Chapter 28: Pancreatitis

INTRODUCTION

• Acute pancreatitis (AP) is an inflammatory disorder of the pancreas characterized by upper abdominal pain and pancreatic enzyme elevations.

• Chronic pancreatitis (CP) is a progressive disease characterized by long-standing pancreatic inflammation leading to loss of pancreatic exocrine and endocrine function.

ACUTE PANCREATITIS: PATHOPHYSIOLOGY

• 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 AP. A cause cannot be identified in some patients (idiopathic pancreatitis).

• Many medications have been implicated (Table 28-1), but drug-induced AP is rare. A causal association is difficult to confirm because ethical and practical considerations preclude 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 edema.

• 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.

CLINICAL PRESENTATION

• Clinical presentation depends on severity of the inflammatory process and whether 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.” Pain usually reaches maximum intensity within 30 minutes ...