Acute pancreatitis

The gold standards are direct inspection at laparotomy and microscopic examination. However, routine diagnostic cornerstones remain abdominal pain, nausea, vomiting, and hyperamylasemia. Clinical signs, although suggestive, are notoriously non-specific. Remote organ failure and metabolic disturbances such as hyperglycemia and hypocalcemia, although rarely present at the onset, should alert the clinician.

Hyperamylasemia has a high sensitivity (>95 per cent) within 24 h of symptom onset but a lower specificity (70 per cent). The magnitude of increase in serum amylase does not correlate with disease severity. Furthermore, normal amylase levels are encountered in cases of hyperlipidemic pancreatitis, acute exacerbations of chronic pancreatitis, and particularly with delayed measurement.

The diagnostic value of isoamylase determination (pancreatic versus salivary) remains controversial, although the lipase assay is as sensitive as but more specific than amylase. Other pancreatic enzymes, such as immunoreactive trypsin, elastase, and phospholipase A2, are elevated in acute pancreatitis but, except in cases of delayed admission, add little to the diagnosis of suspected cases and a normal or only mildly raised amylase. Moreover, these tests are not performed routinely, they are expensive, and their prognostic significance remains doubtful. Rarely, elevation of amylase in pleural or ascitic fluid may coexist with a normal serum level and so is occasionally of some diagnostic utility.

Plain abdominal radiography may reveal adynamic ileus, increased gastrocolic separation, sentinel loops, and the colon cut-off sign at the splenic flexure. It aids diagnosis of other potentially confounding abdominal emergencies, such as hollow viscus perforation or mesenteric infarction. Peritoneal aspiration, smelling the fluid, and Gram staining are useful, since the presence of peritoneal infection on admission is unusual in acute pancreatitis and suggests other pathology that mandates urgent laparotomy.

Although convenient, non-invasive, inexpensive, and repeatable, ultrasound examination can be inconclusive and occasionally misleading. It is highly operator dependent and in 30 to 40 per cent the gland cannot be evaluated, mainly due to excessive overlying bowel gas. It is inaccurate for detection of pancreatic necrosis or regional infection and for delineating the extent of peripancreatic fluid collections.

Abdominal contrast-enhanced CT is the imaging method of choice for cases that pose a diagnostic dilemma. Satisfactory evaluation is obtained in almost all patients, and diagnostic abnormalities (pancreatic swelling, areas of attenuation in the gland, and peripancreatic fluid collections) persist after 1 week in 80 per cent. The specificity of an admission CT is nearly 100 per cent; although sensitivity is about 85 per cent, most episodes undetected by CT are mild. It may provide significant assistance where enzyme levels are normal or falsely elevated. Importantly, CT allows a reliable appraisal of the presence and extent of intra- and extrapancreatic necrosis by high-resolution CT and prolonged bolus scanning techniques (dynamic pancreatography). This provides obvious diagnostic and prognostic information and implications with regard to surgical intervention. Dynamic pancreatograms should usually be obtained within 48 h of admission for severe episodes. Focal areas of diminished enhancement after administration of contrast material allow differential diagnosis between edematous and necrotizing pancreatitis with an overall accuracy rate exceeding 90 per cent. The size of these defects correlates closely with the amount of devitalized pancreatic tissue assessed at operation and confirmed by histomicroangiographic studies. Ancillary CT signs of necrotizing pancreatitis include marked glandular enlargement, lowered pancreatic density values on precontrast CT, and extensive extrapancreatic extension of inflammation. Although the degree of pancreatic necrosis correlates with the extent of peripancreatic fluid collections, these are not mutually inclusive.

Failure to diagnose acute pancreatitis is generally ascribed to an atypical presentation, namely the absence of abdominal pain. This may occur during artificial ventilation with analgesia/sedation, or because shock, severe gastrointestinal bleeding, diabetic coma, or respiratory failure may be the presenting manifestations of a painless episode or conceal abdominal pain. In rare instances (up to 5 per cent) a definite diagnosis can only be made at laparotomy.

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