Acute pancreatitis can range from a mild, self-limiting process that responds to supportive care to severe disease with multiple organ failure and high mortality. Its incidence is increasing,1 and pancreatitis is one of the most common causes of hospital admission for gastrointestinal illness.2 Although most patients experience minor episodes characterized by mild parenchymal edema without organ dysfunction, response to conservative management, and complete recovery,3 approximately 20% to 25% of patients develop clinically severe acute pancreatitis. More severe episodes may progress to pancreatic necrosis, systemic inflammatory response syndrome (SIRS), multiorgan failure, clinical deterioration, and even death.4 Historically, mortality has been up to 15% in the setting of necrotizing pancreatitis and as high as 30% with infected pancreatic necrosis.5 Recent years have seen advances in the classification and management of acute pancreatitis including evidence-based guidelines and a notable shift toward nonoperative management of even the most severe cases of infected pancreatic necrosis.
Given the wide spectrum of severity, patients with pancreatitis must receive highly individualized care. Mild acute pancreatitis can generally be managed with resuscitation and supportive care including a search for etiologic factors such as gallstones. Patients with severe pancreatitis and pancreatic necrosis may require maximal support in intensive care and occasionally surgical or endoscopic debridement of the pancreas. The indications for intervention in patients with severe pancreatitis have evolved significantly in the past 2 decades. Whereas early surgical debridement was used for most patients with pancreatic necrosis in the past, a far more conservative approach was adopted with recognition that surgical debridement was not necessary in the setting of most cases of pancreatic necrosis without infection.6 Revision of the 1992 Atlanta Classification of acute pancreatitis7 to provide a newer classification to more precisely describe the clinical behavior and imaging characteristics of acute pancreatitis8 has allowed more uniform categorization of the disease in recent years. At the same time, the development of minimally invasive and nonsurgical approaches to necrotizing pancreatitis has led to increased consensus that most patients, including even those with the greatest disease severity, may avoid surgical debridement.9 This chapter reviews contemporary management strategies in acute pancreatitis, including assessment of severity, nutritional support, the role of antibiotics, and indications for intervention.
Acute pancreatitis has been attributed to a range of etiologic factors (Table 68-1). Intra-acinar activation of trypsinogen, with subsequent activation of other pancreatic enzymes, is thought to play a central role in pathogenesis of the disease. A local inflammatory response is associated with liberation of oxygen-derived free radicals and cytokines including interleukin (IL)-1, IL-6, IL-8, tumor necrosis factor alpha (TNF-α), and platelet-activating factor. These mediators play an essential role in transformation of the local inflammatory response to a systemic illness.
TABLE 68-1ETIOLOGIC FACTORS IN ACUTE PANCREATITIS