Acute pancreatitis (AP) is an inflammatory disorder of the pancreas characterised by upper abdominal pain and pancreatic enzyme elevations.
Chronic pancreatitis (CP) is a progressive disease characterised by long-standing pancreatic inflammation leading to loss of pancreatic exocrine and endocrine function.
WHAT ARE THE CAUSES OF PANCREATITIS?
Gallstones and alcohol abuse account for most cases in the United States. Diabetes mellitus and autoimmune disorders such as inflammatory bowel disease are also associated with an increase in acute pancreatitis. A cause cannot be identified in some patients (idiopathic pancreatitis).
Many medications have been implicated (Table 1–1), but drug-induced acute pancreatitis is considered to be rare. A causal association is difficult to confirm because ethical and practical considerations prevent rechallenge.
AP is initiated by premature activation of trypsinogen to trypsin within the pancreas, leading to activation of other digestive enzymes and autodigestion of the gland.
Activated pancreatic enzymes within the pancreas and surrounding tissues produce damage and necrosis to pancreatic tissue, surrounding fat, vascular endothelium, and adjacent structures. Lipase damages fat cells, producing noxious substances that cause further pancreatic and peripancreatic injury.
Release of cytokines by acinar cells injures those cells and enhances the Inflammatory response. Injured acinar cells liberate chemoattractants that attract neutrophils, macrophages, and other cells to the area of inflammation, causing systemic inflammatory response syndrome (SIRS). Vascular damage and ischemia cause release of kinins, which make capillary walls permeable and promote tissue oedema.
Pancreatic infection may result from increased intestinal permeability and translocation of colonic bacteria.
Local complications in severe AP include acute fluid collection, pancreatic necrosis, infection, abscess, pseudocyst formation, and pancreatic ascites. Systemic complications include respiratory failure and cardiovascular, renal, metabolic, hemorrhagic, and CNS abnormalities.
WHAT ARE THE SIGNS AND SYMPTOMS OF PANCREATITIS?
Clinical presentation depends on the severity of the inflammatory process and whether the damage is confined to the pancreas or involves local and systemic complications.
The initial presentation ranges from moderate abdominal discomfort to excruciating pain, shock, and respiratory distress. Abdominal pain occurs in 95% of patients and is usually epigastric, often radiating to the upper quadrants or back. Onset is usually sudden, and intensity is often described as “knife-like” or “boring.” The pain usually reaches maximum intensity within 30 minutes and may persist for hours or days. Nausea and vomiting occur in 85% of patients and usually follow the onset of pain.
Signs include marked epigastric tenderness on palpation with rebound tenderness and guarding in severe cases. The abdomen is often distended and tympanic with decreased or absent bowel sounds in severe disease.
Vital signs may be normal, but hypotension, tachycardia, and low-grade fever are often observed, especially with widespread pancreatic inflammation and necrosis. Dyspnea and tachypnea are signs of acute respiratory complications.
Jaundice and altered mental status may be present; other signs of alcoholic liver disease may be present in patients with alcoholic pancreatitis.
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