Gastroenterology and Hepatology Board Review: Pearls of Wisdom, Third Edition
Section VI GALLBLADDER, BILE DUCTS, AND PANCREAS
CHAPTER 38. Acute and Chronic Pancreatitis
Enrique Molina, MD and Jamie S. Barkin, MD, MACP, MACG
What are the most common causes of acute pancreatitis?
Gallstones and alcohol. Idiopathic acute pancreatitis accounts for 8%–25% of cases; however, up to two-thirds of these patients may have microlithiasis or sphincter of Oddi dysfunction identified by inspection of bile and sphincter of Oddi manometry, respectively. Other causes include hypertriglyceridemia, hypercalcemia, trauma, iatrogenic trauma (eg, post endoscopic retrograde cholangiopancreatography [ERCP]), autoimmune pancreatitis, pancreatic tumors (both primary and metastatic), medications, vasculitis, and certain viral and bacterial infections. Pancreas divisum has been suggested as a cause of acute pancreatitis, although this remains controversial.
True/False: The most important therapy of acute pancreatitis is volume resuscitation.
True. Appropriate and timely fluid resuscitation in acute pancreatitis is critical as it is associated with reduced morbidity and mortality, including a reduced incidence of systemic inflammatory response syndrome (SIRS) and organ failure. Appropriate early resuscitation requires at least 250–300 mL/hour of IV fluids for the first 48 hours of hospitalization; however, patients with severe volume depletion may require up to 500–1000 mL/hour of IV hydration. Crystalloids are the preferred parenteral fluid in most cases.
True/False: Patients with coexisting alcohol dependence and cholelithiasis should undergo prophylactic cholecystectomy in order to prevent an episode of acute pancreatitis.
False. Cholecystectomy has not been shown to prevent recurrent episodes of pancreatitis in patients with coexisting alcohol dependence. The pancreatitis nearly always follows the course of alcohol-related pancreatitis.
What is the mortality rate of gallstone-associated pancreatitis?
Approximately 12% during the first attack; however, it varies depending on the severity of the attack. Mortality tends to decrease with subsequent attacks.
What is the role of shock wave lithotripsy in acute pancreatitis caused by obstructive pancreatic stones?
Extracorporeal shock wave lithotripsy of obstructive pancreatic duct stones may prevent further attacks in patients with recurrent episodes of acute pancreatitis.
True/False: Prophylactic pancreatic stent placement during ERCP reduces the risk of post-ERCP pancreatitis.
What etiology of acute pancreatitis documented by CT scan should be suspected in patients without measurable elevation in serum amylase levels?
Severe hypertriglyceridemia may result in false-negative serum values of amylase and lipase. While measured serum amylase activity is frequently normal, urinary amylase concentration is markedly elevated. Recurrences may be prevented by treatment aimed at avoiding elevations in serum triglycerides greater than 1000 mg/dL.
Which of the following etiologies of pancreatitis is most likely to result in the eventual development of chronic pancreatitis: biliary pancreatitis, hypercalcemia-induced pancreatitis, or post-ERCP pancreatitis?
Hypercalcemia often leads to the development of chronic pancreatitis (with an estimated incidence of 0.1%–3.3%).
What is the cause of the increased incidence of acute pancreatitis during pregnancy?
Cholelithiasis or microlithiasis is present in about 90% of cases; however, nonbiliary sources should be sought as they are associated with worse outcomes. Hypercalcmeia of hyperparathyroidism may be falsely lowered due to hypoalbuminemia or magnesium tocolysis. Most episodes of biliary pancreatitis occur in the third trimester or in the early postpartum period. Elective cholecystectomy after the first trimester is generally recommended. The overall prognosis is good; however, the first trimester episodes of acute pancreatitis are associated with a high risk of fetal loss of about 20%.
What percentage of acute pancreatitis is medication-related?
5%. However, drug-induced pancreatitis is probably underestimated because of the difficulty in determining definitively the causative agent. Epidemiologic data suggest the risk of pancreatitis is highest for mesalamine and azathioprine. Other drugs that are definitely associated with acute pancreatitis include 6-mercaptopurine, sulfonamides, thiazide diuretics, furosemide, estrogens, tetracyclines, valproic acid, pentamidine, didanosine, intravenous lipid infusion, and L-asparaginase. Other drugs with a less certain association include chlorthalidone, ethacrynic acid, phenformin, nonsteroidal anti-inflammatory agents, nitrofurantoin, methyldopa, corticosteroids, angiotensin converting enzyme (ACE) inhibitors, cimetidine, ranitidine, acetaminophen, metronidazole, lamivudine, carbamazepine, rifampin, and salicylates.
What compounds have a dose-related effect in drug- and poison-induced pancreatitis?
Ethyl alcohol, organophosphorus insecticides, and intravenous lipid infusions.
What percentage of patients with intraductal papillary mucinous neoplasms (IPMNs) develop acute pancreatitis?
Acute pancreatitis occurs in up to 34% of patients with IPMNs, with branch duct IPMN being the most commonly associated with acute pancreatitis. Severe pancreatitis is uncommon but recurrent acute pancreatitis is common and should be considered in older patients.
What etiologies must be considered in posttransplant patients with acute pancreatitis?
Secondary hyperparathyroidism, hyperlipidemia, viral infections, vasculitis, and immunosuppressive therapy (particularly corticosteroids, azathioprine, and L-asparaginase). Posttransplant pancreatitis is associated with a high mortality.
What infections may cause acute pancreatitis in immunocompetent hosts?
Overall, infection-associated pancreatitis is uncommon; however, several viruses have been implicated and include mumps, coxsackie, and hepatitis A and B. Bacterial causes include Mycoplasma, Salmonella, and Mycobacterium tuberculosis. Intraductal parasitic infections, particularly ascaris, fasciola, and clonorchis, have also been described.
What are the two most common causes of acute pancreatitis in AIDS patients?
Drugs and infections. Drugs commonly implicated in these patients include pentamidine, trimethoprim-sulfamethoxazole, and didanosine. Cytomegalovirus accounts for the majority of infection-related cases. Other infectious agents implicated include Cryptococcus neoformans, M. tuberculosis, and herpes simplex virus. Disseminated infections with M. avium complex, Toxoplasma gondii, Pneumocystis carinii, Leishmania species, and Candidaspecies may involve the pancreas but rarely cause clinical symptoms.
What is the most common cause of acute pancreatitis in children?
Trauma is the most common cause of acute pancreatitis in children, often resulting from bicycle handle bar injury and steering wheel injury (in older children). A not uncommon sequela of trauma includes pancreatic duct stricture, which may result in recurrent and chronic pancreatitis. Blunt, rather than penetrating, trauma may induce pancreatitis and usually involves compression of the body of the pancreas against the spine. In adults, this frequently results from seat belt injury and may result in a pancreatic body stricture causing acute recurrent pancreatitis.
True/False: A patient with so-called “idiopathic” acute pancreatitis should undergo pancreatic duct imaging.
True. This is done primarily to evaluate for ultrasound-negative choledocholithiasis and cholelithiasis (microlithiasis); choledochoceles; obstruction of pancreatic duct by calculi, strictures, small pseudocysts, annular pancreas, or carcinoma; ampullary tumors; sphincter of Oddi dysfunction; and (more controversial) pancreas divisum. Magnetic resonance cholangiopancreatography (MRCP) is a noninvasive imaging modality which also allows direct visualization of the pancreaticobiliary system without intrapancreatic ductal contrast medium injection and thus avoids the most frequent complication of ERCP—acute pancreatitis. Its diagnostic accuracy in centers with sufficient expertise rivals that of ERCP.
What clinical prognostic scoring criteria are used to assess the severity of patients with acute pancreatitis?
Ranson’s criteria and APACHE-II grading systems are used to assess the degree of severity of patients’ pancreatitis. The CT severity index (CTSI) uses CT scan features of acute pancreatitis and pancreatic necrosis to calculate severity; however, this is based on local complications and does not reflect the SIRS found in patients with acute pancreatitis. A new prognostic scoring system, the bedside index for severity in acute pancreatitis (BISAP), has been validated and is as accurate as the APACHE-II and Ranson’s criteria for prognosis and uses five criteria: blood urea nitrogen (BUN), mental status, age, presence of SIRS, and presence of pleural effusions.
Describe Ranson’s criteria.
Ranson’s criteria, used in assessing the severity and prognosis of ethanol-associated pancreatitis, can only be applied at 48 hours after hospitalization, and this is the major drawback to its use. Fewer than three positive signs indicate mild disease with a mortality rate near zero. The mortality rate increases to 10%–20% when three to five signs are present and is > 50% with six or more signs. A variant of these criteria is utilized to assess the severity of non-alcohol-related pancreatitis.
Describe the APACHE-II scoring system as used for acute pancreatitis.
The APACHE-II scoring system can be calculated at the time of hospital admission and is based on a point system depending on the patient’s age, chronic illness, and a number of physiologic variables. It is, however, a cumbersome and clinically less practical system. A score of > 8 suggests the presence of severe pancreatitis.
True/False: The magnitude of hyperamylasemia correlates with the severity of pancreatitis.
False. The serum amylase level typically rises 2–12 hours after onset of symptoms and slowly declines over 3–5 days. Conversely, elevations of serum lipase levels tend to rise later and persist longer. The magnitude of hyperamylasemia has no prognostic value in acute pancreatitis; levels may remain normal in up to 10% of cases of fatal pancreatitis.
What are nonpancreatic sources of hyperamylasemia and hyperlipasemia?
Diseases of the salivary glands, lungs, fallopian tubes, ovarian cysts, gallbladder, and small bowel may result in elevations of serum amylase as may tumors of the colon, lung, and ovary. Any condition associated with increased small bowel permeability (perforation, infarction, or obstruction) or renal disease resulting in diminished renal clearance of pancreatic enzymes may cause elevations in both amylase and lipase in the absence of clinical pancreatitis. Patients with chronic hepatitis C infection, diabetic ketoacidosis, and inflammatory bowel disease (IBD) may also present with increased enzymes of nonpancreatic origin. Macroamylasemia and macrolipasemia may also result in elevations of serum pancreatic enzymes.
What are macroamylasemia and macrolipasemia?
These are conditions in which amylase or lipase complexes with immunoglobulin (IgA, IgG) and/or polysaccharides. These large molecules do not undergo glomerular filtration; therefore, serum amylase/lipase levels are increased but urinary amylase levels and the amylase-creatinine clearance ratio are low. Diagnosis can be established by measuring the molecular weight of amylase and lipase, or by immunologic assays. These conditions have been associated with celiac disease, HIV, cirrhosis, rheumatoid arthritis, ulcerative colitis, monoclonal gammopathy, and non-Hodgkin’s lymphoma.
What pulmonary manifestations may be found in patients with acute pancreatitis?
Approximately 10%–20% of patients with acute pancreatitis will have pleural effusions. They are usually left-sided and are exudative with high fluid amylase levels. Early arterial hypoxemia may also occur and results from right-to-left shunting due to microthrombi of the pulmonary vasculature. Finally, adult respiratory distress syndrome occurs in up to 20% of patients with severe acute pancreatitis.
True/False: All acute peripancreatic fluid collections that develop in the course of acute pancreatitis should be drained.
False. More than half of all peripancreatic fluid collections associated with acute pancreatitis will resolve spontaneously within 6 weeks. They may occur as a result of sympathetic effusion or extravasated pancreatic exocrine secretions secondary to duct rupture. Intervention may be considered when the collection persists beyond 6 weeks after the onset of pancreatitis and results in symptoms or complications resulting from mass effect or infection.
True/False: All pancreatic pseudocysts developing after an episode of acute pancreatitis should undergo drainage.
False. Pancreatic pseudocyst occurs in approximately 15% of patients after acute pancreatitis. Pseudocysts do not have a true epithelial lining but are instead surrounded by granulation tissue and collagen. Eighty-five percent are located in the body or tail and 15% in the head of the pancreas. Pseudocysts that are asymptomatic and not increasing in size should be observed. Those that are expanding in size, usually above 6 cm, and are symptomatic should be considered for drainage.
True/False: A CT scan should always be obtained in a patient with acute pancreatitis.
False. A CT scan with rapid bolus intravenous contrast should be obtained in patients with acute pancreatitis who: 1) fail to improve clinically, 2) have evidence of organ failure, or 3) are suspected of having infected pancreatic necrosis. Sterile necrosis may be distinguished from infected necrosis by needle aspiration of fluid. A CT scan should not be performed early in the course of acute pancreatitis in patients with volume depletion and/or renal impairment.
What is the significance of pancreatic necrosis identified by an IV contrast-enhanced abdominal CT scan?
The presence of pancreatic necrosis portends a more unfavorable outcome. Areas of pancreatic necrosis fail to enhance during CT scanning after rapid bolus injection of contrast material. The diagnosis of pancreatic necrosis is established when there are focal or diffuse zones of nonenhanced pancreatic parenchyma > 3 cm or involving > 30% of the pancreas. Patients with pancreatic necrosis have a 30%–50% chance of developing infection of the necrosis; the extent of the necrosis correlates with worsening prognosis. CT scan findings are generally not helpful in differentiating sterile from infected necrosis, although the presence of gas bubbles is suggestive of infected necrosis. CT-guided needle aspiration with Gram stain and culture of the aspirate allows diagnosis of suspected infected necrosis.
What are the causes of early mortality in acute pancreatitis?
The most common cause of early mortality in acute pancreatitis is SIRS, defined as body temperature < 36°C or > 38°C, heart rate > 90 beats per minute, tachypnea, leukopenia, or leukocytosis; SIRS can be complicated by acute lung injury, acute kidney injury, shock, and multiple organ failure. When acute renal failure occurs in the setting of prolonged hypovolemia and shock, acute tubular necrosis ensues and the mortality rate approaches 50%. In addition, adult respiratory distress syndrome, intraabdominal hemorrhage, and acute cholangitis can account for early mortality in acute pancreatitis.
What are the causes of late mortality in acute pancreatitis?
Septic complications, particularly infected pancreatic necrosis and abscess formation, and pneumonitis tend to occur after the first week of illness.
True/False: The mortality rate of patients with pancreatitis who develop infected pancreatic necrosis is increased fourfold compared with patients with similar extent of sterile necrosis.
True. The mortality rate is increased considerably in patients with infected necrosis (38% compared with 9% of patients with sterile necrosis). Blood cultures are neither sensitive for isolation of responsible microorganisms nor specific for site of infection. Sonographic or CT-guided percutaneous aspirates of suspected areas of necrosis are the procedures of choice when infected necrosis is suspected.
What is the most common organism isolated in infected pancreatic necrosis?
Escherichia coli is isolated in about 50% of percutaneous aspirates. Gram stain or culture of these pancreatic aspirates may identify a single microorganism or a polymicrobial infection. Other common organisms include Enterococcus (19%), Staphylococcus (18%), Proteus (10%), Klebsiella (10%), Pseudomonas (10%), Streptococcus faecalis (7%), and Bacteroides (6%) species. These organisms likely reach the pancreas by translocation across the colonic wall followed by local lymphatic, rather than hematogenous, spread.
True/False: Patients with infected pancreatic necrosis who are stable should undergo immediate surgical drainage.
False. Treatment with antibiotics is still the initial treatment of choice if the condition of the patient is stable, since over 75% of patients are able to avoid surgery. However, if there is no response to antibiotics, then therapeutic intervention by either percutaneous, endoscopic, laparoscopic, or open surgical approach should be pursued. The preferred surgical intervention is necrosectomy; however, it should be performed as late as possible (approximately 1 month after diagnosis of acute pancreatitis). For patients with a pancreatic abscess, drainage is recommended.
True/False: The role for prophylactic antibiotics in patients with acute necrotizing pancreatitis has been conclusively defined.
False. Indiscriminate use of antibiotics is neither advocated nor supported by the preponderance of the scientific evidence in the effort to prevent pancreatic infection.
What other organ system complications outside the abdomen may be affected by acute pancreatitis?
Polyserositis of articular synovium, pleura, or pericardium may also occur. Subcutaneous fat necrosis may cause a skin rash resembling erythema nodosum. Fat necrosis adjacent to synovium may result in arthritis revealing synovial fluid with many leukocytes and high lipase concentration. Evidence of distant fat necrosis, while clinically evident in only 1% of cases of acute pancreatitis, may be seen in up to 10% of patients on autopsy. Purtscher’s retinopathy is a rare complication of acute pancreatitis and is manifested by sudden blindness due to occlusion of the posterior retinal artery with aggregated granulocytes.
What are the potential causes of acute pancreatitis in patients with IBD?
The increased incidence of acute pancreatitis in Crohn’s disease can be explained on the basis of the high predisposition to cholesterol and pigment stones as a result of ileal disease, anatomic abnormalities of the duodenum (with obstructive pancreatitis), immunologic disturbances associated with IBD, and primary sclerosing cholangitis with associated biliary stones. Medications including sulfasalazine, 5-aminosalicylic acid, azathioprine, and 6-mercaptopurine, used in the treatment of Crohn’s disease and ulcerative colitis, can cause acute pancreatitis.
What complications of acute pancreatitis may result in acute upper gastrointestinal bleeding?
Gastric variceal hemorrhage and hemosuccus pancreaticus. Isolated gastric varices resulting from splenic vein thrombosis may complicate acute pancreatitis, so-called left-sided portal hypertension. Splenectomy with gastric devascularization is curative. Usually, hemosuccus pancreaticus refers to bleeding in the pancreas into the pancreatic duct and then into the duodenum. It typically arises from erosion of a pseudocyst into adjacent vasculature. Selective mesenteric arteriography during active bleeding distinguishes hemosuccus pancreaticus from hemobilia, identifies the source of arterial or venous bleeding, and determines if the blood traverses a pancreatic pseudocyst or abscess prior to drainage into the pancreatic duct. Selective arterial embolization during angiography may control bleeding.
What clinical findings are suggestive of intrapseudocyst hemorrhage?
Abdominal pain associated with a sudden increase in the size of the pseudocyst, a localized bruit over the pseudocyst, and a sudden decrease in hemoglobin and hematocrit without obvious external blood loss.
True/False: Pancreas divisum is associated with an increased incidence of acute recurrent pancreatitis.
False, although controversial. Pancreas divisum is a congenital failure of fusion of the ventral and dorsal pancreatic anlagen resulting in drainage of the dorsal duct draining via the minor ampulla and the ventral duct via the major ampulla. It is the most common congenital anatomic variant (5%–10%) of the human pancreas. The majority of patients are not predisposed to develop pancreatitis; however, it is believed that the combination of pancreas divisum with a small accessory ampullary orifice may lead to pancreatitis. Clues to pancreatic divisum as a cause of pancreatitis include a dilated dorsal pancreatic duct and stones within the dorsal duct.
What is the most common cause of chronic pancreatitis in adults?
Chronic alcohol abuse accounts for 70%–80% of chronic pancreatitis. The type of alcohol and pattern of drinking have no influence on the risk of developing chronic pancreatitis. It may be influenced by genetic predisposition in the host.
True/False: Alcohol consumption and cigarette smoking are independent risk factors for chronic pancreatitis.
What is tropical pancreatitis?
It is a nutritional pancreatitis seen in African and Asian countries resulting from severe protein-calorie malnutrition. It is characterized by hypoalbuminemia, marked emaciation, bilateral parotid gland enlargement, and hair and skin changes resembling kwashiorkor. The pathophysiology of this form of chronic pancreatitis is felt to be due to nutritional antioxidant deficiencies (zinc, copper, selenium). Severe chronic calcific pancreatitis with large intraductal stones may develop and diabetes typically occurs several years after the onset of abdominal pain. Nutritional repletion may lead to a return to normal pancreatic exocrine function if instituted before extensive atrophy and fibrosis of the gland occurs.
What genetic factors influence the development of chronic pancreatitis?
Hereditary pancreatitis, inherited through an autosomal dominant gene of incomplete penetrance, has been described in different areas of the world (New Zealand, United States, Ireland, France). It affects both sexes equally and typically presents as episodes of acute pancreatitis in childhood by age 10 to 12. These patients progress from episodes of acute pancreatitis to chronic pancreatitis and have an increased incidence of pancreatic carcinoma. Mutations of the cystic fibrosis transmembrane conductance regulator (CFTR) gene, the cationic trypsinogen gene (PRSS1), and pancreatic secretory trypsin inhibitor (PSTI), otherwise known as SPINK1, can lead to the development of chronic pancreatitis. Concomitant mutation of both CFTR and SPINK1 enhances the risk of pancreatitis above that of CFTR mutations alone (600-fold versus 40-fold).
Which serologic marker is elevated in autoimmune pancreatitis?
Serum IgG4 is usually elevated more than two times the upper limit of normal (> 140 mg/dL). Only about 1% of patients with pancreatic cancer have a serum IgG4 above 280 mg/dL.
What are the diagnostic criteria of autoimmune pancreatitis?
The “HISORt” criteria proposed by the Mayo Clinic are commonly used, and include the presence of one or more of the following: Diagnostic histology (see below), pancreatic imaging (diffusely enlarged pancreas with featureless borders and delayed enhancement with or without a capsule-like rim; narrowed main and dorsal pancreatic duct), serology (elevated IgG4), other organ involvement (biliary strictures, parotid/lacrimal gland involvement, mediastinal lymphadenopathy, retroperitoneal fibrosis), and response to steroid treatment.
What are the histologic features of autoimmune pancreatitis?
Type 1 autoimmune pancreatitis is characterized by a lymphoplasmacytic sclerosing pancreatitis or > 10 IgG4 positive cells with at least two of the following: periductal lymphoplasmacytic infiltrate, obliterative phlebitis, and acinar fibrosis. Type 2 autoimmune pancreatitis is characterized by idiopathic duct centric pancreatitis or a granulocytic epithelial lesion in the pancreatic duct with minimal IgG4 positive cells in the pancreatic parenchyma.
What is the long-term prognosis of autoimmune pancreatitis?
There is a recurrence rate of approximately 41%.
True/False: The diagnosis of chronic pancreatitis may be excluded in patients without abdominal pain.
False. Although pain is the most common presenting symptom of patients with chronic pancreatitis, it may be absent in up to 15% of patients with alcohol-related chronic pancreatitis and in up to 23% of patients with nonalcoholic chronic pancreatitis.
What specialized test directly measures pancreatic exocrine function?
In chronic pancreatitis, exocrine secretion is decreased. The secretin stimulation test measures the volume of secretion and the concentration of bicarbonate (collected via aspiration of duodenal contents) in response to injection of secretin. Bicarbonate levels < 50 mEq/L are consistent with the diagnosis of chronic pancreatitis. This test is invasive, requiring duodenal tube insertion for collection of secretions, and has a reported sensitivity of approximately 80%–90%.
True/False: Steatorrhea is an early symptom of chronic pancreatitis.
False. Ninety percent of exocrine function is typically lost before steatorrhea develops. A secretin test may be abnormal when 60% of the exocrine function is lost. Patients with so-called early chronic pancreatitis can have symptoms of bloating, abdominal discomfort, abdominal pain, or change in bowel habits when 60%–90% of the pancreatic function is lost. Thus, early chronic pancreatitis can mimic a wide variety of gastrointestinal disorders.
What indirect tests of pancreatic secretory function are available?
Serum trypsinogen, fecal chymotrypsin, fecal elastase, and 72-hour quantitative fecal fat determination. They all lack sensitivity except in patients with advanced chronic pancreatitis, when patients typically have already developed steatorrhea. Furthermore, these tests do not influence management in most cases.
True/False: Plain abdominal radiographs are helpful in the diagnosis of chronic pancreatitis.
True. While plain abdominal radiographs cannot exclude the diagnosis, the presence of focal or diffuse pancreatic calcification (seen in approximately 30% of cases) makes the diagnosis of advanced chronic pancreatitis almost certain and obviates the need for additional testing.
What osseous abnormalities are associated with chronic pancreatitis?
Approximately 5% of patients with chronic pancreatitis demonstrate medullary infarcts or aseptic necrosis of the femoral or humeral head. The long bones of the hands and feet are affected most often. These abnormalities result from medullary fat necrosis during episodes of acute pancreatitis.
When is ERCP useful in the diagnosis of chronic pancreatitis?
Changes of early chronic pancreatitis may not be seen on ERCP. ERCP assesses ductular changes, such as irregularity, dilatation, tortuosity, stenosis, and ductal calculi, which occur in advanced chronic pancreatitis. ERCP is also useful in differentiating chronic pancreatitis from pancreatic cancer. Endoscopic ultrasound (EUS) is also capable of diagnosing chronic pancreatitis on the basis of both ductal and parenchymal changes and, thus, may be able to detect chronic pancreatitis earlier than ERCP.
What are the most common complications of chronic pancreatitis?
• Chronic abdominal pain, often leading to narcotic dependence, is the most common complication of chronic pancreatitis.
• Pancreatic exocrine insufficiency with steatorrhea.
• Pseudocysts occur in up to 25% of patients with chronic pancreatitis. In contrast with acute pseudocysts, chronic pseudocysts almost never resolve spontaneously. Hemorrhage into a pseudocyst with subsequent conversion into a pseudoaneurysm is potentially the most serious complication of chronic pancreatitis.
What is pancreatic ascites?
Pancreatic ascites occurs as a consequence of persistent leakage of pancreatic fluid from a pseudocyst or a disrupted pancreatic duct. Its incidence in chronic pancreatitis is less than 1%, but may occur in up to 15% of patients with pseudocysts. It may be distinguished from ascites secondary to cirrhosis by the finding of high ascitic fluid amylase levels greater than serum levels and high fluid protein or albumin levels.
True/False: The presence of signs of fat-soluble vitamin deficiencies is highly suggestive of chronic pancreatitis.
False. While the absorption of fat-soluble vitamins (A, D, E, and K) is diminished, marked deficiency is relatively uncommon. The clinical presence of easy bruisability, bone pain, and decreased night vision resulting from deficiencies of vitamins K, D, and A, respectively, is more suggestive of small intestinal disease with malabsorption.
True/False: Patients with pancreatic exocrine insufficiency secondary to chronic pancreatitis are predisposed to nephrolithiasis.
True. Patients with untreated steatorrhea have high concentrations of long-chain fatty acids in the colon, which bind intraluminal calcium and form insoluble calcium soaps. Consequently, less calcium is available to bind to and precipitate unabsorbed dietary oxalate as calcium oxalate and more oxalate is absorbed and excreted in the urine. Hyperoxaluria and oxalate stone formation may then develop.
How should hyperoxaluria be treated in patients with chronic pancreatitis?
Low dietary oxalate intake, low dietary long-chain triglycerides, pancreatic enzyme substitution, and increased intake of either calcium (3 g/day) or aluminum in the form of antacids (3.5 g/day).
True/False: Patients with chronic pancreatitis may have vitamin B12 malabsorption.
True. The probable mechanism is due to competitive binding of cobalamin by cobalamin-binding proteins (usually destroyed by pancreatic proteases). It is correctable with administration of pancreatic enzymes and occurs in 40% of patients with advanced chronic pancreatitis.
True/False: Retinopathy may occur in patients with chronic pancreatitis.
True. Nondiabetic peripheral retinopathy may occur due to a deficiency of vitamin A and/or zinc. Diabetic retinopathy and other microvascular complications of diabetes are less common. However, the prevalence of diabetic retinopathy and neuropathy in patients with chronic pancreatitis is comparable to that of patients with idiopathic diabetes mellitus if corrected for the duration of diabetes.
What nonsurgical and surgical modalities of pain control are available in chronic pancreatitis?
Cessation of alcohol intake, nonnarcotic analgesics, and celiac plexus block. Pancreatic enzyme supplementation should be utilized in all patients with chronic pancreatitis to correct exocrine insufficiency. Their utility in the management of pain in chronic pancreatitis remains controversial. The non-enteric-coated preparation is preferable for treatment of the pain associated with chronic pancreatitis. Correctable causes of pain such as the presence of a pseudocyst, duodenal or biliary narrowing, and pancreatic ductal stricture/stone should be sought. Surgery offers better longer-lasting pain control compared to endoscopic therapy. Lateral pancreaticojejunostomy (modified Puestow) is preferred in patients with ductal obstruction in the head of the pancreas with distal duct dilatation, whereas partial pancreatic resection should be considered in patients without ductal dilatation, so-called small-duct disease or localized distal (tail) disease.
How much lipase is necessary in the form of pancreatic enzyme supplementation for treatment of steatorrhea?
Malabsorption does not usually occur if more than 5% of normal maximal enzyme output is delivered to the duodenum. This requires 28,000 IU of lipase during a 4-hour postprandial period. Pancreatic enzymes are available in two forms: enteric and non-enteric-coated preparations. The advantage of enteric-coated compounds (eg, Creon, Zenpep, and Pancrease, as opposed to Viokase) is that they do not dissolve in the stomach and are less susceptible to acid-pepsin inactivation. Exogenous enzymes should be given with meals and with snacks. Their dose may need to be titrated upward.
• • • SUGGESTED READINGS • • •
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American Gastroenterological Association (AGA) Institute on “Management of Acute Pancreatits” Clinical Practice and Economics Committee; AGA Institute Governing Board. AGA Institute medical position statement on acute pancreatitis. Gastroenterology. 2007;132(5):2019-2021.
Banks PA, Freeman ML; Practice Parameters Committee of the American College of Gastroenterology. Practice guidelines in acute pancreatitis. Am J Gastroenterol. 2006;101(10):2379-2400.
Bornman PC, Botha JF, Ramos JM, et al. Guideline for the diagnosis and treatment of chronic pancreatitis. S Afr Med J. 2010;100 (12 Pt 2):845-860.
American Gastroenterological Association Medical Position Statement: treatment of pain in chronic pancreatitis. Gastroenterology. 1998 Sep;115(3):763-764.
Clain JE, Pearson RK. Evidence-based approach to idiopathic pancreatitis. Curr Gastroenterol Rep. 2002;4(2):128-134.