AUTHOR AND EDITOR INFORMATION

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• Radiograph
• CT SCAN
• Ultrasound
• Nuclear Medicine
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• Intervention
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• References

INTRODUCTION

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Background

Acute acalculous cholecystitis (AAC) represents inflammation of the gallbladder in the absence of demonstrated calculi. The disease process of AAC is distinct from that of the calculous variety, in which the primary initiating event is believed to be obstruction of the cystic duct. Acalculous cholecystitis typically occurs as a secondary event in patients who are hospitalized and are acutely ill with another disease.^{1, 2}

The diagnosis often is difficult and is often delayed because of comorbidities that decrease sensitivity and specificity of both clinical and imaging evaluation. A high degree of suspicion is required on the part of the physician. A much higher rate of complications is observed in patients with acalculous cholecystitis (eg, gangrene, perforation) because of the more fulminant course and coexistent disease. As a result, some authors propose the term necrotizing cholecystitis to reflect the fact that acalculous cholecystitis does not simply represent cholecystitis without stones.

Related eMedicine topics:
Acalculous Cholecystitis (from Gastroenterology)
Cholecystitis, Acute
Gallbladder Disease

Related Medscape topics:
Specialty Site Radiology
Specialty Site Gastroenterology
Resource Center Gallbladder and Biliary Disease
Resource Center Minimally Invasive Gastrointestinal Surgery
CME Transdermal Rather Than Oral Hormone Therapy May Help Avoid Cholecystectomy
CME New Guidelines Address Management of Common Bile Duct Stones

Pathophysiology

The pathophysiology of acalculous cholecystitis is multifactorial and is incompletely defined. At least 3 mechanisms appear to work in concert to produce the disease, including (1) systemic mediators of inflammation and trauma, (2) biliary stasis, and (3) generalized or localized ischemia. In turn, the mechanisms often result in functional or secondary mechanical obstruction of the cystic duct from inflammation and bile viscosity.

In some settings, extrinsic compression may contribute to the development of stasis. When it occurs, infection usually represents a secondary event and involves gram-negative enteric flora. In some patients, infection may be the primary event. Acute acalculous cholecystitis (AAC) has been described in association with infection by Salmonella (ie, typhoid fever), Staphylococcus, and Brucella species; in AIDS patients, cholecystitis has been described in association with infection by cytomegalovirus and Cryptosporidium organisms.^{3, 4, 5}

In animal models, acalculous cholecystitis has been shown to develop after administration of systemic mediators of inflammation. Small-vessel necrosis in the gallbladder serosa and muscularis has been demonstrated after activation of factor XII–dependent pathways, platelet activating factor, endotoxin, or interleukin 2. This frequently is associated with gallbladder atony, which in turn predisposes patients to biliary stasis.

Biliary stasis results in more viscous bile, an increase in the concentration of the detergent bile salts, and sludge formation, which increases the bile histotoxicity to the gallbladder mucosa. Fasting, use of parenteral nutrition, use of narcotic analgesics, and the postoperative state all predispose patients to biliary stasis and are commonly seen in patients with ACC.

Generalized or localized ischemia further predisposes patients to biliary stasis; it may result in gallbladder wall necrosis and perforation. Hypovolemic shock, cardiogenic shock, and septic shock predispose patients to ischemia and are contributing factors. At times, ischemia is the primary cause; it may occur in the setting of small-vessel vasculitis or following therapeutic particulate embolization.

Individuals presenting with ACC in the outpatient setting typically are older patients with microvascular disease and other comorbidities.

Frequency

United States

In 7-22% of cases of cholecystitis, calculi are absent. The variability is mostly a result of differences in patient populations; a higher incidence is seen in burn and trauma centers and in pediatric populations. As many as 90% of cases of postoperative acute cholecystitis are acalculous in origin. Although in the critical care setting, cholecystitis frequently is acalculous, the overall incidence in this setting is estimated to be only 0.2%. In such cases, a high index of suspicion is required to make the diagnosis.

Mortality/Morbidity

Complications are much more common in the acalculous variety of cholecystitis than in the calculous variety because of the variable pathophysiology, comorbid conditions, and the frequent delay in diagnosis and treatment. Perforation or gangrene occurs in 40-60% of patients. Gangrene may be either diffuse or focal and is frequently associated with perforation. Approximately 40% of cases of cholecystitis that are complicated by perforation are of the acalculous variety. In more than one half of cases of emphysematous cholecystitis, the disease is of the acalculous type; often, these cases are associated with gangrene.

The mortality rate varies widely in the literature from 9-66%; mortality is attributed to delay in diagnosis, more frequent complications, and concurrent disease processes.

Race

No racial predilection has been identified for acalculous cholecystitis.

Sex

In most reported series regarding acalculous cholecystitis, the male-to-female ratio is 2-3:1.

Age

The average age of patients with acalculous cholecystitis is greater than 50 years.

Clinical Details

Acute acalculous cholecystitis most commonly occurs in hospitalized patients who did not have gallbladder disease previously but who have severe concomitant medical and surgical conditions. Known populations at risk include postoperative patients (especially patients who have undergone abdominal surgery), patients with extensive burns, patients with trauma, and patients receiving prolonged parenteral nutrition. Other reported associations include prolonged fasting, use of high-dose opioid analgesics, and mechanical ventilation.

A small subset of patients present in the outpatient setting with symptoms that are easier to localize. Clinical and imaging evaluation are much more accurate in this setting. These patients are diagnosed earlier in the disease course and have a better prognosis.

In the pediatric population, acute cholecystitis is rare; approximately one half of cases occur in the absence of demonstrated calculi. These patients are more likely to present in the outpatient setting and most often are treated with cholecystectomy.

The most frequent physical and laboratory findings include fever, right upper quadrant (RUQ) pain, nausea, leukocytosis, and elevation of liver-associated enzymes and bilirubin. All of these clinical parameters are nonspecific. In almost all instances in which it can be evaluated, abdominal pain is present; however, it is often not localized to the RUQ. Fever is present in two thirds of patients, and leukocytosis and liver function abnormalities are present in approximately 80%.

Preferred Examination

Early imaging evaluation is required for patients with acalculous cholecystitis, and frequently, multiple diagnostic tests are performed. No single imaging study is ideal. The 3 primary imaging modalities often are complementary, with ultrasound (US) or CT providing anatomic information and evaluation of adjacent structures and cholescintigraphy providing functional information.^{6, 7}

US and cholescintigraphy should be the initial imaging tests performed to evaluate possible acute acalculous cholecystitis (AAC).

CT is preferred if other diseases in the differential diagnosis are more likely or if CT needs to be performed for another indication.

Limitations of Techniques

All available modalities have a significant false-positive and false-negative rate and generally are better at excluding, rather than confirming, the presence of acalculous cholecystitis.

Although it is unusual for acalculous cholecystitis to occur in patients with a normal gallbladder, on both US and cholescintigraphy examinations, the gallbladder may be found to be normal early in the course of the disease. For patients who continue to experience clinical deterioration and for whom clinical evaluation is not possible or fails to demonstrate an alternative source, many authors recommend maintaining a low threshold for instituting empiric, minimally invasive therapy in the form of percutaneous cholecystostomy.

DIFFERENTIALS

Section 3 of 11  

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Other Problems To Be Considered

The differential diagnosis for patients suspected of having acalculous cholecystitis is broad because comorbid conditions typically are present, the ability to evaluate the patient's symptoms is reduced, and the most common clinical and laboratory manifestations of acalculous cholecystitis are nonspecific. Almost any infectious or inflammatory process may result in nonspecific findings. In patients with more localized symptoms, the primary diseases in the differential diagnosis are calculous cholecystitis, ascending cholangitis, acute hepatitis, and pancreatitis.

RADIOGRAPH

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Findings

Plain film radiography is of limited use in the diagnosis of acute acalculous cholecystitis. Emphysematous cholecystitis may occur as a complication of acute cholecystitis; more than one half of such cases occur in the setting of acalculous disease. This form of complicated cholecystitis typically is seen in older male patients with diabetes. On upright abdominal radiographs, acute acalculous cholecystitis (AAC) may be evinced by the presence of an air-fluid level in the right upper quadrant; such a finding represents gas in the gallbladder lumen. The presence of intramural gas is indicated by findings of a curvilinear gas collection that conforms to the gallbladder wall. Gas is visualized only in more severe cases on plain film. US and CT are much more useful. The presence of gas is often associated with gangrene and perforation (see Images 1, 9, 14).

CT SCAN

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• CT SCAN
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Findings

CT often is performed as the diagnostic examination of choice in patients presenting with abdominal pain in the critical care setting or in patients with fever or leukocytosis of undefined etiology. CT offers the advantage of evaluating the entire chest and abdomen; it has the disadvantage of requiring transport to the scanner. One should be familiar with the CT signs that suggest acalculous cholecystitis in the appropriate clinical setting (see Images 2, 3, 10).

The diagnosis of acute acalculous cholecystitis (AAC) with CT requires that 2 major diagnostic criteria be met or, alternatively, that 1 major criterion and 2 minor criteria be met. These criteria are as follows:

• Major criteria
  • Gallbladder wall thickening greater than 3 mm
  • Subserosal halo (ie, gallbladder wall edema)
  • Pericholecystic fatty inflammation
  • Pericholecystic fluid (without ascites or hypoalbuminemia)
  • Mucosal sloughing
  • Intramural gas
• Minor criteria
  • Gallbladder distention (>5 cm transverse)
  • High-attenuation bile (sludge)

The normal gallbladder wall is barely perceptible as a thin enhancing rim on contrast-enhanced CT. In the absence of gallstones, imaging relies on ancillary findings of cholecystitis.

CT findings for patients with AAC are as follows:

• Gallbladder wall thickening
• Mucosal irregularity
• Luminal distention
• Increased bile density (biliary sludge)
• Intramural or intraluminal gas
• Intraluminal hemorrhage
• Localized pericholecystic fluid collections
• Inflammatory infiltration of pericholecystic fat
• Indistinctness of the liver-gallbladder interface

Degree of Confidence

Although mucosal sloughing and intramural gas are specific findings, they are observed infrequently. Isolated local pericholecystic fluid collections and pericholecystic inflammatory changes are relatively specific and suggest advanced disease, but they lose specificity in the setting of ascites, recent abdominal surgery, or anasarca.

Reported sensitivity and specificity vary but generally have been greater than 90-95%. As with other imaging modalities, the specificity of many of these findings is decreased in the typical populations at risk for acalculous cholecystitis because of comorbid conditions, such as recent surgery or trauma, multisystemic organ failure, ascites, or hypoalbuminemia.

ULTRASOUND

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Findings

Usually, sonography is the first examination performed in cases of possible acalculous cholecystitis. US has the advantages of being readily available, portable to the bedside, and able to identify other adjacent pathologies. Primary disadvantages of US include the high incidence of nonspecific abnormal examinations and the inability to survey the entire abdomen (see Images 6-8, 11-12).^{8, 9, 10}

The normal gallbladder has sonolucent bile and a thin wall; no localized pain is present. Sonographic signs compatible with acalculous cholecystitis include the following:

• Gallbladder wall thickening
• Sonographically localized tenderness over the gallbladder
• Subserosal edema
• Pericholecystic fluid
• Gallbladder distension
• Biliary sludge
• The presence of gas

Failure of the gallbladder to contract after the infusion of cholecystokinin has been reported as an additional criterion, but the response often is too variable to be of use in these patients.

The diagnosis of acute acalculous cholecystitis (AAC) with US requires that 2 major diagnostic criteria be met or, alternatively, that 1 major criterion and 2 minor criteria be met. These criteria are as follows:

• Major criteria
  • Gallbladder wall thickening greater than 3 mm
  • Striated gallbladder (ie, gallbladder wall edema)
  • Sonographic Murphy sign (ie, localized gallbladder tenderness)
  • Pericholecystic fluid (without ascites or hypoalbuminemia)
  • Mucosal sloughing
  • Intramural gas
• Minor criteria
  • Gallbladder distention (>5 cm transverse)
  • Echogenic bile (sludge)

Gallbladder wall thickness should be measured in the transverse plane, provided the gallbladder has not collapsed. The presence of ascites or decreased oncotic pressure (as occurs in patients with hypoalbuminemia) confuses the finding, unless the finding is markedly discordant. Similarly, the presence of pericholecystic fluid is not meaningful in the presence of generalized ascites; however, the occurrence of pericholecystic fluid as a localized finding often signifies advanced disease or perforation. The sonographic Murphy sign is the most specific sonographic finding, but often it cannot be evaluated because of the patient's clinical condition.

Following diagnostic needle aspiration of the gallbladder, results of bile Gram stain and culture are often normal; the sensitivity is less than 50%, and the results of culture are delayed. Therefore, the test is of limited value for the diagnosis of AAC. Culture is performed routinely at the time of therapeutic cholecystostomy and may guide antibiotic selection.

Degree of Confidence

The reported sensitivity and specificity of sonography in the evaluation of acalculous cholecystitis vary from 23-95% and 40-95%, respectively; this degree of variance occurs because of differences in patient populations, clinical courses, and imaging technologies employed over time. The sensitivity and specificity are greater than 90% in the subset of patients with acalculous cholecystitis who present in the outpatient setting.

Overall, the sensitivity and specificity approach 70%. As the proportion of patients in the critical care environment increases, the diagnostic accuracy decreases. Several studies have documented a high incidence of abnormal gallbladder sonograms in the ICU environment in asymptomatic patients who were not suspected of having acalculous cholecystitis.

At least 1 abnormal finding was seen in 50-85% of patients in this setting; 3 abnormal findings were seen in as many as 57% of patients. None of these patients had localized gallbladder tenderness by sonography. Serial sonography has been of benefit in some studies; the fact that the appearance on short-term follow-up images progressively worsens increases the specificity for diagnosis.

NUCLEAR MEDICINE

Section 7 of 11  

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Findings

Hepatobiliary scintigraphy (HBS) is a physiologic test that evaluates hepatic bile formation, excretion, and ductal functional patency.

Imaging typically is performed with dynamic image acquisition for up to 4 hours following the intravenous (IV) administration of 5 mCi of a technetium-99m-labeled iminodiacetic acid derivative. Peak liver uptake is at 5-10 minutes, with subsequent gallbladder visualization by 20 minutes and duodenal visualization by 30 minutes (see Images 4-5).

If nonvisualization or questionable visualization of the gallbladder occurs but adequate hepatic uptake and excretion into the bowel are seen, IV morphine sulfate (0.04 mg/kg) may be administered at 30-40 minutes, with imaging carried out for up to 1 hour. This raises intrabiliary pressure by inducing contraction of the sphincter of Oddi and filling of the gallbladder, provided the cystic duct remains patent. A lateral view may be helpful if a question remains concerning gallbladder filling; the gallbladder is located anteriorly in this projection.

Some have attempted to improve accuracy by pretreating the patient with cholecystokinin infusion before performing HBS, so as to empty the distended gallbladder. HBS may be nondiagnostic in patients with liver failure and intrahepatic cholestasis of any cause because of the inability to conjugate and excrete the radiotracer.

Additional useful findings on cholescintigraphy include the presence of an area of increased pericholecystic radiotracer accumulation in the gallbladder fossa. This rim sign is associated with complications such as gangrene. Radiotracer extravasation rarely may be visualized in the setting of perforated gangrenous cholecystitis if the cystic duct remains patent.

Degree of Confidence

Hepatobiliary scintigraphy (HBS) is accurate in the diagnosis of calculous cholecystitis because the primary event is believed to be cystic duct obstruction. In cases of acalculous cholecystitis, functional obstruction usually occurs in the disease process but is variable and is not the primary process. Not surprisingly, the sensitivity and specificity of HBS are decreased in this setting.

In general, diagnostic quality studies with augmentation yield a sensitivity of 80-90% and a specificity of 90-100%.

False Positives/Negatives

The false-positive rate without pharmacologic augmentation is as high as 40% in some series, decreasing the specificity of the test. With morphine augmentation, the false-positive rate is decreased and the specificity is improved.

False-negative results (gallbladder filling in presence of acalculous cholecystitis) also may occur. Early filling of the gallbladder (within the first 30 min) excludes the diagnosis of acalculous cholecystitis, but with delayed filling after augmentation, the false-negative rate may be as high as 20%.

ANGIOGRAPHY

Section 8 of 11  

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Findings

No role exists for angiography in the diagnosis of acalculous cholecystitis.

INTERVENTION

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Once the diagnosis of acute acalculous cholecystitis is made, the gallbladder should be removed or drained.

Therapeutic options for acalculous cholecystitis include open cholecystectomy, laparoscopic cholecystectomy, surgical cholecystostomy, percutaneous cholecystostomy or aspiration, and endoscopic transcystic drainage.^{11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21}

Surgical cholecystectomy

Surgical cholecystectomy remains the definitive treatment. For patients presenting in the outpatient setting or those with minimal comorbidity, it is the procedure of choice. Unfortunately, for most patients with ACC, the disease is discovered while the patient is in the critical care setting or is recovering from major surgery or trauma; in these patients, the risk of operative mortality is high. Such patients are often best managed with less invasive treatments.

Percutaneous cholecystostomy

If performed before the occurrence of complications, such as frank necrosis or perforation, percutaneous cholecystostomy may be life-saving, definitive therapy. Initial imaging findings consistent with complicated cholecystitis or progression of signs and symptoms after PCC should still prompt cholecystectomy.

• PCC procedure
• • PCC is an image-guided procedure performed under local anesthesia at the bedside or in the interventional suite. US is used to guide placement of a drainage catheter into the gallbladder. CT is occasionally used if no suitable ultrasonographic window is found. Drainage may be accomplished by use of a single-step trocar drainage technique or needle access followed by serial dilation and catheter placement over a guidewire. A 6-10F locking pigtail drainage catheter with large side holes is used. Although somewhat controversial, a transhepatic tract is typically favored. This has been shown to decrease the risk of catheter dislodgement and to minimize the potential for bile leakage.
  • After catheter placement, the gallbladder is drained and left to external drainage with daily monitoring of outputs. In the presence of viscous bile, regular flushing with 5 mL of sterile saline helps maintain catheter patency. Catheter output may be minimal until the patient improves, with decreased biliary stasis and restoration of functional cystic duct patency.
• Indications
• • PCC is indicated when imaging and clinical findings suggest acalculous cholecystitis as the diagnosis. In some instances, imaging results are inconclusive or discordant, and clinical evaluation is nonspecific. In the absence of other treatable etiologies, a reasonable approach is to proceed with PCC on an empiric basis to see if the patient improves. In this setting, PCC is as much a diagnostic test as a treatment. In most cases in which patients show a response, definitive clinical improvement is seen within 72 hours after drainage.
• Contraindications and complications
• • Contraindications to PCC include uncorrectable coagulopathy and massive ascites that cannot be drained adequately. Complications of PCC include bleeding, bile peritonitis, vagal reactions, catheter dislodgment, and damage to adjacent structures. The procedural complication rate is 5-10%.
  • Technical success is achieved in 95-100% of patients; clinical response is achieved in 70-85%. The 30-day mortality rate remains high at 10-30% but almost always results from underlying conditions. Many series reporting on PCC include both patients with calculous disease and those with acalculous disease who are not suitable candidates for surgery.
• Follow-up care
• • Follow-up cholecystogram is performed if there is a question of catheter function, if the patient fails to respond, or if catheter removal is under consideration.
  • Minimum criteria and considerations for removing PCC tubes are as follows:
  • • Three weeks of drainage time
    • Patent cystic duct and common bile duct
    • Initial primary risk factors corrected
    • Signs and symptoms of AAC resolved
    • No or minimal ascites
• Tract maturation
• • After 3 weeks, almost all PCC tracts are mature and will not result in significant peritoneal leakage. PCC tract maturation depends on the catheter material, catheter dwelling time, the nutritional status of the patient, and the presence of steroids. If risk factors for delayed maturation are present or if early tube removal is considered, a tractogram (sinogram) may be performed easily over a guidewire at the time of the cholecystogram (see Image 13).
  • A tractogram is performed by removing the drainage catheter over a guidewire and placing a short sheath of equivalent size into the gallbladder. While slowly withdrawing the sheath over the wire through the tract, dilute contrast is injected to allow evaluation of the integrity of the tract. If extensive peritoneal leakage is identified, a new drain may be placed over the guidewire. It is best to have the initial underlying risk factors, such as parenteral nutrition and sepsis, corrected to minimize the risk of the recurrence of cholecystitis.

• Needle aspiration
• • Therapeutic needle aspiration of the gallbladder with an 18-gauge transhepatic needle has been reported to be successful in the treatment of acute cholecystitis in high-risk surgical patients. A study by Chopra et al found simple aspiration to be effective in 77% of patients with AAC; by contrast, PCC was effective in 90% of patients.²²
  • PCC was used as a salvage procedure in patients who failed to respond clinically within 72 hours after aspiration alone; the results were equally good, and the overall complication rate was lower. This study excluded ICU patients with acalculous cholecystitis, for whom the diagnosis is more difficult and the therapeutic outcome less favorable and more difficult to assess. The findings suggest that needle aspiration is a reasonable first step in high-risk patients with AAC outside of the critical care environment.

Transpapillary endoscopic cholecystostomy

In patients in whom percutaneous drainage cannot be performed safely, transpapillary endoscopic cholecystostomy is another option. In this technique, the cystic duct is selected during endoscopic retrograde cholangiopancreatography (ERCP), and either a double pigtail biliary stent or a nasobiliary catheter is placed into the gallbladder. Technical success has been achieved in up to 90% of patients, although many of the reported series have involved less critically ill patients or those with more chronic symptoms. Potential advantages include a decrease in the risk of bleeding, of bile peritonitis, and of injury to adjacent organs. Disadvantages are the need for sedative medications, the risks associated with aspiration, an increase in the risk of pancreatitis, and associated risks related to ERCP.

Medical/Legal Pitfalls

• Failure to maintain a high index of clinical suspicion (a high index of suspicion facilitates early diagnosis and early initiation of therapy and optimizes outcome).

Special Concerns

Right upper quadrant pain.
American College of Radiology.  1996 (revised 2005).  5 pages.  NGC:004781
 
Treatment of gallstone and gallbladder disease.
Society for Surgery of the Alimentary Tract, Inc.  1996 (revised 2003 Feb 1).  4 pages.  NGC:003756

MULTIMEDIA

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• Nuclear Medicine
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• Intervention
• Multimedia
• References

Media file 1:  Abdominal radiograph of acalculous emphysematous cholecystitis demonstrating curvilinear air pattern conforming to the shape of the gallbladder wall.
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Media file 2:  CT images of emphysematous cholecystitis (same patient as Image 1).
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Media type:  CT

Media file 3:  CT cine loop of acalculous cholecystitis demonstrates irregular gallbladder wall, pericholecystic inflammation, and perihepatitis in gallbladder fossa. Necrotic gallbladder was present at surgery.
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Media type:  CT

Media file 4:  Normal hepato-iminodiacetic acid scan. Prompt hepatic concentration of radiopharmaceutical is noted, along with early visualization of the gallbladder and drainage into the duodenum.
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Media type:  Movie

Media file 5:  Hepato-iminodiacetic acid scan of acalculous cholecystitis. Prompt uptake of radiopharmaceutical is noted in the liver, along with drainage into the bowel without gallbladder visualization by 90 minutes.
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Media file 6:  Ultrasound of ICU patient with fever of unclear etiology. Ultrasound findings of acalculous cholecystitis include marked gallbladder wall thickening and pericholecystic fluid. Localized tenderness could not be evaluated.
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Media type:  Image

Media file 7:  Transverse ultrasound demonstrates marked gallbladder wall thickening and pericholecystic fluid collection in a patient with AIDS who was managed conservatively. No localized tenderness was noted, and hepato-iminodiacetic acid scan demonstrated delayed filling but otherwise was normal. Patient recovered with treatment of underlying pneumonia, and ultrasound findings normalized within 2 weeks.
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Media type:  Image

Media file 8:  A 53-year-old man status post–endoscopic stenting for pancreatic cancer with progressive fever, leukocytosis, and right upper quadrant pain. Ultrasound demonstrates gallbladder distention, biliary sludge, borderline wall thickness, and localized tenderness consistent with acalculous cholecystitis.
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Media type:  Image

Media file 9:  Images from percutaneous transhepatic cholecystostomy tube placement using coaxial technique demonstrating transhepatic needle access, irregular gallbladder wall, and occluded cystic duct (same patient as Image 8). Note the safety wire adjacent to the definitive 6F drainage catheter.
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Media file 10:  Despite drainage, the patient (same patient as Images 8 and 9) continued to experience right upper quadrant pain and leukocytosis. Ultrasound and CT studies demonstrate transhepatic cholecystomy catheter in good position, but interval development of markedly worsening gallbladder wall edema and pericholecystic inflammatory changes have occurred. At surgery, gangrenous gallbladder was found and resected successfully.
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Media type:  CT

Media file 11:  Ultrasound images from percutaneous cholecystomy using the trocar technique. Ultrasound guides transhepatic access to the gallbladder with a 6F trocar drainage catheter. After access, the catheter is fed forward to reform the distal pigtail within the gallbladder lumen and is locked in this configuration.
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Media file 12:  Cine image of pigtail catheter moving freely within the gallbladder, which confirms adequate placement, along with free return of bile from the catheter.
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Media file 13:  Cine loop percutaneous cholecystostomy tractogram demonstrates immature tract 3 weeks after percutaneous cholecystostomy. Free spillage of contrast into the peritoneal space is noted. Drainage was continued for an additional 2 weeks prior to catheter removal.
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Media file 14:  Cholecystogram 4 weeks status post–cholecystomy tube placement for acalculous cholecystitis demonstrating a patent cystic and common duct and the absence of calculi. All clinical signs and symptoms had resolved.
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Media type:  X-RAY

REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

1. Kalliafas S, Ziegler DW, Flancbaum L, Choban PS. Acute acalculous cholecystitis: incidence, risk factors, diagnosis, and outcome. Am Surg. May 1998;64(5):471-5. [Medline].
2. Shridhar Ganpathi I, Diddapur RK, Eugene H, Karim M. Acute acalculous cholecystitis: challenging the myths. HPB (Oxford). 2007;9(2):131-4. [Medline].
3. Katsinelos P, Pilpilidis I, Papaziogas B, Chatzimavroudis G, Paroutoglou G, Mimidis K, et al. Fatal acute acalculous cholecystitis as an early complication after radiation therapy.. Chirurgia (Bucur). Mar-Apr 2008;103(2):223-6. [Medline].
4. Iaria C, Arena L, Di Maio G, Fracassi MG, Leonardi MS, Famulari C, et al. Acute acalculous cholecystitis during the course of primary Epstein-Barr virus infection: a new case and a review of the literature. Int J Infect Dis. Jul 2008;12(4):391-5. [Medline].
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Article Last Updated: Oct 16, 2008