Acute pancreatitis may vary in severity, from mild, self-limiting pancreatic inflammation to pancreatic necrosis with life-threatening sequelae. In the majority of the more than 185,000 patients who develop acute pancreatitis each year in the United States, the process is limited to mild parenchymal edema without distant organ dysfunction and an uneventful recovery.1 Although the overall mortality rate with acute pancreatitis is 2-10%, this is primarily related to patients with more severe disease. Approximately 10� 30% of patients develop severe illness with pancreatic inflammation progressing to pancreatic and peripan-creatic necrosis. The severity of the local response can lead to development of the systemic inflammatory response syndrome (SIRS) and multiorgan failure, with considerable morbidity and mortality.
The management of patients with mild acute pancreatitis is generally standardized and is primarily limited to identification and management of etiologic factors, resuscitation, and supportive care. Patients with severe and necrotizing pancreatitis require more intensive therapy, possibly including aggressive surgical management for debridement of infected pancreatic necrosis or to address other local complications of the disease. The precise indications for surgery in these patients have been controversial, although in recent years many investigators have adopted a more conservative stance toward early intervention.45 This review provides current diagnostic and therapeutic strategies in acute pancreatitis, with particular attention to recent developments in our understanding of severity assessment, nutrition, prophylactic antibiotics, indications for and timing of surgery, and the role of minimally invasive techniques.
Despite advances in the understanding of the pathophysiology of pancreatitis and improvements in
imaging technology, diagnostic modalities for acute pancreatitis have not changed drastically in recent years. Clinical signs and symptoms, such as upper abdominal pain, back pain, vomiting, fever, tachycardia, and leukocytosis, are relatively nonspecific. The periumbilical and flank bruising seen with hem-orrhagic pancreatitis (Cullen and Grey-Turner signs) are uncommon and nonspecific for any particular etiology. Diagnosis therefore typically depends on a high level of clinical suspicion and the demonstration of elevated plasma concentrations of pancreatic enzymes. Levels of both amylase and lipase peak within the first 24 hours of symptoms, and amylase has a slightly shorter half-life in plasma. As a result, lipase levels may have a slightly greater sensitivity than amylase levels, particularly when measured late (>24 hours) after initial presentation.6 Moreover, hyperamylasemia is neither specific for pancreatitis7 nor perfectly sensitive, as normoamylasemia has been described in acute pancreatitis.8 Other pancreatic enzymes have not been shown to have any advantage over amylase and lipase for diagnostic purposes. Of note, plasma levels of pancreatic enzymes serve a purely diagnostic and not a prognostic role; absolute levels have no direct correlation with disease severity.
An early goal in management is to identify patients with severe pancreatitis to institute directed therapy early in the course of the disease. Although progress has been made in this area, an objective and reproducible measure of disease severity has not been universally accepted.9 Clinical evaluation at presentation is not always straightforward. Initial signs and symptoms of necrotizing pancreatitis are only different in degree from edematous pancreatitis; likewise, severe and mild forms of disease share the same etiologies.10 Despite considerable experimental effort to identify differences in the pathogenesis of edematous and necrotizing pancreatitis,11 this has not resulted in a successful model of predicting which patients, at initial presentation, will progress to severe disease.