Acute Pancreatitis
Mrudula Kumar
Daniel K. Mullady
BACKGROUND
Acute pancreatitis is inflammation of the pancreas associated with varying degrees of autodigestion, edema, necrosis, and hemorrhage of pancreatic tissue. The principal symptom is abdominal pain, mainly in the epigastric region. Nausea and vomiting are common. In a patient with characteristic abdominal pain, the diagnosis is confirmed by elevated serum amylase and lipase levels (greater than three times normal) and/or evidence of pancreatic inflammation on cross-sectional imaging. There are many causes of acute pancreatitis, but gallstones and alcohol account for nearly 70% of cases (Table 50.1). The clinical course varies from mild, self-limited episodes to severe pancreatitis with associated multiorgan dysfunction, local complications such as infected peripancreatic fluid collections, or extrapancreatic complications such as venous thrombosis. Up to 20% of patients presenting with pancreatitis have a severe course. The overall mortality rate from the presence of severe pancreatitis with infectious complications is approximately 10% to 20% and can increase to more than 50% in the presence of persistent organ failure. Predicting severity is of highest importance, and all patients should be treated as severe until proven otherwise with aggressive intravenous fluid (IVF) resuscitation and pain control.
EVALUATION
The evaluation of a patient with suspected pancreatitis should begin with a careful history with attention to symptom onset, prior pancreatitis, alcohol use, gallstone disease, and review of medications. On physical examination, patients typically have epigastric tenderness but can have a diffusely tender abdomen. Bowel sounds may be absent indicative of ileus. Patients may also have systemic inflammatory response syndrome (SIRS) with fever, tachycardia, and tachypnea. Findings suggesting severe disease include diminished breath sounds, hypoxia, and altered mental status. Cullen’s sign (periumbilical ecchymosis) and Grey Turner’s sign (flank ecchymosis) are rare findings and indicate hemorrhagic pancreatitis.
Per the Atlanta Symposium, the diagnosis of acute pancreatitis requires two of the following: (1) abdominal pain, (2) amylase and/or lipase elevation greater than three times the upper limit of normal, and (3) pancreatic inflammation on cross-sectional imaging. Serum lipase levels are more sensitive in the diagnosis of acute pancreatitis and remain elevated for longer than serum amylase. Other initial laboratory values should include liver function tests, complete blood cell count, serum urea nitrogen
(BUN), and creatinine. Elevations in liver enzymes (particularly transaminases) with or without associated hyperbilirubinemia suggest the presence of bile duct stones or compression of the common bile duct by pancreatic edema.
(BUN), and creatinine. Elevations in liver enzymes (particularly transaminases) with or without associated hyperbilirubinemia suggest the presence of bile duct stones or compression of the common bile duct by pancreatic edema.
TABLE 50.1 Causes of Acute Pancreatitis | |||||||||||||||||||||||||||
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An abdominal ultrasonography should be performed, especially in suspected gallstone pancreatitis, to assess for cholelithiasis or choledocholithiasis. Cross-sectional imaging is not mandatory as part of the initial evaluation but can be performed if there is concern for complications. Contrast-enhanced computed tomography (CECT) is the best modality for evaluating pancreatic inflammation, necrosis, and peripancreatic fluid collections. The most common findings on imaging in uncomplicated pancreatitis are enlargement of all or part of the pancreas with blurring of the margins and inflammatory changes. CECT done at the initial presentation may underestimate disease severity, as it can take up to 72 hours for necrosis to develop. Therefore, CECT should be delayed unless there is a concern for other complications or if the diagnosis is in doubt.
For recurrent acute pancreatitis (two or more episodes), a detailed work-up, including IgG4, triglyceride, and calcium levels, is warranted. A thorough review of patient’s medication profile should be examined, as iatrogenic causes account for 2% of pancreatitis. An endoscopic ultrasonography can be performed to evaluate for pancreatic cancer in patients who do not have an identified etiology. Empiric cholecystectomy should be considered in patients with no identifiable cause for recurrent acute pancreatitis, even if liver function tests and gallbladder imaging are normal.
PREDICTION OF SEVERITY
Early prediction of severity in acute pancreatitis is vitally important in identifying patients at increased risk for morbidity and mortality. This can be challenging as there is no single, reliable way to predict severity. Current severity indices are based on clinical and radiographic parameters. An important clinical factor is persistent organ failure at >48 hours. Persistent pain, respiratory failure, and renal failure generally indicate severe disease.
Various grading and scoring systems have been developed to risk-stratify acute pancreatitis patients. Historically, the Ranson criteria and Glasgow scoring systems
have been used, but these are cumbersome and can take 48 hours to complete. More recently, the Acute Physiology and Chronic Health Examination II (APACHE II) has been used to predict severity in acute pancreatitis, but it is not pancreas specific. Patients with an APACHE II score >8 usually have severe disease. A new prognostic scoring system, the bedside index for severity in acute pancreatitis (BISAP), has been proposed as a simple method for early identification of patients at risk for in-hospital mortality and is as accurate as other scoring systems (Table 50.2). One point is assigned for each of the following signs within 24 hours of presentation: BUN level >25 mg/dL, impaired mental status, SIRS, age >60, and pleural effusion on imaging studies. A BISAP score ≥3 is associated with an increased risk of complications. Other single factors on admission that are associated with a severe course include hemoconcentration (hematocrit >44%), obesity, C-reactive protein (CRP) >150 mg/dL, albumin <2.5 mg/dL, calcium <8.5 mg/dL, and early hyperglycemia (Table 50.3).
have been used, but these are cumbersome and can take 48 hours to complete. More recently, the Acute Physiology and Chronic Health Examination II (APACHE II) has been used to predict severity in acute pancreatitis, but it is not pancreas specific. Patients with an APACHE II score >8 usually have severe disease. A new prognostic scoring system, the bedside index for severity in acute pancreatitis (BISAP), has been proposed as a simple method for early identification of patients at risk for in-hospital mortality and is as accurate as other scoring systems (Table 50.2). One point is assigned for each of the following signs within 24 hours of presentation: BUN level >25 mg/dL, impaired mental status, SIRS, age >60, and pleural effusion on imaging studies. A BISAP score ≥3 is associated with an increased risk of complications. Other single factors on admission that are associated with a severe course include hemoconcentration (hematocrit >44%), obesity, C-reactive protein (CRP) >150 mg/dL, albumin <2.5 mg/dL, calcium <8.5 mg/dL, and early hyperglycemia (Table 50.3).
TABLE 50.2 BISAP Score for Predicting Severity and Complications in Acute Pancreatitis
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