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In most patients the disease is mild and patients recover after a few days. However, 20% develop severe (necrotising) pancreatitis with complications or organ failure, which has a high mortality. Having many episodes of acute pancreatitis may lead to [[chronic pancreatitis]]. | In most patients the disease is mild and patients recover after a few days. However, 20% develop severe (necrotising) pancreatitis with complications or organ failure, which has a high mortality. Having many episodes of acute pancreatitis may lead to [[chronic pancreatitis]]. | ||
<section begin="clinical biochemistry" /> | |||
== Etiology == | == Etiology == | ||
The most common causes are alcoholism and gallstones in the biliary tract distal to the pancreatic duct. These two factors are responsible for 80% of all cases of acute pancreatitis. | The most common causes are alcoholism and gallstones in the biliary tract distal to the pancreatic duct. These two factors are responsible for 80% of all cases of acute pancreatitis. | ||
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* [[ERCP]] | * [[ERCP]] | ||
* Drugs | * Drugs | ||
<section end="clinical biochemistry" /> | |||
Other causes are Vascular ([[shock]], arteroembolism, polyarteritis nodosa), mutations (PRSS1, SPINK1), etc. | Other causes are Vascular ([[shock]], arteroembolism, polyarteritis nodosa), mutations (PRSS1, SPINK1), etc. | ||
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On contrast CT, the pancreas is focally or diffusely enlarged. In oedematous pancreatitis there is heterogenous contrast enhancement. In necrotic pancreatitis there is a lack of contrast enhancement. CT may also show a gallstone if present, as well as any complication. Like on ultrasonography, there may be peripancreatic fluid and the pancreatic margins may be indistinct. | On contrast CT, the pancreas is focally or diffusely enlarged. In oedematous pancreatitis there is heterogenous contrast enhancement. In necrotic pancreatitis there is a lack of contrast enhancement. CT may also show a gallstone if present, as well as any complication. Like on ultrasonography, there may be peripancreatic fluid and the pancreatic margins may be indistinct. | ||
<section end="radiology" /> | <section end="radiology" /><section begin="clinical biochemistry" /> | ||
=== Etiology === | === Etiology === | ||
After the diagnosis is made, the underlying cause must be sought. This includes a thorough history to look for risk factors, serum triglyceride level, calcium level, and abdominal ultrasound for gallstone. [[Endoscopic ultrasound]] may be used if initial investigations does not reveal the etiology. | After the diagnosis is made, the underlying cause must be sought. This includes a thorough history to look for risk factors, serum triglyceride level, calcium level, and abdominal ultrasound for gallstone. [[Endoscopic ultrasound]] may be used if initial investigations does not reveal the etiology. | ||
=== Severity assessment === | === Severity assessment === | ||
The severity of the pancreatitis must be assessed, both based on clinical assessment and the SIRS score. Severe acute pancreatitis (as determined by the presence of [[haemodynamic instability]], [[hypoxaemia]], [[acid-base disorder]], [[altered mental status]], etc.) should be managed in an [[intensive care unit]]. High <abbr>[[CRP]]</abbr> (> 100 mg/L) suggests necrotising pancreatitis. Important to note that serum lipase/amylase are not predictors of severity, and so the degree of enzyme elevation does not correlate with the severity of the disease. | The severity of the pancreatitis must be assessed, both based on clinical assessment and the SIRS score. Severe acute pancreatitis (as determined by the presence of [[haemodynamic instability]], [[hypoxaemia]], [[acid-base disorder]], [[altered mental status]], etc.) should be managed in an [[intensive care unit]]. High <abbr>[[CRP]]</abbr> (> 100 mg/L) suggests necrotising pancreatitis. Important to note that serum lipase/amylase are not predictors of severity, and so the degree of enzyme elevation does not correlate with the severity of the disease. |