Health Questions and Answers

Acute Pancreatitis

What are the causes of acute pancreatitis (AP)?

  • Mechanical: gallstones, microlithiasis (biliary sludge), sphincter of Oddi dysfunction, papillary stenosis, duodenal diverticula, pancreas divisum, trauma
  • Toxins: alcohol, drugs, scorpion venom
  • Infectious: viral, bacterial, parasitic
  • Metabolic: hypertriglyceridemia, hypercalcemia
  • Ischemic: thromboembolic, vasculitis, hypotension, dehydration
  • Genetic: cystic fibrosis, hereditary
  • Tumors: ampullary, pancreatic, intraductal papillary mucinous tumors (IPMT)
  • Other: idiopathic, postoperative, postendoscopic retrograde cholangiopancreatography (ERCP), pregnancy

What are the most common causes of acute pancreatitis?
Gallstones and alcohol abuse are the most common causes of AP in the United States, each accounting for at least 30-35% of cases. The leading etiology depends on the population studied; for instance, alcoholism may predominate in many inner cities.
Idiopathic AP, in which a source is not identified, ranks as the third leading cause of AP. Recent studies, however, have demonstrated the presence of microlithiasis in up to two thirds of these patients when they undergo further investigation with repeated gallbladder ultrasound or bile crystal analysis. The theory that many cases of idiopathic AP are caused by microlithiasis is supported by a reduction in recurrences of AP in patients who undergo endoscopic sphincterotomy or cholecystectomy when compared with untreated patients (10% vs. 73%, p<.01). Chemical dissolution with ursodeoxycholic acid can also prevent recurrences.

Which drugs have been reported to cause acute pancreatitis?
The list can be remembered by using the mnemonic “NO IDEA”:
N
NSAIDs (sulindac, salicylates)
O
Other (valproate)
I
IBD drugs (sulfasalazine, 5-aminosalicylic acid)
Immunosuppressants (l-asparaginase, azathioprine, 6-mercaptopurine)
D
Diuretics (furosemide, thiazides)
E
Estrogens
A
Antibiotics (metronidazole, sulfonamides, tetracycline, nitrofurantoin, stibogluconate)
AIDS drugs (didanosine, pentamidine)

Drug-induced pancreatitis can occur immediately upon initiation of the drug or be delayed by months.

How is pregnancy associated with acute pancreatitis?
Coexisting cholelithiasis or microlithiasis is present in about 90% of cases. Other causes include hyperlipidemia and medications. Most episodes occur in the third trimester or postpartum period. The overall prognosis is good.

Which infectious agents have been implicated in causing acute pancreatitis? Viruses (i.e., mumps, coxsackievirus, cytomegalovirus, varicella-zoster, herpes simplex, Epstein-Barr, hepatitis A, hepatitis B); bacteria (i.e., Mycoplasma, Legionella, Leptospira, Salmonella, tuberculosis, brucellosis); fungi (i.e., Aspergillus, Candida albicans); and parasites (Toxoplasma, cryptosporidium, ascaris, Clonorchis sinensis)

How do Clonorchis sinensis and ascaris cause acute pancreatitis?
These parasites cause AP by blocking the main pancreatic duct and obstructing drainage of pancreatic secretions.

Is there an increased incidence of acute pancreatitis in patients with acquired immunodeficiency syndrome (AIDS)?
Yes. Up to 10% of patients with AIDS develop AP. The cause is usually multifactorial, with drugs and infections being the most common.

How does trauma cause acute pancreatitis?
AP can be caused by either blunt trauma or penetrating trauma. Blunt trauma occurs usually from compression of the pancreatic body against the spine. In adults, this may be seen during an automobile accident with a steering wheel or seat-belt injury. Trauma is the most common cause of AP in children, usually as a result of bicycle handle-bar injury. Less frequently, AP can also be caused by penetrating trauma, for instance, gunshot or stab wounds with damage to the pancreas.
Traumatic pancreatitis can range from mild contusion to severe crush injury with transection of the gland. Possible sequelae from trauma include acute duct rupture with pancreatic ascites or pancreatic duct strictures that result in recurrent and chronic pancreatitis.

What is pancreas divisum? Is it associated with an increased incidence of recurrent acute pancreatitis?
Pancreas divisum is the most common congenital variant of the pancreatic anatomy, occurring in approximately 5-10% of the population. It results when the embryologic dorsal and ventral pancreases fail to fuse, causing most of the pancreatic exocrine secretions to drain through the duct of Santorini (dorsal duct) and through the smaller minor papilla into the duodenum. Normally, pancreatic drainage flows through the duct of Wirsung (ventral duct) and through the larger major papilla into the duodenum. Pancreas divisum is usually diagnosed by endoscopic retrograde pancreatography (ERP) but may also be diagnosed by magnetic resonance cholangiopancreatography (MRCP), with or without secretin and endoscopic ultrasound (EUS).
Whether pancreas divisum causes recurrent AP is controversial. Ninety-five percent of people with pancreas divisum are asymptomatic, and their anomaly is discovered incidentally. It is, however, generally accepted that the combination of pancreas divisum along with a stenotic minor papilla leads to dorsal pancreatic duct obstruction and pancreatitis. Therapeutic options for these patients are decompression of the obstructed pancreatic duct with endoscopic sphincterotomy or surgical sphincteroplasty of the minor papilla. Stenting across the minor papilla may serve as a diagnostic test of sphincter dysfunction, if episodes of AP or pain occur frequently.

What is the relationship between hypertriglyceridemia and acute pancreatitis?
Hypertriglyceridemia may cause up to 4% of AP cases. Usually, serum triglyceride levels above 1000 mg/dL are required to induce an attack of AP. Treatment with diet and lipid-lowering agents can reduce recurrence when the initial episode has resolved.

What is the relationship between hypercalcemia and acute pancreatitis?
Hypercalcemia from any cause (e.g., hyperparathyroidism, metastatic bone disease, sarcoidosis) may lead to AP. Possible mechanisms include calcium activation of trypsinogen to trypsin within the pancreas, and calcification with possible stone formation in the pancreatic duct.
How is the diagnosis of acute pancreatitis made?
The diagnosis of AP is based on clinical assessment, biochemical analysis, and radiologic evaluation. In general, AP is clinically characterized by acute onset of epigastric abdominal pain that radiates into the back in a patient with risk factors such as alcohol and biliary disease. Compatible laboratory data include at least a threefold elevation in the serum amylase and/or lipase. Presentation may be mild to severe, depending on the amount of pancreatic inflammation and injury to regional or distant organs. The role of imaging with computed tomography (CT) is twofold, to find pancreatic inflammation and to exclude another source of pathology.
How does serum amylase compare to serum lipase in the diagnosis of acute pancreatitis?
Serum amylase rises typically within 6-12 hours of AP onset and declines gradually over 3-5 days. Serum lipase is elevated within the first 24 hours of AP and remains elevated for a longer period than serum amylase. Therefore, it may be more valuable than serum amylase in patients with delayed onset of suspected AP. Sensitivity of serum amylase and lipase are similar; however, some feel that specificity is greater with serum lipase given that most lipase stems from the pancreas. Fractionation of elevated total serum amylase into pancreatic-type (p-type) and salivary-type (s-type) isoamylase is available in most laboratories and may help in the diagnosis of AP. Recall that abdominal pathology (i.e., intestinal obstruction) can cause elevation of pancreatic isoamylase.
What are the nonpancreatic sources of hyperamylasemia and hyperlipasemia?
Hyperamylasemia may be seen in diseases of the salivary glands, lungs, fallopian tubes, ovarian cysts, gallbladder, small bowel, and appendix. Certain malignancies may also be associated with hyperamylasemia, including tumors of the pancreas, colon, lung, and ovary. Elevations in serum amylase may also be seen in macroamylasemia (see later), metabolic acidosis, and anorexia nervosa.
Although most serum lipase originates from the pancreas, other possible sources include the stomach, intestine, liver, and tongue. Serum lipase is also elevated in macrolipasemia. Conditions that increase intestinal permeability (inflammation, perforation, obstruction) or decrease renal clearance can also result in hyperamylasemia or hyperlipasemia.
What are macroamylasemia and macrolipasemia?
These are entities in which amylase or lipase is bound to a serum immunoglobulin, thus forming a large molecule that does not readily undergo renal clearance. This results in elevation of the serum amylase or lipase level. In macroamylasemia, the serum amylase is high; however, urine amylase and amylase:creatinine clearance ratio (ACR) are low (usually ACR <1%). Associated conditions include celiac disease, inflammatory bowel disease, lymphoma, and connective tissue disease.
What cause of acute pancreatitis should be suspected in patients who present with normal serum amylase levels?
Hypertriglyceridemia. One possible mechanism is that hypertriglyceridemia interferes with the laboratory measurement of the actual amylase level by preventing the calorimetric reading of the assay endpoint. Diluting the serum allows for true values of serum amylase to be measured. Whether this dilution reduces interference of light transmission by the lactescent plasma or decreases the concentration of a circulating amylase inhibitor associated with triglyceride elevation is unclear.

What is the relationship between hypercalcemia and acute pancreatitis?
Hypercalcemia from any cause (e.g., hyperparathyroidism, metastatic bone disease, sarcoidosis) may lead to AP. Possible mechanisms include calcium activation of trypsinogen to trypsin within the pancreas, and calcification with possible stone formation in the pancreatic duct.

How is the diagnosis of acute pancreatitis made?
The diagnosis of AP is based on clinical assessment, biochemical analysis, and radiologic evaluation. In general, AP is clinically characterized by acute onset of epigastric abdominal pain that radiates into the back in a patient with risk factors such as alcohol and biliary disease. Compatible laboratory data include at least a threefold elevation in the serum amylase and/or lipase. Presentation may be mild to severe, depending on the amount of pancreatic inflammation and injury to regional or distant organs. The role of imaging with computed tomography (CT) is twofold, to find pancreatic inflammation and to exclude another source of pathology.

How does serum amylase compare to serum lipase in the diagnosis of acute pancreatitis?

Serum amylase rises typically within 6-12 hours of AP onset and declines gradually over 3-5 days. Serum lipase is elevated within the first 24 hours of AP and remains elevated for a longer period than serum amylase. Therefore, it may be more valuable than serum amylase in patients with delayed onset of suspected AP. Sensitivity of serum amylase and lipase are similar; however, some feel that specificity is greater with serum lipase given that most lipase stems from the pancreas. Fractionation of elevated total serum amylase into pancreatic-type (p-type) and salivary-type (s-type) isoamylase is available in most laboratories and may help in the diagnosis of AP. Recall that abdominal pathology (i.e., intestinal obstruction) can cause elevation of pancreatic isoamylase.

What are the nonpancreatic sources of hyperamylasemia and hyperlipasemia?

Hyperamylasemia may be seen in diseases of the salivary glands, lungs, fallopian tubes, ovarian cysts, gallbladder, small bowel, and appendix. Certain malignancies may also be associated with hyperamylasemia, including tumors of the pancreas, colon, lung, and ovary. Elevations in serum amylase may also be seen in macroamylasemia (see later), metabolic acidosis, and anorexia nervosa.  Although most serum lipase originates from the pancreas, other possible sources include the stomach, intestine, liver, and tongue. Serum lipase is also elevated in macrolipasemia. Conditions that increase intestinal permeability (inflammation, perforation, obstruction) or decrease renal clearance can also result in hyperamylasemia or hyperlipasemia.

What are macroamylasemia and macrolipasemia?

These are entities in which amylase or lipase is bound to a serum immunoglobulin, thus forming a large molecule that does not readily undergo renal clearance. This results in elevation of the serum amylase or lipase level. In macroamylasemia, the serum amylase is high; however, urine amylase and amylase:creatinine clearance ratio (ACR) are low (usually ACR <1%). Associated conditions include celiac disease, inflammatory bowel disease, lymphoma, and connective tissue disease.

What cause of acute pancreatitis should be suspected in patients who present with normal serum amylase levels?

Hypertriglyceridemia. One possible mechanism is that hypertriglyceridemia interferes with the laboratory measurement of the actual amylase level by preventing the calorimetric reading of the assay endpoint. Diluting the serum allows for true values of serum amylase to be measured. Whether this dilution reduces interference of light transmission by the lactescent plasma or decreases the concentration of a circulating amylase inhibitor associated with triglyceride elevation is unclear.

Does the magnitude of hyperamylasemia or hyperlipasemia correlate with the severity of acute pancreatitis?
No. The magnitude of elevation in pancreatic enzymes does not generally correlate with the severity of pancreatitis and has no prognostic value.

What is the most reliable marker for diagnosing biliary acute pancreatitis?

A greater than threefold elevation of serum alanine aminotransferase (ALT) level has a positive predictive value of 95% for biliary AP. Bilirubin and alkaline phosphatase levels are not specific for biliary tract origin of AP. Amylase:lipase ratios and the magnitude of their elevation are also not helpful in distinguishing the cause of AP.

How is acute pancreatitis classified?

The most widely accepted classification system is based on the collaboration of 40 international experts on AP known as the 1992 Atlanta Symposium. AP is divided into mild and severe disease.

  • Mild AP is defined as minimal or no organ dysfunction and is usually associated with a self-limited course and an uneventful recovery. Severe AP consists of multiorgan failure and/or local complications, including pseudocyst or necrosis with possible superimposed infection.
  • Severe AP may be predicted by clinical criteria, including Ranson’s criteria and APACHE-II prognostic scoring systems (see later).

Distinction is also made between interstitial pancreatitis and necrotizing pancreatitis based on the findings of a contrast-enhanced dynamic CT. Interstitial pancreatitis is characterized by interstitial edema and inflammation, with no macroscopic parenchymal necrosis. Mortality is approximately 1%. This CT finding is usually associated with mild AP. Conversely, necrotizing pancreatitis is characterized by macroscopic focal or diffuse necrosis with nonviable parenchyma. Mortality for sterile necrosis approaches 10-15% and increases to 30-35% if the necrosis becomes infected. Patients with pancreatic necrosis have a 30-50% chance of developing infection of the necrosis.

What prognostic scoring systems are used to assess the severity of acute pancreatitis?

Clinical prognostic scores include Ranson’s criteria, simplified Glasgow criteria, and APACHE-II system. Additionally, a CT severity index can be used.

Ranson’s criteria consist of 11 indices used to assess the severity of AP. Five indices are measured on admission, and the remaining six indices are measured at 48 hours after admission. Thus, one of the limitations of this system is that a full 48 hours is required after admission prior to fully assessing disease severity. In addition, since the 1970s when the Ranson system was developed, subsequent studies have suggested that Ranson’s criteria are more predictive of ethanol-associated AP and less so for biliary AP. The score calculated from Ranson’s criteria correlates with mortality (score <3 = 5%, score 3-5 = 10%, score ≥6 = more than 60%). Ranson score ≥6 is also associated with more complications from AP, including necrosis and infected necrosis.

What is the role of serum markers in assessing the severity of acute pancreatitis?

Recent studies suggest that hemoconcentration on admission with a hematocrit ≥44% and failure of hematocrit to decrease at 24 hours may be predictive of necrotizing AP and organ failure.

What are the major systemic complications of acute pancreatitis?

Hypotension secondary to cardiovascular collapse may occur due to significant third-spacing of fluids, peripheral vasodilatation from circulating vasoactive kinins, and depressed left ventricular function.

Acute renal failure due to renal hypoperfusion and shock may lead to acute tubular necrosis, with a mortality rate approaching 50%.

Pleural effusions are usually left-sided (although bilateral and right-sided effusions do occur) and exudative with a high amylase level. Early arterial hypoxia results from microthrombi of the pulmonary vasculature with subsequent right-to-left shunt. Acute respiratory distress syndrome (ARDS) occurs in up to 20% of patients with severe AP.

Gastrointestinal (GI) bleeding may result from stress-induced gastritis and ulceration. Isolated gastric varices may form from splenic vein thrombosis. Splenectomy is the treatment of choice for bleeding gastric varices. Pseudoaneurysm and hemosuccus pancreaticus are also causes of GI bleeding in AP. Dynamic contrast-enhanced CT is the most useful initial diagnostic test, which may show a pseudocyst with contrast within it (so-called target sign). Selective mesenteric arteriography with embolization is the treatment of choice.

Pancreatic encephalopathy manifested by agitation, disorientation, confusion, hallucinations, and possible coma may occur.

Fat necrosis affecting subcutaneous tissue, bone, peritoneum, retroperitoneum, mediastinum, pleura, and pericardium may occur. Subcutaneous fat necrosis causes circumscribed, tender, red nodules over the skin, resembling erythema nodosum. Involvement of joints may result in arthritis.

Purtscher’s retinopathy, a rare complication of AP, leads to sudden blindness secondary to occlusion of the posterior retinal artery with aggregated granulocytes.

When is infection of pancreatic necrosis suspected?

Suspect infected pancreatic necrosis when the patient is not improving clinically, despite aggressive, supportive care, and there is persistence of systemic toxicity (fever >101°F, leukocytosis >20,000/mm3) or organ failure. Infection does not occur usually until 5-7 days after the onset of AP; however, it can be its presenting symptom. Infection is diagnosed by CT-guided percutaneous aspiration of the necrotic pancreas with Gram stain and culture of the aspirate for aerobic/anaerobic bacteria and fungi. Visualization of retroperitoneal gas bubbles on CT also suggests infection from gas-forming organisms.

What is the most common organism isolated in infected pancreatic necrosis?

Infected pancreatic necrosis may be due to a single organism (75-80% of the time) or a polymicrobial infection. The organisms probably infect the pancreas by translocation across the bowel wall with subsequent local lymphatic, hematogenous, or biliary spread.

Escherichia coli is isolated in 51% of percutaneous aspirates that are infected. Other organisms include Enterococcus spp. (19%), Staphylococcus spp. (18%), Klebsiella spp. (10%), Proteus spp. (10%), Pseudomonas spp. (10%), Streptococcus faecalis (7%), Bacteroides spp. (6%), and, rarely, fungi like Candida spp.

How is acute pancreatitis treated?

Treatment of AP depends on the severity of disease and the presence of complications. Mild AP is treated with supportive care, which includes intravenous hydration, parenteral analgesics, and nothing by mouth. Nasogastric suction may be used in cases of ileus or intractable nausea and vomiting. There is no indication for prophylactic antibiotics in mild AP.

Severe AP has higher morbidity and mortality as well as risk of developing systemic complications. These patients should be monitored in the Intensive Care Unit. Close attention should be paid to volume status because large amounts of fluid may third-space and accumulate in the injured pancreatic bed. Therefore, fluid resuscitation is a foundation of supportive therapy. If there is pancreatic necrosis, prophylactic antibiotics with good pancreatic tissue penetration may be utilized to prevent secondary infection and septic complications. There is no consensus regarding use of antibiotic prophylaxis in patients with severe AP without demonstrable necrosis by CT. Antibiotics with adequate pancreatic penetration include imipenem, third-generation cephalosporins, piperacillin, mezlocillin, fluoroquinolones, and metronidazole. Prophylactic antibiotic use may promote development of fungal infections, therefore use of prophylactic fungal therapy may also be advised. Other possible ways to prevent infection of necrotizing pancreatitis include selective digestive tract decontamination and use of enteral rather than parenteral feeding. Because the gut is the source of bacteria causing pancreatic infection, use of oral nonabsorbable antibiotics (norfloxacin, colistin, and amphotericin) for gut decontamination may reduce secondarily infected pancreatic necrosis. Enteral feeding eliminates complications like line sepsis and thrombophlebitis seen commonly with parenteral nutrition, and reduces bacterial translocation through decreasing gut permeability.

Patients with infected pancreatic necrosis should undergo urgent surgical debridement with continued antibiotic coverage. The surgical techniques vary, and debridement may be done in conjunction with closure of the abdomen with external drainage alone or with local saline lavage, or with open packing of the abdomen and repeated debridement. Because of the prolonged hospitalization associated with surgical debridement, recent advances with endoscopic drainage of infected pancreatic necrosis, or with catheters placed by interventional radiology, have been described. Their application presently remains limited.

In patients with persistent sterile pancreatic necrosis, there is no clear consensus on treatment. Most experts advise medical management for 4-6 weeks and monitor for resolution. No studies have clearly shown an advantage for surgical debridement, although some favor this approach in severely ill patients with continued organ dysfunction.

When, and by what route, should nutritional support be initiated in patients with acute pancreatitis?

Oral feeding should be initiated as soon as possible in patients with pancreatitis. Clinically, this translates to when the patient is hungry and is without nausea, vomiting, or evidence of gastrointestinal ileus. It is irrelevant if pain is present or if there is elevation of serum pancreatic enzymes. If oral feedings are not tolerated, then nutritional supplementation should be considered.

The decision to use parenteral or enteral nutrition is controversial, although there is mounting evidence that enteral feeding is more beneficial. Enteral nutrition, given via a jejunal feeding tube placed beyond the ligament of Treitz, has the advantage over parenteral nutrition of preserving bowel function and integrity. This can reduce bacterial translocation and theoretically decrease the incidence of pancreatic infection. Enteral nutrition is also less expensive than parenteral nutrition, has fewer problems with stress-induced hyperglycemia, and has a lower incidence of septic complications (i.e., catheter sepsis). A recent study showed that although enteral infusions of elemental diets did not rest the pancreas in healthy subjects, the enzyme secretory responses to elemental diets were suppressed in all patients with AP.

When should endoscopic retrograde cholangiopancreatography be performed in biliary acute pancreatitis?

Early ERCP with endoscopic sphincterotomy for stone extraction and biliary decompression has proved beneficial for patients with biliary pancreatitis and evidence of persistent or progressive biliary obstruction with cholangitis or biliary sepsis. Of note, the best clinical predictor of persistent common bile duct stones is an elevated serum total bilirubin level (>1.35 mg/dL) on hospital day 2 (sensitivity 90%, specificity 63%). However, the routine use of prelaparoscopic cholecystectomy ERCP in all patients with presumed gallstone pancreatitis is not justified. Patients without evidence of ongoing biliary obstruction or sepsis should have intraoperative cholangiogram at time of laparoscopic cholecystectomy, with bile duct exploration or postoperative ERCP as indicated.

Should patients undergo a cholecystectomy after an episode of biliary acute pancreatitis?

Yes. There is a 25% risk of recurrent AP, cholecystitis, or cholangitis within 6 weeks of the initial episode of biliary AP if cholecystectomy is not done.

How soon should a cholecystectomy be performed after an attack of biliary acute pancreatitis?

In patients with mild AP (Ranson’s criteria <3), laparoscopic cholecystectomy performed within the first week of admission is generally considered safe. Studies have shown no difference in mortality or length of postoperative stay when early cholecystectomy is compared with laparoscopic cholecystectomy performed later. However, in patients with more severe AP (Ranson’s criteria ≥3), laparoscopic cholecystectomy should be delayed for more than a week after admission given that patients tended to have a shorter postoperative stay if operated on later.

Should patients with coexisting alcoholism and cholelithiasis undergo cholecystectomy to prevent further attacks of acute pancreatitis?

No. Cholecystectomy does not prevent recurrent attacks of AP in patients with coexisting alcoholism because the disease almost always follows the pattern of alcohol-related pancreatitis.

What are acute fluid collections?

Acute fluid collections (AFC) occur in more than 50% of patients with moderate-to-severe AP. They are an accumulation of transudative or exudative fluid secondary to the local inflamed pancreatic tissue. They lack a clear wall of granulation tissue and are irregularly shaped. In general, they do not communicate directly with the pancreatic duct, and therefore do not have high pancreatic enzyme concentrations, as do pseudocysts. Acute fluid collections may occur as early as 48 hours after the onset of AP, with most resolving spontaneously by 4-6 weeks. However, 10-15% may develop a capsule and progress to pseudocyst formation.

What are pseudocysts?

Pancreatic pseudocysts are an accumulation of fluid containing necrotic tissue, debris, blood, and high concentrations of pancreatic enzymes. They develop usually 4 weeks after onset of AP and represent extravasated pancreatic secretions with an inflammatory response, often in communication with the pancreatic duct. They appear round or oval in shape and are surrounded by a capsule of granulation tissue and collagen. Unlike pancreatic cysts, pancreatic pseudocysts lack a true epithelial lining. Approximately 85% are located in the body or tail, with 15% found in the head of the pancreas. They may also occur in the lesser peritoneal sac and can extend into the paracolic gutters, pelvis, mediastinum, and, rarely, to the neck or scrotum.

When should a pseudocyst be suspected?
A pseudocyst should be suspected in the following scenarios: Serum amylase remains persistently high.

  1. An episode of AP fails to resolve.
  2. The patient has persistent abdominal pain after clinical resolution of AP.
  3. An epigastric mass is felt after an episode of AP.

What are the indications for pseudocyst drainage?

An asymptomatic pseudocyst does not require treatment regardless of size and may be followed every 3-6 months with abdominal ultrasound. Indications for pseudocyst drainage include presence of symptoms, progressive enlargement, presence of complications (i.e., infection, hemorrhage, rupture, obstruction), and suspicion of malignancy.

How are pancreatic pseudocysts drained?

Pseudocysts may be drained endoscopically, percutaneously under radiologic guidance, or surgically. Endoscopic or percutaneous drainage is successful in 85% of cases. Endoscopic drainage can be done when the pseudocyst is adherent to the wall of the stomach or duodenum, creating an endoluminal bulge, in which case an endoscopic cyst-gastrostomy or cyst-duodenostomy is performed. Bleeding is a potential complication, and use of endoscopic ultrasonography is recommended to avoid puncturing large blood vessels in the drainage area. Moreover, if there is continuity between the main pancreatic duct and pseudocyst, endoscopic placement of a transpapillary pancreatic duct stent into the pseudocyst may be done for drainage. Percutaneous catheter drainage under radiologic guidance is preferred for high-risk patients, immature pseudocysts with thin walls, and infected pseudocysts. It is not to be used in the presence of a main pancreatic duct obstruction close to the ampulla secondary to the risk of developing a permanent external fistula. Surgical drainage still remains the gold standard. It is warranted when: (1) there are complications of bleeding or fistula formation, (2) endoscopic or percutaneous drainage fails, (3) multiple or giant pseudocysts are present, and (4) if malignancy is suspected to obtain excisional histopathology.

What are possible complications of an untreated pancreatic pseudocyst?

Secondary infection occurs in approximately 10% of pseudocysts. CT scan may suggest infection by demonstrating gas bubbles within the pseudocyst. Diagnosis is made by percutaneous aspiration with Gram stain and culture.

Pseudocyst rupture occurs in <3% of patients. Clinical presentation varies widely from an acute abdomen to a silent event producing pancreatic ascites or pleural effusion.

Pancreatic ascites, secondary to leakage from a pseudocyst (70%) or pancreatic duct (10-20%), is characterized by ascitic fluid with a high amylase level (usually >1000 U/dL) and protein (usually >2.5 g/dL). Medical management consists of total parenteral nutrition and octreotide (50-200 μg subcutaneously every 8 hours). ERCP can demonstrate the site of leakage, and endoscopic stenting of the main pancreatic duct may allow resolution of the ascites. Surgical approach remains the gold standard of treatment, if the aforementioned are unsuccessful.

Pancreatic fistulas develop usually from external drainage of a pseudocyst. They may close spontaneously or with the aid of octreotide, which decreases fistula output. Surgery may be necessary for persistent high-output fistulas (>200 mL/day).

Obstruction of the GI tract, urinary system, vena cava, or portal vein by a pseudocyst necessitates drainage.

Jaundice is associated with pseudocyst in approximately 10% of cases. Its causes include hepatic dysfunction, extrahepatic biliary obstruction, and stenosis of the intrapancreatic portion of the distal common bile duct from pancreatitis and choledocholithiasis.

Pseudoaneurysm occurs when the pseudocyst erodes into an adjacent vessel (5-10% of patients). Clinical signs include an expanding pseudocyst with pain, hypotension, and a falling hematocrit. If the pseudocyst communicates with the pancreatic duct, massive GI bleeding with hematemesis or melena occurs secondarily to bleeding directly through the pancreatic duct into the duodenum (hemosuccus pancreaticus). Intraperitoneal bleeding results from pseudoaneurysm rupture.

What is a pancreatic abscess?

A circumscribed collection of pus located usually in or near the pancreas. It is caused by secondary infection of a pancreatic pseudocyst or an area of pancreatic necrosis. It is a late event, occurring at least 4 weeks after the onset of AP. The mortality rate associated with pancreatic abscess is generally less than that of infected necrosis. Treatment includes percutaneous catheter or surgical drainage, with possible debridement of necrotic tissue.

References
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  27. Tenner S, Dubner H, Steinberg W: Predicting gallstone pancreatitis with laboratory parameters: A meta analysis. Am J Gastroenterol 89:1863-1866, 1994.
  28. Venu RP, Brown RD, Marrero JA, et al: Endoscopic transpapillary drainage of pancreatic abscess: Technique and results. Gastrointest Endosc 51:391-395, 2000.

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