Poor prognostic factor in a patient with pancreatitis includes-
Correct Answer: Leucocytosis>20,000/|iL
Description: Clinical features The typical presentation is with severe, constant upper abdominal pain, of increasing intensity over 15-60 minutes, which radiates to the back. Nausea and vomiting are common. There is marked epigastric tenderness, but in the early stages (and in contrast to a perforated peptic ulcer), guarding and rebound tenderness are absent because the inflammation is principally retroperitoneal. Bowel sounds become quiet or absent as paralytic ileus develops. In severe cases, the patient becomes hypoxic and develops hypovolaemic shock with oliguria. Discoloration of the flanks (Grey Turner's sign) or the periumbilical region (Cullen's sign) is a feature of severe pancreatitis with haemorrhage. The differential diagnosis includes a perforated viscus, acute cholecystitis and myocardial infarction. A collection of fluid and debris may develop in the lesser sac, following inflammatory rupture of the pancreatic duct; this is known as a pancreatic fluid collection. It is initially contained within a poorly defined, fragile wall of granulation tissue, which matures over a 6-week period to form a fibrous capsule . pseudocysts' are common and usually asymptomatic, resolving as the pancreatitis recovers. Pseudocysts greater than 6 cm in diameter seldom disappear spontaneously and can cause constant abdominal pain and compress or erode surrounding structures, including blood vessels, to form pseudoaneurysms. Large pseudocysts can be detected clinically as a palpable abdominal mass. Pancreatic ascites occurs when fluid leaks from a disrupted pancreatic duct into the peritoneal cavity. Leakage into the thoracic cavity can result in a pleural effusion or a pleuro-pancreatic fistula. Investigations The diagnosis is based on raised serum amylase or lipase concentrations and ultrasound or CT evidence of pancreatic swelling. Plain X-rays should be taken to exclude other diagnoses, such as perforation or obstruction, and to identify pulmonary complications. Amylase is efficiently excreted by the kidneys and concentrations may have returned to normal if measured 24-48 hours after the onset of pancreatitis. A persistently elevated serum amylase concentration suggests pseudocyst formation. Peritoneal amylase concentrations are massively elevated in pancreatic ascites. Serum amylase concentrations are also elevated (but less so) in intestinal ischaemia, perforated peptic ulcer and ruptured ovarian cyst, while the salivary isoenzyme of amylase is elevated in parotitis. If available, serum lipase measurements are preferable to amylase, as they have greater diagnostic accuracy for acute pancreatitis. Ultrasound scanning can confirm the diagnosis, although in the earlier stages the gland may not be grossly swollen. The ultrasound scan is also useful because it may show gallstones, biliary obstruction or pseudocyst formation. Contrast-enhanced pancreatic CT performed 6-10 days after admission can be useful in assessing bility of the pancreas if persisting organ failure, sepsis or clinical deterioration is present, since these features may indicate that pancreatic necrosis has occurred. Necrotising pancreatitis is associated with decreased pancreatic enhancement on CT, following intravenous injection of contrast material. The presence of gas within necrotic material suggests infection and impending abscess formation, in which case percutaneous aspiration of material for bacterial culture should be carried out and appropriate antibiotics prescribed. Involvement of the colon, blood vessels and other adjacent structures by the inflammatory process is best seen by CT. Ceain investigations stratify the severity of acute pancreatitis and have impoant prognostic value at the time of presentation . In addition, serial assessment of CRP is a useful indicator of progress. A peak CRP of >210 mg/L in the first 4 days predicts severe acute pancreatitis with 80% accuracy. It is woh noting that the serum amylase concentration has no prognostic value. Ref Davidson edition23rd pg 839
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