Pancreatitis
BACKGROUND
The pancreas is approximately 6 to 10 inches long, is located directly behind the stomach, and has distinct endocrine and exocrine functions. The endocrine portion of the pancreas is composed of islets of Langerhans cells that constitute about 2% of the organ. These cells produce and secrete hormones including insulin, glucagon, and somatostatin. The exocrine portion of the pancreas is composed of acinar cells (80% of the organ) and ductal cells (18% of the organ). Acinar cells produce digestive enzymes that are sequestered until physiologic impulses stimulate their release into the pancreatic ductal system where they are transported to the small intestine. The digestive enzymes are enzymatically inert until activated in the small intestine by various peptides. Disruption of this physiologic process, by any of a variety of etiologies, is the basis for our current understanding of acute and chronic pancreatitis. This chapter primarily focuses on acute pancreatitis, which is more commonly seen in emergency care. Pertinent aspects of chronic pancreatitis are also addressed.
ACUTE PANCREATITIS
The incidence of acute pancreatitis is estimated to be as high as 38 per 100,000 patients and accounts for more than 220,000 hospital admissions in the United States annually.1 Most cases are clinically mild and self-limited; a minority of cases are severe and are associated with critical illness, prolonged hospitalization, infection, organ failure, and death.
Acute pancreatitis occurs from premature activation of digestive enzymes within the pancreatic parenchyma leading to an autodigestive and inflammatory process. Evolution into a life-threatening systemic process begins when acinar cell injury leads to expression of endothelial adhesion molecules that further potentiates the inflammatory response. Local microcirculatory failure and ischemia–reperfusion injury ensue, with some patients developing systemic complications such as systemic inflammatory response syndrome (SIRS), acute respiratory distress syndrome, and multiorgan failure.
The most common causes of acute pancreatitis are gallstones and excess alcohol ingestion. These account for about 45% and 35% of cases, respectively.2,3 Hypertriglyceridemia accounts for up to 5% of cases. Other causes include hypercalcemia, autoimmune diseases, infections, medications, trauma, and complications after endoscopic retrograde cholangiopancreatography (ERCP) (Table 26.1). Controversial etiologies include pancreatic divisum and sphincter of Oddi dysfunction. Idiopathic pancreatitis occurs in up to 20% of patients, and by definition, the cause is not established by history, physical exam, routine laboratory tests, or imaging.
TABLE 26.1 Causes of Acute Pancreatitis
History and Physical Exam
The typical presentation includes a constant (as opposed to waxing and waning) upper abdominal pain located primarily in the epigastric area with radiation to the back. The onset of pain is rapid and typically reaches maximum intensity within 10 to 20 minutes. Pain that lasts only a few hours is unlikely to be pancreatitis. About 90% of patients will also complain of nausea and vomiting.
Mild pancreatitis may involve minimal abdominal tenderness without guarding. In severe disease, abdominal tenderness can be elicited with superficial palpation. Abdominal distention and reduced bowel sounds can occur secondary to ileus. Extravasation of hemorrhagic pancreatic exudate can lead to ecchymosis in one or both flanks (Turner sign) or the periumbilical regions (Cullen sign). Severe disease should be suspected with abnormal vital signs that can include fever, tachycardia, tachypnea, and hypotension. These signs represent a transition from localized retroperitoneal inflammation to one of systemic inflammation. Pleural effusions and mental status changes are also hallmarks of severe disease. The presence of jaundice may suggest an underlying alcoholism or choledocholithiasis.
Diagnostic Evaluation
Acute pancreatitis is diagnosed when two of the following three criteria are met: (1) characteristic abdominal pain, (2) serum amylase or lipase greater than three times the upper limit of normal, and, if needed, (3) radiologic imaging consistent with the diagnosis.4 Amylase and lipase are the most frequently used serum-based tests for pancreatitis. The most common source of amylase is not the pancreas, but salivary glands. In contrast, 90% of lipase is made from the pancreas, making it a more specific marker. Amylase rises within 6 to 24 hours of acute pancreatitis and peaks in 48 hours, normalizing in 3 to 7 days. Lipase has a longer half-life than amylase, with levels increasing within 4 to 8 hours, peaking at 24 hours, and falling over 8 to 14 days.5 The degree of elevation is not a marker of disease severity, and mild elevation of these serum markers—less than three times the upper limit of normal—is not specific for pancreatitis.
The use of computed tomography (CT) or magnetic resonance imaging (MRI) should only be considered when the first two diagnostic criteria are not met and (1) the pretest probability for pancreatitis remains high or (2) there is a high pretest probability for another abdominal process. Otherwise, CT and MRI have no role and may exacerbate renal injury from use of intravenous contrast.6 Such imaging can be considered 7 days later should the diagnosis remain uncertain or to assess disease severity and identify complications related to severe pancreatitis. Following clinical and laboratory parameters allows adequate initial assessment of disease severity. For patients with an established history of chronic pancreatitis or recent acute pancreatitis, imaging may be considered as part of the initial emergency department assessment for specific treatable complications of pancreatitis including, but not limited to, enlarging pseudocysts, arterial pseudoaneurysms, and/or new common bile stones.
Differential Diagnosis
The differential diagnosis includes biliary colic, acute cholecystitis, acute cholangitis, biliary dyskinesia, peptic ulcer disease, dyspepsia, acute mesenteric ischemic, and bowel obstruction. Nongastrointestinal disorders, including acute myocardial infarction, aortic dissection, pulmonary embolism, acute spinal disorders, and renal calculi, should also be considered.
Complications
The majority of cases (80% to 90%) of pancreatitis are mild and self-limiting; 10% of cases, however, develop severe disease, defined as the presence of significant fluid collections, infectious complications including abscess formation, infected necrosis, and/or extrapancreatic organ failure. These patients typically exhibit SIRS or sepsis physiology.
Fluid collections around the pancreas affect over half of patients. Most will resolve, but for those that persist, a fibrogenic anti-inflammatory response will lead to containment of these fluid collections, resulting in the formation of a pseudocyst. A pancreatic pseudocyst is a fluid collection that persists beyond 4 weeks. Other complications include infections (arising from pancreatic necrosis or within pseudocysts), thrombosis (splenic, superior mesenteric, and/or portal vein), arterial pseudoaneurysms, and gastrointestinal bleeding. The mortality rate for patients with severe pancreatitis is approximately 30%. Death within the first 2 weeks of illness is usually due to multiorgan failure. Death after 2 weeks typically stems from infection.
Management Guidelines
Once a diagnosis of acute pancreatitis is made, a risk stratification calculation should be performed. Clinical risk scoring systems, such as Ranson’s and APACHE II, have traditionally been used. However, both are cumbersome and require 48 hours before a meaningful interpretation can be made. The Bedside Index for Severity in Acute Pancreatitis (BISAP) score is a newer validated scoring system that requires five data points of collection in the emergency room.7,8 This includes a blood urea nitrogen (BUN) >25 mg/dL, impaired mental status, SIRS, age >60, and the presence of a pleural effusion (Table 26.2). The presence of three or more features at admission is associated with a 7- to 12-fold increase in organ failure. Such patients should be managed in the intensive care unit.
TABLE 26.2 Risk Stratification Scoring System for Severity of Acute Pancreatitis
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