Peter A D Steel, MA, MBBS,
Staff Physician, Department of Emergency
Medicine, Joan and Sanford I Weill Medical College of Cornell
and Columbia University College of Physicians and Surgeons,
New York Presbyterian Hospitals
Nothing to disclose.
Coauthor(s)
Rahul Sharma, MD, MBA, FACEP,
Assistant Professor, Weill Medical College of
Cornell University; Assistant Director for Operations,
Department of Emergency Medicine, New York Presbyterian
Hospital-Weill Cornell Medical Center
Nothing to disclose.
Specialty Editor(s)
Eugene Hardin, MD, FAAEM, FACEP,
Former Chair and Associate Professor,
Department of Emergency Medicine, Charles Drew University of
Medicine and Science; Former Chair, Department of Emergency
Medicine, Martin Luther King Jr/Drew Medical
Center
Nothing to disclose.
Francisco Talavera, PharmD, PhD,
Senior Pharmacy Editor,
eMedicine
eMedicine Salary Employment
John D Halamka, MD, MS,
Associate Professor of Medicine, Harvard
Medical School, Beth Israel Deaconess Medical Center; Chief
Information Officer, CareGroup Healthcare System and Harvard
Medical School; Attending Physician, Division of Emergency
Medicine, Beth Israel Deaconess Medical
Center
Nothing to disclose.
Samuel M Keim, MD,
Associate Professor, Department of Emergency
Medicine, University of Arizona College of
Medicine
Nothing to disclose.
Chief Editor
Barry E Brenner, MD, PhD, FACEP,
Professor of Emergency Medicine, Professor of
Internal Medicine, Program Director, Emergency Medicine,
University Hospitals, Case Medical Center
Nothing to disclose.
Background
Biliary colic and cholecystitis are in the spectrum of biliary tract disease. This spectrum ranges from asymptomatic gallstones to biliary colic, cholecystitis, choledocholithiasis, and cholangitis.
Gallstones can be divided into 2 categories: Cholesterol stones (80%) and pigment stones (20%). Most patients with gallstones are asymptomatic. Stones may temporarily obstruct the cystic duct or pass through into the common bile duct, developing symptomatic biliary colic, developing in 1-4% of patients with gallstones annually. Cholecystitis occurs when obstruction at the cystic duct is prolonged (usually several hours) resulting in inflammation of the gallbladder wall. Acute cholecystitis develops in approximately 20% of patients with biliary colic if they are left untreated.[1] Choledocholithiasis occurs when the stone becomes lodged in the common bile duct, with the potential sequelae of cholangitis and ascending infections.
Biliary sludge is a reversible suspension of precipitated particulate matter in bile in a viscous mucous liquid phase. The most common precipitates are cholesterol monohydrate crystals and various calcium-based crystals, granules, and salts.[2] A portion of biliary sludge contains comparatively large particles (1-3 mm) called microliths, the formation of which is an intermediate step in the formation of gallstones (about 12.5%).[3]
Cholecystitis is inflammation of the gallbladder wall caused by obstruction of the cystic duct. This inflammation may be sterile or bacterial. Gallstones usually (>90%) cause this obstruction (calculous cholecystitis) but may infrequently be acalculous or caused by sludge (1.7%).[3] This obstruction results in gallbladder distention, gallbladder wall edema, and ischemia. Inflammatory mediators, specifically prostaglandins, are released, resulting in increased gallbladder inflammation. The wall of the gallbladder may undergo necrosis and gangrene (gangrenous cholecystitis) and ultimately perforate, with the development of an abscess in the right upper quadrant or liver or generalized peritonitis.
Bacterial infection is thought to be a consequence, not a cause, of cholecystitis. In the early stages of acute cholecystitis, bile is sterile. Approximately 20-75% of bile cultures are eventually positive, with the most common organisms being Escherichia coli and Klebsiella, Enterococci, and Enterobacter species. Bacterial superinfection with gas-forming organisms may lead to gas in the wall or lumen of the gallbladder (emphysematous cholecystitis).
Common bile duct stones (choledocholithiasis, 10%) are either secondary (from the gallbladder) or primary (formed in bile ducts).
Prevalence of cholelithiasis is affected by many factors, including race, ethnicity, gender, age, medical problems, and fertility. Between 10% and 20% of adults (approximately 20 million people) in the United States have gallstones, which result in direct costs of more than $6.3 billion.[1, 4] Each year, only 1-3% of people with stones develop biliary colic. Acute cholecystitis eventually develops in about 20% of these symptomatic patients if they are left untreated.[5]
International
People of Hispanic or northern European countries are more likely to have stones.
Mortality/Morbidity
Asymptomatic gallstones result in morbidity and mortality when they become symptomatic.
The incidence of acute cholecystitis is falling, likely due to increased acceptance by patients of laparoscopic cholecystectomy as a treatment of symptomatic gallstones.[6]
Mortality can be as high as 15% in immunocompromised patients.
Complicated cholecystitis has a 25% mortality rate (eg, gangrene, empyema of gallbladder). Perforation of the gallbladder occurs in 3-15% of patients with cholecystitis and is associated with a 60% mortality rate.
In patients with diabetes who have biliary colic, acute cholecystitis occurs more frequently compared with the nondiabetic population. Further, diabetic patients with cholecystitis are more likely experience complications.[7]
Race
Racial or ethnic influences are important in gallbladder disease. Fair people of northern European descent are more likely to have gallstones.
African Americans are at decreased risk for gallstones unless they have a hematologic reason for stones (eg, sickle cell anemia).
Asians with stones are more likely than other populations to have pigmented stones. In elderly Pima Indians, incidence of gallstones is approximately 75%. Increased incidence of stones may be observed in people of Hispanic ethnicity.
Sex
The phrase "fair, female, fat, and fertile" summarizes the major risk factors for development of gallstones. Although gallstones and cholecystitis are more common in women, men with gallstones are more likely to develop cholecystitis (and more severe cholecystitis) than women with gallstones.[8]
Whether women who are pregnant or have multiple pregnancies are more likely to develop stones or whether they are simply more symptomatic with stones is unknown.
The incidence of sludge or stone formation during pregnancy is 5.1% in the second trimester, 7.9% in the third trimester, and 10.2% 4-6 weeks postpartum.[9]
Some oral contraceptives or estrogen replacement therapy may increase the risk of gallstones.
Age
Age increases rates of gallstones, cholecystitis, and common bile duct stones. Elderly patients are more likely to go from asymptomatic gallstones to serious complications of gallstones without gallbladder colic.
Children are more likely than adults to have acalculous gallstones. If stones exist, they are more likely pigmented stones from hemolytic diseases (eg, sickle cell diseases, spherocytosis, G-6-PD deficiency) or chronic diseases (eg, total parenteral nutrition, burns, trauma).
Teenagers have the same etiologies of gallstones as adults, with a higher incidence in girls.
Typical gallbladder colic is 1-5 hours of constant pain, most commonly in the epigastrium or right upper quadrant. Pain may radiate to the right scapular region or back. Peritoneal irritation by direct contact with the gallbladder localizes the pain to the right upper quadrant. Pain is severe, dull or boring, and constant (not colicky). Patients tend to move around to seek relief from the pain. Onset of pain develops hours after a meal, occurs frequently at night, and awakens the patient from sleep. Associated symptoms include nausea, vomiting, pleuritic pain, and fever.
Up to 70% of patients with cholecystitis report having experienced similar episodes in the past that spontaneously resolved. Persistence of biliary obstruction leads to cholecystitis and persistent right upper quadrant pain. Character of pain is similar to gallbladder colic except that it is prolonged and lasts hours (usually >6 h) or days. Nausea, vomiting, and low-grade fever are associated more commonly with cholecystitis
Indigestion, belching, bloating, and fatty food intolerance are thought to be typical symptoms of gallstones; however, these symptoms are just as common in people without gallstones and frequently are not cured by cholecystectomy.
Most gallstones (60-80%) are asymptomatic at a given time. Smaller stones are more likely to be symptomatic than larger ones. Almost all patients develop symptoms prior to complications.
Symptoms of cholecystitis are steady pain in the right hypochondrium or epigastrium, nausea, vomiting, and fever. Acute attack often is precipitated by a large or fatty meal.
Vital signs parallel the degree of illness. Patients with cholangitis are more likely to have fever, tachycardia, and/or hypotension. Patients with gallbladder colic have relatively normal vital signs. In a retrospective study, only 32% of patients with cholecystitis had fever. Fever may be absent, especially in elderly patients.
Patients with cholecystitis are usually more ill appearing than simple biliary colic patients, and they usually lie still on the examination table since any movement may aggravate any peritoneal signs.
Abdominal examination in gallbladder colic and cholecystitis is remarkable for epigastric or right upper quadrant tenderness and abdominal guarding. The Murphy sign (an inspiratory pause on palpation of the right upper quadrant) can be found on abdominal examination. Singer et al found that a positive Murphy sign was extremely sensitive (97%) and predictive (PPV, 93%) for cholecystitis.[10] However, in elderly patients, this sensitivity may be decreased.
When observed, peritoneal signs should be taken seriously. Most uncomplicated cholecystitis does not have peritoneal signs; thus, search for complications (eg, perforation, gangrene) or other sources of pain.
Gallbladder gangrene can be a complication in up to 20% of cases of cholecystitis and is usually in diabetics, elderly, or immunocompromised persons.
A palpable fullness in the RUQ may be appreciated in 20% of cases after 24 hours of symptoms, but is rarely present early in the clinical course.
As in all patients with abdominal pain, perform a complete physical examination, including rectal and pelvic examinations in women.
In elderly patients and those with diabetes, occult cholecystitis or cholangitis may be the source of fever, sepsis, or mental status changes.
Jaundice is unusual in the early stages of acute cholecystitis and may be found in fewer than 20% of patients. Frank jaundice should raise suspicion of concomitant choledocholithiasis or Mirizzi's syndrome (obstruction of the bile duct as a result of external compression of a stone in the gallbladder or cystic duct).
A very high bilirubin should prompt the physician to pay special attention to the common bile duct and pancreatic region.
Risk factors for biliary colic and cholecystitis include pregnancy, elderly population, obesity,
certain ethnic groups (Northern European and Hispanic), weight loss, and liver transplant patients.[11]
Risk factors for acalculous cholecystitis include diabetes, HIV, vascular disease, total parenteral nutrition, prolonged fasting, or being an ICU patient.
Drugs associated with cholecystitis include octreotide and ceftriaxone.[12, 13]
Labs with cholelithiasis and gallbladder colic should be completely normal. WBC, aspirate aminotransferase (AST), alanine aminotransferase (ALT), bilirubin, and alkaline phosphate may be helpful in the diagnosis of cholecystitis. However, presence of normal lab values does not exclude cholecystitis.
Because biliary obstruction is limited to the gallbladder in uncomplicated cholecystitis, elevation in the serum total bilirubin and alkaline phosphatase concentrations may not be present. A study by Singer et al examined the utility of laboratory values in acute cholecystitis diagnosed by hepatic 2,6-dimethyliminodiacetic acid (HIDA) scan.[10] No difference was found in mean WBC, AST, ALT, bilirubin, and alkaline phosphate between patients diagnosed with cholecystitis and those without.
An elevated WBC is expected but not reliable. In a retrospective study, only 61% of patients with cholecystitis had a WBC greater than 11,000. A WBC greater than 15,000 may indicate perforation or gangrene.
Comprehensive metabolic panel with bicarbonate may exhibit the following:
AST, ALT, and alkaline phosphate levels may be elevated; however, as with other laboratory tests, these levels are not sensitive for excluding cholecystitis. When the AST and ALT are elevated significantly, a common bile duct stone is more likely.
An elevation of AST, ALT, or alkaline phosphate should raise the possibility of other biliary system pathology such as cholangitis, choledocholithiasis, or the Mirizzi syndrome (obstruction of the common bile duct by an impacted stone in the distal cystic duct).
Note calcium level (Ranson criteria) if evidence of biliary pancreatitis exists.
Other abnormalities (eg, renal insufficiency) are not related to cholecystitis but may indicate a comorbid condition.
Mild elevation of amylase up to 3 times normal may be found in cholecystitis, especially when gangrene is present.
Prothrombin time (PT) and activated partial thromboplastin time (aPTT) are not expected to be elevated unless sepsis or underlying cirrhosis is present. Coagulation profiles are helpful if the patient needs operative intervention.
For febrile patients, send 2 sets of blood cultures to attempt to isolate the organism in the presence of bacteremia from bacterial superinfection.
Although expected to be normal, urinalysis is essential in the workup of patients with abdominal pain to exclude pyelonephritis and renal calculi.
Conduct a pregnancy test for women of childbearing age.
Ultrasonography and nuclear medicine studies are the best imaging studies for the diagnosis of both cholecystitis and cholelithiasis. Ultrasonography is usually favored as the first test, whereas hepatobiliary scintigraphy is usually reserved for the 20% of patients in whom the diagnosis is unclear after ultrasonography has been performed.
Plain radiography, CT scans, and endoscopic retrograde cholangiopancreatography (ERCP) are diagnostic adjuncts.
Abdominal radiographs
The advantages of abdominal radiographs include their readily availability and low cost. However, abdominal radiographs have low sensitivity and specificity in evaluating biliary system pathology, but they can be helpful in excluding other abdominal pathology such as renal colic, bowel obstruction, perforation. Between 10 and 30% of stones have a ring of calcium and, therefore, are radiopaque. A porcelain gallbladder also may be observed on plain films.
Emphysematous cholecystitis, cholangitis, cholecystic-enteric fistula, or postendoscopic manipulation may show air in the biliary tree. Air in the gallbladder wall indicates emphysematous cholecystitis due to gas-forming organisms such as clostridial species and Escherichia coli.
Computed tomography scan
CT scan is not the test of choice and is recommended only for the evaluation of abdominal pain if the diagnosis is uncertain. CT scan can demonstrate gallbladder wall edema, pericholecystic stranding and fluid, and high-attenuation bile.
A helical CT scan with fine cuts through the biliary tract has not been well studied and may be useful.
Advantages of CT include the following:
For complications of cholecystitis and cholangitis, gallbladder perforation, pericholecystic fluid, and intrahepatic ductal dilation, CT scan may be adequate.
CT scan provides better information of the surrounding structures than sonogram and HIDA. CT scan is also noninvasive.
Disadvantages of CT include the following:
CT scan misses 20% of gallstones because the stones may be of the same radiographic density as bile.
CT scan is also more expensive and takes longer since the patient usually has to drink oral contrast.
Also, given the radiation dose, it may not be ideal in the pregnant patient.
Ultrasonography
View Image
The ultrasound only shows gallstones within the gallbladder but no evidence of cholecystitis (ie, gallbladder wall thickening, pericholecystic fluid, ....
Ultrasonography is the most common test used in the ED for the diagnosis of biliary colic and acute cholecystitis. It is 90-95% sensitive for cholecystitis and 78-80% specific. For simple cholelithiasis, it is 98% sensitive and specific.
Ultrasonography may be diagnostic for biliary disease, help exclude biliary disease, or may reveal alternative causes of the patient's symptoms.
Findings include gallstones or sludge and one or more of the following conditions:
Gallbladder wall thickening (>2-4 mm) - False-positive wall thickening found in hypoalbuminemia, ascites, congestive heart failure, and carcinoma
Gallbladder distention (diameter > 4 cm, length >10 cm)
Pericholecystic fluid from perforation or exudate may be seen as a hypoechoic or anechoic region seen along the anterior surface of the gallbladder within the hepatic parenchyma.
Air in the gallbladder wall (indicating gangrenous cholecystitis)
Sonographic Murphy sign (86-92% sensitive, 35% specific), pain when the probe is pushed directly on the gallbladder (not related to breathing)
Some ED sonographers recommend the diagnosis of cholecystitis if both a sonographic Murphy sign and gallstones (without evidence of other pathology) are present.
In a study by Ralls et al, involving 497 patients with suspected acute cholecystitis, the positive predictive value of the presence of stones and a positive ultrasonographic Murphy's sign was 92%, and that of stones and thickening of the gallbladder wall was 95%. The negative predictive value of the absence of stones combined with either a normal gallbladder wall or a negative Murphy's sign was 95%.[14]
Additional findings in the presence or absence of gallstones: Dilated common bile duct or dilated intrahepatic ducts of the biliary tree indicate common bile duct stones. In the absence of stones, a solitary stone may be lodged in the common bile duct, a location difficult to visualize sonographically.
Advantages of sonography include the following:
Images other structures (eg, aorta, pancreas, liver)
Rapidly performed at the bedside and by the ED physician (see Bedside Ultrasonography, Gallbladder Disease)
No radiation (important in pregnancy)
Disadvantages of sonography include the following:
Operator dependent and patient dependent
Inability to image the cystic duct
Decreased sensitivity for common bile duct stones
Biliary scintigraphy
Depending on the ED, either sonography or nuclear medicine testing is the test of choice for cholecystitis. HIDA scans have sensitivity (94%) and specificity (65-85%) for acute cholecystitis. They are sensitive (65%) and specific (6%) for chronic cholecystitis. Oral cholecystography is not practical for the ED.
HIDA and diisopropyl iminodiacetic acid (DISIDA) scans are functional studies of the gallbladder. Technetium-labeled analogues of iminodiacetic acid (IDA) or diisopropyl IDA-DISIDA are administered intravenously (IV) and secreted by hepatocytes into bile, enabling visualization of the liver and biliary tree.
Normal scans are characterized by normal visualization of gallbladder in 30 minutes.
With cystic duct obstruction (cholecystitis), the HIDA scan shows nonvisualization (ie, considered positive) of the gallbladder at 60 minutes and uptake in the intestine as the bile is excreted directly into the duodenum. This finding has a sensitivity of 80-90% for acute cholecystitis.
Obstruction of the common bile duct causes nonvisualization of the small intestine.
The rim sign is a blush of increased pericholecystic radioactivity, tracer adjacent to the gallbladder, present in approximately 30% of patients with acute cholecystitis and in 60% with acute gangrenous cholecystitis.
False-negative results (filling in 30 min) are found in 0.5% of studies, and filling between 30-60 minutes is associated with false-negative rates of 15-20%.
False-positive results (10-20%) occur when the gallbladder does not visualize despite a nonobstructed cystic duct. Causes include fasting patients receiving total parenteral nutrition; severe liver disease, which leads to abnormal uptake of the tracer; cystic-duct obstruction induced by chronic inflammation, and biliary sphincterotomy, which decreases resistance to bile flow leading to excretion of the tracer into the duodenum. The specificity of the test can be improved by intravenous administration of morphine, known as morphine cholescintigraphy, which induces spasm of this sphincter, increasing back pressure to fill the gallbladder.[15]
Advantages of HIDA/DISIDA scans include the following:
Assessment of function
Normal-appearing gallbladder (by ultrasound); obstructed cystic duct abnormal on DISIDA scan but not ultrasound.
Simultaneous assessment of bile ducts
Disadvantages of HIDA/DISIDA scans include the following:
High bilirubin (>4.4 mg/dL) possibly decreases sensitivity
Recent eating or fasting for 24 hours also possibly affects study
ST-segment elevations are an uncommon finding in acute cholecystitis. The pathophysiological mechanism of these ECG changes is unclear but has been shown to be correctable with appropriate hepatobiliary management. Prompt recognition of cholecystitis will prevent the performance of unnecessary diagnostic and therapeutic cardiac interventions.[16]
Endoscopic retrograde cholangiopancreatography
ERCP provides both endoscopic and radiographic visualization of the biliary tract. It can be diagnostic and therapeutic by direct removal of common bile duct stones.
Ultrasonography is 50-75% sensitive for choledocholithiasis. CT and HIDA scans are not better. Therefore, when a dilated common bile duct is found or elevated LFTs are present, suspicion should remain high for common bile duct stones, and an ERCP should be considered.
Debate exists as to when an ERCP should be performed. In general, since cholecystitis is caused by obstruction of the ducts, the risk of common bile duct stones is approximately 10%. Given its potential for complications, ERCP should be used when there is a high potential for intervention and it should not be used solely as a diagnostic modality.
Some studies have classified people as low risk for common bile duct stones based on (1) lack of jaundice, (2) elevated transaminase levels, and (3) a common bile duct diameter of less than 8 mm. In this population, the risk of common bile duct stones may be as low as 1%. In patients with any of the risk factors, the rate of stones was 39%. Therefore, in general, people with any of the risk factors for common bile duct stones should undergo operative or ERCP evaluation of the common bile duct.
Major complications of ERCP include pancreatitis and cholangitis.
Patients with gallbladder colic or cholecystitis usually present in the prehospital setting with severe abdominal pain. Transport patients with minor symptoms to the hospital with an IV in place and monitor. However, the diagnosis of cholecystitis is not a prehospital diagnosis.
In patients with severe pain (eg, differential includes abdominal aortic aneurysm, myocardial infarction) and in patients with hypotension and/or fever who may have cholecystitis or cholangitis, prehospital care should include the following:
As with all emergencies, airway, breathing, and circulation take priority and should be assessed immediately.
Primary goal of ED care is stabilization of the patient and an expedient diagnosis.
Suspect gallbladder colic in patients with less than 4-6 hours of right upper quadrant pain that radiates to the back. Consider acute uncomplicated cholecystitis in patients with pain of longer duration and with or without low-grade fever. Severe cholecystitis can develop into sepsis or cholangitis, especially in patients with diabetes or elderly patients, in whom the diagnosis may be delayed.
After assessment of the ABCs, perform the standard opening gambit of IV, pulse oximetry, oxygen, ECG, and monitoring. Send labs when the IV is placed; include blood cultures if the patient is febrile.
Replace volume loss with normal saline, then maintenance fluids. Make patients nothing by mouth (NPO). Nasogastric suction may be needed in patients with persistent vomiting or abdominal distention.
In patients who are unstable or have severe pain, consider a bedside ultrasound to exclude an abdominal aortic aneurysm and assist in the diagnosis of cholecystitis. Signs on ultrasound scan include the presence of gallstones, a sonographic Murphy's sign, gallbladder wall thickening and pericholecystic fluid. Competent emergency physician-performed bedside ultrasonography for the detection of acute cholecystitis has been shown to have a negative predictive value (NPV) of 95%, not markedly different from radiologist-performed formal ultrasonography.[17]
In 2007, the unvalidated "Tokyo guidelines" were published, a set of clinical and radiological diagnostic criteria for acute cholecystitis to address the controversy regarding the optimal criteria for clinical diagnosis. Patients exhibiting one of the local signs of inflammation, such as Murphy's sign, or a mass/pain/tenderness in the right upper quadrant, as well as one of the systemic signs of inflammation, such as fever, elevated white blood cell count, and elevated C-reactive protein level, are diagnosed as having acute cholecystitis. Imaging findings characteristic of acute cholecystitis confirm the diagnosis.[18]
Once diagnosis of acute cholecystitis is made, it usually is treated by hospitalization. This may include medical and/or surgical therapy. Some patients may be treated as outpatients.
The guidelines of the Infectious Diseases Society of America recommend that antimicrobial therapy be instituted if infection is suspected on the basis of laboratory and clinical findings (>12,500 WCC; temp >38.5°C) and radiographic findings (eg, air in the gallbladder or gallbladder wall).[19]
Antibiotics are also recommended for routine use in patients who are elderly or have diabetes or immunodeficiency and for prophylaxis in patients undergoing cholecystectomy to reduce septic complications even when infection is not suspected.[1]
Pain control considerations are as follows:
Several studies now have shown that early pain control in ED patients with abdominal pain does not hinder the diagnosis. Therefore, administer pain control early, without waiting for the diagnosis or surgical consult. A courtesy call to the surgical consultant prior to administration of narcotics offers the expedient opportunity to examine the patients without narcotics, which occasionally diminishes surgical resistance to prediagnosis narcotic use.
Pain control should be with opiate analgesics such as meperidine (Demerol). Morphine is generally not recommended since it can increase the tone of the sphincter of Oddi.
Anticholinergic antispasmodics, such as dicyclomine (Bentyl), are also recommended in the initial management of acute biliary colic and cholecystitis.
Anti-inflammatory medications such as ketorolac or indomethacin have been reported to be effective in relieving pain from gallbladder distention. Because the release of prostaglandins results in gallbladder distension, inhibition of these prostaglandins may help alleviate some of the symptoms. However, they may not be as effective when biliary colic is complicated by infection.
Antiemetics such as metoclopramide or prochlorperazine can be used.
Historically, cholecystitis was operated on emergently, resulting in increased mortality. Currently, practice is to cool off the gallbladder and perform a cholecystectomy after several days or readmit the patient at a later date.
Emergent cholecystectomy is usually performed in 20% of cases of acute cholecystitis that has become complicated (ie, gangrene, perforation).
In high surgical risk patients, placement of a percutaneous cholecystostomy is an acceptable alternative and can be performed at the bedside with ultrasound guidance.
Prescribe an urgent gastroenterology consultation for ERCP for patients with evidence of choledocholithiasis (ie, common bile duct stones seen on sonography, dilated common bile ducts, elevated LFTs, pancreatitis).
Surgical consult is appropriate, and depending on the institution, either medicine or surgery may admit the patient for conservative care.
Although surgical therapy is treatment of choice for acute cholecystitis, many patients require hospitalization for stabilization and "cooling off" of the gallbladder prior to surgery. Indications for urgent surgical intervention include patients with complications such as empyema, emphysematous cholecystitis, or perforation. Medical therapy of gallbladder colic includes antiemetics and pain control. In mild cholecystitis, in which inflammation is the primary process, antibiotics are prophylactic but usually are used. In acute cholecystitis, broad-spectrum antibiotic coverage is used.
The following dosages are general recommendations. Please check current sources prior to administration.
Clinical Context:
Has antimuscarinic and anticholinergic effects on smooth muscle. Moderately effective in reducing pain of gallbladder colic and cholecystitis. Used in many institutions as first-line pain control for this disease, with narcotics as second-line pain controllers. May not be given IV.
Clinical Context:
Use similarly to dicyclomine for anticholinergic effects. Acts in smooth muscle, CNS, and secretory glands, where blocks action of acetylcholine at parasympathetic sites.
When dicyclomine (Bentyl) is not effective, a narcotic is appropriate. The narcotic of choice is meperidine due to potential problems of increased tone of sphincter of Oddi with morphine.
Clinical Context:
Narcotic analgesic with multiple actions similar to those of morphine. However, may produce less constipation, smooth muscle spasm, and depression of cough reflex than similar analgesic doses of morphine.
Clinical Context:
Antidopaminergic agent effective in treatment of emesis. Blocks postsynaptic mesolimbic dopaminergic receptors in brain and reduces stimuli to brainstem reticular system.
Clinical Context:
Antidopaminergic drug that blocks postsynaptic mesolimbic dopamine receptors, has anticholinergic effect, and can depress reticular activating system, possibly responsible for relieving nausea and vomiting.
Treatment of acute cholecystitis usually requires single-agent therapy, but for more serious infections, combination drug treatment has increased broad-spectrum coverage. Debate exists as to whether the most effective antibiotics must have high biliary concentrations. Antibiotics should be guided to target the most common organisms found in biliary tract pathology. These include E coli, Klebsiella species, and Streptococcus species.
Single-agent regimens include the following: piperacillin and tazobactam, ampicillin and sulbactam, mezlocillin, imipenem, meropenem, ticarcillin, and clavulanate.
Good combinations include the following: penicillin (including piperacillin, ampicillin, or penicillin) and metronidazole; the above plus an aminoglycoside (gentamicin or tobramycin); and aminoglycoside and third-generation cephalosporin.
Clinical Context:
Drug combination usually used in combination therapy. Antibiotic regimen needs to cover enteric microbes, including most common organisms: E coli (39%), Klebsiella species (54%), Enterobacter (34%), enterococci (34%), and group D streptococci.
Clinical Context:
During growth phase, interferes with bacterial cell wall synthesis, causing death in susceptible microorganisms. Has antipseudomonal activity.
Clinical Context:
For treatment of multiple organism infections in which other agents do not have wide-spectrum coverage or are contraindicated due to potential for toxicity. Reserve for very ill patients. May be used alone or in combination.
Clinical Context:
Second-generation cephalosporin indicated for management of infections caused by susceptible gram-positive cocci and gram-negative rods. Many infections caused by gram-negative bacteria, resistant to some cephalosporins and penicillins, respond to cefoxitin.
Clinical Context:
Aminoglycoside antibiotic used for gram-negative bacterial coverage. Commonly used in combination with both an agent against gram-positive organisms and one that covers anaerobes.
Single daily dosing has not been well studied in cholangitis. Do not use if evidence of renal insufficiency exists.
Cholecystectomy may be performed after the first 48 hours or after the inflammation has subsided. In approximately 30% of patients with uncomplicated cholecystitis, medical therapy is not sufficient and these patients usually need cholecystectomy within 24-72 hours. Unstable patients may need more urgent intervention with ERCP, percutaneous drainage, or cholecystectomy.
Laparoscopic cholecystectomy is very effective and has few complications. Approximately 5% of cases must be converted to an open cholecystectomy. In acute cholecystectomy, the conversion rate can be as high as 30%. The rate of conversion is higher for acute cholecystitis compared with uncomplicated cholelithiasis, in both acute or delayed intervention.[20, 21] Predictors of the need for open conversion include a white cell count of more than 18,000 at the time of presentation, a duration of symptoms of more than 72-96 hours and an age older than 60 years.[22]
Immediate laparoscopic cholecystectomy (within 24 h) is now being increasingly performed by surgeons because it has been shown to be safe, not more difficult than laparoscopic cholecystectomy performed later, and shortens the hospital length of stay.[23]
Patients who are not good surgical risks but who are toxic may benefit from percutaneous gallbladder drainage and placement of a T tube if common bile duct stones are suspected. The alternative is ERCP to attempt endoscopic opening of the common bile duct or cystic duct.
Delayed surgical intervention can be used for patients who have high-risk medical conditions and are unstable for surgery and in patients in whom the diagnosis in doubt. Mortality may be up to 15% in patients with acute cholecystitis who were at high risk (as per APACHE criteria).[24]
In patients younger than 60 years, the mortality rate for emergent cholecystectomy is approximately 3%, whereas mortality in early or elective cholecystectomy approaches 0.5%.
For acute cholecystitis, some patients may be treated on an outpatient basis. The patients must meet the following criteria:
Afebrile and normal vital signs
Minimal amount of pain and tenderness
No markedly abnormal labs, normal common bile duct on sonography, and no pericholecystic fluid or biliary air
No underlying medical problems (eg, diabetes, cirrhosis, vascular condition, steroids), advanced age, or pregnancy
Next day follow-up visit
Discharge on oral antibiotics and a small number of pain medications. In pregnancy, since symptoms may be recurrent, refer women to their OB/GYN as well as a surgeon. Second trimester cholecystectomy is the safest time period because the risk of premature labor is lower, and the uterus does not push on the gallbladder.
Other therapies: For simple gallbladder colic, other therapies rarely are performed because they require long-term therapy (oral dissolution), cause complications (shock wave therapy), and ultimately do not prevent the recurrence of gallstones.
Oral dissolution therapy: Bile acid therapy consists of ursodeoxycholic acid sometimes in combination with chenodeoxycholic acid. With this treatment, cholesterol saturation of bile is decreased, and dissolution of small gallstones (< 5 mm) is possible with 6-12 months of therapy; however, over one half recur. This treatment has several disadvantages including the time frame of up to 2 years. Fewer than 10% of patients with symptomatic gallstones are candidates for this therapy. The doses are not listed because this treatment option is chosen rarely, and it is not in the purview of the ED.
Extracorporeal shock-wave lithotripsy: This is another little-used therapy due to the recurrence of stones. This therapy is not popular because only small, < 2 cm, stones can be fragmented and also a recurrence of gallstones occurs in up 30% of patients within 5 years.
Dissolution therapy: Percutaneous contact dissolution by injection of methyl tert-butyl ether into the gallbladder to dissolve stones rarely is used.
There is evidence to support early laparoscopic cholecystectomy (< 24 h of diagnosis of biliary colic) decreasing the morbidity during the waiting period for laparoscopic cholecystectomy, in addition to decreasing the rate of conversion to open cholecystectomy and the hospital length of stay.[25]
Complications of cholecystitis and/or biliary colic may include the following:
Cholangitis
Sepsis
Pancreatitis
Gallbladder perforation
Gallbladder perforation occurs in 10% of patients with cholecystitis. When perforation is localized, it may be seen as pericholecystic fluid by ultrasound. Abscess formation is common.
Free perforation also can occur, releasing bile and inflammatory matter intraperitoneally, causing peritonitis.
Gallstone ileus
When perforation occurs next to a hollow viscus, a gallbladder enteric fistula can be formed.
Fistulas into the duodenum are most common. When gallstones are passed directly through the fistula into the small bowel, if they are greater than 2.5 cm, they can obstruct the ileocecal valve. This causes gallstone ileus.
Mortality can be up to 20% because diagnosis is difficult.
Treatment includes cholecystectomy, CBC exploration, and closure of the fistulous tract.
Emphysematous gallbladder of infection by gas-forming organisms (eg, Clostridium species) is more common in patients with diabetes and men. Mortality is 15%. Perforation of the gallbladder occurs in 3-15% of cholecystitis with up to 60% mortality.
Gangrenous or empyema of the gallbladder carries 25% mortality.
The ultrasound only shows gallstones within the gallbladder but no evidence of cholecystitis (ie, gallbladder wall thickening, pericholecystic fluid, common bile duct dilatation, sonographic Murphy sign).
){kind=link}