Acute Pancreatitis
I. Acute 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.
A. 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.
B. 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.
II. COMPLICATIONS
A. 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.
B. 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).
C. Pseudocysts.
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.
D. Pancreatic abscesses.
The secondary infection of a pancreatic phlegmon or pseudocyst by enteric flora results in pancreatic abscess.
E. 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.
F. 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.
G. 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, results in renal dysfunction of varying severity.
H. Circulatory shock
may occur in severe instances due to third-spacing of fluid and intravascular hypovolemia. If intravenous (IV) fluid replacement is inadequate, hypovolemia and hypotension may intensify the pancreatitis.
III. ETIOLOGY.
There are many conditions implicated as causative factors in the pathogenesis of acute pancreatitis (Table 45-1).
A. Alcoholism and biliary tract disease.
The two most common etiologic factors associated with pancreatitis are alcoholism and biliary tract disease (gallstones). These two factors account for 75% to 85% of all cases. In countries in which the incidence of alcoholism and excessive alcohol use is high, such as the United States, Australia, and South Africa, alcohol is the etiologic factor in more than 50% of patients. In contrast, in countries in which alcoholism is less prevalent, such as Britain and Israel, biliary tract disease is the most common cause of acute pancreatitis. The mortality of gallstone-associated pancreatitis is approximately 8% during the first attack and 1% during subsequent attacks. Chronic pancreatitis with pancreatic insufficiency rarely, if ever, occurs, even after multiple episodes of pancreatitis associated with gallstones.
TABLE 45-1 Causes of Acute Pancreatitis | ||||||||||||||
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TABLE 45-2 Drugs Associated with Pancreatitis | ||||||||||||||||||||||||||||||||
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There is a well-documented association between excessive alcohol consumption and pancreatitis. In most patients, the disease recurs many times, leading to chronic pancreatitis with irreversible functional and structural damage of the organ. Even though the mortality is considerably less than that of gallstone disease-associated pancreatitis, all the complications of acute pancreatitis may develop during the acute attacks.
B. Postoperative pancreatitis
is infrequent but has a high mortality. It occurs after cardiopulmonary bypass, thoracic, and abdominal surgical procedures. Operations on and near the pancreas such as gastrectomy, biliary tract surgery, and splenectomy are involved in most of the cases.
C. Endoscopic retrograde pancreatography.
Pancreatitis may occur in less than 1% of cases after endoscopic retrograde pancreatography (ERCP). However, hyperamylasemia is common after ERCP.
D. Blunt abdominal trauma
is the most common cause of pancreatitis in children and young adults.
E.
Some metabolic disorders are implicated as causes of pancreatitis.
1. Hypertriglyceridemia
may precede and cause pancreatitis. Patients with some lipoprotein abnormalities, especially Frederickson type I, type IV, and type V hyperlipoproteinemia, are at increased risk of development of pancreatitis. An abrupt increase in serum triglycerides to greater than 2,000 mg/dL can precipitate a bout of acute pancreatitis. This can occur in patients with underlying hypertriglyceridemia who ingest either large amounts of lipid and moderate amounts of alcohol or large amounts of alcohol or who use birth control pills. Serum amylase may be normal in lipemic serum. Dilutions should be requested to ascertain the correct level of serum amylase.
2. Hypercalcemia
from any cause can lead to acute pancreatitis. Causes of hypercalcemia include hyperparathyroidism, parathyroid adenoma or carcinoma, myeloma, excessive doses of vitamin D, familial hypocalciuric hypercalcemia, and hypercalcemia in patients receiving total parenteral nutrition (TPN) or using calcium carbonate-containing antacids. Acute pancreatic necrosis is frequent during hyperparathyroid crisis. Increased concentrations of calcium ions in pancreatic secretion and pancreatic tissue might promote activation of trypsinogen, initiating the proteolytic cascade.
F. Organ transplantation.
Pancreatitis may complicate renal and liver transplantation.
G. Pregnancy.
Women in whom acute fatty liver of pregnancy develops in the third trimester may also develop acute pancreatitis. However, 90% of instances of pancreatitis during pregnancy are associated with gallstones.
H. Infections.
Viral agents, including mumps, hepatitis B, and Coxsackie virus group B, and some bacteria (e.g., Mycoplasma pneumoniae) have been implicated as causes for acute pancreatitis. Opportunistic protozoan, bacterial, and fungal pathogens, which may involve the pancreas, include Cryptosporidium, cytomegalovirus, Legionella pneumophila, and Salmonella species, Mycobacterium avium, and tuberculosis.
I. Connective tissue diseases.
Pancreatitis may occur in patients with some connective tissue diseases, such as systemic lupus erythematosus (SLE), especially those complicated with vasculitis.
J. Vasculitis,
present in other disorders such as Henoch-Schönlein purpura, thrombocytopenic purpura, and necrotizing angiitis, may also be implicated as a cause of acute pancreatitis.
K. Drugs
have been associated with the development of pancreatitis in some patients. Table 45-2 lists the drugs in two groups: those for which there is a definite association and those for which the association is probable.
L. Anatomic abnormalities.
Pancreatitis has been reported in patients with a number of anatomic abnormalities in the vicinity of the ampulla of Vater, possibly associated with its obstruction, such as duodenal Crohn’s disease, duodenal diverticula, choledochocele, choledochal cysts, duodenal intussusception, and sphincter of Oddi dysfunction.
M. Pancreas divisum
is a special condition that may lead to recurrent bouts of pancreatitis. Pancreas divisum results when the ducts of the embryologic ventral and dorsal parts of the pancreas fail to fuse. Wirsung’s duct, which normally drains the entire pancreas, only drains the uncinate process in these patients. The rest of the pancreas is drained by the duct of Santorini through the minor papilla. In many of the patients with pancreas divisum and recurrent pancreatitis, the minor papilla has been found to be stenotic and may be implicated as the predisposing condition for the development of pancreatitis.
N. Duodenal ulcer.
Penetration of a duodenal ulcer into the pancreas may result in local pancreatic inflammation. Even though there may be an elevation of serum amylase, extensive pancreatitis usually does not develop.
O. Hereditary pancreatitis
in an autosomal dominant transmission pattern has been described in a number of families. Symptoms usually appear between the ages of 5 and 15 years and progress to chronic pancreatitis. There may be an increased incidence of pancreatic adenocarcinoma in these families.
P. Miscellaneous causes.
There are numerous other reported causes of pancreatitis including scorpion bite by Tityus trinitatis found in the West Indies and pancreatic duct obstruction by parasites
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