Acute pancreatitis remains an important diagnosis in emergency medicine, accounting for more than 220,000 hospital admissions a year.^1-4 The frequency of hospitalizations has increased 100% in the last 2 decades and is predicted to continue to increase, likely related to the growing obesity epidemic.^3,5,6 Emergency physicians are often challenged with the diagnosis of acute pancreatitis, and this article seeks to offer evidence-based guidelines for the diagnosis and management of this disease.

Epidemiology

Acute pancreatitis can be separated into mild and severe pancreatitis.

Severe pancreatitis is defined by the presence of local complications (pseudocysts, necrosis, abscess) or organ failure (renal failure, pulmonary insufficiency, shock).^1,4,7,8 Mild pancreatitis occurs in about 80% of patients, is self-limited, and resolves without complication. The remaining 20% of patients develop severe pancreatitis.^2,8,9

The mortality for pancreatitis overall is 5%.^1,3 The mortality of severe pancreatitis is 14%-25%.^2,8,10 The presence of multiorgan failure increases this value to 47%.^1,3,10 About half of the deaths occur within 2 weeks as the result of multiorgan failure, and the remainder occur later from complications of infection.¹⁰

Pathophysiology

Acute pancreatitis is caused by inappropriate activation of trypsin. This leads to pancreatic autodigestion and the activation of a variety of other digestive enzymes. Local inflammatory mediators are released, leading to distant ­extra-pancreatic organ dysfunction, including shock, acute respiratory distress syndrome (ARDS), and renal failure.^1,2,8

The inciting factor that leads to inappropriate trypsin activation varies according to the etiology of acute pancreatitis. Gallstone pancreatitis develops when a gallstone lodges in either the pancreatic or common bile duct, leading to increased intraductal pressure, bile reflux, and trypsin activation.^8,9

Idiopathic pancreatitis is the third-leading cause of acute pancreatitis (after gallstone and alcohol disease) and is increasingly thought to be from biliary microlithiasis.^3,8,10

Other etiologies of acute pancreatitis include hypertriglyceridemia (serum levels greater than 1,000 mg/dL), drug-induced pancreatitis, trauma, postendoscopic retrograde cholangiopancreatography (ERCP), pancreas divisum, tumor, and infection.^8,10,11

Risk Factors

The two most common and important risk factors for acute pancreatitis are gallstones and alcohol consumption.¹⁰ In developed countries, the cause of acute pancreatitis is biliary in 38% of cases and alcohol abuse in 36%.^2,8,9 Gallstone pancreatitis is most likely to develop in patients older than 60 years and with small gallstones (less than 5 mm or microlithiasis).^4,10 Only 3.4% of patients with cholelithiasis develop pancreatitis.¹⁰

Alcohol is a dose-dependent risk factor after the threshold of 4-5 drinks daily is exceeded. Even among patients with the highest alcohol intake, the risk is only 2%-3%.^6,10 Smoking is another important risk factor for pancreatitis, and its effects are additive with alcohol.^3,6 Patients with HIV are 35-800 times more likely to develop acute pancreatitis when compared to a population without HIV.¹⁰

Signs and Symptoms

Patients typically present with the rapid onset of unremitting, severe epigastric pain that radiates to the back. Epigastric abdominal pain is present in 95% of these patients.¹² The classically taught Cullen (periumbilical ecchymosis) and Gray-Turner (flank ecchymosis) signs are present in only 3% of patients but have been associated with a mortality of 37%.⁸ Nausea or vomiting is present in 90% of patients.⁸

Diagnostic Tests

The American College of Gastroenterology guidelines state that two of these three findings should be present for the diagnosis of acute pancreatitis: 1) elevated serum lipase or amylase greater than or equal to three times the upper limit; 2) characteristic abdominal pain; 3) computed tomography (CT) evidence of acute pancreatitis.^1,11

The two main enzymes that aid in laboratory diagnosis of acute pancreatitis are amylase and lipase. Amylase rises within 6-24 hours and normalizes in 3-7 days.¹³ Lipase rises within 4-8 hours and stays elevated for 8-14 days.¹³ There are many advantages of lipase over amylase. Lipase remains elevated longer and is at least as sensitive and more specific than amylase.^14-16 Lipase levels of greater than five times the upper limit of normal have 100% specificity for the diagnosis of acute pancreatitis.¹³

Traditionally, amylase was recommended as the diagnostic test of choice because it was cheaper and more widely available than lipase.¹⁵ Given recent developments that have made lipase widely available and its superior test characteristics, lipase is now the laboratory measurement of choice for the diagnosis of acute pancreatitis, and there is little additional benefit from also obtaining a serum amylase level.^14,15

The degree of elevation of serum lipase or amylase at admission does not predict severity of disease.¹⁷

Urine trypsinogen-2 is a newer test that may be useful as point of care testing in settings where laboratory testing for serum pancreatic enzymes is not readily available.¹⁸

Additional laboratory tests that are useful for the diagnosis of acute pancreatitis are liver function tests and hematocrit. In patients with no history of alcohol consumption, the presence of alanine aminotransferase (ALT) elevation three times the upper limit of normal has a 95% positive predictive value for acute gallstone pancreatitis.^1,4,8,19 Normal liver function tests do not exclude the diagnosis of biliary pancreatitis, as this can occur in up to 20% of patients.8 Hemoconcentration (defined as hematocrit greater than 44%) and failure of hematocrit to decrease at 24 hours are important predictors of severe pancreatitis.⁷

Furthermore, the absence of hemoconcentration at admission or during the first 24 hours excludes the occurrence of pancreatic necrosis in most patients^1,2,20 and is strongly predictive of a benign clinical course.¹

Urinary trypsinogen activation peptide is a newer test that has been shown recently to be more accurate at predicting severe acute pancreatitis, compared with hematocrit.²¹ As it becomes more widely available, it may be an important adjunct to clinical findings in predicting severity of disease.

CT scan at admission is rarely indicated if the diagnosis of acute pancreatitis has been made on the basis of elevated pancreatic enzymes and characteristic abdominal pain. It is reasonable to obtain a CT scan to rule out other intra-abdominal etiologies1 and to assess for complications of acute pancreatitis (such as necrosis, pseudocyst, abscess) when the time course is appropriate.

Remember that pseudocysts take about 4 weeks and pancreatic abscesses about 5 weeks to form after initial onset of symptoms.¹

Pancreatic necrosis is best evaluated by obtaining a contrast-enhanced CT scan 2-4 days after admission, as CT done on admission may underestimate severity.^1,7,8

Once the diagnosis of acute pancreatitis is made, the etiology should be determined. The recurrence rate of alcoholic pancreatitis is about 50%; in biliary pancreatitis, it is up to 61%.^1,7,10 Prior to hospital discharge, it is imperative that these two leading causes of pancreatitis are fully evaluated.

Social history should be reviewed thoroughly, specifically to quantify alcohol use. If there is no history to support alcohol as the etiology, the patient should undergo a gallbladder ultrasound during his or her hospitalization. Furthermore, if biliary pancreatitis is diagnosed, there should be a definitive treatment plan (i.e., cholecystectomy or ERCP with sphincterotomy) in effect at the time of discharge to prevent recurrent episodes.^1,3,4,7

Numerous severity scoring systems exist for acute pancreatitis.^3,7,8 The early recognition of severe acute pancreatitis is important, given the significantly increased mortality and morbidity.^2,8,10

The traditionally used severity scoring systems, Ranson and APACHE II, have limited value in the emergency department setting. The Ranson score cannot be calculated until 48 hours after admission.⁷ The APACHE II scoring system is complex and time consuming to calculate.⁷

Singh and colleagues recently developed a new severity scoring system, the bedside index for severity in acute pancreatitis (BiSAP), which may be more practical for use in the emergency department.²² It is a five-point scoring system that assigns one point each for the following criteria: older than 60 years, pleural effusion, systemic inflammatory response syndrome (SIRS), altered mental status, and blood urea nitrogen greater than 25 mg/dL.²² The presence of three or more points correlates with morbidity and mortality, with similar accuracy to APACHE II.^3,7

The Harmless Acute Pancreatitis Score (HAPS) allows the emergency physician to quickly and accurately identify patients who are low risk for the development of severe acute pancreatitis. The absence of rebound tenderness and/or guarding, a normal hematocrit, and a normal serum creatinine predict with 98% accuracy patients who will have a mild course.³ This could have important implications when an emergency physician is considering allocating limited resources, such as intensive care unit beds.

Treatment

The mainstay of treatment for acute pancreatitis is supportive care. This includes aggressive fluid management, adequate opiate analgesia, early nutrition, and oxygen administration.⁸ Fluid resuscitation is an especially important aspect of treatment.^1,3,19,23 Hypovole­mia plays a central role in pancreatic necrosis by compromising pancreatic microcirculation.⁷ Fluids should be bolused initially to achieve hemodynamic stability, followed by rates of 250-500 cc/hr to replete fluid losses.^4,7 Crystalloid is generally preferred. Colloid may be considered in specific situations when hematocrit is less than 25% or albumin is less than 2 g/dL.^23,24

The choice of parenteral analgesic should be based on provider comfort and patient relief. Traditional teaching has been to avoid morphine as it causes spasm of the sphincter of Oddi and to favor meperidine, which has no such effect.^8,25 Meperidine, however, has fallen out of favor because of its adverse effect profile. No outcomes-based evidence has emerged that morphine is contraindicated in acute pancreatitis.^8,25

Acute pancreatitis is a hypercatabolic state and therefore adequate nutrition is critical.3 Oral feeding can be considered in patients as early as 24 hours.³ It is now recognized that enteral nutrition offers advantages over parenteral nutrition.^1,4,7 These include preservation of the gut barrier, prevention of bacterial translocation, decreased cost, and avoidance of catheter-related complications.^1-4,7

Antibiotic prophylaxis is another area of acute pancreatitis that is under scrutiny. Most experts agree that in mild pancreatitis, there is no indication for antibiotics.^4,7 Severe acute pancreatitis offers more of a challenge. In the emergency department, it is often impossible to distinguish SIRS secondary to acute pancreatitis from that caused by bacterial sepsis.

In patients with acute abdominal pain, fever, and systemic toxicity, it is reasonable to initiate broad-spectrum antibiotics pending a complete infectious work-up, which may include eventual fine-needle aspiration of areas of pancreatic necrosis to distinguish sterile from infected necrosis.^1,3 Once infectious etiologies including pancreatic abscess and pseudocyst are ruled out, antibiotics should be discontinued.¹ Recommended antibiotics include carbapenems,² which have high pancreatic tissue penetration, or the combination of ciprofloxacin and metronidazole.^1,7

Emergency physicians should be familiar with the optimal timing of ERCP in the evaluation of acute pancreatitis. In patients with presumed biliary pancreatitis, the presence of choledocholithiasis or cholangitis mandates an urgent ERCP (within 24 hours of admission).^1,7 Unrelieved obstruction can lead to worsening pancreatitis.^2,4

Conclusion

Acute pancreatitis remains a disease with significant morbidity and mortal­ity. The emergency physician’s role in prompt recognition, assessment of severity, and initiation of supportive care is central to the treatment of this disease.

References

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