Emphysematous Cholecystitis
No Results
No Results
processing….
Emphysematous cholecystitis, known less commonly as clostridial cholecystitis, is an acute infection of the gallbladder wall caused by gas-forming organisms (eg, Clostridium or Escherichia coli) that is generally considered a surgical emergency. [1] An infrequent, insidious, and rapidly progressive form of acute cholecystitis, emphysematous cholecystitis is characterized by early gangrene, perforation of the gallbladder and high mortality. Although this condition develops in approximately 1% of all cases of acute cholecystitis, compared with typical acute cholecystitis, emphysematous cholecystitis is associated with much higher rates of gangrene and perforation of the gallbladder and significantly increased rates of mortality (15-25%).
An estimated 500,000 cholecystectomies are performed per year in the United States. Assuming all patients with emphysematous cholecystitis come to surgery, this would indicate that 5000 cholecystectomies are performed per year for emphysematous cholecystitis. Although the number of patients who are treated successfully without surgery is certainly small, the number of patients who die without surgery is unknown.
Usually, the diagnosis is made by the radiographic presence of air within the gallbladder wall or lumen (see the image below). Elderly males, especially diabetics, are particularly susceptible to clostridial cholecystitis (emphysematous cholecystitis). The computed tomography (CT) scan below shows a patient with emphysematous cholecystitis.
See Can’t-Miss Gastrointestinal Diagnoses, a Critical Images slideshow, to help diagnose the potentially life-threatening conditions that present with gastrointestinal symptoms.
For more information, see Cholecystitis.
Four pathogenetic factors are proposed in the development of emphysematous cholecystitis.
In most cases, the cystic artery is the sole arterial supply of the gallbladder. Occlusion or stenosis results in compromised viability of the gallbladder, in which arteriosclerosis is the usual causative abnormality, although the condition has been described after an embolic event. The evidence that vascular insufficiency is a root cause of emphysematous cholecystitis is circumstantial, that is, association with diabetes mellitus, greater incidence in males, high frequency of gangrene, and occurrence in older patients. However, exceptions exist for each of these.
Vascular compromise of the cystic artery renders the gallbladder ischemic and facilitates the proliferation of gas-forming organisms and bacterial translocation in the devitalized tissue with low oxygen saturation. Bacteriocidal bile is rendered alkaline, facilitating infection of the bile. Histopathologic reviews of emphysematous gallbladders reveal a higher incidence of endarteritis obliterans compared with the typical acute cholecystitis secondary to cholelithiasis.
A case of emphysematous cholecystitis that developed following hepatic artery embolization appeared to substantiate the theory that vascular compromise is the main pathogenic factor. [2] In another report, gallbladder torsion progressed to emphysematous cholecystitis, probably due to ischemic necrosis (secondary to torsion) facilitating infection and translocation of gas-forming bacteria. [3]
Emphysematous cholecystitis has also been reported as an adverse event caused by sunitinib, administered for the treatment of gastrointestinal stromal tumor (GIST), probably due to the thromboembolic side effect of this class of drugs (vascular endothelial growth factor [VEGF] receptor inhibitors). [4]
Gallstones are observed in 28-80% of patients with emphysematous cholecystitis. Impaction of stones in the cystic duct leads to localized edema of the gallbladder wall, which contributes to the vascular compromise of the gallbladder. Nevertheless, emphysematous cholecystitis in the presence of acalculous cholecystitis is well established, occurring nearly 3 times more frequently in the emphysematous form, suggesting that there is a basic difference in the pathogenesis between emphysematous cholecystitis and acute cholecystitis secondary to gallstones. [5] Indeed, the proportion of patients with acalculous cholecystitis in association with emphysematous cholecystitis exceeds that of patients with ordinary acute calculous cholecystitis.
These observations raise doubt about the role of gallstones in the pathogenesis of emphysematous cholecystitis. [6, 5]
Diabetes mellitus is detected in 38-55% patients with emphysematous cholecystitis, and the mean age of patients is 59 years. Both the metabolic abnormality and older age probably contribute to the increased risk of infection.
Microorganisms commonly isolated are clostridial species, Escherichia coli, and Klebsiella species. Less frequently, enterococci and anaerobic streptococci are among the other organisms detected. Although the intramural gas observed in patients with emphysematous cholecystitis seems to result from gas-forming bacteria, whether these bacteria represent the primary cause of the disorder or are secondary invaders remains unclear. Concomitant emphysematous cholecystitis and emphysematous pyelonephritis raise the possibility of septic seeding of the gallbladder wall. Infectious complications following endoscopic retrograde cholangiopancreatography (ERCP) have also been reported. [7, 8]
In an analysis of bile in 109 cases of emphysematous cholecystitis, 95 of 109 (87%) had a positive culture, of which 46% were clostridial species (79% of the clostridial cultures grew Clostridium welchii and 33% grew E coli, often as a copathogen with Clostridia. [5]
In a separate series of 20 patients with emphysematous cholecystitis, Tellez et al reported gallbladder culture results in which E coli grew in 40%, Bacteroides fragilis in 30%, C perfringens in 20%, and Proteus vulgaris, Aerobacteraerogenes, as well as Klebsiella, Streptococcus, Staphylococcus, and Enterococcus species in 40%. [9]
The bacteriologic patterns of simple (ie, nonemphysematous) cholecystitis are vastly different—only 12% of the positive cultures of typical acute cholecystitis grew clostridia. [5] Thus, there is nearly a 4-fold difference in the incidence of clostridial infection in patients with emphysematous cholecystitis compared with those with ordinary acute cholecystitis. [5]
It is thought that these organisms acquire pathogenicity when they proliferate in a devascularized gallbladder. Specifically, clostridium produces several different exotoxins, the most prevalent being oxygen-stable lecithinase-C, an alpha-toxin which is hemolytic, tissue-necrotizing and lethal. [10] This alpha-toxin induces profound shock via increased capillary permeability, cardiotoxicity, and leukocyte dysfunction.
Despite the potentially lethal nature of this disease, patients with emphysematous cholecystitis—typically a man older than 60 years, often with type II diabetes mellitus—often have deceptively mild clinical findings that are frequently indistinguishable from acute cholecystitis. The insidious nature of this disease may mislead the clinician, and the patient may unsuspectingly rapidly deteriorate with sudden cardiovascular collapse and even death.
The most common clinical complaints initially are right upper quadrant pain and fever. The pain is localized to the right upper quadrant and often radiates to the back, but it is unrelated to position or physical activity. The patient may also complain of generalized abdominal pain consistent with peritonitis. Nausea and vomiting occur less frequently.
In addition, an antecedent history of self-limited episodes of pain may be present. However, the clinician must be aware that elderly patients may develop acute intra-abdominal disorders with little or no localizing symptoms or signs. [11]
The physical examination usually reveals an elderly patient with fever and tachycardia, who may be obtunded depending on the presence of septic shock. These individuals may also be hypotensive, depending on the severity of the disease. If concomitant choledocholithiasis or common duct obstruction and/or intrahepatic disease is present, the patients can also appear jaundiced.
When evaluating the abdominal region, there is generally tenderness in the right upper quadrant, but there may also be diffuse tenderness consistent with peritonitis. In certain cases, there could be overlying erythema of the right side secondary to perforation of the gallbladder with intraperitoneal abscess. [12] In addition, an enlarged tense gallbladder may be noted, which is best demonstrated by light palpation. Bowel sounds are diminished or absent, especially if peritonitis has supervened. Transient relief of right upper quadrant pain followed by the appearance of peritoneal signs is the hallmark of perforation.
Major fluid sequestration (ie, “third-spacing” of fluid), florid septic shock, or peritonitis may occur as later clinical presentations.
Staging of the disease is image based (see Abdominal Ultrasonography). Diagnostic visualization on plain radiographs of the abdomen is thought to represent late-stage disease (see Abdominal Radiography). CT imaging differentiates pre-perforation disease from post-perforation disease (see CT Scanning of the Abdomen). [6]
Two levels of differential diagnosis should be considered: clinical and radiologic.
The clinical differential diagnosis is that of acute cholecystitis (nonemphysematous), both calculous and acalculous, as well as bacterial sepsis, peritonitis, and abdominal sepsis.
The radiologic differential diagnosis is that of finding gas in the biliary tree, which may be due to a biliary-enteric fistula (spontaneous or surgical); may occur after ERCP, especially following a sphincterotomy; or may be due to cholangitis caused by gas-forming organisms. [13, 14] Imaging studies are the key diagnostic maneuvers.
Although urinalysis, chest radiography, and electrocardiography add little to establish a diagnosis, these studies should be obtained as part of the preoperative assessment of the patient.
Patients have leukocytosis that is, at times, strikingly high, but this feature cannot differentiate clostridial cholecystitis (emphysematous cholecystitis) from simple cholecystitis.
Liver tests results are usually normal or slightly elevated (eg, aspartate aminotransferase [AST], alanine aminotransferase [ALT]), reflecting the patient’s febrile state and potentially reflecting concurrent choledocholithiasis (seen in up to 10% of patients). Very abnormal liver test results, especially elevated alkaline phosphatase (ALP), bilirubin, or gamma-glutamyl transpeptidase (GGTP), suggest a common duct obstruction or intrahepatic disease.
Serum glucose can also be elevated, because many patients with emphysematous cholecystitis are also diabetic.
The key radiographic finding in emphysematous cholecystitis is air inside the gallbladder and/or in the gallbladder area (seen in 95% of patients) or in the biliary tree (15%). [9]
Abdominal radiographs show the classic picture of a gallbladder wall containing gas (see the images below). The gallbladder is often fluid-filled, and gas that has leaked into its lumen collects in the least dependent portion. [15] The absence of a gas-filled gallbladder wall on an abdominal radiograph does not exclude a diagnosis of emphysematous cholecystitis. [14, 16]
Inflammation and gas formation may extend to the pericholecystic tissues and extrahepatic ducts. This picture has been regarded as specific for emphysematous cholecystitis, but the sensitivity is unknown.
Pneumoperitoneum may be present, but this is rare. Occasionally, pneumobilia can be the sole radiographic finding. [5]
With the advent of other imaging techniques, especially computed tomography (CT) scanning, the importance of plain radiographs of the abdomen has declined (see CT Scanning of the Abdomen). Changes noted on CT scans and ultrasonograms of the abdomen (see Abdominal Ultrasonography) can be observed before the classic abnormalities are visible on plain abdominal radiograph. [6] Furthermore, the presence of abnormal findings on a plain film of the abdomen may indicate advanced disease, [6] as the classic picture observed on abdominal radiographs is believed to represent a late phase in the evolution of emphysematous cholecystitis and may presage a poorer outcome.
Abdominal radiographs are less sensitive than ultrasonograms and CT scans [17] and may be negative in up to 60% of cases. This consideration has altered both the diagnostic workup and the surgical options; early diagnosis requires CT scanning, and the presence or absence of gas outside the gallbladder will influence the choice of the surgical approach. [6]
Ultrasonography is the most common imaging modality currently employed to visualize the gallbladder, especially in those patients with the clinical suspicion of acute cholecystitis. This modality helps detect acute emphysematous cholecystitis earlier than plain abdominal radiography and identifies the condition in 90-95% of cases.
Emphysematous cholecystitis is classically described ultrasonographically in 3 stages. [13]
Gas is present in the gallbladder lumen. There is a dense band of hyperreflective echoes with distal reverberations when the gallbladder is full of gas or a band of reverberations in the gas-filled portion of the gallbladder with the usual signs of cholecystitis in the bile-filled portion when the gallbladder is partially full of gas.
Gas is present in the gallbladder wall. There is an area of high reflectivity in the gallbladder wall with reverberations that may change position with patient movements or a bright hyperreflective ring emanating from the entire gallbladder circumference.
Gas is present in the pericholecystic tissue and is seen inside the gallbladder, within its wall and outside the gallbladder in the surrounding tissues, indicating gangrene and perforation.
In some cases, there may be multiple tiny echogenic foci in the gallbladder lumen, arising from the dependent part of the gallbladder and “floating” to the nondependent wall, reminiscent of bubbles rising in a glass of champagne. [18, 19, 20]
Curvilinear gaseous artifacts in the gallbladder, the “ring-down effect” or “comet tail,” are diagnostic of emphysematous cholecystitis, but the frequency with which these are observed is not clear. [19]
One disadvantage of ultrasonography is that extensive gallbladder wall gas can be interpreted as nonvisualization of the gallbladder, resulting in false-negative results from the scans. [6] In addition, the characteristic ultrasonographic findings of intraluminal or intramural gas may be highly echogenic reflectors on ultrasonography, which can be mistaken for a porcelain gallbladder or stones adherent to the gallbladder wall. These findings are not diagnostic of emphysematous cholecystitis. The alert clinician questions the paradoxical absence (ie, ultrasonographic nonvisualization) of a gallbladder in the clinical setting of a patient who likely has gallbladder disease. [6, 21]
Although ultrasonography is highly specific (90-95%) to diagnose acute clostridial cholecystitis (emphysematous cholecystitis), its sensitivity is lower. Computed tomography scanning may help in certain equivocal cases. However, if the diagnosis is made by ultrasonography, the patient should proceed to surgery without delay and CT scanning is unwarranted.
Evaluation with abdominal computed tomography (CT) scanning is now considered the primary imaging modality to confirm acute emphysematous cholecystitis, as it is the most sensitive and specific imaging modality for identifying gas in the gallbladder lumen or wall (see the images below). [22, 23, 24] CT scanning demonstrates emphysematous changes in the gallbladder wall that are diagnostic of this condition and is highly sensitive for tiny bubbles of air which may not be seen on ultrasonography. CT scanning can also provide precise information regarding the location and extent of air and fluid collections, such as extension into the pericholecystic tissues and the hepatic ducts. Gas in the peritoneum indicates perforation. [25]
CT scanning should be performed early in the evaluation when the clinical picture warrants, and it is indicated in cases in which an ultrasonographic or abdominal radiographic evaluation is equivocal. Initial use of CT scanning may eliminate the need for further imaging studies and facilitates appropriate clinical management. [26, 27]
Magnetic resonance imaging (MRI) can provide extensive information on intramural necrosis as well as intraluminal gas. Gas in the gallbladder lumen and wall appear as signal void areas. [28] Characteristic MRI findings of emphysematous cholecystitis are numerous floating signal void bubbles in the upper dependent portions of the gallbladder (gallstones are usually in the lower dependent portion) (see the image below).
In a report, a gas-fluid level was shown by a signal void in the nondependent portion of the gallbladder contrasted against an intermediate signal intensity in the dependent portion. Gas within the wall was demonstrated by a rim of low signal intensity. Extraluminal gas, suggesting perforation, may cause small magnetic field inhomogeneous collections referred to as “blooming” artifacts. [29]
Following the invasion of the wall by gas-forming bacteria, the different layers of the gallbladder wall become separated (full-thickness necrosis), leading to the characteristic tissue crepitus. Histologically, colonies of bacteria can be observed forming intramural abscesses, and obliteration of the cystic artery is seen secondary to endarteritis obliterans. Gallbladder contents are often purulent. Even with prompt intervention, necrosis and gangrene are observed in 75% of gallbladders at surgery, and nearly 20% of the gallbladders perforate. [5]
Although sporadic cases of presumed emphysematous cholecystitis treated only with antibiotics and supportive measures are described, it should be emphasized that definitive management of this condition requires surgical intervention. [6, 30] Thus, prompt surgical cholecystectomy, with excision of the gallbladder with its highly infectious content, is the mainstay of treatment because of the observation that septic shock and death progresses quickly with this disease process, particularly in the elderly and diabetic individuals.
Broad-spectrum antibiotics should be initiated immediately preoperatively and can be continued postoperatively until the patient clinically improves. Then these agents can be tailored according to the bacteriologic samples obtained during the surgical procedure.
Intravenous antibiotics of choice are those that have beta-lactamase inhibitor activity or combinations that provide coverage for anaerobic and gram-negative organisms. A good choice is ampicillin/sulbactam (Unasyn) or piperacillin/tazobactam (Zosyn) with or without metronidazole (Flagyl) depending on the level of Bacteroides coverage desired.
Antibiotic regimens are suggested with the following caveats: (1) antibiotics are not definitive therapy for this condition, and (2) antibiotic regimens should be evaluated in light of changing bacterial sensitivities, changing antibiotic options, and changing patient characteristics.
Fluid replacement and correction of electrolyte deficits and metabolic imbalances should be initiated in preparation for surgery. It is to be emphasized that these temporary and preparatory maneuvers are not intended to reverse the basic disease process.
Consultation with surgical and internal medicine specialists is indicated in all cases of emphysematous cholecystitis. In addition, if available, the services of an interventional radiologist is indicated when percutaneous gallbladder drainage is considered an option. This would be especially true in a patient who is seriously ill and/or has multiple comorbidities.
Consultation with infectious disease specialists is indicated for optimal selection of antibiotics, and consultation with other medical subspecialists depends on the array of comorbid conditions present.
Interventional radiologic techniques allow drainage and decompression followed by interval excision of the gallbladder. These techniques are particularly useful for patients with complications, such as perforation, and for those with high surgical risk. [31]
This procedure is an option mainly for patients in such poor clinical condition that they cannot tolerate general anesthesia. Cholecystostomy (done under local anesthesia by the interventional radiologists under ultrasonographic guidance) is considered a temporary measure to control sepsis. Once the sepsis is controlled and the patient improves, an interval (ie, 4-6 wk later) cholecystectomy can be performed for definitive therapy.
With increasing experience with percutaneous drainage, surgical survival appears to have improved. However, the following important issues remain unresolved:
With improving diagnostic techniques, specifically ultrasonography and computed tomography scanning, the disease process is likely to be at an early stage of its evolution. For this reason, it may have been amenable to a combination of radiologic drainage, concomitant antibiotic therapy, and interval cholecystectomy in a well-prepared, stable patient.
The case descriptions do not clarify the appropriate interval between interventional drainage and surgical excision of the gallbladder.
At the very least, current experience suggests that interventional radiologic drainage can be performed without increasing the overall mortality rate, and it appears to be a reasonable temporizing option in a seriously ill patient.
Hopefully, the favorable impact of interventional radiology will be confirmed. It does not yet obviate the need for ultimate surgical removal of the gallbladder. Further experience is required to determine the role of percutaneous transhepatic gallbladder drainage. The final management algorithm for emphysematous cholecystitis has yet to been written.
Management of emphysematous cholecystitis is surgical. Antibiotics and fluid replacement are started immediately to stabilize the patient, but because of the risk of perforation and its impact on survival, clinicians tend to proceed to surgery with deliberate speed. Overall, surgical mortality rates vary from 15% to 25%.
Traditionally, early open cholecystectomy was performed. Laparoscopic cholecystectomy for acute emphysematous cholecystitis was first described in 1994, and experience with this technique continues to increase. Although laparoscopic cholecystectomy is feasible, the number of cases does not allow valid comparisons with open cholecystectomy for mortality and complications. A preoperative diagnosis of perforation would likely preclude a laparoscopic approach, thereby requiring a preoperative computed tomography (CT) scanning or magnetic resonance imaging (MRI) of the abdomen. [32, 33]
As long as fundamental surgical principles are maintained (and depending on the patient and surgeon skill/comfort level) laparoscopic cholecystectomy is a safe and effective treatment for this disease process. [32, 33, 34] The surgeon should be aware that higher conversion rates have been reported due to the anatomic distortion caused by acute inflammation, [35] although, with current techniques, emphysematous cholecystitis can be treated initially as a laparoscopic procedure while maintaining a low threshold for conversion. Due to the degree of inflammation, the surgeon should consider postoperative drainage of the gallbladder fossa (eg, Jackson-Pratt drain) to potentially decrease the risk of postoperative fluid collections and abscess formation.
If the patient has concurrent common bile duct stones, common bile duct exploration can be done transcystically or via choledochotomy, open or laparoscopic, to clear the common bile duct. An alternative choice is to refer the patient postoperatively to the biliary endoscopist for ERCP to clear the common bile duct of stones.
Hyperbaric oxygenation (HBO) has been described as an adjuvant therapy to surgery for emphysematous cholecystitis. [10] In a small study from Croatia, patients with acute emphysematous cholecystitis were exposed to HBO within 8 hours after surgery at a pressure of 3.0 bars 3 times daily for 90 minutes, with an air break of 15 minutes within the first 24 hours and for the next 5 days twice daily under the same conditions.
The rationale for HBO on clostridia and other anaerobes is based on the formation of free radicals in the absence of free radical degrading enzymes (eg, superoxide dismutases, catalases, and peroxidases). Achieving tissue partial oxygen pressure above 250 mm Hg is necessary to stop bacterial growth and inactivate exotoxins.
Note: Although HBO may be beneficial as adjunctive therapy, it is not considered an adequate alternative to surgical cholecystectomy.
The episode of emphysematous cholecystitis itself should not impose any dietary requirements. However, the patient should not be given anything by mouth until a decision has been made regarding surgery. Any gallbladder stimulation secondary to oral intake is likely to exacerbate the pathophysiologic process.
Once cholecystectomy has been successfully performed, the patient can be started on a diet depending on the clinical scenario. Upon discharge, dietary recommendations reflect the presence of active comorbid diseases.
Early postoperative activity is dictated by surgical considerations. Upon discharge after the operation, the patients should experience no limitation of activity that was not present before the episode.
Patients should be observed for the development of pseudomembranous enterocolitis manifested by diarrhea. This diagnosis is established by demonstrating C difficile toxin in the stool. Treatment is usually started with metronidazole and switched to vancomycin if metronidazole fails to elicit a response.
Patients should also be observed for the development of early postoperative complications, such as a leak from the cystic duct stump and retained common duct stone, as well as the development of common duct stricture and/or postcholecystectomy diarrhea (see Complications).
Patients should be educated to watch for features of bile duct obstruction, including changes in the color of the skin, eyes, urine, and stool, which may indicate a retained common duct stone or stricture.
The most feared complication of emphysematous cholecystitis is potentially lethal septic shock, which can occur in up to 25% of cases. Untreated emphysematous cholecystitis can progress to soft-tissue gas gangrene due to hematogenous spread of microorganisms to the muscles and eventual septic shock and death. [25] Once the diagnosis of acute emphysematous cholecystitis is made, the patient should be resuscitated, broad-spectrum antibiotics should be initiated, and the patient should undergo operative treatment without any delay. If the patient’s condition progresses to septic shock and cardiovascular collapse, the mortality is significantly higher.
Morbidity can be as high as 50%, often related to the sequelae of septic shock. Other postoperative complications include postoperative abscess, bile leak, bile duct injury, and wound infection. Placing a closed-suction drainage (eg, Jackson-Pratt drain) at the time of operation may help decrease the rate of fluid collections and subsequent abscess formation postoperatively. Bile duct injury may be avoided by intraoperative cholangiogram to help delineate the biliary tree anatomy, especially in cases with dense inflammation causing distortion of the anatomy in Calot’s triangle. [36]
Emphysematous cholecystitis evolves to gangrenous cholecystitis in 75% of the cases. [9] Once gangrenous cholecystitis is present, perforation of the gallbladder is inevitable, occasionally giving rise to pneumoperitoneum and frank peritonitis. Both gangrene and perforation are relatively infrequent in simple acute cholecystitis secondary to gallstones. In fact, the incidence of gangrene is 30-fold more frequent and the incidence of perforation is 5-fold more frequent in emphysematous cholecystitis compared to ordinary acute cholecystitis. [5]
There is no significant difference in the mortality and in the sequence of gangrene and perforation in acute emphysematous cholecystitis between diabetic and nondiabetic individuals. [9] Gangrene and perforation have also been noted in patients with emphysematous cholecystitis who were symptomatic for less than 72 hours, reinforcing the concept that the initial presentation may be misleading to the clinician and that the patient can rapidly deteriorate clinically with hemodynamic collapse and septic shock.
The overall mortality from emphysematous cholecystitis ranges from 15% to 25%, usually due to a delay in the diagnosis. These rates are 5 times the operative mortality rates for nonemphysematous cholecystitis. In addition to the septic character of the disease, comorbidities attendant to advanced age and diabetes mellitus also add to the risk of mortality. [5]
Although most patients have the typical clinical presentation as previously described (see Presentation), there are some issues the clinician must be aware of.
Older patients may not present with significant abdominal pain or fever, even in the presence of frank peritonitis.
Acute emphysematous cholecystitis is a separate entity compared with acute cholecystitis secondary to cholelithiasis. The epidemiologic profile and the disease course (rapid progression) are different. The clinician can be misled by a deceptively mild initial presentation. Once the diagnosis is made radiographically, the patient should undergo operative treatment without delay.
A plain film of the abdomen may not be diagnostic. A normal finding on a plain film does not exclude the diagnosis of emphysematous cholecystitis. [6, 14, 16] In addition, the gallbladder may not be readily observed on ultrasonographic examination. Indeed, the apparent absence of a visualized gallbladder on ultrasonograms in a patient with biliary tract features should prompt the clinician to proceed to an abdominal CT scan. [6, 21] Ultimately, a CT scan is the most reliable diagnostic test.
Delay in the diagnosis or treatment and any intraoperative/technical misadventures may expose the clinician to legal liability. An intraoperative cholangiogram to help delineate the biliary anatomy—which may be distorted due to the extensive inflammation—may help decrease the rate of bile duct injury.
Mathew G, Pfeifer C. Gallbladder, Cholecystitis, Clostridial (Gangrenous, Emphysematous). StatPearls [Internet]. 2019 Jan 14. [Medline]. [Full Text].
Coldwell DM, Hottenstein DW, Ricci JA, Wengert PA. Emphysematous cholecystitis as a complication of hepatic arterial embolization. Cardiovasc Intervent Radiol. 1985. 8(1):36-8. [Medline].
Tanaka S, Kubota D, Oba K, et al. Gallbladder torsion-induced emphysematous cholecystitis in a 16-year-old boy. J Hepatobiliary Pancreat Surg. 2007. 14(6):608-10. [Medline].
de Lima Lopes G Jr, Rocha Lima CM. Emphysematous cholecystitis in a patient with gastrointestinal stromal tumor treated with sunitinib. Pharmacotherapy. 2007 May. 27(5):775-7. [Medline].
Mentzer RM Jr, Golden GT, Chandler JG, et al. A comparative appraisal of emphysematous cholecystitis. Am J Surg. 1975 Jan. 129(1):10-5. [Medline].
Gill KS, Chapman AH, Weston MJ. The changing face of emphysematous cholecystitis. Br J Radiol. 1997 Oct. 70(838):986-91. [Medline].
Alvarez C, Hunt K, Ashley SW, Reber HA. Emphysematous cholecystitis after ERCP. Dig Dis Sci. 1994 Aug. 39(8):1719-23. [Medline].
Stack R, McLoughlin J, Gillis A, Ryan BM. Post-ERCP emphysematous cholecystitis in a young woman: a rare and potentially fatal complication. Case Rep Gastrointest Med. 2017 Mar 21. 2017:1971457. [Medline]. [Full Text].
Garcia-Sancho Tellez L, Rodriguez-Montes JA, Fernandez de Lis S, Garcia-Sancho Martin L. Acute emphysematous cholecystitis. Report of twenty cases. Hepatogastroenterology. 1999 Jul-Aug. 46(28):2144-8. [Medline].
Kraljevic D, Druzijanic N, Tomic I, Juricic J, Petri N. Hyperbaric oxygenation as adjuvant therapy to surgery of emphysematous cholecystitis. Hepatogastroenterology. 1999 Mar-Apr. 46(26):775-7. [Medline].
Liao CY, Tsai CC, Kuo WH, et al. Emphysematous cholecystitis presenting as gas-forming liver abscess and pneumoperitoneum in a dialysis patient: a case report and review of the literature. BMC Nephrol. 2016 Mar 1. 17:23. [Medline]. [Full Text].
Kanehiro T, Tsumura H, Ichikawa T, Hino Y, Murakami Y, Sueda T. Patient with perforation caused by emphysematous cholecystitis who showed flare on the skin of the right dorsal lumbar region and intraperitoneal free gas. J Hepatobiliary Pancreat Surg. 2008. 15(2):204-8. [Medline].
Bloom RA, Libson E, Lebensart PD, et al. The ultrasound spectrum of emphysematous cholecystitis. J Clin Ultrasound. 1989 May. 17(4):251-6. [Medline].
Lorenz RW, Steffen HM. Emphysematous cholecystitis: diagnostic problems and differential diagnosis of gallbladder gas accumulations. Hepatogastroenterology. 1990 Dec. 37 Suppl 2:103-6. [Medline].
Sousa I, Fernandes A, Tavora I. Emphysematous cholecystitis: imaging diagnosis of an emergent condition. Acta Med Port. 2016 Nov. 29(11):761. [Medline]. [Full Text].
Chuang C, Hsieh H, Wu H, et al. Management of emphysematous cholecystitis. Chir Gastroenterol. 2007. 23:75-78.
Johnson H Jr, Sloane RE, Perlman DM. Pneumobilia as the sole radiographic finding in emphysematous cholecystitis. Int Surg. 1984 Oct-Dec. 69(4):365-7. [Medline].
Nemcek AA Jr, Gore RM, Vogelzang RL, Grant M. The effervescent gallbladder: a sonographic sign of emphysematous cholecystitis. AJR Am J Roentgenol. 1988 Mar. 150(3):575-7. [Medline].
Parulekar SG. Sonographic findings in acute emphysematous cholecystitis. Radiology. 1982 Oct. 145(1):117-9. [Medline].
Wu CS, Yao WJ, Hsiao CH. Effervescent gallbladder: sonographic findings in emphysematous cholecystitis. J Clin Ultrasound. 1998 Jun. 26(5):272-5. [Medline].
Mammen L, Watkins GE. Emphysematous cholecystitis. Applied Radiology Online. 10 October 2000. [Full Text].
Andreu J, Perez C, Caceres J, Llauger J, Palmer J. Computed tomography as the method of choice in the diagnosis of emphysematous cholecystitis. Gastrointest Radiol. 1987. 12(4):315-8. [Medline].
Grayson DE, Abbott RM, Levy AD, Sherman PM. Emphysematous infections of the abdomen and pelvis: a pictorial review. Radiographics. 2002 May-Jun. 22(3):543-61. [Medline].
Mora-Guzman I, Martin-Perez E. Perforated emphysematous cholecystitis and Streptococcus bovis. Rev Esp Enferm Dig. 2018 Nov 13. 111:[Medline]. [Full Text].
Safioleas M, Stamatakos M, Kanakis M, et al. Soft tissue gas gangrene: a severe complication of emphysematous cholecystitis. Tohoku J Exp Med. 2007 Dec. 213(4):323-8. [Medline].
Bennett GL, Balthazar EJ. Ultrasound and CT evaluation of emergent gallbladder pathology. Radiol Clin North Am. 2003 Nov. 41(6):1203-16. [Medline].
van Dam PM, Posthouwer D. An 86-year-old man with acute abdominal pain. BMJ Case Rep. 2016 Feb 11. 2016:[Medline].
Watanabe Y, Nagayama M, Okumura A, et al. MR imaging of acute biliary disorders. Radiographics. 2007 Mar-Apr. 27(2):477-95. [Medline].
Koenig T, Tamm EP, Kawashima A. Magnetic resonance imaging findings in emphysematous cholecystitis. Clin Radiol. 2004 May. 59(5):455-8. [Medline].
Chiu HH, Chen CM, Mo LR. Emphysematous cholecystitis. Am J Surg. 2004 Sep. 188(3):325-6. [Medline].
Slot WB, Ooms HW, Van der Werf SD, et al. Percutaneous gallbladder drainage in emphysematous cholecystitis. Neth J Med. 1995 Feb. 46(2):86-9. [Medline].
Banwell PE, Hill AD, Menzies-Gow N, et al. Laparoscopic cholecystectomy: safe and feasible in emphysematous cholecystitis. Surg Laparosc Endosc. 1994 Jun. 4(3):189-91. [Medline].
Hazey JW, Brody FJ, Rosenblatt SM, et al. Laparoscopic management and clinical outcome of emphysematous cholecystitis. Surg Endosc. 2001 Oct. 15(10):1217-20. [Medline].
Chen MY, Lu C, Wang YF, Cai XJ. Emphysematous cholecystitis in a young male without predisposing factors: A case report. Medicine (Baltimore). 2016 Nov. 95 (44):e5367. [Medline].
Eldar S, Sabo E, Nash E, Abrahamson J, Matter I. Laparoscopic cholecystectomy for the various types of gallbladder inflammation: a prospective trial. Surg Laparosc Endosc. 1998 Jun. 8(3):200-7. [Medline].
Massarweh NN, Flum DR. Role of intraoperative cholangiography in avoiding bile duct injury. J Am Coll Surg. 2007 Apr. 204(4):656-64. [Medline].
Katagiri H, Yoshinaga Y, Kanda Y, Mizokami K. Emphysematous cholecystitis successfully treated by laparoscopic surgery. J Surg Case Rep. 2014 Apr 18. 2014(4):[Medline]. [Full Text].
Kamer E, Karaisli S, Cuneyit I, Peskersoy M. A pathology requiring urgent cholecystectomy : emphysematous cholecystitis. Acta Gastroenterol Belg. 2018 Jul-Sep. 81(3):449-50. [Medline].
Koole SN, Lohman BG, van Unen JM. Emphysematous cholecystitis due to Clostridium perfringens successfully treated by cholecystectomy. Acta Chir Belg. 2016 Feb. 116(1):54-7. [Medline].
Yagi Y, Sasaki S, Terada I, et al. Massive pneumoretroperitoneum arising from emphysematous cholecystitis: a case report and the literature review. BMC Gastroenterol. 2015 Sep 8. 15:114. [Medline]. [Full Text].
Alan A Bloom, MD Associate Clinical Professor of Medicine, Albert Einstein College of Medicine; Attending Physician, Department of Gastroenterology, Veterans Affairs Hospital, Bronx
Alan A Bloom, MD is a member of the following medical societies: American College of Physicians, American Gastroenterological Association, American Medical Association, American Society for Gastrointestinal Endoscopy, New York Academy of Medicine, New York Academy of Sciences
Disclosure: Nothing to disclose.
Prospere Remy, MD Assistant Professor of Medicine, Albert Einstein College of Medicine; Attending Physician, Department of Internal Medicine, Bronx-Lebanon Hospital Center
Prospere Remy, MD is a member of the following medical societies: American College of Physicians, American Society for Gastrointestinal Endoscopy
Disclosure: Nothing to disclose.
BS Anand, MD Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine
BS Anand, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy
Disclosure: Nothing to disclose.
BS Anand, MD Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine
BS Anand, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American Gastroenterological Association, and American Society for Gastrointestinal Endoscopy
Disclosure: Nothing to disclose.
Burt Cagir, MD, FACS Assistant Professor of Surgery, State University of New York Upstate Medical University; Consulting Staff, Director of Surgical Research, Robert Packer Hospital; Associate Program Director, Department of Surgery, Guthrie Clinic
Burt Cagir, MD, FACS is a member of the following medical societies: American College of Surgeons, American Medical Association, Association of Program Directors in Surgery, and Society for Surgery of the Alimentary Tract
Disclosure: Nothing to disclose.
Amber A Guth, MD, FACS
Disclosure: Nothing to disclose.
H Leon Pachter, MD, FACS Chair, George David Stewart Professor, Department of Surgery, New York University Medical Center
H Leon Pachter, MD, FACS is a member of the following medical societies: American Association for the Surgery of Trauma, American College of Surgeons, American Surgical Association, American Trauma Society, New York Academy of Sciences, Society for Surgery of the Alimentary Tract, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.
Manish Parikh, MD Assistant Professor of Surgery, Department of Surgery, New York University School of Medicine; Attending Surgeon, Director Laparoscopic and Bariatric Surgery, Bellevue Hospital
Manish Parikh, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Surgeons, and Society of American Gastrointestinal and Endoscopic Surgeons
Disclosure: Nothing to disclose.
Tushar Patel, MB, ChB Professor of Medicine, Ohio State University Medical Center
Tushar Patel, MB, ChB is a member of the following medical societies: American Association for the Study of Liver Diseases and American Gastroenterological Association
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Medscape Salary Employment
Emphysematous Cholecystitis
Research & References of Emphysematous Cholecystitis|A&C Accounting And Tax Services
Source
0 Comments