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Hyperstimulation of pancreas exocrine secretion appears to be the mechanism of action in both instances. Acute pancreatitis may occur in the postoperative period of various surgical procedures (eg, abdominal or cardiopulmonary bypass surgery, which may damage the gland by causing ischemia). Postoperative acute pancreatitis is often a difficult diagnosis to confirm, and it has a higher complication rate than pancreatitis associated with other etiologies.

The mechanism is unclear. Vascular factors, such as ischemia or vasculitis, can play a role in causing acute pancreatitis. Vasculitis can predispose patients to pancreatic ischemia, especially in those with polyarteritis nodosa and systemic lupus erythematosus. Autoimmune pancreatitis, a relatively newly described entity, is an extremely rare cause of acute pancreatitis (prevalence, 0.

When it does cause acute pancreatitis, it is usually in young people (approximately age 40 years) who may also suffer from other autoimmune diseases. The pathogenesis is unclear, but it is potentially related to immunoglobulin (Ig) G4 autoimmune disease. In 1998, 183,000 patients with acute pancreatitis were admitted. This trend in rising incidence has been recognized over the past several decades.

In Finland, the incidence is 73. Similar incidence rates have been reported in Australia. The incidence of disease outside North America, Europe, and Australia is less well known.

In Europe and other developed nations, such as Hong Kong, more patients tend to have gallstone pancreatitis, whereas in the United States, alcoholic pancreatitis is most common. The median age at onset depends on the etiology. For people aged 35-75 years, the rate doubles for males and quadruples for females.

Generally, acute pancreatitis affects males more often than females. Idiopathic pancreatitis has no clear predilection for either sex. The hospitalization rates of patients with acute pancreatitis per 100,000 population are 3 times higher for blacks than whites.

These racial differences are more pronounced for males than females. The risk for African Americans aged 35-64 years is 10 times higher than for any other group.

African Americans are at a higher risk than whites in that same age group. Patients with biliary pancreatitis tend to have a higher mortality than patients with alcoholic pancreatitis. This rate has been falling over the last 2 decades as improvements in supportive care have been initiated.

Type 2 diabetes mellitus has also been associated with higher severity and mortality in the setting of acute pancreatitis. In patients with pancreatic necrosis without organ failure, the mortality approaches zero. In the first week of illness, most deaths result from multiorgan system failure. In subsequent weeks, infection plays a more significant role, but organ failure still constitutes a major cause of mortality. Acute respiratory distress syndrome (ARDS), acute renal failure, cardiac depression, hemorrhage, and hypotensive shock all may be systemic manifestations of acute pancreatitis in its most severe form.

Identifying patients in the greatest need of aggressive medical treatment by differentiating their disease severity as mild or severe is recommended. Different strategies have been used to assess the severity of acute pancreatitis and predict outcome (see Workup and Staging). Several clinical scoring systems (eg, Ranson criteria, Glasgow, Imrie) are available. The APACHE II scoring system, though cumbersome, appears to be the best validated (see the APACHE II Scoring System calculator).

Biological markers have also been used for this purpose. Genetic markers are being studied and have not yet come into clinical use. Dynamic CT scanning of the abdomen is widely available and useful in predicting the outcome of acute pancreatitis. Suppiah et al examined the prognostic value of the neutrophil-lymphocyte ratio (NLR) in 146 consecutive patients with acute pancreatitis. The NLR is calculated from the white cell differential and provides an indication of inflammation.