymphocytic leukemia (CCL) is a subtype of nonHodgkin lymphoma (NHL) with the main characteristic
being a progressive accumulation of old and nonfunctional
lymphocytes. Symptoms of CLL are nonspecific and include
weakness, fatigue, fever without illness, night sweats, and frequent bacterial and viral infections. The most frequent finding is lymphadenopathy. When the spleen is enlarged, it may
be massive or barely palpable below the costal margin. Splenectomy is indicated to improve cytopenias and was shown
to be 75% effective in a combined group of patients who had
either CLL or nonmalignant Hodgkin disease (HD). Splenectomy may thus facilitate chemotherapy in patients whose cell
counts are prohibitively low before spleen removal. Palliative
splenectomy also is indicated for symptomatic splenomegaly.
The remaining disease processes are not likely to improve
with splenectomy. (See Schwartz 11th ed., p. 1528.)
Answer: C
Hereditary spherocytosis (HS) is the most common type of
hemolytic anemia for which splenectomy is indicated and
the third most common type of congenital hemolytic anemia
overall. Patients with typical HS forms may have mild jaundice. Splenomegaly usually is palpable on physical examination. Laboratory examination reveals varying degrees of
anemia: patients with mild forms of the disease may not have
anemia; patients with moderate to severe forms may have
hemoglobin levels as low as 4 to 6 g/dL. The mean corpuscular volume is typically low to normal or slightly decreased.
For screening, a combined elevated mean corpuscular hemoglobin concentration and an elevated erythrocyte distribution
width are an excellent predictor. Other laboratory indicators
of HS include those providing evidence of rapid red blood cell
destruction, including elevated reticulocyte count, elevated
lactate dehydrogenase level, and increased level of unconjugated bilirubin. Spherocytes are readily apparent on peripheral blood film. (See Schwartz 11th ed., p. 1524.)
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