Casey M. Glass
Cholelithiasis or alcohol abuse account for 90% of all cases of acute pancreatitis in the United States.
Many other causes account for the remaining cases of acute pancreatitis (Table 44-1).
The cause of up to 20% of acute pancreatitis cases remains unclear after evaluation.
Biliary colic is pain related to intermittent gallbladder obstruction from stones, typically lasting less than 5 hours. Gallstones are usually clinically silent with only 1% to 4% of affected persons developing symptoms in any year or 10% and 20% in 5 and 20 years, respectively.
Cholecystitis is inflammation of the gallbladder, most often due to obstruction from gallstones. Up to 10% of cases of acute cholecystitis are complicated by perforation.
Acalculous cholecystitis occurs in the absence of gallstones. Advanced age, critical illness, long-term total parenteral nutrition (TPN), diabetes, immunosuppres-sion, and childbirth are risk factors.
Cholangitis is bacterial infection of the biliary tree as a result of biliary obstruction. It is a serious illness with a high mortality rate if untreated.
Choledocholithiasis is the presence of stones in the common bile duct.
TABLE 44-1 Causes of Acute Pancreatitis
Gallstones (including microlithiasis)
Alcohol (acute and chronic alcohol consumption)
Endoscopic retrograde cholangiopancreatography
Autoimmune disease (eg, systemic lupus erythematosus, Sjögren syndrome)
Genetic factors (PRSS1, SPINK1, CFTR)
Postoperative complications (abdominal or cardiac surgery)
Bacterial infections (Legionella, Leptospira, Mycoplasma, Salmonella)
Viral infections (mumps virus, coxsackievirus, cytomegalovirus, echovirus, hepatitis B virus)
Parasitic infections (Ascaris, Cryptosporidium, Toxoplasma)
Posterior penetrating ulcer
Pancreatic or ampullary tumor
Pancreas divisum with ductular narrowing on pancreatogram
Oddi sphincter dysfunction
Abbreviations: CFTR = cystic fibrosis transmembrane conductance regulator; PRSS1 = protease, serine, 1 (trypsin 1); SPINK1 = serine peptidase inhibitor, Kazal type, 1.
The central cause of acute pancreatitis is believed to be unregulated intracellular activation of trypsin. Trypsin activates digestive enzymes leading to pancreatic inflamation and necrosis.
In severe cases of acute pancreatitis, local activation of inflammatory mediators can cause systemic symptoms, systemic inflamatory response syndrome, organ failure, and death (Table 44-2).
The causes of the gallstone formation are unclear. Large fasting and residual gallbladder volumes are associated with increased risk for stone formation. Cholesterol stones (70%) form from increased concentration of cholesterol in the bile. Mixed pigment stones (20%) form from bilirubin-calcium salts and are assoicated with biliary sludge, enteric infection, cholangitis, and parasites. Pure pigment stones (10%) form from bilirubin polymers and are associated with hemolysis, advnaced age, alcoholism, pancreatitis, cirrhosis, and TPN.
Gallstone passage from the gallbladder to the cystic duct and common bile duct causes pain and nausea seocndary to increased luminal pressure in the obstructed gallbladder or duct.
Persistent biliary obstruction leads to visceral ischemia, transmural inflammation, and peritoneal irritation.
Polymicrobial infection as a component of acute cholecystitis is common. Pathogens include gram-negative bacteria (Escherichia coli, 36%; and Klebsiella, 15%) and gram-positive bacteria (Enterococcus, 6%; Staphylococcus, 3%; and Streptococcus, 2%).
TABLE 44-2 Complications of Acute Pancreatitis
Patients suffering from acute pancreatitis typically present with nausea, vomiting, and epigastric pain. Pain may localize to the right or left upper quadrant or radiate to the back.
Pain from acute pancreatitis usually begins abruptly and lasts for days.
In the setting of acute pancreatitis, vital sign abnormalities are variably present and correlate with severity of disease.
In patients with acute pancreatitis, physical examination typically demonstrates epigastric tenderness. Bowel sounds may be diminished. Cullen or Turner signs are present only in the most severe cases.
Jaundice is not typically present in acute pancreatitis and, when noted, is associated with gallstone pancreatitis.
Patients suffering from biliary colic complain of RUQ pain associated with nausea and vomiting. The pain may radiate to the right back or shoulder or occasionally the left back. The pain does not persist for more than 5 to 6 hours.
Patients with acute cholecystitis complain of similar pain as those with biliary colic but with more persistent symptoms. They may exhibit Murphy’s sign (respiratory arrest with palpation of the RUQ).
Patients with chronic cholecystitis have milder symptoms that may occur frequently.
Patients with choledocholithiasis often note pain radiating to the middle of the back and have epigastric tenderness to palpation.
Ascending cholangitis is associated with RUQ pain, fever, and jaundice (Charcot triad), although all three are present in less than half of cases.
DIAGNOSIS AND DIFFERENTIAL
Differential diagnosis of acute pancreatitis, acute cholecystitis, cholangitis, and choledocholithasis includes lower lobe pneumonia, rupture of a pseudocyst, peritonitis, peptic ulcer disease, referred cardiac pain, small bowel obstruction, renal colic, dissecting aortic aneu-rysm, diabetic ketoacidosis, and gastroenteritis.
The diagnosis of acute pancreatitis is based on history and examination findings consistent with the diagnosis.
Objective criteria for acute pancreatitis require two of the following three components: (1) characteristic abdominal pain, (2) serum amylase/lipase levels greater than three times the upper limit of normal, or (3) computed tomography (CT) or ultrasonography (US) findings consistent with pancreatitis.
Lipase is the laboratory test of choice for diagnosis of acute pancreatitis. At cutoff levels of 600 IU/L, the specificity is above 95% and sensitivity is 55% to 100%. A normal lipase does not exclude the diagnosis of pancreatitis, especially in patients with chronic pancreatitis.
Amylase is less accurate than lipase in the diagnosis of acute pancreatitis. Amylase is found in many tissues throughout the body including the pancreas and salivary glands. Amylase greater than 3 times the upper limit of normal has a specificity of 95% and a sensitivity of 61% for acute pancreatitis.
Abnormal liver function tests suggest a biliary cause of acute pancreatitis.
CBC, serum chemistries, and serum lactate dehy-drogenase (LDH) can be helpful in determining the severity of acute pancreatitis. Prospective scoring systems to predict severe pancreatitis include the acute pancreatitis APACHE II score or Ranson’s criteria (Table 44-3).
No single laboratory or radiographic test is effective at ruling in or ruling out cholecystitis.
The most sensitive finding for acute cholecystitis is a positive Murphy’s sign.
Leukocytosis is neither sensitive nor specific for cholecystitis.
Abnormal liver function tests are suggestive of common bile duct stone, cholangitis, or Mirizzi’s syndrome (compression of the common hepatic duct by a common bile duct stone).
Plain radiographs of the abdomen are usually not helpful in the evaluation of pancreatitis or biliary pathology.
US is helpful in the identification of gallstones or dilatation of the biliary tree. It is the test of choice for diagnosis of biliary pathology. It has a sensitivity up to 94% and specificity of 78% for the diagnosis of acute cholecystitis. Common US findings in acute cholecystitis are a sonographic Murphy’s sign (pain over the gallbladder), gallstones, wall thickening (>3–5 mm), and pericholecystic fluid (Fig. 44-1). US is also helpful for identifying common duct pathology. The normal diameter of the common bile duct is approximately 7 mm.
FIG. 44-1. Abdominal US image showing acute cholecystitis with pericholecystic fluid (white arrow), gallbladder wall thickening (white pluses), and enlarged short-axis dimension (white dots). (Courtesy of Mustafa Secil, MD.)
CT is the study of choice for visualizing the pancreas, the confirmation of pancreatic inflammation, and the identification of phlegmons, abscesses, or pseudo-cysts. It cannot be used to rule out acute pancreatitis as it may be normal in mild pancreatitis (Fig. 44-2). CT scanning scores can be used to estimate the severity of acute pancreatitis. CT has a sensitivity of up to 95% and specificity of 96% for detection of acute cholecystitis (Fig. 44-3).
FIG. 44-2. Abdominal CT scan showing mild pancreatitis with the borders of the gland becoming indistinct, with hazy soft tissue stranding consistent with inflammation surrounding the pancreas (arrows).
FIG. 44-3. Enhanced abdominal CT image showing acute cholecystitis with enlarged gallbladder with fluid (white arrow), gallbladder wall thickening (white pluses), and enlarged short-axis dimension (white dots). (Courtesy of Mustafa Secil, MD.)
Hepatobiliary iminodiacetic acid (HIDA) scan is an adjunctive test when initial studies for gallbladder disease are indeterminate.
Endoscopic retrograde cholangiopancreatography (ERCP) is rarely used in the ED, but can be useful when the etiology of acute pancreatitis remains unclear after initial evaluation. ERCP can be therapeutic for common duct stones or gallstone pancreatitis.
The utility of magnetic resonance imaging (MRI) in acute pancreatitis is unclear. MRI can be an alternative diagnostic imaging method for acute cholecystitis with high sensitivities for identifying wall thickening, pericholecystic fluid, and adjacent fat stranding.
TABLE 44-3 Ranson’s Criteria*
EMERGENCY DEPARTMENT CARE AND DISPOSITION
The mainstays of acute pancreatitis treatment are pain and nausea control, hydration, and bowel rest.
All patients with acute pancreatitis should have regular reassessment of vital signs and oxygen saturation.
Adminster IV hydration to maintain urine output greater than 0.5 cc/kg/h.
Patients with acute pancreatitis and mild symptoms who are tolerating clear fluids may be discharged home, provided they have minimal laboratory abnormalities and normal vital signs.
Acute pancreatitis associated with organ dysfunction, respiratory distress, and hypotension should be treated aggressively.
Gallstone pancreatitis is an indication for urgent ERCP.
Antibiotics are not indicated for acute pancreatitis unless a specific source of infection is suspected. If associated infection is noted (infected phlegmon, pseudocyst, sepsis), treatment with imipenem-cilastin500 milligrams IV or meropenem 1 gram IV is appropriate. Alternative treatment may include ciprofloxacin 400 milligrams IV with metronidazole 500 milligrams IV.
Patients with acute pancreatitis and significant systemic complications, shock, or extensive pancreatic necrosis will necessitate an intensive care setting.
Incidental identification of gallstones requires no treatment. Patients should be warned about symptoms of biliary colic and cholecystitis.
Patients with biliary colic require outpatient referral to a general surgeon.
Patients with acute cholecystitis require surgical consultation and admission for choelcstectomy or percutaneous drainage.
Antibiotics should be given as soon as acute cholecystitis is confirmed. Initial treatment regimens include ceftriaxone or cefotaxime 1 gram IV in conjunction with metronidazole 500 milligrams IV, or a quinolone plus metronidazole IV for patients who are beta-lactam allergic. Patients with severe disease require extended coverage with medications such as piperacillin/tazobactam 3.75 grams IV.
Patients with ascending cholangitis require fluid resuscitation, broad-spectrum antibiotics, and emergent consultation for surigcal or endoscopic decompression of the biliary tract.
Patients with choledocholithiasis or gallstone panre-actitis require urgent ERCP for stone removal.
For further reading in Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7th ed., see Chapter 82, “Pancreatitis and Cholecystitis,” by Ridvan Atilla and Cem Oktay.