General Surgery (Board Review Series) 1st Edition

17

Pancreas and Spleen

Thomas G. Gleason

1. Pancreas
2. Embryology
3. The pancreas develops from

• the dorsal pouch(the endodermal lining of the duodenum) and the ventral pouch (the hepatic diverticulum).

1. The ventral pouch

• migrates posteriorly and clockwise to fuse with the dorsal pouch.

1. Failure of normal clockwise rotation

• results in an annular pancreas.

2. The ventral duct normally fuses

• with the distal dorsal duct to form the main pancreatic duct, the duct of Wirsung.

1. Pancreas divisum (Figure 17-1)

• occurs when these ducts do not fuse (in 25% of people).

1. The unfused proximal dorsal duct

• forms the accessory duct of Santorini.

1. Anatomy
2. The pancreas consists ofthe

• head (with uncinate process).
• neck.
• body.
• tail.

2. Blood supply(Figure 17-2)
3. The head

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• is supplied by the anterior and posterior pancreaticoduodenalarteries and veins.

Figure 17-1. Pancreatic divisum. No connection between the main pancreatic and accessory pancreatic ducts. (Reprinted with permission from Howard JM, Jordan, Jr GL, Reeber HA: Surgical Diseases of the Pancreas. Baltimore, Williams & Wilkins, 1987, p 22.)

1. The proximal body

• is supplied by the superior and inferior pancreaticarteries and veins originating from the celiac or splenic arteries.

1. The distal body and tail

• are supplied by the short branches of the splenicand gastroepiploic arteries and veins and the dorsal pancreatic artery.

Figure 17-2. Arterial supply of the pancreas. (Reprinted with permission from Howard JM, Jordan, Jr GL, Reeber HA: Surgical Diseases of the Pancreas. Baltimore, Williams & Wilkins, 1987, p 26.)

3. Nodal groups

. The pancreatic head

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• drains into the subpyloric, portal, mesocolic, and aortocaval nodes.

1. The body and tail

• drain into the retroperitoneal celiac, mesocolic, mesenteric, and aortocaval nodes.

1. Histology and physiology
2. Exocrine cells
3. Acinar cells

• contain digestive enzymes (e.g., amylase, lipase, phospholipase A₂, trypsin, chymotrypsin, elastase).

1. Ductal cells

• secrete an electrolyte solution high in bicarbonate(HCO₃^-).

2. Pancreatic secretions
3. Cholecystokininand acetylcholine

• stimulate enzyme secretion.

2. Most peptidasesare secreted in inactive forms: trypsin, chymotrypsin, elastase, kallikrein, carboxypeptidase A and B.
3. The peptidases are activated intraluminally by enterokinase.
4. Nucleases, lipase, and amylase are secreted in their active forms.
5. Secretinand vagal efferents

• stimulate HCO₃^-secretion—the substrate is a clear, isotonic, basic solution (pH 8), with 30–120 mEq/L HCO₃^-.

3. Endocrine cells: islets of Langerhans
4. Alpha cellsproduce glucagon.
5. Beta cellsproduce insulin.
6. Delta cellsproduce somatostatin.
7. F cellsproduce pancreatic polypeptide.
8. Islets also produce

• vasoactive intestinal peptide (VIP).
• serotonin.
• pancreastatin.
• calcitonin gene related peptide (CGRP).
• neuropeptide Y.
• gastrin-releasing peptide.

1. Pancreatitis
2. Acute pancreatitis
3. Etiology
4. The most common causesof pancreatitis are alcohol abuse and gallstones.
5. Other causesinclude

• endoscopic retrograde cholangiopancreatography (ERCP).
• trauma.
• hyperlipidemia.

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• medications (e.g., azathioprine, furosemide, glucocorticoids, cimetidine).
• Ascaris lumbricoidesand Opisthorchis sinensis.
• viruses (e.g., coxsackie, mumps)
• hypercalcemia.
• scorpion bite.

2. Enzymes contributingto saponification, hemorrhage, and necrosis include

• trypsin.
• lipase.
• phospholipase A₂.
• elastase.

3. Signs and symptoms

. Patients typically present with

• abdominal pain.
• nausea.
• vomiting.
• anorexia.

1. Signs of complex diseaseinclude

• retroperitoneal hemorrhage of the flank (Grey Turner sign).
• umbilicus (Cullen sign).
• inguinal ligament (Fox sign).

4. Diagnosis

• Work-up should focus on identifying the cause and severity of illness.

1. Laboratory studiesshould include

• amylase.
• lipase.
• values needed for establishing Ranson's criteria(Table 17-1).

1. Ranson's criteria

• are used as a prognostic indicator in pancreatitis.

2. Patients with more than 3 Ranson's criteriaare at high risk for developing complicated pancreatitis (abscess or necrosis).
3. Mortalitysharply rises with more than 3 Ranson's criteria (see Table 17-1)
4. Abdominal imaging(i.e., computed tomography [CT] scan with intravenous [IV] contrast) may show

• a sentinel loop.
• edematous pancreas.
• nonenhancement of the pancreas (necrotic pancreatic tissue).

1. Ultrasound

• is used to identify gallstone disease and biliary ductal dilation.

1. ERCP

• helps evaluate pancreatic ductal anatomy and pathology.

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5. Treatment

• is nonoperativeunless complications develop (i.e., necrosis or infection).

1. Aggressive fluid resuscitation

• is an essential part of treatment.

1. Intubation and mechanical ventilation

• should be instituted if significant pulmonary dysfunction occurs (e.g., partial pressure of oxygen [pO₂] less than 60 mm Hg).

1. Nasogastric decompression

• is used to relieve vomiting.

1. Nutritional support

• is an important adjunct, but controversy exists about which form is ideal.

1. Most agree that early in a course of complicated acute pancreatitis total parenteral nutrition (TPN) is indicated.
2. If patients tolerate enteral feeding, it should initially occur distal to the ampulla of Vater via a nasoenteric tube or jejunostomy.
3. ERCP with endoscopic sphincterotomy(ES)

• is indicated in patients with gallstone pancreatitis and biliary obstruction.

1. The use of prophylactic antibiotics(i.e., imipenem-cilastatin)

• lowers the infection rate.
• may lower the mortality rate in necrotizing pancreatitis(see II C 2).

Table 17-1. Ranson's Criteria and Predicted Mortality

Less than 24 Hours Age > 55 White blood cells (WBC) > 16 × 103/µL Lactate dehydrogenase (LDH) > 350 IU/L Asparate aminotransferase (AST) > 250 IU/L Glucose > 200 mg/dL Less than 48 Hours Fluid sequestration > 6 L Base deficit > 4 PO2 < 60 mm Hg Hematocrit (Hct) decrease > 10% Ca2+ < 8 mg/dL Blood urea nitrogen (BUN) increase > 5 mg/dL Predicted Mortality Number of Criteria Percent Mortality 3–4 signs 28% 5–6 signs 40% > 7 signs 100%

1. Gallstone pancreatitis

• is characterized by pancreatitis identified in the setting of cholelithiasis.

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1. Blockage of the pancreatic duct

• appears to play an important role.

2. Uncomplicated pancreatitis with concomitant biliary obstruction

• should be treated by preoperative ERCP with ESand stone extraction.

1. Laparoscopic cholecystectomy

• should then be performed, once the acute pancreatitis resolves.

1. Intraoperative cholangiography(IOC)

• should be performed to confirm the absence of common bile duct obstruction.

3. Gallstone pancreatitis without biliary obstruction

• should initially be treated medically, followed by laparoscopic cholecystectomy before discharge.

1. Complicated acute pancreatitis
2. Pancreatic abscesses

• are typically polymicrobial.

1. Well-circumscribed abscesses

• should be drained percutaneously.

1. Operative drainageshould be reserved

• for failed attempts at percutaneous drainage.
• with infected pancreatic necrosis or multiloculated, poorly defined fluid collections.

2. Necrotizing pancreatitis

. Sterile (uninfected) necrosis

1. These patients should be treated nonoperativelyduring the first several weeks to better delineate viable and nonviable pancreatic tissue.
2. Necrotic tissue or fluid collectionsshould be sampled percutaneously with CT-guidance if the patient develops bacteremia, sepsis, or deterioration.
3. Administering antibioticswith imipenem-cilastatin decreases the infection rate in patients with sterile pancreatic necrosis.
4. Infected necrosis
5. If CT-guided aspirates demonstrate infection, débridement of necrotic pancreatic tissue (necrosectomy) and operative drainage (open or closed) are indicated.
6. Many patients require reoperation for further débridement.
7. IV antibioticsdirected at the organisms cultured from the pancreatic bed are indicated.
8. Peritoneal lavage

• has been proposed as an adjunctive therapy for necrotizing pancreatitis.

3. Enterocutaneous or enteroperitoneal fistulae

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• develop in over 20% of patients with pancreatic necrosis.
• Over 50%of enterocutaneous fistulae will resolve spontaneously after adequate drainage is established (see Chapter 13).

1. Pancreas divisum (see Figure 17-1)
2. The majority of patients with pancreas divisum

• have no clinical manifestations.

2. A minority of patients with accessory duct (duct of Santorini) stenosis

• develop recurrent acute pancreatitis.

3. These patients can be treated

• endoscopically or surgically.

1. Endoscopic treatmentincludes

• dilation.
• sphincterotomy, stent placement, or both.

1. Surgical therapy

• entails a transduodenal sphincteroplasty.

1. Chronic pancreatitis

• corresponds with irreversible parenchymal fibrosis.

1. Manifestationsof chronic pancreatitis may include

• recurrent bouts of acute pancreatitis.
• chronic abdominal pain.
• anorexia and weight loss.
• malabsorption and steatorrhea.
• diabetes.

2. The majority of casesin the United States are caused by alcohol abuse.
3. The diagnosisis based on clinical and radiographic findings.

• CT findingstypically demonstrate an atrophied gland, areas of dilated pancreatic duct, and calcifications.

4. Primary treatment
5. Abstinence from alcohol

• will help prevent acute exacerbations.

1. Supportive care

• will include pain control and nutritional support.

5. Relative indications for surgeryinclude

• refractory, disabling pain.
• concern of concomitant malignancy.
• biliary obstruction.
• complications of pseudocysts (e.g., bowel obstruction, splenic artery pseudoaneurysm, splenic vein thrombosis).

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6. Operative techniquesused for chronic pancreatitis

. Drainage procedures

1. The Duval procedureis a retrograde drainage with distal resection and end-to-end pancreaticojejunostomy.
2. The modified Peustow procedureis a side-to-side pancreaticojejunostomy.
3. The Frey procedureis a longitudinal pancreaticojejunostomy with partial pancreatic head resection.
4. Resection procedures
5. Distal pancreatectomyis useful in chronic pancreatitis secondary to distal pancreatic trauma.
6. A modified Whipple procedure(Figure 17-3) may be appropriate for an inflammatory mass of the pancreatic head.
7. Total pancreatectomyis rarely indicated for diffuse chronic pancreatitis with a nondilated pancreatic duct.
8. Splanchnicectomy

• or celiac ganglionectomy or ganglion ablation may be useful for pain control.

Figure 17-3. Anastomoses of a standard pancreaticoduodenectomy (Whipple procedure). (Reprinted with permission from Bell RH, Rikkers LF, Mulholland MW: Digestive Tract Surgery. Philadelphia, Lippincott-Raven, 1995, p 866.)

1. Pancreatic pseudocysts

• are nonepithelialized, encapsulatedpancreatic fluid collections.

1. Typically, pseudocysts mature

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• from pancreatic fluid collections several weeks after bouts of acute pancreatitis.

2. Symptomsinclude pain, fever, weight loss, and bowel obstruction by external compression.
3. A CT scanis often diagnostic (Figure 17-4).
4. Small cysts(< 5 cm)

• will usually resolve spontaneously.

5. Large cysts(> 6 cm)

• are more likely (75%) to require drainage, but they should be allowed to mature a capsule for at least 6 weeksbefore attempted drainage.

1. Image-guided percutaneous drainage

• has a failure or reaccumulation rate of at least 30%–40%.

1. Operative drainage techniques(e.g., cystgastrostomy)

• have significantly lower recurrence rates than percutaneous techniques.

1. Endoscopic cystgastrostomy or cystenterostomy

• are newer techniques that may be used for draining these cysts, but recurrence rates are not yet defined.

Figure 17-4. CT scan of a pancreatic pseudocyst. G = gallbladder; P = pseudocyst; S = stomach compressed by pseudocyst. (Reprinted with permission from Daffner RH: Clinical Radiology: The Essentials, 2nd ed. Baltimore, Williams & Wilkins, 1999, p 333.)

1. Pancreatic fistulae
2. Pancreatitis-associated pleural effusions

• may require ERCP with pancreatic stent placement to control pancreatic drainage.

2. Pancreatic ascites

• When persistent, these should similarly be treated by pancreatic ductal stenting.

3. Low-output (< 200 mL/day) pancreaticocutaneous fistulae

• typically resolve spontaneously.

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1. Treatment

• is similar to treatment of small bowel fistulae (see Chapter 13).

1. Octreotide

• may help decrease the volume of a fistula and convert a high-output (> 200 mL/day) into a low-output fistula.

1. Pancreatic insufficiency

• generally refers topancreatic exocrine insufficiency, but often occurs with endocrine insufficiency.

1. It generally occurs in the setting of

• long-standing chronic pancreatitis.
• after total pancreatectomy (over 90% of exocrine function must be lost).

2. Symptoms

• include malabsorption and steatorrhea.

3. Diagnosis

• To confirm diagnosis, fecal fat testingand the secretin or cholecystokinin test are used most frequently.

4. Treatment

• includes a high-carbohydrate, high-protein diet with pancreatic enzyme replacement.

III. Pancreatic Carcinoma

1. Epidemiology and pathology
2. The incidence
3. Pancreatic carcinoma

• occurs in approximately 1/10,000 people.
• is twice as common in African Americans and 1.5 times as common in men versus women.

1. This carcinoma typically develops in the seventh decade of life.
2. Tobacco useappears to be a risk factor for its development.
3. Ninety percent of pancreatic carcinomasare of ductal cell origin.
4. Sixty to seventy percent of adenocarcinomasarise in the head of the pancreas.
5. The majority (60%–65%) of periampullary cancersare pancreatic.
6. Pancreatic adenocarcinomastypically metastasize to the lymph nodes, liver, and peritoneal surfaces.
7. Five-year survival ratesrange from 0%–10% in the United States. Most patients die within one year.
8. Other neoplasmsof the exocrine pancreas have a more favorable prognosis than adenocarcinomas.
9. Papillary-cystic neoplasms

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• of the pancreas are usually cured by resection.

1. Serous cystadenomas

• are generally benignand are treated with resection to exclude malignancy.

1. Mucinous cystadenomas

• often contain malignantcells and, like cystadenocarcinomas, have a 60% 5-year survival rate after surgery.

1. Pancreatic lymphomas

• are rare (1%–2% of pancreatic cancers) and are treated with chemotherapy.

1. Metastatic tumors

• of the pancreas are rare but can arise from renal cell carcinomas or other non-Hodgkin's lymphomas.

1. The tumor-node-metastasis (TNM) staging system

• for pancreatic cancers is outlined in Table 17-2.

Table 17-2. Tumor-Node-Metastasis (TNM) Staging System of Pancreatic Carcinoma

Stage Primary Tumor Nodal Disease Distant Metastases I T1 or T2 N0 M0 II T3 N0 M0 III T1, T2 or T3 N1 M0 IV T1, T2 or T3 N0 or N1 M1 Primary tumor T1 No extension beyond the pancreas T2 Limited direct extension (e.g., to duodenum, bile ducts, or stomach) T3 Extension incompatible with resection Nodal disease N0 None N1 Regional nodal disease Distant metastases M0 None M1 Distant metastatic disease

1. Presentation and diagnosis
2. Most patients presentwith weight loss, jaundice, or both.
3. Other manifestationsinclude

• abdominal pain.
• nausea and anorexia.
• jaundice.
• hepatomegaly.
• vomiting secondary to duodenal obstruction.

3. Laboratory signsinclude

• elevated conjugated bilirubin.

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• elevated alkaline phosphatase.
• mild elevations of amylase.

4. Nonspecific tumor markersinclude

• mucin-associated carbohydrate antigens (e.g., CA 19–9).
• carcinoembryonic antigen (CEA).
• mutated c-K-ras.

5. Important imaging modalitiesinclude

• contrast-enhanced dynamic CT.
• magnetic resonance cholangiopancreatography (MRCP).
• ERCP.
• percutaneous transhepatic cholangiography (PTHC).
• radiolabeled octreotide scanning.
• endoscopic ultrasound.

6. Radiographic studies

• may reveal a classic “double duct sign”(Figure 17-5) when both the pancreatic and common bile ducts are dilated.

Figure 17-5. Carcinoma of the head of the pancreas near the ampulla of Vater. CT scan demonstrates dilation of both the pancreatic and bile ducts (“double duct sign”). (Reprinted with permission from Howard JM, Idezuki Y, Ihse I, Prinz RA: Surgical Diseases of the Pancreas, 3rd ed. Baltimore, Williams & Wilkins, 1987, p 141.)

7. Fine-needle aspiration (FNA)remains somewhat controversial.

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• It does, however, appear to have reasonable sensitivity (~70%) and excellent specificity (100%).

1. Treatment of pancreatic adenocarcinoma

• Curecan only be achieved with surgical resection.
• Resectabilityis definitively determined intraoperatively, although spiral CT and MRI can predict vascular involvement.

1. Laparotomy allows palpation of the

• pancreatic head.
• superior mesenteric artery.
• superior mesenteric vein.
• portal veins.
• nodal beds.

1. Laparoscopy is less invasive

• but requires the use of ultrasound to evaluate for vascular invasion and nonvisible nodal beds.

1. Contraindicationsto curative resection include

• liver metastases.
• peritoneal metastases.
• nodal metastases beyond the zone of resection(e.g., periaortic).
• tumor invasionof the superior mesenteric artery.
• The type of resection dependson tumor location.

1. Tumors of the head

• require a Whipple procedure[see II E 6 b (2)].

1. Tumors of the tail and body

• are treated by distal or extended distal(near-total) pancreatectomy.

1. Total pancreatectomy

• for pancreatic cancer is generally avoided.
• Pre- or postoperative adjuvant chemoradiotherapy
• (5-fluorouraciland external beam radiation) may increase 2-year survival rates.
• Complications of pancreaticoduodenectomyinclude
• delayed gastric emptying.
• pancreatic fistula(10%–20%).
• infection.
• bile leak.
• pancreatitis.
• Postoperative prognosis may be affected by
• lymph node involvement.
• vascular invasion.
• a clear margin of resection.
• the need for blood transfusions.

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• Patients with unresectable tumors
• may require palliative surgery to treat intractable jaundice or duodenal obstruction.

1. Jaundice

• can be palliated by internal or external biliary stents or a biliary bypass (choledochojejunostomy).

1. Duodenal obstruction

• can be treated by gastrojejunostomy.

1. Endocrine Pancreatic Neoplasms

Table 17-3. Endocrine Tumors of the Pancreas

Tumor Features Usual Site Diagnosis % Malignant Treatment Insulinoma Whipple's triad Pancreas, evenly distributed Fasting glucose and insulin levels 10% Enucleation or resection Gastrinoma Peptic ulcers, diarrhea Gastronoma triangle Secretin stimulation test 50% Resection, omeprazole VIPoma Watery diarrhea, hypokalemia, achlorhydria Distal pancreas Elevated PP and VIP in setting of diarrhea > 50% Resection, distal pancreatectomy, octreotide Glucagonoma Diabetes, necrolytic migratory erythema Body and tail of pancreas Skin biopsy, fasting glucagon level > 80% Resection, distal or extended distal pancreatectomy Somatostatinoma Diabetes, steatorrhea, gallstones Periampullary head of pancreas Fasting somatostatin level > 90% Resection of bulky disease, cholecystectomy Nonfunctional Large mass: pain, weight loss, jaundice Throughout pancreas Abdominal imaging: CT/MRI 50%–90% Resection, chemotherapy VIPoma = vasoactive intestinal peptide tumor; PP = pancreatic polypeptide; CT = computed tomography; MRI = magnetic resonance imaging.

• are rare, occurring at a rate of 5 cases per million people per year.

1. Endocrine pancreatic tumors

• arise from neural crest cells called amine precursor uptake and decarboxylation (APUD) cells.
• may be functionalor nonfunctional, presenting as a space-occupying lesion (Table 17-3).

1. Functional tumors
2. Insulinomas

• are the most common endocrine tumor of the pancreas.
• Most (90%) insulinomas are benign.

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3. Symptoms
4. Most patients present with catecholamine surge–related symptoms, such as palpitations, diaphoresis, and tachycardia induced by hypoglycemia and relieved by carbohydrates.
5. Whipple's triadis typically documented:

• symptomatic hypoglycemia during fasting.
• serum glucose measurements of less than 50 mg/dL.
• relief of symptoms when administered glucose.

4. Diagnosis

• Insulinomas are diagnosed by concomitantly measuring insulinand glucose levels during a monitored fasting period of 12–18 hours.
• Measuring proinsulinor C-peptide levels can exclude the possibility of surreptitious insulin.

5. Fewer than 10% of patients with insulinoma

• have the multiple endocrine neoplasia (MEN) I syndrome, but those that do often have multiple insulinomas (see Chapter 20).

1. Gastrinomastypically present with

• abdominal pain.
• intractable peptic ulcer disease (PUD).

1. Of patients with recurrent PUD, 2% have gastrinomas.
2. Occurrence

• Seventy-five percent of gastrinomas occur sporadically.
• Twenty-five percent occur in patients with MEN type 1 (see Chapter 20).

1. Gastrinomas are associated with

• amplification of the HER-2/neuproto-oncogene.

1. Initial diagnosis

• is confirmed with the secretin stimulation test.

1. Gastrinomas typically(90%) are found

• within the gastrinoma triangle(Figure 17-6).

1. Halfof these tumors are malignant.
2. Vasoactive intestinal peptide tumors (VIPomas)

• present with the Verner-Morrisonor WDHA syndrome (watery diarrhea, hypokalemia, and achlorhydria.)

1. Diagnosis

• of these tumors is typically made by excluding other causes of diarrhea and documenting elevated VIP levels.

1. Ten percent of VIPomas are extrapancreatic (i.e., retroperitoneum, thorax).
2. Over 50%of VIPomas present with metastatic disease to lymph nodes or liver.
3. Glucagonomaspresent with

• severe dermatitis.
• diabetes.

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• stomatitis.
• weight loss.

1. The dermatitis

• is called necrolytic migratory erythema.
• tends to wax and wane in severity, spreading in a serpentine-like fashion.

1. Skin biopsyaids in diagnosis

• but elevated fasting glucagon levelsare more conclusive.

1. These tumors tend to be

• fairly large.
• easily seen by contrast-enhanced CT.

1. Somatostatinomas

• have less distinguishable symptomatology often including steatorrhea, diabetes, hypochlorhydria, and gallstones.
• These tumors are very rare, occurring in fewer than 1 in 40 million people per year.

Figure 17-6. Gastrinoma triangle. (Reprinted with permission from Greenfield LJ, Mulholland MW, Oldham KT, Zelenock GB: Surgery: Scientific Principles and Practice, 2nd ed. Philadelphia, Lippincott-Raven, 1997, p 839.)

2. Nonfunctional tumors
3. These tumors present

• with symptoms of pain, weight loss, and jaundice because they are large and space-occupying.

1. Nonfunctional endocrine tumors

• tend to have a protracted, indolent course relative to pancreatic carcinomas.

1. Pancreatic polypeptidelevels

• may be elevated in these patients, but this is not specific for these tumors.

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1. Treatment
2. All pancreatic endocrine tumors

• are primarily treated by resection.

1. Metastatic diseaseprecludes curative resection.
2. The type of resection indicated

• depends on the tumor histologyand location (see Table 17-3).

2. Insulinomascan usually be enucleated although some may require formal resection.
3. Gastrinomasand somatostatinomas typically require pancreaticoduodenectomy.
4. VIPomasand glucagonomas usually require distal pancreatectomy.
5. Nonfunctional tumorsmay require either a Whipple procedure or a distal pancreatectomy.
6. Octreotide

• (or omeprazole for gastrinoma) may be helpful in ameliorating symptoms in patients with VIPomas and glucagonomas.

3. Chemotherapy

• (e.g., streptozocin and doxorubicin) may be helpful with nonfunctional pancreatic endocrine tumors and insulinomas.

4. Radiotherapyhas not improved survival.
5. Survival rates
6. Insulomas

• Over 90% are curablewith resection.

2. Gastrinomas

• Sixty to seventy percent are curable with resection.

3. Somatostatinomas

• Most are incurable.

4. Nonfunctional tumors

• After resection, the 5-year survival rateis 50%.

1. Spleen
2. Embryology
3. The spleen arisesfrom mesenchymal cells in the dorsal mesogastrium.
4. Accessory spleensoccur in 20% of people and are most frequently found within the splenic hilum or the splenic ligaments.
5. Anatomy
6. The arterial blood supplyis primarily via the splenic artery, which does not branch until it enters the hilum.
7. Short gastric vessels

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• emanate from the left gastroepiploic artery supplying some arterial blood.

1. The venous drainage vessels

• parallel the arterial supply with the splenic vein abutting the posteroinferior aspect of the pancreas.

2. The splenic parenchyma consists of

• red pulp(erythrocytes).
• white pulp(lymphocytes and monocytes).

3. Blood either passesthrough capillaries directly into venous sinusoids (closed circulation), or into the red pulp (open circulation).
4. Physiology of the spleen
5. The red pulpof the spleen acts as a filter to remove damaged or aged erythrocytes.
6. The white pulpof the spleen harbors leukocytes that serve to mount both nonspecific and specific immune responses.
7. Within the spleen macrophages phagocytose

• cellular, particulate debris and poorly opsonized bacteria.

1. The lymphocyte population

• produces a large percentage of nonspecific opsoninsincluding tuftsin, properdin, and fibronectin.

1. Antigen processing

• occurs in the spleen upon interaction between macrophages and helper T cells.

1. Diseases Treated by Splenectomy (Table 17-4)
2. Splenic trauma

• is the primary indicationfor splenectomy.

1. Splenic injuries

• are gradedby severity (Table 17-5).

2. Indications for operative interventionassociated with splenic trauma include

• hemodynamic instability.
• arterial “blushing” or “pooling of contrast” on abdominal CT.
• active bleedingconfirmed by falling blood counts and the need for blood transfusions (> 2 units packed red blood cells [PRBC]).

3. Patients with grade IV or V injuries

• generally require splenectomy.

4. Primary repair of the spleen (splenorrhaphy)

• should be attempted only in hemodynamically stable patients.

1. Hereditary spherocytosis (HS)
2. HS is a hereditary disease

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• transmitted by an autosomal dominanttrait.
• characterized by the formation of poorly deformable erythrocyte membranes.

Table 17-4. Indications for Splenectomy

Disease Description and Caveats Trauma Resection with hilar involvement, significant parenchymal disruption, active bleeding ITP Steroid therapy; IV gamma globulin and plasmapheresis are primary therapies; resection reserved for refractory disease TTP Resection as last resort after failed medical therapy Myeloproliferative diseases Resection for symptomatic splenomegaly—may reduce transfusion requirements Lymphoma Resection occasionally indicated for symptomatic splenomegaly Hereditary spherocytosis Resection is curative Felty's syndrome Resection improves responses to infection and treats symptomatic splenomegaly Splenic abscess CT-guided percutaneous drainage occasionally successful, otherwise resection Parasitic cysts Resection indicated Sarcoidosis, Gaucher's disease Resection for symptomatic splenomegaly may improve symptoms Splenic vein thrombosis Resection cures the sinistral portal hypertension ITP = idiopathic thrombocytopenic purpura; IV = intravenous; TTP = thrombotic thrombocytopenic purpura; CT = computed tomography.

2. Red blood cells

• are sequesteredand destroyed by the spleen.

3. Patients

• become anemic.
• become jaundiced.
• develop splenomegaly.

4. Splenectomyis curative and should be delayed until age 4.

Table 17-5. Grading System for Classification of Splenic Injuries

Grade Description of Injury I Subcapsular hematoma > 10% surface area, capsular tear > 1 cm II Subcapsular/intraparenchymal hematoma 10%–50% surface area/> 5 cm diameter, laceration 1 cm–3 cm depth III Large (> 50% surface area, > 5 cm diameter) subcapsular/intraperitoneal hematoma, expanding or ruptured hematoma, > 3 cm laceration involving trabecular vessel IV Laceration involving hilar or segmental vessel V Hilar avulsion or shattered spleen

1. Idiopathic thrombocytopenic purpura (ITP)

• occurs as a result of the development of anti-platelet antibodies(immunoglobulin [Ig]G) that direct platelet destruction and sequestration in the spleen.

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1. The clinical manifestations

• occur as a result of thrombocytopenia:purpura, ecchymoses, bleeding from mucosal surfaces, and hematuria.
• The spleen is notenlarged.

2. Treatment
3. Initial treatmentshould include

• corticosteroidsand IV gamma globulin directed at binding and neutralizing the antiplatelet antibodies.

1. For refractory cases

• that do not respond to steroids, Vinca alkaloids, cyclophosphamide, danazol, and plasmapheresis have been used.

1. Splenectomy

• is frequently effective.
• is reserved for patients who fail medical therapy or require continued steroid therapy to maintain adequate platelet counts.

1. Platelet transfusions

• should notbe given preoperatively.
• shouldbe given after the splenic blood supply is ligated.

1. Thrombotic thrombocytopenic purpura (TTP)

• is characterized by diffuse aggregation of platelets.
• Hyaline membrane deposits throughout capillary systems, causing profound thrombocytopenia.

1. A pentad syndrome

• of fever, purpura, hemolytic anemia, hematuria, and neurologic changesis typical.

2. Hemolytic uremic syndrome (HUS)

• of children has a similar presentation and disease course.

3. Treatment
4. Plasmapheresisis the mainstay of treatment.
5. Splenectomyis reserved for patients with disease refractory to plasmapheresis and is frequently unsuccessful at effectively treating TTP.
6. Splenic abscesses

• are typically caused by hematogenous spread of a bacterial infection (endocarditisand IV drug abuse most common).
• may be amenable to CT-guided percutaneous drainage but may require splenectomy.

VII. Hypersplenism

• refers to a condition associated with splenomegaly, decreased and/or dysfunctional circulating platelets, and responsive bone marrow hypertrophy.

1. Types
2. Primary hypersplenism

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• is very rare and is a diagnosis of exclusion.

2. Secondary hypersplenismis more common and is associated with several diseases, such as

• myeloproliferative diseases.
• infections (e.g., mononucleosis).
• portal hypertension.
• congestive heart failure.
• Felty's syndrome (arthritis, splenomegaly, neutropenia).
• amyloidosis.
• sarcoidosis.
• malignancies (e.g., lymphomas).
• acquired immunodeficiency syndrome (AIDS).
• Gaucher's disease.
• polycythemia vera.
• systemic lupus erythematosus.

1. Splenectomy is generally indicated

• in patients with primary hypersplenism.
• in symptomatic splenomegaly associated with secondary hypersplenism (see Table 17-4).

VIII. Overwhelming Postsplenectomy Infection (OPSI)

1. After splenectomy

• patients are at risk for developing a life-threatening bacterial infection (0.5%).

1. Mortality

• from OPSI can be as high as 80%–90%.

1. Causes of OPSI

• are most often related to encapsulated organisms, particularly pneumococcalspecies (Streptococcus pneumoniae).

1. Prophylaxis

• should include vaccinationagainst Pneumococcal species, Meningococcal species, and Haemophilus influenza B.
• Vaccinationsshould ideally be given 10 days before splenectomy.
• After splenectomy childrenshould also receive prophylactic penicillin through adolescence.

1. Infections

• in postsplenectomy patients should be aggressively diagnosed and treated.

P.424

Review Test

Directions: Each of the numbered items or incomplete statements in this section is followed by answers or by completions of the statement. Select the ONE lettered answer or completion that is BEST in each case.

1. A 52-year-old man presented to his primary care physician 3 months ago with severe epigastric pain after an episode of hematemesis. Esophagogastroduodenoscopy (EGD) at that time revealed two large peptic ulcers in the first portion of the duodenum. He was placed on omeprazole after Helicobacter pylorititers were negative. After 6 weeks he returned to his physician with improved but continued pain. Repeat EGD revealed that the original ulcers were significantly smaller but there were several new ulcers both in the duodenum and in the antrum of the stomach. What is the next most appropriate step in the management of this patient?

(A) Repeat EGD in 6 weeks

(B) Abdominal ultrasound

(C) Highly selective vagotomy

(D) Vagotomy and pyloroplasty

(E) Secretin stimulation test

1–E. This patient may have Zollinger-Ellison syndrome (gastrinoma with intractable peptic ulcer disease), although this must be initially confirmed. A secretin stimulation test is often diagnostic. In patients with ZE syndrome, secretin administration increases serum gastrin levels, in contrast to the normal physiologic inhibition of gastrin secretion by secretin. Repeating the esophagogastroduodenoscopy (EGD) is unnecessary at this time because the patient does not seem to be actively bleeding. Abdominal ultrasound would not be particularly helpful, but once diagnosed, a gastrinoma can at times be localized by endoscopic ultrasound. Neither ulcer operation (vagotomy or pyloroplasty) is indicated before ruling out a gastrinoma.

2. A patient with a suspected gastrinoma has a markedly elevated serum gastrin level and the level failed to drop appropriately after secretin administration. Abdominopelvic computed tomography (CT) scan failed to reveal any pancreatic mass. Endoscopic ultrasound was also unrevealing. Which of the following would be the most appropriate next step in managing this patient?

(A) Distal pancreatectomy

(B) Vagotomy and pyloroplasty

(C) Mobilization of the duodenum and intraoperative ultrasound

(D) Whipple procedure (pancreaticoduodenectomy)

(E) Metronidazole, omeprazole, and clarithromycin therapy

2–C. Gastrinomas are located in the gastrinoma triangle in the majority of cases. They can often be seen by abdominal computed tomography (CT), magnetic resonance imaging (MRI), or endoscopic ultrasound. Other localizing modalities include selective portal venous gastrin sampling or radiolabeled octreotide scanning. Alternatively, as in this question, it is reasonable to explore the abdomen, initially focusing on the gastrinoma triangle by exposing and examining the duodenum and pancreatic head using intraoperative ultrasound. Neither distal pancreatectomy nor a Whipple procedure should be performed before more aggressive attempts are made at localizing the tumor. Ulcer operations are not indicated in patients with Zollinger-Ellison syndrome; even those with unresectable or metastatic tumors should be treated with omeprazole. This patient does not have Helicobacter pylori, thus antibiotic therapy would not be appropriate.

3. A 45-year-old man presents to the emergency room complaining of severe epigastric pain that radiates to his back and left scapula. He has had severe nausea and vomiting associated with the pain for 3 days. Nothing seems to relieve his pain. He drinks about a fifth of bourbon a day. He has not had a bowel movement in several days. He also complains of a very dry mouth. He is afebrile and normotensive with a heart rate of 110 beats/min. He is mildly tender on abdominal examination. His serum amylase level is 650 IU/L. Which of the following is the most appropriate initial step in the management of this patient?

(A) Exploratory laparotomy and pancreatic débridement

(B) Discharge and close follow up as outpatient

(C) Obtain an abdominopelvic computed tomography (CT) scan

(D) Perform esophagogastroduodenoscopy (EGD)

(E) Admit for intravenous (IV) hydration and withhold oral feeding

3–E. This patient has acute pancreatis most likely secondary to alcoholism. He does not appear to have peritonitis nor is he in extremis. He has signs of intestinal ileus and is assuredly dehydrated. The initial management of a patient with acute pancreatitis should be fluid resuscitation and restriction of oral intake. Surgery for acute pancreatitis is reserved for patients with complications of pancreatitis or infected pancreatic necrosis. Discharging a severely dehydrated patient with acute pancreatitis would not be safe. Esophagogastroduodenoscopy would not be helpful in the initial management of this patient and would not be well tolerated. An abdominopelvic computed tomography (CT) scan is useful in evaluating patients with severe, acute pancreatitis, to help in identifying signs of pancreatic necrosis and fluid collections, but it is not indicated initially in patients with uncomplicated pancreatitis.

4. A 57-year-old man with a history of biliary colic presents with a 2-day history of severe epigastric and left upper quadrant (LUQ) pain, intractable nausea, and vomiting. He was admitted to an outside hospital for intravenous (IV) hydration, but over the first 24 hours of his hospital course he became progressively more ill. Abdominopelvic computed tomography (CT) scan demonstrated an enlarged common bile duct, a markedly edematous pancreas with portions of the pancreas which do not enhance, and several liters of ascites. His left flank became markedly ecchymotic, and his abdomen became progressively more distended. He was then transferred to the intensive care unit at your tertiary care hospital. Despite infusion of 10 L of crystalloid over the last 12 hours, he remains hypotensive. Laboratory studies reveal a white blood cell count of 24,000, a Po₂of 55 mm Hg, a blood glucose of 280 mg/dL, bilirubin of 4.3, and a lactate dehydrogenase of 495 IU/L. Based on Ranson's criteria, which of the following indicates this patient's mortality risk upon entering the intensive care unit?

(A) 0%

(B) 20%

(C) 40%

(D) 80%

(E) 100%

4–C. This patient has hemorrhagic necrotizing pancreatitis which is made evident by his Grey Turner sign (left flank ecchymosis) and the computed tomographic findings. With a history of biliary colic, the pancreatitis is likely secondary to gallstones. He has at least six of Ranson's criteria, notably (1) age over 55, (2) fluid sequestration > 10 L, (3) white blood cell count > 16,000, (4) Po₂ < 60, (5) glucose > 200, (6) lactase dehydrogenase > 350. His mortality risk is at least 40%.

5. A patient with necrotizing pancreatitis would benefit most from which of the following therapeutic measures?

(A) Placement of a pulmonary artery catheter

(B) Blood transfusion

(C) Endoscopic pancreatic stent placement

(D) Emergent surgical exploration

(E) Initiation of broad spectrum antibiotic therapy with imipenem/cilastatin

5–E. While placement of a pulmonary artery catheter may help manage the fluid resuscitation of this patient, its use has not been shown to significantly improve patient outcome. Blood transfusion may be appropriate to improve oxygen-carrying capacity in the setting of retroperitoneal hemorrhage, but without blood loss or hemolysis there is no benefit to transfusion. Placement of an endoscopically placed pancreatic stent in the setting of necrotizing pancreatitis would likely worsen the pancreatitis. Emergent surgical exploration is not recommended in the initial treatment of patients with sterile necrotizing pancreatitis because patient survival has not been improved by this approach. The patient with necrotizing pancreatitis should be assumed to have sterile necrosis until proven otherwise. Those patients who have culture-proven bacterial sepsis or signs of deterioration despite aggressive supportive care should undergo a fine-needle aspiration of pancreatic fluid collections or necrotic debris for Gram stain and culture to prove the presence of infected necrosis. The presence of infected necrosis then dictates surgical débridement. The use of imipenem/cilastatin in patients with necrotizing pancreatitis has been shown to decrease infection-related complications and, therefore, would benefit the patient.

6. A patient with a high-output pancreatic fistula is most likely to suffer from which one of the following metabolic derangements?

(A) Hyponatremia

(B) Hyperkalemia

(C) Respiratory alkalosis

(D) Metabolic acidosis

(E) Metabolic alkalosis

6–D. Patients with high-output pancreatic fistulae can develop a profound metabolic acidosis secondary to loss of bicarbonate in the pancreatic secretions. These patients may partially compensate by increasing their minute ventilation, however this compensation is not enough to cause an alkalosis. Octreotide therapy is often helpful in decreasing the volume of output from the fistula, and thus decreasing the amount of lost bicarbonate. These patients generally do not develop significant hyponatremia or hyperkalemia.

7. A 39-year-old woman presents with severe epigastric pain, nausea and vomiting. She states she has been anorexic for 2 days. She weighs 240 lb and gave birth to her fourth child 2 years ago. Examination reveals mild tachycardia and abdominal tenderness in the epigastrium and the left upper quadrant (LUQ). Ultrasound examination demonstrates multiple large gallstones in the gallbladder and a dilated common bile duct. The pancreas was poorly visualized secondary to her body habitus. Her serum bilirubin is measured at 3.8 mg/dL, amylase at 1,200 IU/L, lipase at > 6,000 IU/L, and white blood cell count at 17,500. In addition to intravenous (IV) hydration, which of the following is the most appropriate approach to managing this patient?

(A) Antibiotics and endoscopic retrograde cholangiopancreatography (ERCP) with endoscopic sphincterotomy

(B) Antibiotics and exploratory laparotomy

(C) Observation

(D) Antibiotics and observation

(E) Antibiotics and laparoscopic cholecystectomy

7–A. This patient has gallstone pancreatitis with both laboratory and ultrasound evidence suggesting an impacted gallstone at the ampulla of Vater. The most appropriate care would involve fluid resuscitation followed by endoscopic stone extraction, cholangiopancreatography, and sphincterotomy. Any time endoscopic retrograde cholangiopancreatography (ERCP) is performed, the patient should be given prophylactic antibiotics because of the associated risk of cholangitis. Based on the information given, neither exploratory laparotomy nor cholecystectomy is indicated at this time. The patient's gallbladder should be removed electively after resolution of her gallstone pancreatitis to prevent recurrence. Observation in the setting of an impacted gallstone is likely to worsen the severity of pancreatitis and lead to cholangitis.

8. A 73-year-old man is brought to your clinic by his wife because of her concerns of his “wasting away.” He describes having lost 60 lb over the last 6 months. He appears cachectic with a scaphoid abdomen. You note a fullness to his epigastrium. Abdominopelvic computed tomography (CT) reveals a mass in the head of the pancreas and a 3-cm hypodense lesion in the liver. Which of the following is appropriate in the management of this patient?

(A) Pancreaticoduodenectomy (Whipple procedure)

(B) Image-guided percutaneous biopsy of the liver lesion

(C) Radiotherapy

(D) Choledochojejunostomy

(E) Total pancreatectomy

8–B. This patient likely has pancreatic carcinoma with a metastasis to the liver. First, the liver lesion should be biopsied before embarking on resection of the primary tumor. This could be achieved either percutaneously, laparoscopically, or by laparotomy. If feasible, percutaneous needle biopsy is the least invasive and the most desirable as a first step in planning the care of this patient. A Whipple procedure is generally not indicated in patients with stage IV pancreatic carcinoma. Total pancreatectomy is no longer recommended for pancreatic carcinoma. Biliary bypass (choledochojejunostomy) is not indicated in patients with metastatic pancreatic carcinoma who do not have biliary obstruction. Radiotherapy for end-stage pancreatic carcinoma is ineffective.

9. A 41-year-old woman with human immunodeficiency virus (HIV) presents to her physician with complaints of bleeding gums and easy bruising throughout her extremities. Examination reveals a palpable spleen below the left costal margin, multiple soft tissue ecchymoses of her extremities, and multiple petechiae on her hands and feet. Blood counts reveal a platelet count of 27,000/µL. Evaluation of the plasma reveals antiplatelet antibodies. Which of the following is the most appropriate initial therapy?

(A) Glucocorticoids

(B) Platelet infusions

(C) Splenectomy

(D) Methotrexate

(E) Danazol

9–A. Patients with human immunodeficiency virus (HIV) are at increased risk of developing idiopathic thrombocytopenic purpura (ITP), which is what this patient has. Patients typically develop antiplatelet antibodies that appear to facilitate platelet sequestration and destruction in the spleen. Initial therapy includes using steroids and intravenous (IV) immunoglobulin (Ig)G therapy to induce a remission. Patients will typically respond to the steroids by an increase in their platelet counts. If the platelet counts begin to fall upon steroid withdrawal, splenectomy is indicated. Refractory cases that do not respond to steroids may respond to other agents like cyclophosphamide and danazol. Platelet infusions should generally not be given to patients with ITP before splenectomy because these platelets will quickly be sequestered in the spleen and will not function. Immediately after splenectomy, platelets may be given. Life-threatening hemorrhage should be treated with emergent IgG therapy. Methotrexate is an antineoplastic agent and therefore not appropriate in this case.

10. A 54-year-old woman presents with complaints of intermittent episodes of marked diaphoresis and palpitations. She describes feeling like her heart is racing during these episodes, and it makes her feel quite anxious. She has learned that eating food will relieve her symptoms. Screening laboratory tests reveal a blood glucose level of 55 mg/dL. The woman weighs 122 lb and appears otherwise healthy. A fasting glucose level performed the next day was 50 mg/dL and her serum insulin level was markedly above fasting norms. Abdominopelvic computed tomography (CT) demonstrated a discrete, 1-cm tumor in the body of the pancreas. Which of the following is the most appropriate therapy for this patient?

(A) Oral propranolol therapy

(B) Wide local excision of the tumor

(C) Distal pancreatectomy

(D) Enucleation of the tumor

(E) Pancreaticoduodenectomy

10–D. This woman has an insulinoma. She is experiencing catecholamine surges at times of profound hypoglycemia as a compensatory mechanism to promote glycogenolysis and release of glucose stores. Propranolol may help ameliorate the palpitations and anxiety, but it will not address the underlying problem. Over 90% of insulinomas are benign, and most can be successfully enucleated. The lesion described is small and enucleation should be curative. Distal pancreatectomy is possible, but is more resection than is necessary, and pancreaticoduodenectomy would not address her tumor.

11. A 38-year-old woman with no history of alcohol use or cholelithiasis has suffered from intermittent epigastric abdominal pain, nausea, and vomiting for most of her adult life. She takes no medicines. Recently, evaluations have included esophagogastroduodenoscopy, an upper gastrointestinal barium study, and an abdominal ultrasound that have all been unrevealing. She now presents with the same constellation of symptoms. Examination is unremarkable, however laboratory studies reveal an amylase of 1200 IU/L and a lipase of 4400 IU/L. Repeat abdominopelvic computed tomography (CT) scan reveals only an edematous pancreatic head. Which of the following is the next most reasonable diagnostic or therapeutic modality?

(A) Endoscopic ultrasound

(B) Percutaneous transhepatic cholangiography (PTHC)

(C) Enteroclysis

(D) Hepatobiliary scintigraphy (HIDA scan)

(E) Endoscopic retrograde cholangiography (ERCP)

11–E. This patient has signs of acute pancreatitis based on her clinical presentation, laboratory, and radiologic evaluation. With no history of alcohol consumption or gallstones other causes must be ruled out. Pancreas divisum is often a cause of intermittent acute pancreatitis in patients in whom other causes have been ruled out. The best way to identify an anatomical cause of this patient's acute pancreatitis is by endoscopic retrograde cholangiography (ERCP). Moreover, ERCP has the advantage over other imaging techniques by allowing treatment options at the time of the investigation (i.e., endoscopic sphincterotomy or pancreatic duct stent placement). Repeat ultrasound would offer no additional information. Percutaneous transhepatic cholangiography (PTHC) is more difficult in the absence of a dilated biliary tree and does not often provide good detail of the pancreatic ductal anatomy. Enteroclysis will not address the question of etiology of pancreatitis. Hepatobiliary scintigraphy does not provide any image of the pancreatic ducts.

12. A 22-year-old woman presents to the emergency room after having fallen off a galloping horse. She complains of left lower chest wall pain and is mildly short of breath. She is hemodynamically stable. There is a large bruise over her left flank. Chest radiograph demonstrates several fractured ribs on the lower left side. Abdominopelvic computed tomography (CT) scan reveals a 1 × 3 cm²subcapsular splenic hematoma and some fluid adjacent to the spleen. Which of the following is the most appropriate next step in the management of this patient?

(A) Emergent splenectomy

(B) Splenorrhaphy

(C) Pneumococcal vaccine administration

(D) Chest wall splinting

(E) Bedrest and observation

12–E. This patient has a grade II splenic injury and is hemodynamically stable. This warrants a conservative management with close observation and bedrest for a defined period of time (3–7 days). Emergent splenectomy would be premature and likely subject this patient to the risks of laparotomy and splenectomy unnecessarily. Splenorrhaphy would be an appropriate option (as would splenectomy) if this patient did not tolerate conservative management (i.e., she continued to bleed and required blood transfusions while being observed). The pneumococcal vaccine should only be given if the patient undergoes splenectomy. Chest wall splinting is unnecessary, would further restrict her chest wall motion, and would not address her splenic injury.

13. A 26-year-old man presents to his primary physician with complaints of intermittent, crampy epigastric pain, nausea, and vomiting shortly after eating. He usually vomits undigested food and this relieves the pain and nausea. He has preferred to eat soft foods his whole life, and he often relies on liquids. He is otherwise healthy and well-developed. Upper gastrointestinal barium study reveals a markedly narrowed second portion of the duodenum. Laboratory studies are unremarkable. Which of the following is the most likely diagnosis for this patient?

(A) Gallstone pancreatitis

(B) Pancreatic carcinoma

(C) Pancreas divisum

(D) Annular pancreas

(E) Cholelithiasis

13–D. This patient has symptoms of gastric outlet obstruction or, as in this case, duodenal obstruction. Several of these diseases could result in duodenal obstruction. However, the fact that he is young, otherwise healthy, and has avoided solid foods all his life suggests he has a congenital problem. He does not describe symptoms of biliary colic nor does he have signs of cancer. Episodic pain is not typical during bouts of acute pancreatitis, and pancreas divisum does not cause duodenal obstruction. Annular pancreas fits best with his history, his constellation of present symptoms, and his upper gastrointestinal study.

14. A 44-year-old woman was hospitalized 3 weeks earlier with acute pancreatitis believed to be secondary to the azathioprine therapy, which was used as maintenance immunosuppressive for her transplanted kidney. The azathioprine therapy was discontinued, and she gradually recovered. She presents to clinic today with a new complaint of early satiety, intermittent nausea, and one episode of postprandial vomiting. Abdominopelvic computed tomography (CT) reveals a 5-cm, round, fluid collection within the lesser sac. Which of the following is the most appropriate therapy for the management of this patient?

(A) Observation and follow-up CT in 3–6 weeks

(B) Laparotomy and cystgastrostomy

(C) Gastroscopy and endoscopic cystgastrostomy

(D) Percutaneous drainage

(E) Restart azathioprine therapy

14–A. This patient, who recovered from an episode of acute pancreatitis 3 weeks ago, appears to have an evolving pancreatic pseudocyst. The majority of small pseudocysts (< 5 cm) will resolve spontaneously. Those larger are likely to require intervention. Pseudocysts should not be drained until they have a mature capsule, which generally takes 6–8 weeks from the time of the acute pancreatitis. Therefore, none of the drainage procedures (laparotomy and cystgastrostomy; gastroscopy and endoscopic cystgastrostomy; percutaneous drainage) are appropriate only 3 weeks after the resolution of the acute pancreatitis. The inciting agent—azathioprine—should not be restarted this early. It can be substituted with other agents if necessary.

15. Patients having undergone splenectomy are at increased risk of developing overwhelming sepsis from which of the following organisms?

(A) Helicobacter pylori

(B) Klebsiella pneumoniae

(C) Bacteroides fragilis

(D) Staphylococcus aureus

(E) Enterococcus faecium

15–B. Overwhelming postsplenectomy infection (OPSI) is an uncommon event, occurring at a rate of 0.3%–1.8% among adults over an 8-year follow-up. The mortality rate of postsplenectomy sepsis is approximately 50%, and thus it must be taken very seriously. Encapsulated organisms are the usual causes. Among the organisms listed only Klebsiella pneumoniae is encapsulated.

16. A 48-year-old, alcoholic male has been hospitalized over the last 20 years more than 30 times for episodes of acute pancreatitis. He now presents to the emergency department complaining of mid-back pain and horribly malodorous and frequent soft stools. He describes that the stools float in the toilet. He also explains that he has lost 30 lb over the last 6 months. Which of the following therapeutic measures is the best option to improve this patient's health maintenance?

(A) Total pancreatectomy

(B) Oral pancreatic enzyme replacement

(C) Total parenteral nutrition

(D) Octreotide therapy

(E) High-fat diet

16–B. This patient has chronic pancreatitis and signs of pancreatic insufficiency with steatorrhea and weight loss secondary to malabsorption. Total pancreatectomy is not likely to improve the patient's health. Oral pancreatic enzyme replacement will treat both this patient's fatty stools and his malabsorption. He should also initiate a high-carbohydrate, high-protein diet to stabilize his weight. Although total parenteral nutrition may help this patient's malnourishment acutely, it is not a good option as it would restrict his activities, require a central venous catheter, carry a significant risk of morbidity, not provide optimal nutrition, and be quite costly. Octreotide therapy would likely make this patient's symptoms worse, as it would inhibit any remaining pancreatic exocrine function. A high-fat diet would worsen this patient's steatorrhea.

17. A 57-year-old, male alcoholic with chronic pancreatitis has had several episodes of acute pancreatitis in the last year. Today he presents to the emergency department with hematemesis. After admission to the intensive care unit and resuscitation, esophagogastroduodenoscopy (EGD) reveals large gastric varices, one of which is actively bleeding. The bleeding varix is successfully banded, but over the next 12 hours the patient's hematocrit continues to fall despite blood transfusions, and fresh blood continues to drain from a nasogastric tube. Upon review of an abdominal computed tomography (CT) scan performed 1 month ago you note a markedly calcified pancreas, large gastric varices, and no enhancement of the splenic vein. Which of the following is the most appropriate next step in the management of this patient?

(A) Emergent splenectomy

(B) Repeat EGD and sclerotherapy

(C) Sengstaken-Blakemore tube placement

(D) Excision of the gastric varices

(E) Intravenous (IV) vasopressin

17–A. This patient developed splenic vein thrombosis secondary to pancreatitis. He has since developed sinistral portal hypertension with massive gastric varices formed from the enlarged short gastric veins, which now drain the splenic blood supply completely. Splenectomy will cure this patient's left-sided portal hypertension. It should be understood that emergent laparotomy in the setting of variceal bleeding carries a high mortality rate. Repeat esophagogastroduodenoscopy (EGD) in a patient with actively bleeding, large gastric varices that have failed one attempt at banding is not likely to be successful, will delay definitive therapy, and will increase his mortality risk. Sengstaken-Blakemore tubes are useful as a temporizing measure in patients with intractable esophageal varices, however they do not work well with gastric varices. Excision of the varices is not curative and risks inappropriate gastric devascularization. Intravenous (IV)) vasopressin may be temporizing, but does not address the underlying pathology and has not been shown to reduce mortality in this setting.

18. A 33-year-old woman presents with complaints of frequent paroxysms of profuse diaphoresis and a “racing heart.” She has seen several physicians about these concerns, but none have “helped her.” Occasionally, these episodes result in her fainting. She generally feels better if she eats right after the onset of symptoms. A portable glucometer demonstrates that she has a normal blood glucose level in your clinic. Reports from other physicians demonstrate that she has had several low blood glucose levels and elevated insulin levels documented. She explains that her symptoms do not occur every day. Which of the following laboratory tests may aid in establishing her diagnosis?

(A) Glucagon level

(B) Lactate dehydrogenase level

(C) Erythrocyte sedimentation rate

(D) C-peptide level

(E) Somatostatin stimulation test

18–D. This patient may be feigning illness by administering insulin surreptitiously. This possibility can be excluded by measuring either proinsulin or C-peptide (an insulin precursor) levels. None of the other tests would be likely to aid in the diagnosis. Somatostatin is an inhibitory enzyme, not a stimulating one.