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Acute Pancreatitis

Last updated on May 12, 2023

Acute PancreatitisAcute pancreatitis is a discrete episode of inflammation resulting from intrapancreatic activation of digestive enzymes. It is a disease with a wide spectrum of severity, complications, and outcome.

Acute edematous or interstitial pancreatitis. In this stage, the pancreatic inflammation and disease is mild and self-limited in most patients. The inflammation results in interstitial edema. The parenchymal damage is minimal, and the organ recovers its function after resolution of the inflammation.

Hemorrhagic or necrotizing pancreatitis. In some patients, the inflammation may be extensive and progress to coagulation necrosis of the gland and the surrounding tissues, leading to hemorrhagic or necrotizing pancreatitis. The mass of inflamed pancreas containing necrotic tissue is referred to as a phlegmon.


Spread of the inflammatory process

The retroperitoneal location of the pancreas and the absence of a well-developed pancreatic capsule allow the inflammatory process to spread freely. The activated pancreatic enzymes dissect through the tissue planes and affect any of the following organs: the common bile duct, duodenum, splenic artery and vein, spleen, pararenal spaces, mesocolon, colon, mesentery of the small bowel, celiac and superior mesenteric ganglia, lesser omental sac, posterior mediastinum, and diaphragm.

The peritoneal surfaces may be involved with the inflammatory process, leading to exudation and fluid accumulation in the peritoneal cavity (pancreatic ascites) and the lesser omental sac. Involvement of the diaphragmatic lymphatics may lead to sterile pleural effusion and pneumonitis.

Local effects of pancreatic enzymes and vasoactive materials include an intense chemical burn of tissue leading to leakage of protein-rich fluid from the systemic circulation into peritoneal and retroperitoneal spaces. This phenomenon may lead to hypovolemia. Systemic effects of these circulating materials include cardiovascular instability, respiratory failure, and renal failure.

Hemorrhage within or around the gland may dissect along tissue planes and lead to a bluish discoloration in the periumbilical area (Cullen’s sign) or in the costovertebral angle (Turner’s sign).


Necrotic tissue, blood, pancreatic juice, and fat from disrupted cells may accumulate within or adjacent to the pancreas, forming pseudocysts. Pseudocysts may resolve spontaneously as the inflammation subsides. If the pseudocyst is large or if there is a communication between the pseudocyst and a ruptured pancreatic duct with continued secretion of pancreatic juices into the enclosed space, the pseudocyst may not resolve.

Pancreatic abscesses

The secondary infection of a pancreatic phlegmon or pseudocyst by enteric flora results in pancreatic abscess.

Fat necrosis may occur in peritoneal, retroperitoneal, and distant locations such as in subcutaneous or intramedullary areas. Calcium salts (soaps) of free fatty acids liberated from fatty tissue may precipitate in these areas.

Polyserositis and the adult respiratory distress syndrome. The entry of the activated pancreatic enzymes (e.g., trypsin, elastase, phospholipase A) into the circulation allows these potent digestive enzymes to attack distant sites.

Polyserositis involving pericardial, pleural, and synovial surfaces may occur. Left-sided pleural effusion is common. The pulmonary alveolar-capillary membrane may be disrupted, forming hyalin membranes lining the alveolar surface. A transudate fills the alveolar space and leads to a noncardiogenic pulmonary edema or adult respiratory distress syndrome.

Disseminated intravascular coagulation and microthrombi. The release of activated pancreatic enzymes into the circulation may result in disseminated intravascular coagulation with formation of intravascular microthrombi. These thrombi may affect the function of many organ systems. Pulmonary intravascular microthrombi result in intrapulmonary right-to-left shunting and hypoxia. Microthrombi in the glomerular capillaries, deposited in the mesangium and the glomerular basement membrane, result in renal dysfunction of varying severity.

Circulatory shock may occur in severe instances due to third-spacing of fluid and intravascular hypovolemia. If intravenous (intravenous) fluid replacement is inadequate, hypovolemia and hypotension may intensify the pancreas.

Etiology of Acute Pancreatitis


The exact mechanism of the events that trigger the intrapancreatic activation of zymogens to active enzymes leading to autodigestion and inflammation remains unknown. However, there is evidence that more than one mechanism is involved. It is thought that ischemia, anoxia, trauma, infections, and endo- and exotoxins set the stage for activation of trypsinogen to trypsin with further activation of other zymogens to active enzymes, including phospholipase A, elastase, and lipase.

The enzymes, along with the detergent effect of bile acids, then digest cell membranes and elastic fibers of blood vessels, leading to vascular damage with interstitial edema, hemorrhage, and parenchymal cell and fat necrosis of the pancreatic and peripancreatic tissues. Vasoactive substances such as bradykinin and histamine that are released lead to vasodilatation and increased permeability resulting in more edema and inflammation.

One popular theory to explain the initiation of the autodigestion cascade suggests obstruction to the outflow of pancreatic juice (i.e., with gallstone impaction at the ampulla resulting in intraductal hypertension) and inhibition of acinar cell zymogen secretion by exocytosis. In this setting, the zymogen-containing vacuoles in the acinar cells fuse with lysosomes, which contain proteases.

This results in enzyme activation within the combined vacuoles. These vacuoles rupture into the acinar cell, resulting in acinar cell injury and death with consequent intra- and extraparenchymal injury. Reflux of duodenal contents into the pancreatic duct, presence of a common channel (communicating pancreatic and common bile duct) with or without impacted gallstone, and occlusion of pancreatic blood vessels are other popular theories. Other forms of ischemia may also lead to intracellular zymogen activation and result in parenchymal damage.

Prognostic factors in acute pancreatitis

Acute pancreatitis is a disease of varying severity. In most individuals, the disease is mild or moderate with full recovery of the patient. However, in some individuals, the disease may be fulminant with very high morbidity and mortality. Thus, it is important to identify factors that increase the likelihood of a fatal outcome in patients with acute pancreatitis. Tables PROGNOSTIC FACTORS IN ACUTE PANCREATITIS and CLINICAL CRITERIA FOR SEVERE PANCREATITIS summarize some of those factors. An increased mortality is observed when three or more risk factors are present. These include hypotension, need for massive fluid and colloid replacement, respiratory failure, and hypocalcemia. Patients at high risk should be treated in an intensive care unit and may require surgical intervention.

Diagnosis of Acute Pancreatitis

Diagnostic studies of Acute Pancreatitis

Differential diagnosis

Table DIFFERENTIAL DIAGNOSIS OF ACUTE PANCREATITIS summarizes the differential diagnosis of acute pancreatitis. It may be difficult to distinguish between acute cholecystitis, ascending cholangitis, and pancreatitis, because they may present with similarly elevated serum amylase and abnormal liver tests. Ultrasound and dimethylphenylcarbamylmethyliminodiacetic acid (HIDA) scan may be helpful in differentiating between these diseases. Gut ischemia, infarction, viscus perforation, aortic dissection, mechanical intestinal obstruction, myocardial infarction, and acute appendicitis need to be promptly diagnosed and surgically treated.



In most patients (85%-90%) with acute pancreatitis, the disease is self-limited and resolves spontaneously. These patients are medically treated with supportive care with special attention given to analgesia, maintenance of normal intravascular volume, frequent monitoring of vital signs, and treatment of possible complications of the disease.

Meperidine (Demerol) in a dosage of 50 to 100 mg every 4 to 6 hours intravenous or intramuscular is better tolerated than morphine sulfate, which may induce spasm of the sphincter of Oddi. In cases of severe pain, morphine sulfate may be necessary.

Acutes cholecystitiss
Biliary colic due to choledocholithiasis
Ascending cholangitis
Perforated viscus
Penetrating peptic ulcer
Alcoholic hepatitis
Viral hepatitis
Acute intestinal obstruction
Mesenteric ischemia/infarction
Dissecting aortic aneurysm
Myocardial infarction
Renal colic
Acute appendicitis
Diabetic ketoacidosis
Inflammatory involvement of contiguous organs
Obstructive jaundice
Pancreatic ascites
Intraperitoneal hemorrhage
Thrombosis of splenic vein
Bowel infarction
Gastrointestinal bleeding
Diabetes ketoacidosis
Nonketotic diabetic coma
Pancreatic encephalopathy
Cardiogenic shock
Increased cardiac index
Decreased systemic vascular resistance
Pleural effusions
Pulmonary infiltrates, atelectasis
Adult respiratory distress syndrome
Decreased glomerular filtration rate and renal plasma flow
Acute tubular necrosis
Acute renal failure
Disseminated intravascular coagulation
Increased factor VII or fibrinogen
Skin and musculoskeletal
Erythema nodusum-like lesions
Angiopathic retinopathy

The sequestration of fluid in the peripancreatic and retro- and intraperitoneal areas reduce the circulating plasma volume in most patients. Intravenous electrolyte and colloid solutions should be given generously to replace the fluid deficit. Fluid volume status determination may require Swan-Ganz catheter placement.

It is believed that by putting the pancreas «at rest» by reducing pancreatic secretions, the pancreatic inflammation will be minimized. Patients usually are given nothing by mouth, and the upper gastrointestinal tract is decompressed by nasogastric suction. The rationale for nasogastric suction is to decrease gastric secretion and to prevent gastric contents from entering the duodenum. Nasogastric suction with a double-lumen sump tube is used in patients with nausea, vomiting, and ileus. It may not be necessary for the patient with mild disease.

No drugs have been shown to improve the course of acute pancreatitis. Clinical trials using inhibitors of gastric acid secretion such as histamine-2 blockers or proton-pump inhibitors also are no more effective than nasogastric suction. Somatostatin or its analog octreotide may be beneficial by reducing pancreatic enzyme secretion.

Prophylactic antibiotics are not recommended in intersitial pancreatitis. Antibiotics should be reserved for patients with established infection. It is important to recognize and treat with the appropriate antimicrobial therapy possible secondary infection of the injured pancreatic tissue (phlegmon, pseudocyst, abscess) or an obstructed biliary tract leading to ascending cholangitis.

In several studies, prophylactic antibiotics were found to be helpful in preventing either pancreatic infection or other infections among patients with necrotizing pancreatitis.

Nutritional support of the patient with acute pancreatitis should not be neglected. As the inflammation subsides, small feedings of a diet high in carbohydrate but low in protein and fat may be initiated. It is important to advance the diet slowly. The feedings should be stopped if symptoms return. Pancreatic secretion is stimulated equally in patients given elemental diets and those given regular diets intragastrically or intrajejunally. Parenteral administration of nutrition does not seem to increase pancreatic secretion. Thus, in patients who cannot receive feedings orally, parenteral nutritional support including intralipids should be instituted after the first few days.

Patients with fulminant pancreatitis need intensive monitoring and therapy. These patients have very large fluid requirements. Most patients have respiratory insufficiency and acute respiratory distress syndrome and may require mechanical respiratory support. Hypocalcemia and hypomagnesemia should be promptly treated with intravenous replacement. Renal insufficiency and acute tubular necrosis are not uncommon, and patients may require dialysis.

Patients with severe disease should be closely followed by a surgical team. In patients with a deteriorating clinical condition, emergency laparotomy for drainage of the necrotic pancreas and peripancreatic spaces may be attempted. Some surgeons advocate subtotal pancreatectomy and a procedure to decompress the biliary tract. Alternatively, in clinically deteriorating patients with necrotizing pancreatitis demonstrated on computed tomography scan, computed tomography-guided percutaneous aspiration of the necrotic pancreas may be attempted.

Gram’s stain and culture should be performed on the aspirated material. Bacterial findings necessitate surgical debridement. In selected cases of infected necrosis, vigorous percutaneous drainage with multiple large tubes have been successful in either delaying surgery until the patient is a better surgical candidate or eliminating the need for surgery. Also, in selected incidences of infected necrosis, there may be a role for endoscopic drainage, particularly if the necrosis has organized.

There are several reports in the literature suggesting that potent antibiotics may successfully treat infected necrosis without the need for surgical debridement. In sterile necrosis, nonoperative medical management for the first 3 to 4 weeks is recommended.

Pancreatic pseudocysts are collections of necrotic tissue, fluid, and blood that develop in or near the pancreas over a period of 1 to 4 weeks after the onset of acute pancreatitis. They do not have a true capsule with an epithelial lining. A connection may be present to a disrupted pancreatic duct. Most pseudocysts (90%) are solitary lesions located in the body or tail of the pancreas. The main symptom is abdominal pain.


Most pseudocysts form during a severe episode of acute pancreatitis. Persistence of an elevated serum amylase level for more than a week after the onset of pancreatitis may signal the formation of a pseudocyst. Other causes of pancreatic pseudocyst include abdominal blunt trauma with disruption of a pancreatic duct, inadvertent surgical ductal trauma, and chronic pancreatitis. Neoplastic cysts, such as cystadenoma or cystadenoma-carcinoma, account for 10% of cystic pancreatic masses.

Diagnostic studies

Abdominal Ultrasound and computed tomography scan are the best imaging techniques used in the diagnosis of pancreatic pseudocysts. Serial scans help in following the size and course of the cysts. Endoscopic retrograde cholangiopancreatography may be required to assess the possible connection of the pseudocyst with the pancreatic duct.

Complications and treatment

Most pseudocysts tend to resolve spontaneously. Symptomatic pseudocysts require decompression. This can be achieved by surgery or by percutaneous catheter drainage or by endoscopic techniques. Endoscopic and radiologic methods should be reserved for those institutions with extensive experience in these techniques. The serious complications of pancreatic pseudocysts are infection, perforation, and hemorrhage.


Patients with a pancreatic pseudocyst who have pain, fever, and leukocytosis need to be evaluated for infection. Percutaneous aspiration under Ultrasound or computed tomography guidance with Gram’s stain and culture of the aspirate helps in confirming the diagnosis. Infected pseudocyst or abscess should be drained externally.


Rupture or leak of a pseudocyst into the peritoneal cavity or retroperitoneum may result in shock and requires emergency surgery. The mortality from this complication is very high.


A pseudocyst may erode into a viscus (e.g., stomach, small or large bowel) or a blood vessel with subsequent hemorrhage. Angiography is often necessary prior to surgery for proper diagnosis of this complication.

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