Acute pancreatitis (AP) is defined as the acute nonbacterial inflammatory condition of the pancreas. It is derived from the early activation of digestive enzymes found inside the acinar cells, with variable compromise of the gland itself, nearby tissues and other organs. Although the disease process may be limited to pancreatic tissue, it also can involve peripancreatic tissues or more distant organ sites. AP is a disease with extremely different clinical expressions. It may occur as an isolated attack or may be recurrent (1). It has a variety of causes and can range in severity from mild to severe and life threatening. Most patients suffer a mild and limited disease but about one fifth of cases develop multiple organ disfunction syndrome (MODS), accompanied by high mortality (1). The correct diagnosis of acute pancreatitis should be made in all patients within 48 hours of admission. Mild acute pancreatitis has a very low mortality rate (less than 1 percent), whereas the death rate for severe acute pancreatitis can be 10 to 30 percent depending on the presence of sterile versus infected necrosis. This great variability in presentation, clinical course and complications has given rise to the confusion related to AP related terminology. However, consensus meetings (Atlanta and later working groups) have provided more uniform definitions. For the last 25 years, there has been a global increase in incidence of AP, along with many advances in diagnosis and treatment. This increase was associated with a parallel increase in gallstone and alcohol-related pancreatitis.

Acute pancreatitis is a disease with an overall mortality of approximately 4-6% (which increases to 17-39% in severe disease) and substantive morbidity (2, 3). New mortality data in AP confirm that mortality rates are similar in gallstone and alcohol-induced AP, that mortality is 20% in those hospitalized more than 1month with severe AP (SAP), and that increased mortality occurred in those with hospital-acquired infection and those at least 70 years old (4).

The most common risk factors for acute pancreatic are gallbladder disease (often caused by choledocholithiasis) and chronic alcohol consumption. The etiology factors for acute pancreatitis are listed in table 1 (3, 5, 6). The etiology of acute pancreatitis should be determined in at least 80% of cases and no more than 20% should be classified as idiopathic (7).

Cigarette smoking is an independent risk factor for AP and total exposure correlates with overall risk (4). Sex is strongly associated with the risk of acute pancreatitis: the incidence of alcoholic pancreatitis is higher in men, and the incidence of gallstone pancreatitis is higher in women. Multivariate analyses showed that acute pancreatitis was associated with a stone diameter of less than 5 mm and with mulberry-shaped gallstones.

The hallmark symptom of acute pancreatitis is the acute onset of persistent upper abdominal pain, usually with nausea and vomiting. The usual locations of the pain are the epigastric and periumbilical regions. The pain may radiate to the back, chest, flanks, and lower abdomen. Patients are usually restless and bend forward (the knee-chest position) in an effort to relieve the pain because the supine position may exacerbate the intensity of symptoms (5). Physical examination findings are variable but may include fever, hypotension, severe abdominal tenderness, guarding, respiratory distress, and abdominal distention. Accurate diagnosis is important because many other conditions have similar symptoms, including acute cholecystitis, choledocholithiasis, and penetrating duodenal ulcers. Potentially lifethreatening conditions to consider include a perforated viscus, an ischemic bowel, bowel obstruction, or myocardial infarction (6, 8).

Two types of pancreatitis were defined at the Atlanta symposium in 1992: one light form, usually auto limited; and the other severe, where local complications may appear, such as necrosis and distant organ failure (OF). Fortunately, these complications are uncommon, occurring in approximately 15% of the cases. The situation’s severity will be determined by clinical, analytical and radiological criteria. Because some complications do not appear immediately (necrosis or pseudocysts), a severity definition will be made adequately at the end of the process (9).

Clinical features (abdominal pain and vomiting) together with elevation of plasma concentrations of pancreatic enzymes are the cornerstones of diagnosis. The diagnosis of acute pancreatitis requires at least 2 of the following: typical upper abdominal pain, serum levels of amylase or lipase > 3 times the upper limit of normal, and confirmatory findings from cross-sectional imaging analysis (10, 11). But there is no single laboratory or clinical sign which is pathognomonic for acute pancreatitis; many biomarkers and inflammatory mediators for predicting the severity of acute pancreatitis are being evaluated (5, 12).

The initial laboratory evaluation should include amylase and lipase levels, complete blood count with differential, metabolic panel (blood urea nitrogen, creatinine, glucose, and calcium levels), triglyceride level, urinalysis and arterial blood gases. Amylase and lipase, secreted by the acinar cells of the pancreas, are the most common laboratory markers used to establish the diagnosis of acute pancreatitis. Elevated amylase and lipase levels can be nonspecific, depending on the time since onset of pain, other intra-abdominal processes, and concomitant chronic diseases such as renal insufficiency. Pancreatic enzymes are released into the circulation during an acute attack. Levels peak early, and decline over 3-4 days. An important concept derives from this: the diagnosis of acute pancreatitis should not rely on arbitrary limits of values 3 or 4 times greater than normal, but values should be interpreted in light of the time since the onset of abdominal pain (7). The half life of elevated amylase is shorter than that of lipase. Because it persists longer after the onset of the attack and because the pancreas is the only source of lipase, estimation of plasma lipase has slightly superior sensitivity and specificity and greater overall accuracy than amylase. Amylase levels may be normal in patients with alcoholism who present with acute pancreatitis, especially if they have had previous attacks of alcoholic pancreatitis; thus, serial testing may not be helpful. Plasma lipase is more sensitive and specific than plasma amylase. Recent research has examined potential biologic markers for predicting the severity and prognosis of pancreatitis. Trypsinogens and pancreatic protease involved in the autodigestive processes of acute pancreatitis appear promising. Other investigational serologic markers include trypsinogen activation peptide, C-reactive protein, procalcitonin, phospholipase A2, and the cytokines interleukin-6 and interleukin-8. Currently, these markers have limited clinical availability, but there is significant interest in better understanding markers of immune response and pancreatic injury because these could be valuable tools for reliably predicting the severity of acute pancreatitis (12, 13).

Plain radiographs contribute little to the diagnosis of acute pancreatitis. The recommended initial examination is ultrasonography. Ultrasound may show pancreatic swelling but the pancreas is visualised in only 25-50% of patients with acute pancreatitis. The value of ultrasonography lies in its ability to demonstrate gall bladder stones and dilatation of the common bile duct, as well as other pathology unrelated to the pancreas such as abdominal aortic aneurysm. The sensitivity of the US in the detection of gallstones is > 95% in uncomplicated cases; however in the setting of acute pancreatitis, sensitivity for gallstone detection is only 67-78% due to the ileus and bowel distension. Furthermore, sensitivity in the detection of common bile duct stones is between 25-90% (12, 14).

CT is occasionally indicated for diagnosis, if clinical and biochemical findings are inconclusive, especially when abdominal signs raise the possibility of an alternative abdominal emergency, such as a perforation or infarction of the bowel.

Liver biochemistry is helpful for the diagnosis of biliary pancreatitis. A meta-analysis found that a 3-fold increase of serum alanine transaminase (> 60 μ/l < 48 hours of symptoms) will identify gallstones as the cause in patients with pancreatitis with a positive predictive value of 95%. It should be kept in mind that around 10-15% of patients with biliary pancreatitis present with normal serum liver enzyme and bilirubin levels (14).

Contrast enhanced computed tomography must be performed > 72 h from onset of symptoms to allow delineation of the necrosis. Magnetic resonance imaging is also a reliable staging method with similar sensitivity and specificity to that of contrast enhanced computed tomography.

The revised Atlanta Classification recognizes 3 degrees of severity. Mild disease is defined as acute pancreatitis not associated with organ failure, local complications, or systemic complications. Most patients with mild acute pancreatitis do not require pancreatic imaging analysis and are usually discharged within 3 to 5 days of onset of illness. Moderately severe acute pancreatitis is defined by the presence of transient organ failure, local complications, or systemic complications. Transient organ failure is defined by organ failure that is present for < 48 hours. Patients with moderately severe acute pancreatitis frequently require extended hospitalization but have lower mortality rates than patients with severe acute pancreatitis. Severe acute pancreatitis is defined by the presence of persistent organ failure. Persistent organ failure is defined by organ failure that is present for > 48 hours. Most patients with persistent organ failure have pancreatic necrosis (8-10).

There is agreement that there is still a need for an early objective measure of severity. So far, there has been no precise method for this purpose, although in daily practice, following several clinical guidelines, a number of criteria are being used.

Clinical examination in the first 24 hours of admission although specific lacks sensitivity and hence is unreliable and should be supported by objective measures. Immediate assessment should include clinical evaluation, particularly of any cardiovascular, respiratory, and renal compromise, body mass index, chest x ray. The presence of any organ failure should be documented. After 24 hours in hospital, clinical assessment and documentation of organ failure are required (tab. 2).