Acute Pancreatitis

1 What is acute pancreatitis (AP)?

AP is an inflammatory condition of the pancreas that has a broad spectrum of severity ranging from mild and self-limited to severe and associated with multiorgan failure. Clinically it is associated with the acute onset of abdominal pain and elevation of serum biochemical markers. The underlying pathophysiology is early and inappropriate activation of digestive enzymes within acinar cells.

2 What are the different degrees of AP, and how are they defined?

Mild AP is defined as pancreatic inflammation (of any cause) without persistent organ failure or local complications. Severe acute pancreatitis (SAP) is associated with systemic complications, including multiple-organ failure, and local complications, such as necrosis, abscess, and/or pseudocyst. This degree of pancreatitis requires aggressive therapy in an intensive care setting to prevent significant morbidity or mortality.

3 What are the causes of AP?

Gallstone-related disease and excessive alcohol intake are the two most common causes of AP in the developed world, comprising 70% of all cases. Beyond these, a number of independent factors are thought to cause pancreatitis, including hypertriglyceridemia (serum triglyceride level above 1500 mg/dL), trauma, and hypercalcemia. Evidence is growing that smoking is a risk factor for AP in a time- and dose-dependent manner. A large number of medications have been implicated in causing AP, including angiotensin-converting enzyme inhibitors, furosemide, tetracycline, aminosalicylic acid, corticosteroids, procainamide, thiazides, metronidazole, and ranitidine. Because of the varied duration between exposure and development of symptoms, and the usual lack of a clear mechanism, it is often difficult to identify a drug as the sole cause of AP. True idiopathic cases of AP are diminishing as more genetic causes of the disease are discovered. Endoscopic retrograde cholangiopancreatography (ERCP) causes pancreatitis in approximately 5% of individuals who undergo this procedure.

4 What are the presenting signs and symptoms of AP?

AP is characterized by the sudden onset of abdominal pain, classically located in the epigastrium and usually associated with nausea and/or vomiting. Radiation of pain from the epigastrium through to the back that is alleviated with the patient leaning forward is a typical but not a necessary feature. Tachycardia related to pain or volume depletion and low-grade fever may be present. Two additional findings associated with severe pancreatitis may be present, the Grey Turner and Cullen signs. The Grey Turner sign is an ecchymosis of the flank due to retroperitoneal hemorrhage. When present, it usually occurs 3 to 7 days after the onset of pain and is indicative of severe pancreatitis. The Cullen sign is periumbilical ecchymosis associated with both severe necrotizing pancreatitis and retroperitoneal hemorrhage of various causes.

5 Are amylase and/or lipase measurements helpful in the diagnosis?

The most commonly used diagnostic markers are serum amylase and lipase. Although serum amylase levels have a high sensitivity in the first 24 hours the specificity is very low. In addition to pancreatitis, elevated amylase levels are seen with many other conditions including bowel infarction, renal failure, perforated peptic ulcer, trauma to the salivary glands, and macroamylasemia. In contrast, serum lipase levels are both more specific and more sensitive than amylase measurements. Of note, no correlation exists between the absolute levels of amylase and lipase and the severity of pancreatitis.

6 What is the role of imaging in the diagnosis of AP?

Abdominal plain radiographs may be nonspecific or reveal an ileus if the pancreatitis is severe. Ultrasound evaluation of the pancreas itself is often limited by overlying bowel gas and/or patient discomfort. This test may, however, detect signs of biliary abnormalities in cases where this cause is suspected.

Computed tomography (CT) with oral and intravenous (IV) contrast can offer information regarding severity of disease (see question 9) and development of complications. Features that may be identified on CT include evidence of inflammation (pancreatic parenchymal edema or peripancreatic fat stranding), peripancreatic or intrapancreatic fluid collections, pancreas perfusion, and presence and extent of pancreatic necrosis.

7 Should all patients have imaging studies done at the time of presentation?

The timing of performing CT in the evaluation of AP has been frequently debated and studied. Obtaining CT early in the course of illness has not been shown to establish alternative diagnoses or change clinical management. The need for cross-sectional imaging should be evaluated on a case-by-case basis and reserved for those who do not improve clinically after several days of supportive therapy and/or in whom worrisome symptoms such as fever or leukocytosis develop. Advanced imaging should be considered early in a patient’s course of illness if the diagnosis itself is uncertain or if suspicion exists of a complication from AP that, if identified, would significantly alter management, or if alternative diagnoses requiring surgical management are considered.

8 What if the patient cannot receive contrast for imaging?

Magnetic resonance imaging (MRI) has a growing role in the diagnosis and management of AP and is a reasonable option in patients who cannot receive iodinated contrast for CT. Enhanced MRI requires the administration of gadolinium, which has been implicated in severe toxic side effects (nephrogenic systemic fibrosis) in patients with compromised renal function. Good correlation has been noted, however, when comparing magnetic resonance cholangiopancreatography (MRCP), with or without gadolinium contrast, with CT in the evaluation AP. MRCP also has the added benefit of being able to better define the pancreatic and biliary ductal system in cases where this cause is suspected but the pretest probability is too low to proceed directly to ERCP.

9 How do you determine the severity and prognosis of AP?

Recognizing and differentiating mild AP from SAP is important so that patients can be triaged to the appropriate setting and treatment plan. Over decades, several clinical predictors have emerged. Although all are imperfect, they are considered superior to clinical judgment alone.

Ranson criteria (Table 47-1) were one of the earliest and widely used scoring systems. Their major disadvantage was that they required 48 hours to complete. The Acute Physiology and Chronic Health Evaluation (APACHE) II system, developed to evaluate critically ill patients, has also been used to differentiate mild AP from SAP. The major disadvantage of this system is that many find it cumbersome as it requires 12 physiologic measures to calculate. A CT severity index (Balthazar score, Table 47-2), has been developed and often used to predict severity of pancreatitis on the basis of radiographic features. The bedside index of severity in AP (BISAP) score (Table 47-3) integrates the systemic inflammatory response syndrome (SIRS) criteria and can be calculated relatively quickly on admission.

^{Table 47-1} Ranson Prognostic Signs