acute pancreatitis(redirected from acute haemorrhagic pancreatitis)
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Etymology: Gk, pan, all, kreas, flesh, itis, inflammation
a sudden inflammation of the pancreas caused by autodigestion and marked by symptoms of acute abdomen and escape of pancreatic enzymes into the pancreatic tissues. The condition is associated with trauma, biliary disease or alcoholism. The autodigestion is caused by premature activation of the digestive enzymes. Acute pancreatitis can also be of unknown cause. See also pancreatitis.
acute pancreatitisInflammation of the pancreas of abrupt onset, often accompanied by gallstones and alcohol ingestion.
15-fold increase from 1960s to present, possibly due to widened diagnostic criteria, with 40 admissions/105/year.
Abdominal pain, nausea, vomiting, hypotension.
Contrast-enhanced CT (method of choice), ultrasonography.
Increased amylase, increased lipase.
Supportive bowel rest with parenteral nutrition.
Ranson’s criteria, modified Glasgow criteria, APACHE II.
25% have complications; 9% die of pancreatitis, sepsis, pulmonary failure, etc.
Acute pancreatitis aetiology
• Acute ischaemia—thrombosis, embolism, vasculitis, shock.
• Drugs—thiazide diuretics, azathioprine, oestrogens, sulfonamides, furosemide, methyldopa, pentamidine, procainamide.
• Gallstones—biliary tract disease.
• Genetic—defective genes encoding critical enzymes or proteins.
• Infection—mumps, coxsackieviruses, Mycoplasma pneumoniae.
• Metabolic defects—hypertriglyceridemia, hyperparathyroidism, hypercalcaemia.
• Obstruction—ampullary tumours, congenital defects of pancreas or biliary tree, parasites.
• Toxins—scorpion bites.
• Trauma—blunt, iatrogenic injury during heart surgery or ERCP.
• Vascular defects.
Autodigestion of pancreas by inappropriately activated pancreatic enzymes—e.g., trypsin from trypsinogen—which activates other proenzymes. Possible pathways of enzyme activation:
(1) Pancreatic duct obstruction
Increased intrapancreatic ductal pressure results in accumulation of enzyme-rich interstitial fluid; lipase (one of the few enzymes secreted in activated form) results in fat necrosis, while injured tissues release cytokines, leading to local inflammation, oedema.
(2) Primary acinar cell injury—e.g., mumps, other viral infections, drugs, trauma, ischaemia, shock.
(3) Defective intracellular transport of proenzymes—aberrant cell packaging of enzymes has been shown to occur in alcohol and duct obstruction.
acute pancreatitisInflammation of the pancreas of abrupt onset, often with gallstones and alcohol ingestion Epidemiology 109,000 hospitalizations, 2251 deaths–US; 10-fold ↑ from 1960s to 1980s–reason unclear;
? alcohol abuse; ? widened diagnostic criteria; ± 250 admissions/106 population/yr, higher in certain populations–eg, 4-22% in AIDS Pts Etiology Obstruction, toxins or drugs, trauma, metabolic defects, infection, vascular defects, idiopathic Diagnosis Abdominal pain, ↑ amylase, ↑ lipase, ultrasonography, contrast-enhanced CT Management Supportive, bowel rest with parenteral nutrition Prognosis Ranson's criteria, modified Glasgow criteria, APACHE II Prognosis 25% have complications, 9% die of pancreatitis, sepsis, pulmonary failure, etc. See Chronic pancreatitis.
a·cute pan·cre·a·ti·tis(ă-kyūt' pan'krē-ă-tī'tis)
Inflammation of the pancreas, frequently involving destruction of tissue by pancreatic enzymes. When severe, may lead to local necrosis, hemorrhage, and shock.
Fitz,Reginald Heber, U.S. physician, 1843-1913.
Fitz syndrome - Synonym(s): acute pancreatitis