Authors: Ralph J. Riviello, MD, FACEP, Assistant Professor, Department of Emergency Medicine, Thomas Jefferson University, Philadelphia, PA; William J. Brady, MD, FACEP, FAAEM, Associate Professor, Vice Chair, and Residency Program Director, Department of Emergency Medicine; Associate Professor of Internal Medicine, Department of Internal Medicine, University of Virginia Health System, Charlottesville, VA.
Peer Reviewers: Albert Weihl, MD, FACEP, Program Director, Emergency Medicine Residency, Assistant Professor of Medicine and Surgery, Section of Emergency Medicine, Department of Surgery, Yale University School of Medicine, New Haven, CT; Oliver W. Hayes, DO, FACEP, Associate Professor of Emergency Medicine, Division of Emergency Medicine, Michigan State University, East Lansing, MI.
One million new cases of gallstones, or biliary calculi, arise each year in the United States, resulting in 500,000 operations annually. It is estimated that 10-15% of Americans (i.e., 16-20 million people) have gallstones—at least 20% of females and 8% of males older than age 40 in the United States, according to autopsy series.1-5 Previously thought to be rare in the pediatric population, gallstones now are clinically recognized more frequently and usually are associated with chronic hemolytic disease and structural gastrointestinal or hepatobiliary disorders.6-8 In the majority of patients (50-80%) gallstones are asymptomatic; a minority of patients with gallstones develop symptoms or complications (e.g., acute cholecystitis) over time. Among patients with previously asymptomatic calculi, the incidence of new-onset biliary pain is reportedly 10% at five years, 15% at 10 years, and 18% at 15-20 years. The initial presenting complaint in 90% of these patients is biliary pain, rather than a biliary complication.4,5 Therefore, expectant management with close observation currently is the preferred approach to the asymptomatic patient. Patients with asymptomatic stones should be left alone and, with the exception of those patients at high risk for gallbladder carcinoma, prophylactic cholecystectomy currently is not recommended. With these considerations in mind, this issue discusses the evaluation and treatment for optimizing management of patients with acute biliary tract disorders.
(This article includes a discussion of a device for gallstone therapy that has not been approved for use by the U.S. Food and Drug Administration.)—The Editor
Introduction
An emergent condition arises when gallstones lead to obstruction of the gallbladder and bile ducts, resulting in pancreatitis, cholangitis, symptomatic cholelithiasis (biliary colic), and cholecystitis. Of these four conditions, the emergency physician most frequently encounters acute cholecystitis (which accounts for 20% of gallstone-related procedures) and symptomatic cholelithiasis. Although both syndromes can be quite disabling, acute cholecystitis also represents a threat to life, particularly in the case of elderly patients with significant comorbidity.1
Pathophysiology
Gallstones are crystalline structures formed from both normal and abnormal bile components. Bile is a pigmented, isotonic fluid composed of water (80%), bile acids (10%), lecithin and other phospholipids (4-5%), cholesterol (1%), conjugated bilirubin, electrolytes, mucus, various proteins, and medications. Bile is manufactured in and secreted from the hepatocyte before being transported via the canaliculi, ductiles, and bile ducts to the gallbladder for storage. Bile is required for the absorption of fats and fat-soluble nutrients from the small intestine. During the fasting state, approximately 50% of the bile produced flows directly into the duodenum, and the other half is stored in the gallbladder. While in the gallbladder, stored bile is concentrated and acidified. The bile ducts become increasingly larger, eventually coalescing to form the right and left hepatic ducts, which unite to form the common hepatic duct. The common hepatic duct and the cystic duct from the gallbladder unite to form the common bile duct, which then empties into the duodenum through the ampulla of Vater. Immediately before entering the duodenum, the pancreatic duct frequently merges with the common bile duct. Cholecystokinin, a gastrointestinal hormone secreted from small intestinal mucosal cells when fats and amino acids enter the duodenum, is the major stimulus for release of bile. Cholecystokinin induces dynamic contraction of the gallbladder, relaxation of the sphincter of Oddi, augmented hepatic bile production, and, finally, the release of bile into the duodenum for the sake of digestion. Enterohepatic circulation allows the conservation of approximately 95% of bile.
The principal cause of biliary tract disorders is related to the formation of gallstones. Seventy percent of gallstones are cholesterol stones, comprised of more than 70% cholesterol monohydrate. Such stones are found in the gallbladder, cystic duct, intrahepatic ducts, and common bile duct.3,9 Because the calcium content of cholesterol stones is much lower than that of pigment stones (see below), cholesterol stones are radiolucent. The complex series of steps resulting in the formation of such stones includes cholesterol supersaturation of the bile, the formation of monohydrate crystals with aggregation into successively larger structures, and delayed gallbladder emptying with bile stasis. Risk factors associated with the complex formation of cholesterol calculi include increased age, female sex, pregnancy, parity, obesity, profound weight loss, prolonged fasting, cystic fibrosis, intestinal malabsorption syndromes, total parenteral nutrition, hypertriglyceridemia, diseases of the terminal ileum (e.g., Crohn’s), high spinal cord injury, various medications (particularly oral contraceptive agents, octreotide, estrogens, progestogens, ceftriaxone, and clofibrate), and familial tendency. As exemplified by the Pima Indian tribe, ethnic background also must be considered. This tribe of the southwestern United States has the highest documented incidence of gallstones; up to 75% of females older than 25 have cholelithiasis. Fifty percent of individuals in Scandinavian populations develop stones by age 50.
Twenty percent of gallstones are classified as pigment stones, occurring in both black and brown varieties. Both types result from the abnormal solubility of unconjugated bilirubin in conjunction with the precipitation of calcium salts. Additional risks for the development of pigment stones are associated with Asian descent, chronic biliary tract infection, parasitic infection (e.g., Ascaris lumbricoides), chronic liver disease (particularly related to alcohol), and chronic intravascular hemolysis (e.g., sickle cell anemia, hereditary spherocytosis). Patients with advanced liver disease, pancreatitis, and hemolytic disorders commonly present with black stones, whereas brown stones commonly are noted in patients of Asian descent, typically resulting from parasitic or bacterial (i.e., enteric pathogens) infection. The anatomical distribution of brown pigment stones is similar to that of cholesterol gallstones, whereas black stones occur exclusively in the gallbladder.3,9 Ten percent of gallstones are of a mixed variety, which represent the least commonly encountered type.
Symptomatic cholelithiasis develops with the migration of a stone into either the cystic or common bile duct, where it ultimately becomes lodged. The consequent obstruction leads to increased intraluminal pressure and distention of the hollow viscus, resulting in pain, nausea, and vomiting. Such obstruction may be relieved by strong, repetitive contractions of the entire biliary system.
However, acute cholecystitis may develop if obstruction—particularly in either the cystic duct or the infundibulum of the gallbladder—persists. Acute cholecystitis results from an inflammatory process that may progress to gangrene of the gallbladder wall with or without perforation.3 This inflammatory response is initiated by a combination of chemical, infectious, and mechanical factors. The latter causea rise in intraluminal pressure and distention of the viscus, culminating in visceral ischemia. The release of various mediators (i.e., lysolecithin, phospholipase A, and prostaglandins) produces chemical inflammation and results in direct mucosal injury. The inflammatory response may be complicated by bacterial agents, including Enterobacteriaceae (70%, particularly Escherichia coli and Klebsiella species), enterococci (15%), bacteroides (10%), Clostridium species (10%), group D Streptococcus, and Staphylococcus species.10 (See Table 1.) Predictors of bactibilia include temperature greater than 37.3 °C, serum bilirubin level greater than 8.6 micromol/L, and white blood cell count greater than 14.1 ´ 109/L.11 The extent of the contribution by bacterial pathogens varies, occurring in 35-65% of patients with acute cholecystitis.11
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Clinical Presentation
The typical patient presenting to the emergency department (ED) with symptomatic biliary tract disease is an obese female between the ages of 20 and 40 years. Patients with gallstones present in one of several ways. Those with biliary colic, the most common presentation of cholelithiasis, complain of recurrent episodes of vomiting and abdominal pain. Patients with acute cholecystitis or cholangitis may present with right upper quadrant pain, volume depletion, and systemic toxicity. Gallstones also may cause acute pancreatitis, manifested by epigastric pain radiating to the back with associated emesis and anorexia. In asymptomatic patients undergoing medical evaluation, gallstones may be noted incidentally via ultrasonography or plain film radiography.
Biliary colic is distinguished by abdominal pain (epigastric or right upper quadrant) with radiation to the right posterior shoulder and associated with nausea and vomiting. Patients may cite a history of similar episodes, with increasing intensity and frequency of the exacerbations noted in the recent past. The pain is associated with the ingestion of food, a fatty meal, or a large meal after a period of fasting. This pain commences quite suddenly—approximately 30-60 minutes after ingestion—and ranges from mild to severe, lasting 1-6 hours. Contrary to the intermittent pain suggested by the name "colic," gallstone-related pain is most often constant. It may cease rapidly or gradually, and patients may note a mild abdominal aching or soreness after resolution of the attack for 1-2 days. A history of fever or chills suggests the presence of cholecystitis, cholangitis, or pancreatitis. The physical examination may demonstrate mild right upper quadrant tenderness without evidence of peritoneal irritation, as well as volume depletion due to protracted emesis.4
The pain associated with the onset of acute cholecystitis is usually similar to that produced by biliary colic; however, the pain often persists beyond the typical six hours. Patients may have either a history of similar attacks or documented gallstones. A history of fever and/or chills is common, as well as associated anorexia, nausea, and vomiting. The patient’s pain changes in character and location from visceral (dull and poorly localized mid upper abdominal) to parietal (sharp and localized right upper quadrant) as the inflammatory process progresses. The patient is found to be in moderate to severe distress with signs of systemic toxicity, including temperature elevation, tachycardia, and volume depletion. Evidence of localized peritoneal irritation, distention, and hypoactive bowel sounds accompanies occasional tenderness in the abdominal upper right quadrant. Jaundice, usually not present, may be noted in cases of chronic intravascular hemolysis or in patients with prolonged biliary obstruction with late onset of inflammation.4 Generalized peritonitis with rigidity is rare and, if found, suggests perforation. Murphy’s sign (i.e., increased tenderness to subcostal palpation on inspiration) may be noted. If gallstones are present, a sonographic Murphy’s sign (focal gallbladder tenderness elicited by the ultrasound transducer) has a positive predictive value greater than 95% for acute cholecystitis. (See Table 2.)
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The course of acalculous cholecystitis, which occurs in 5-10% of patients with acute cholecystitis, tends to be more rapid and malignant. Patients frequently are elderly and have a history of diabetes mellitus.12 Other risk factors include multiple trauma, extensive burn injury, prolonged labor, major surgery, systemic vasculitic states, gallbladder torsion, and parasitic or bacterial infections of the biliary tract. Frequently, acalculous cholecystitis occurs as a complication of one of these factors, and patients are gravely ill on initial presentation.4,13,14 In the absence of such conditions, patients with acalculous cholecystitis are indistinguishable from those with calculous cholecystitis.
Diagnosis
Complete blood count often reveals a leukocytosis with predominance of polymorphonuclear forms. However, the possibility of cholecystitis is not excluded by a normal white blood cell count. Additional serum and urine laboratory studies should be obtained; the findings revealed will be similar to those discussed for biliary colic. Ultrasonography will reveal gallstones in the vast majority of cases but may not confirm the diagnosis of acute cholecystitis. However, the presence of stones along with a thickened gallbladder wall, distention of the gallbladder itself, pericholecystic fluid, and a positive sonographic Murphy’s sign has a positive predictive value in excess of 90% for the diagnosis of acute cholecystitis. Conversely, the absence of stones and a normal gallbladder on ultrasound makes the diagnosis of cholecystitis unlikely.17-20,23
Gallstones may be demonstrated by both ultrasonography and oral cholecystography. Oral cholecystography remains a useful adjunctive study in patients suspected of biliary colic with a normal or equivocal sonogram16; however, ultrasonography has emerged as the procedure of choice for the ED diagnosis of gallstones and related biliary obstruction. Ultrasonography of the gallbladder is performed rapidly, without patient preparation, and is very accurate in the identification of calculi, with a sensitivity of 95% for detecting stones greater than 2 mm and greater than 95% when stones are seen with acoustic shadowing. The false-negative and false-positive rates for the ultrasonographic diagnosis of gallstones are 2-4% in most major medical centers. Additionally, ultrasound provides an evaluation of the surrounding tissues.17-20 Emergency physicians themselves are performing limited right upper quadrant ultrasound in many EDs. Recent studies have shown that this practice can provide accurate and rapid diagnosis of biliary tract disorders.21,22 Kendall reported a sensitivity of 96% and a specificity of 88% for sonograms performed by emergency physicians. Additionally, the sonographic Murphy’s sign was present in emergency physician examinations (sensitivity 75%) more often than in radiological examinations (sensitivity 45%). The decreased accuracy of emergency physicians in determining pericholecystic fluid, wall thickness, air in the gallbladder, and ductal dilatation did not result in any adverse outcomes. The reduction in length of ED stay from 223 minutes to 180 minutes was the major advantage of emergency physician ultrasound.21
Radionuclide cholescintigraphy using Tc-iminodiacetic acid analogues (e.g., hepato-iminodiacetic acid [HIDA] and DISIDA scans), with a sensitivity approaching 100% and a specificity of 90%, remains the study of choice for the diagnosis of acute cholecystitis.16-18 The intravenously administered radionuclide, absorbed by the hepatocyte and secreted into the biliary tract, clearly outlines the gallbladder and cystic duct in the normal patient within one hour. Failure to demonstrate the gallbladder within this time frame is consistent with obstruction of the cystic duct and the diagnosis of acute cholecystitis. Use of the HIDA scan is feasible in patients with serum bilirubin levels of less than 5-7 mg/dL; the DISIDA scan is more accurate with serum bilirubin levels above this range. The choice of imaging studies in the evaluation of patients with acute cholecystitis remains controversial; fortunately, both studies are highly accurate. A reasonable approach for the emergency physician is initial ultrasonography followed by scintigraphic studies, if necessary.23 (See Table 3.)
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In patients with biliary colic, further studies may be performed to exclude other causes of upper abdominal pain with nausea and to support the diagnosis. Because the majority of stones are cholesterol and, therefore, radiolucent, plain film radiographs of the abdomen will reveal gallstones in only 10-20% of cases. Pigment and mixed stones, on the other hand, will be radiopaque if they contain at least 4% calcium by weight. Abdominal films are more useful in excluding other causes of pain. Right lower lobe pneumonia and pleural effusions, which are not uncommonly found in patients with pancreatitis, should be ruled out by the close examination of a chest radiograph. A 12-lead electrocardiogram is mandatory to exclude infarction or myocardial ischemia.
In patients with symptomatic cholelithiasis, laboratory studies most often are normal and not particularly useful in the ED evaluation.15 In patients with pigment stones, the hemogram may reveal chronic anemia, with or without evidence of hemolysis. The white blood cell count is typically within normal limits, and the serum bilirubin and alkaline phosphatase levels may be normal or minimally elevated. The serum aminotransferases are most often normal; however, the serum bilirubin will be elevated in cases of hemolysis. Serum studies evaluating the pancreatic amylase and lipase are obtained to rule out an atypical presentation of pancreatitis or co-existing gallstone pancreatitis. Other causes of abdominal pain must be ruled out by examination of the urine and its sediment. Serum or urine pregnancy testing must be obtained to rule out obstetric causes of abdominal pain; a negative pregnancy test additionally enables the emergency physician to proceed safely with radiologic studies, if indicated.
The diagnostic approach is more difficult in patients with acalculous cholecystitis, necessitating a high degree of physician suspicion for this syndrome. Ultrasound and computed tomography (CT) scanning will reveal a large, tense, static gallbladder without evidence of gallstones. Poor filling of the gallbladder will be demonstrated by radionuclide examinations.4,13,14
Differential Diagnosis
According to a review published in the mid-1970s, approximately one-fifth of patients admitted with acute cholecystitis were misdiagnosed. Although the clinical impression is significant in the evaluation of such patients, the results of this study demonstrate the importance of radiologic support for the diagnosis in the form of ultrasonography, nuclear scans, or both. For patients with biliary colic and acute cholecystitis, the differential diagnosis includes gastritis, peptic ulcer (perforated or penetrating), appendicitis, pancreatitis, hepatitis, hepatic abscess, Fitz-Hugh-Curtis syndrome (gonococcal or chlamydial perihepatitis), pelvic inflammatory disease with or without tubo-ovarian abscess, myocardial ischemia or infarction, pyelonephritis, pleuritis, and right lower lobe pneumonia.
Complications
Serious complications associated with cholecystitis include gallbladder empyema and emphysematous (gangrenous) cholecystitis. Patients with cholelithiasis may develop biliary colic, cholecystitis, choledocholithiasis, gallstone pancreatitis, ascending cholangitis, fluid and electrolyte deficits owing to protracted vomiting and anorexia, and upper gastrointestinal hemorrhage from emesis-related Mallory-Weiss tears.
The presentation of patients with pancreatitis due to gallstones is very similar to that of patients with pancreatic inflammation caused by ethanol. Gallstones or alcohol account for the majority (approximately 70%) of cases of acute pancreatitis. Gallstones are involved in 30-70% of patients with acute pancreatitis, depending on the population studied. Obstruction of the ampulla of Vater with reflux of bile into the pancreas leads to gallstone pancreatitis; 15-20% of all patients with gallstones will develop pancreatitis as a result of biliary calculi. Gallstone patients also may manifest findings consistent with acute cholecystitis and acute pancreatitis. The management of such patients includes intravenous fluids, nasogastric decompression, analgesics, and parenteral antibiotics with subsequent surgery.
Urgent biliary decompression (surgical or endoscopic) is mandatory in patients who present in extremis or in those who demonstrate clinical deterioration. Recent studies support the recommendation of endoscopic retrograde cholangiopancreatography (ERCP) with sphincterotomy for patients with severe pancreatitis, continuing biliary colic, cholangitis, obstructive jaundice, stones or dilation of the common bile duct, and liver enzymes that do not decrease rapidly after admission. Elective cholecystectomy is recommended after the pancreatitis has resolved.9,24,25
Approximately 15% of patients with gallstones experience choledocholithiasis. Typically, stones in the common duct originate in the gallbladder, but they may arise in the bile duct as well. Stones that are sufficiently small frequently will pass into the duodenum without pain; however, more frequently, they remain in the common duct. Common duct stones also are defined as retained, if discovered within two years of cholecystectomy, or recurrent if detected more than two years after cholecystectomy. Retained stones most likely were present at the time of cholecystectomy. The presentation of patients with choledocholithiasis includes obstructive jaundice, biliary pain, ascending cholangitis, or pancreatitis. Pain at the time of an attack is comparable to that of biliary colic, and mild to moderate jaundice may be noted. Biliary cirrhosis may result from prolonged obstruction. Laboratory findings include elevated serum bilirubin and alkaline phosphatase levels; the passage of stones into the duodenum is indicated by a transient increase in serum transaminase or amylase.
Although ultrasound may show common duct dilation in 75% of cases and bile duct stones in 50%, the most exact and useful procedure for the diagnosis and treatment of bile duct stones is ERCP. Endoscopic ultrasound (sensitivity, 93-97%; specificity, 97-100%) and magnetic resonance cholangiopancreatography (MRCP) (sensitivity, 71-100%; specificity, 85%) both have a high negative predictive value and offer accurate, noninvasive methods of evaluating patients with suspected choledocholithiasis. Ultimately, endoscopic sphincterotomy and stone extraction followed by laparoscopic cholecystectomy is the preferred treatment for choledocholithiasis.9
Patients with cholangitis present with fever, jaundice, right upper quadrant pain, mental confusion, and distributive shock. Only 25% of patients present with the classic Charcot’s triad of fever, jaundice, and right upper quadrant pain. This life-threatening emergency is the result of complete biliary obstruction in the presence of bacteria. Gram-negative organisms (e.g., E. coli, Klebsiella, Pseudomonas), as well as enterococcal and various anaerobic species (in up to 15% of cases), usually are involved. Obstruction most often is due to choledocholithiasis but also may be caused by biliary tract strictures, surgical anastomotic strictures, various post-procedural complications, and extrinsic compression from malignancy. Intraluminal pressure increases as the obstruction progresses, resulting in bacterial reflux into the lymphatic vessels and hepatic veins with eventual entrance into the systemic circulation. The mortality rate associated with this life-threatening emergency nears 100% in untreated or improperly treated patients. The management of cholangitis patients requires initial volume resuscitation supported by vasopressors in cases unresponsive to crystalloid infusion alone, broad-spectrum parenteral antibiotics (e.g., ampicillin, gentamicin, and metronidazole or ciprofloxacin with or without metronidazole) (See Table 4), and prompt surgical or endoscopic decompression of the biliary tree.9
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Patients with empyema present in similar fashion to those with cholangitis; fever, right upper quadrant pain, altered mentation, and hypotension are involved. Empyema is a life-threatening complication of cholelithiasis that results from complete obstruction of the cystic duct with bacterial infection of the stagnant bile and abscess formation within the gallbladder wall. In the absence of prompt surgical care, outcome for empyema patients is poor. Gram-negative sepsis frequently develops, requiring immediate broad-spectrum antibiotic coverage, fluid resuscitation, and urgent surgical consultation for cholecystectomy.
Only approximately 1% of patients with cholecystitis develop emphysematous cholecystitis—gangrene of the gallbladder. Emphysematous cholecystitis is acalculous in fewer than one-third of patients. With complete cystic duct obstruction, the gallbladder wall becomes ischemic; bacterial infection and gangrene eventually develop. The typical patient is an elderly, diabetic man who presents in extremis with fever, septic shock, and right upper quadrant pain. Owing to gas-forming organisms, air frequently is present in the biliary tree, the gallbladder wall, or the gallbladder itself, as plain film radiographs may demonstrate. The bacteriology of either focal or diffuse gallbladder gangrene includes gram-negative, gram-positive, and anaerobic organisms; polymicrobial infection is not uncommon. The preferred imaging study is abdominal CT scan. Patients with either focal or diffuse gangrene of the gallbladder and patients with empyema are managed in similar fashion. Associated sepsis and the profile of the typical patient give rise to the very high mortality for gangrenous cholecystitis.
Gangrene of the gallbladder wall may occur with diffuse organ involvement or in a limited (i.e., focal) distribution. Patchy ischemia of the gallbladder wall resulting in focal gangrene may be associated with empyema, acute cholecystitis, significant organ distention due to stone-related cystic duct obstruction, torsion with arterial compromise, and certain vasculitic states. This complication of cholecystitis frequently develops in patients with diabetes mellitus.12 Gallbladder wall perforation may occur in a contained or free fashion (into the omentum or into the peritoneal cavity, respectively).
Recent studies have not reproduced the results of earlier studies that reported a much higher rate of conversion from asymptomatic to symptomatic gallstones. A higher conversion rate suggested that the majority of such patients became ill over relatively short periods and that 10-20% of patients presented with serious complications. Additionally, diabetic patients were considered a very high-risk group, mandating aggressive intervention, preferably in the asymptomatic stage. Early, prophylactic cholecystectomy typically was recommended in light of the potential for developing symptomatic cholelithiasis and the associated complications. The contemporary literature, however, does not support these findings. Current opinion states that the patient with a history of asymptomatic gallstones can be expected to develop clinical manifestations and related complications much less frequently than previously believed—10% at five years, 15% at 10 years, and 18% at 15-20 years. Therefore, even among most diabetic patients, a much less aggressive approach—careful, close observation—is followed today.
Treatment
The ED management of patients with biliary colic entails the relief of symptoms and the correction of fluid and electrolyte imbalances. Antispasmodic agents (e.g., glycopyrrolate), opiate analgesics (e.g., meperidine), and antiemetics (e.g., promethazine) are used for patients presenting with abdominal pain and emesis. It is important to note that meperidine produces significantly less spasm of the sphincter of Oddi than that induced by other narcotic agents (e.g., morphine). Gastric decompression with nasogastric suction is warranted in severe cases. Electrolyte imbalance must be corrected by the parenteral route, and volume deficits must be addressed with isotonic intravenous fluids. The patient meets criteria for discharge from the ED with resolution of symptoms, correction of intravascular volume deficits, and restored ability to maintain hydration orally. The gastroenterologist or the surgeon provides definitive care of cholelithiasis. The case should be discussed with the surgical consultant or the patient’s primary care physician before discharge to arrange for timely outpatient follow-up. Oral narcotic-acetaminophen pain medication may be given for the common residual abdominal ache sensation. If the symptomatic cholelithiasis seems to be associated with a particular stimulus such as a fatty meal, this trigger should be avoided. The diagnosis of biliary colic must be questioned if symptoms do not resolve within a four- to six-hour period; such prolonged pain may rather represent early, acute cholecystitis.
Hospital admission is required for patients with acute cholecystitis, biliary colic with intractable pain or inability to take oral medications, and proven or suspected cholangitis. Hospital admission should be considered for high-risk biliary colic patients with common bile duct stones and in pregnant patients with biliary colic.38
Treatment options for patients with symptomatic gallstones include open (traditional) or laparoscopic cholecystectomy, medical dissolution therapy, and gallstone lithotripsy. For patients with biliary colic, open cholecystectomy with intraoperative cholangiography provides a definitive cure; however, the laparoscopic technique rapidly has replaced the traditional open cholecystectomy as the procedure of choice. Laparoscopic surgery provides the advantage of a faster recovery time. The major complication of this technique is gallbladder perforation with an incidence of 10-30%. Risk factors for perforation include previous laparotomies, chronic cholecystitis with thickened walls (7 mm or greater), and gallbladder hydrops. The risk of perforation ranges from 3.5% with one of these risk factors to 25% with all three.27 Cholecystectomy is the best management for patients with frequent or severe attacks of biliary colic, a history of any associated complications of gallstones, large biliary calculi (greater than 2 cm in diameter), a congenitally abnormal hepatobiliary system, diabetes mellitus,28 or a desire for a rapid cure.
Approximately 10-15% of gallstone patients have small (less than 5 mm) floating cholesterol stones within a functioning gallbladder. These patients are candidates for medical dissolution therapy, which includes oral bile acid treatment as well as direct gallbladder irrigation with ether-type solvents. Oral bile acid therapy with chenodiol 750 mg daily for two years resulted in an overall dissolution rate of 10.9-13.5%. The recommended dose of ursodiol—which is more efficacious and has fewer side effects—is 600 mg daily in divided doses over one year. This therapy resulted in a 40-55% complete response rate. The recurrence rate after a successful treatment regimen is about 10%. Recurrence remains a problem with direct irrigation of the gallbladder with ether-type solvents; however, this technique provides a rapid (2-4 hours) means of calculus dissolution.9,29,30 Another option for gallstone patients is a combination of medical dissolution therapy and extracorporeal shock-wave lithotripsy (ESWL). This approach is appropriate for patients with a maximum of three cholesterol stones that are radiolucent and less than 0.2 cm in diameter. These criteria apply to 15% of gallstone patients. ESWL devices have not been approved for use by the U.S. Food and Drug Administration.9,31-33
Calculous and acalculous acute cholecystitis are treated surgically.34-37 As with biliary colic, basic, supportive medical therapy occurs in the ED prior to hospital admission, surgery, or both. Despite the questionable role of acute infection in all cases of early, acute cholecystitis, antibiotic treatment is recommended. Patients with acute cholecystitis require volume resuscitation with intravenous isotonic fluid, pain control with opiate analgesics (after the diagnosis has been confirmed), and bowel rest with antiemetic agents and nasogastric suction. A minority of patients—usually those with either acalculous or emphysematous cholecystitis or a complication of cholecystitis—will present in septic shock and require aggressive resuscitation. Broadened coverage of patients with obvious infection should include ampicillin, gentamicin, and clindamycin or the equivalent. (See Table 5.) Single-agent therapy with a third-generation cephalosporin is adequate in patients presenting without sepsis.
Summary
All patients with acute cholecystitis must be admitted to the hospital for continued intravenous fluid therapy and antibiotics. Approximately 25% of patients will experience either a progression of the inflammatory process or a complication of acute cholecystitis within two to seven days of hospitalization; however, the remainder of medically treated patients will have complete remission of symptoms within this time frame. Surgery typically is performed 24-72 hours after admission, once symptoms have resolved, using the traditional open and laparoscopic cholecystectomy options. The latter technique is preferred; conversion to open cholecystectomy is more likely when gangrenous changes, dense adhesions, and pericholecystic purulence are present. Immediate surgery is mandated for patients with a toxic presentation or clinical deterioration. Percutaneous drainage of the gallbladder can be performed in patients who are not acceptable operative candidates. Few complications are reported, and success rates of 73-100% are attainable. Cholecystectomy can be performed when the patient’s condition has stabilized.
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