Acute Pancreatitis

Acute pancreatitis (AP) is defined as an inflammatory process involving a gland that is normal prior to the attack, and which returns to normal once the derangements that precipitated the attack have been corrected.

AP is a common problem with a rising incidence in the western world - in the US there are about 200,000 admissions/year and about 10,000 deaths/year.

Table 1. Potential factors causing pancreatitis







Drugs (e.g. glucocorticosteroids, azathioprine, hydrochlorothiazide, furosemide, sulfonamides, estrogens, pentamidine, didanosine (DDI), valproic acid)


Hyperalimentation with lipids



Gall stones

Tumours (pancreas CA, common bile duct CA, TU of the ampulla and duodenum, metastases)

Sphincter of Oddi Dysfunction

Post upper gastorintestinal surgery

Post endoscopy

Post abdominal trauma

Duodenal obstruction/scar (e.g. after ulcer disease) Mumps

Coxsackie virus infection

Ascaris infection with mechanical component

Panarteritis nodosa

Post cardiac and pulmonary surgery

Severe arteriosclerosis

Hereditary, idiopathic

Anomalies (pancreas divisum, anulare)


Scorpion sting/gila monster bite

AP is more often seen in the elderly population (50-60 years of age). The most common causes of AP are cholelithiasis (75%) and alcohol abuse (15%). Other causes are metabolic disorders (e.g., hypercalcemia, hy-perlipidemia Type I and V), infections (e.g., parasites, hepatitis, HIV), trauma (e.g., penetrating ulcer, abdominal surgery, endoscopic retrograde cholangiopancreatography [ERCP]), drugs (e.g., azathioprine, furosemide, sul-fonamides, steroids), and structural abnormalities (e.g., pancreas divisum, choldeochocele). In 10-15% of patients no obvious cause can be found, however, biliary microlithiasis might be the most likely cause in these cases (Table 1).

From a pathophysiological point of view, the most likely factors for the sudden onset of AP are: (1) pancreatic hypersecretion, (2) intra- and extravasation of pancreatic secretions, and (3) premature activation of pancreatic enzymes followed by autodigestion and necrosis of the pancreatic gland and peripancreatic tissues.

From the clinical point of view, AP can be divided into a mild and severe form almost paralleled by the patho-physiological finding of an interstitial (edematous) and necrotizing form [6, 7].

The mild form of AP (approximately 50% of the cases) is characterized by mild symptoms and transitory elevation of amylase levels that recover rapidly without complications. In general, the gland may be enlarged due to a moderate edema, and peripancreatic fluid collections can be present; however, in 30% of the cases no morphological changes can be appreciated. In cholelithiasis, a segmental pancreatitis - mainly of the pancreatic head -is found in up to 20% of cases (Fig. 1).

While ultrasound (US) may reveal a normal to mildly enlarged gland with homogeneous (hypoechoic) echogenicity, sufficient visualization by US is possible in only 60-70% of cases. In contrast-enhanced computed tomography (CT) as well as in magnetic resonance imag

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