Acalculous cholecystitis accounts for 10% of cases of all cases of acute cholecystitis.

In comparison to ordinary acute cholecystitis, acalculous cholecystitis has a higher likelihood of gangrene and perforation and as well as significantly higher morbidity and mortality rate.

It is more common in the elderly and in male patients.

Patients are usually severely debilitated, due to severe trauma, sepsis, shock, burns or other disease conditions.

Acalculous cholecystitis may complicate hypotension in trauma, surgery, child birth, burns, septicemia or hyperalimentation and in AIDS or bone marrow transplantation or in association with diabetes mellitus. 

The trauma, burns or surgery usually precede the on-set of cholecystitis by two weeks. 

The histology is like that of acute cholecystitis.

Visit: Acute cholecystitis ; Emphysematous cholecystitis.

Acute acalculous cholecystitis as the initial presentation of primary Epstein-Barr virus infection.J Pediatr Surg. 2007 Jan;42(1):E11-3.

The case of a 13-year-old girl with primary Epstein-Barr virus (EBV) infection and concomitant cholestatic hepatitis, which initially presented as acute acalculous cholecystitis (AAC), is described. The diagnosis of AAC was documented by clinical and ultrasonographic criteria, whereas acute EBV infection was confirmed serologically. AAC may develop during the course of acute EBV infection, especially in patients with cholestatic hepatitis.

Cellular turnover and expression of hypoxic-inducible factor in acute acalculous and calculous cholecystitis.Crit Care. 2007 Oct 31;11(5):R116.

ABSTRACT: BACKGROUND: Epithelial corrective and destructive mechanisms have not been studied in inflammatory gallbladder disease. METHODS: Epithelial apoptosis, cell proliferation, and expression of hypoxic-inducible factor (HIF-1 alpha) were compared in acute acalculous cholecystitis (AAC) (n=30), acute calculous cholecystitis (ACC) (n=21) and normal gallbladders (n=9) removed in open cholecystectomy. The immunohistochemical stainings included antibodies to Ki-67 (proliferation), M30 (apoptosis) and HIF-1 alpha. Proliferation and apoptosis were expressed as percentages of positive cells. HIF-1 alpha expression was expressed as absent, weak or strong. RESULTS: Apoptosis (median, 25th, 75th percentiles) was significantly increased in AAC, 1.31 % (0.75 %, 1.8 %), P<0.001, and ACC, 1.10% (0.63 %, 1.64 %), P=0.001, compared to controls, 0.20 % (0.07 %, 0.45 %). Proliferation rate was significantly increased in AAC, 8.0 % (4.0 %, 17.0 %), P< 0.001, and ACC, 14 % (7.5 %, 26.5 %), P=0.001, compared to controls, 1.0 % (1.0 %, 3.0 %). Strong HIF-1 alpha staining was observed in 57 % of AAC, in 100 % of ACC and in 44 % of control specimens (P<0.001). Intense HIF-1 alpha expression was associated with increased cell proliferation (P=0.002). CONCLUSIONS: Cell proliferation and apoptosis were increased in AAC and ACC, compared to normal gallbladders. The expression of hypoxic-inducible factor was lower in AAC than in ACC.

Tight junction proteins in gallbladder epithelium: different expression in acute acalculous and calculous cholecystitis.J Histochem Cytochem. 2007 Jun;55(6):567-73. Epub 2007 Feb 5.

There is a paucity of information of tight junction (TJ) proteins in gallbladder epithelium, and disturbances in the structure of these proteins may play a role in the pathogenesis of acute acalculous cholecystitis (AAC) and acute calculous cholecystitis (ACC). Using immunohistochemistry, we investigated the expression of TJ proteins claudin-1, -2, -3, and -4, occludin, zonula occludens (ZO-1), and E-cadherin in 9 normal gallbladders, 30 gallbladders with AAC, and 21 gallbladders with ACC. The number of positive epithelial and endothelial cells and the intensity of the immunoreaction were determined. Membrane-bound and cytoplasmic immunoreactivities were separately assessed. We found that TJ proteins were uniformly expressed in normal gallbladder epithelium, with the exception of claudin-2, which was present in less than half of the cells. In AAC, expression of cytoplasmic occludin and claudin-1 were decreased, as compared with normal gallbladder. In ACC, expression of claudin-2 was increased, and expression of claudin-1, -3, and -4, occludin, and ZO-1 were decreased, as compared with normal gallbladder or AAC. We conclude that there are significant differences in expression of TJ proteins in AAC and ACC, supporting the idea that AAC represents a manifestation of systemic inflammatory disease, whereas ACC is a local inflammatory and often infectious disease.

Acute acalculous cholecystitis in a child returning from the Ivory Coast. Pediatr Emerg Care. 2007 Apr;23(4):242-3

Acute cholecystitis is an uncommon occurrence in children. Acute acalculous cholecystitis (AAC) has various etiology; among them are a wide variety of infectious agents. We report the case of a 7-year-old child who presented AAC due to plasmodium falciparum infection. The causes of AAC are discussed.

Acute acalculous cholecystitis: pathophysiology and treatment.Ann Ital Chir. 2006 Jul-Aug;77(4):309-11.

The absence of reliable correlation between clinical features and pathological evolution and the molteplicity of risk factors, often related to various pathophysiological pathways, make of acute acalculous cholecystitis a clinical entity well distinct from other affecting gallbladder. In spite of the slight incidence, its occurrence among serious multiple trauma patients may reach 90%. The arguability of diagnostic criteria and the missed or delayed recognition, then affecting timing of surgery are important in determining morbidity and mortality of this condition. The Authors reviewed 16 patients operated for acute acalcolous cholecystitis. US, although sometimes underestimate the severity of affection and cause false negatives, had been the first choice investigation because of its rapidity, facility of execution and repeatability. TC adds subsequent information when US images were doubtful and reveleated pericholecystic involvement more carefully. Hepatobiliary scintigraphy has high diagnostic accuracy but needs of too long execution time. Reasons of early cholecystectomy lay on clinical and experimental evidences that focal or diffuse ischemic damage of gallbladder's wall may affect natural history of the illness and infectious overwhelming is a late event. Surgical intervention has been performed in 16 patients, must within 24 hours. Morbility has been very low, mortality scored 18.7%.

Acute acalculous cholecystitis in a child with systemic lupus erythematosus. Pediatr Nephrol. 2006 Jun;21(6):873-6.

A 10-year-old boy with systemic lupus erythematosus (SLE) developed abrupt right upper quadrant pain and vomiting during the course of his active disease. Antiphospholipid antibody was negative and the C3 level was low. Abdominal sonography showed cholecystitis with sludge balls in the gallbladder. He was treated by high-dose prednisolone with ceftriaxone and metronidazole IV for 3 days but due to poor response, cholecystectomy was performed and no stone was identified. Histopathologic examination showed vasculitis in the medium-sized arteries of the gallbladder wall. He was doing well at the 9-month follow-up after the operation. This report describes the first pediatric case of SLE with acalculous cholecystitis caused by vasculitis of the gallbladder.

Acute acalculous cholecystitis following open heart surgery.Am Surg. 1993 Feb;59(2):74-7.

We undertook a retrospective study designed to ascertain the frequency of acute acalculous cholecystitis (AAC) following open heart surgery. In the study period 1982-1990, 22 of 6393 patients following open heart surgery were recognized to have developed AAC, an incidence of 0.34%. The majority of patients (16/22) presented within the first postoperative week. Vague right upper quadrant physical findings, nonspecific changes in the liver function chemistries and unexplained sepsis frequently led to radiologic evaluations. Ultrasonography was the most valuable radiologic study, with a diagnosis sensitivity of 82%. Technetium cholescintography can serve as a useful adjunct when interpreted in the context of other clinical findings. Cholecystectomy was performed in 20 patients and cholecystostomy in two. Nine (41%) patients had gangrenous gallbladders with frank perforation in two. A specific preoperative diagnosis was made in 19 patients (86%). Fifteen patients survived for a mortality rate of 32%. In 12 of 15 survivors (80%), the diagnosis of AAC was established and laparotomy performed within 48 hours of first clinical suspicion. Gangrene and perforation were seen in 87% of patients in whom surgery was delayed. AAC is a life-threatening condition especially in critically ill patients. Experience suggests that early diagnosis and operative intervention are the key elements of treatment. Delay of operative management on the grounds of recent cardiac surgery is not justified.

Acute acalculous cholecystitis.Zhonghua Yi Xue Za Zhi (Taipei). 1993 Apr;51(4):266-70.

To demonstrate the importance of early detection and diagnosis of acute acalculous cholecystitis, 34 patients with this disease, were studied retrospectively. Twenty patients had a delay between the onset of symptoms and operative intervention, exceeding 48 hours; five of them were found to have a perforated gallbladder during operation; however, no such complication was encountered in the 14 patients who underwent surgical treatment within 48 hours of onset. Sixteen patients had post-operative complications, and four patients who died produced in a mortality rate 11% (4/34). Three mortality cases had coexisting cardiovascular disease and the operation was also delayed for more than 48 hours.

Familial acalculous gallbladder disease.South Med J. 1993 Feb;86(2):183-6.

Four patients, all sisters, presented a long-standing history of pain in the gallbladder region and no calculi. All were first thoroughly investigated and then relieved of their symptoms by cholecystectomy. This prompted an investigation of their family over three generations, which revealed a surprisingly large number of relatives, mostly female, with acalculous gallbladder disease. Our review of various syndromes causing pain in the gallbladder region, including biliary dyskinesia, cystic duct syndrome, and chronic acalculous cholecystitis, makes a case for the existence of familial incidence of noncalculous and calculous gallbladder disease, possibly related to the disturbance of the autonomic nervous system affecting emptying of the gallbladder.

Acalculous cholecystitis in bone marrow transplant patients.Cancer. 1993 Jan 15;71(2):354-8.

BACKGROUND. Acalculous cholecystitis (ACC) is an uncommon disorder of the biliary tract, accounting for approximately 6% of acute cholecystitis cases. In this study, cholecystitis was seen in 8 of 770 bone marrow transplant recipients, with ACC occurring in five (63%). METHODS. Records of 592 allogenic and 150 autologous BMT patients were reviewed for risk factors associated with ACC. RESULTS. Only the number of blood transfusions administered and the use of total parenteral nutrition were associated with ACC development. ACC occurred in 4 of 42 (9%) allogeneic recipients who required exchange transfusion for ABO incompatibility. ACC developed in one autogolous recipient alongside venoocclusive disease of the liver. There was no association between ACC development and preparative regimen, cyclosporine usage, graft versus host disease, or cytomegalovirus infection. CONCLUSIONS. ACC occurs more frequently in patients after ABO incompatible BMT requiring exchange transfusion than in other transplant recipients.

A case of acute hemorrhagic gangrenous acalculous cholecystitis with bile peritonitis during anti-coagulant therapy after coronary-artery bypass grafting.Nippon Kyobu Geka Gakkai Zasshi. 1993 Jan;41(1):83-7.

Acute acalculous cholecystitis is a relatively rare complication occurring after surgery on organs other than the bile duct system. It is often misinterpreted to be a post-operative symptom, and can progress into a very serious condition with high risk of mortality if gangrene and perforation develop. Its occurrence after open heart surgery is relatively rare. We experienced a case of acute hemorrhagic, gangrenous acalculous cholecystitis that developed after coronary-artery bypass grafting. The patient, a 78-year-old man, complained post-operatively of a right upper abdominal pain. The diagnosis of acute gangrenous acalculous cholecystitis was established on the basis of abdominal sonography and CT, and emergency operation performed was successful. Etiological factors in this case may have included post-operative stasis of bile, swelling of the gallbladder, hypotension during cardiopulmonary bypass, and post-operative anti-coagulant therapy administered after open heart surgery. These factors induced intracystic hemorrhage followed by sudden exacerbation, which resulted in gangrenous cholecystitis followed by perforative biliary peritonitis.

Hepatobiliary manifestations in AIDS in adults. Place of cholecystectomy. Presse Med. 1992 Nov 28;21(40):1901-4.

In AIDS patients an acalculous cholecystitis may be responsible for abdominal pain subsiding after cholecystectomy. But the indications for cholecystectomy are not clear: cholecystitis is usually associated with diffuse cholangitis and this might cause the symptoms. Since 1985, 8 AIDS patients have undergone cholecystectomy for acute cholecystitis. Ultrasonography revealed a 5 to 12 mm thickening of the gallbladder wall in all of them and gallbladder stones in two; four patients had cholangitis. The decision to operate was based on persistent pain associated with fever, poor general condition and muscular rigidity at palpation. Four patients had septic shock at the time of surgery; one died in the immediate postoperative period. In all other patients pain and septic syndrome subsided. Two patients died of AIDS complications 20 days after surgery; the remaining five died of AIDS 6, 9, 10, 12 and 14 months respectively after surgery; in two of them cholestasis had reappeared due to cholangitis. To summarize, in the 8 AIDS patients studied cholecystectomy was performed for clinical deterioration. Gallbladder pathology was responsible for the abdominal pain and the febrile general condition which was relieved by cholecystectomy.

Diagnosis of gallbladder perforation in acute acalculous cholecystitis in critically ill patients.Intensive Care Med. 1992;18(4):245-6.

In the presence of ascites ultrasound is not appropriate to distinguish between gallbladder perforation and acute acalculous cholecystitis. However, the correct and early diagnosis of gallbladder perforation is important for the treatment and prognosis. We report 4 critically ill patients with ascites. All patients had evidence of gallbladder perforation by ultrasound and underwent cholecystectomy: 2 patients had gallbladder perforation, but 2 had acalculous cholecystitis without perforation. Markedly elevated serum alkaline phosphatase was the only discriminating finding indicating gallbladder perforation.

Acute acalculous cholecystitis caused by Salmonella typhi in a 6-year-old child.Eur J Pediatr Surg. 1992 Oct;2(5):301-3.

A rare case of acute acalculous cholecystitis caused by Salmonella typhi in a 6-year-old child is presented. The clinical signs were fulminant, with diffuse peritonitis being suspected. Cholecystostomy and i.v. ceftriaxone proved efficacious and the girl was discharged in less than two weeks. The appropriate literature is reviewed.

Acute acalculous cholecystitis. A review.J Clin Gastroenterol. 1992 Oct;15(3):238-41.

Acute acalculous cholecystitis is an uncommon but very serious illness, that, if undiagnosed, may lead to gallbladder perforation and death. The condition has numerous causes that result in bile stasis and ischemia leading to inflammation and infection in the gallbladder wall. The bedside diagnosis may be difficult, especially in critically ill patients. Current imaging techniques including ultrasonography, computer tomography, and radionuclide cholescintigraphy are very helpful. Depending on the clinical situation, the gallbladder should either be drained by a surgical or percutaneous cholecystostomy under local anesthesia or removed.

Acute acalculous cholecystitis as a postoperative complication-- the stress gallbladder.Rozhl Chir. 1991 Nov;70(10-11):495-7.

Acute acalculous cholecystitis (AACH) is a relatively rare disease in relation to postoperative complications. The majority of AACH are cured by conservative treatment along with the basic disease but if there are further complications relaparotomy and an adequate operation is necessary, as in the presented case.

Ischemia is one mechanism implicated in the pathogenesis of acute acalculous cholecystitis. Gallbladder specimen arteriography was performed to define the comparative status of cystic artery runoff in the macroscopically normal gallbladder (n = 10), in acute gallstone-associated cholecystitis (n = 10), and in acute acalculous cholecystitis (n = 7). Standardized film exposure and quantity of contrast medium administered permitted objective intergroup comparison. Compared to the macroscopically normal gallbladder, specimens of acute gallstone-associated cholecystitis exhibited arterial dilatation and extensive venous filling. In contrast, multiple arterial occlusions, with absent or minimal venous filling, were consistent features of acute acalculous cholecystitis; the degree of arteriographic abnormality for acute acalculous cholecystitis corresponded to the severity of gallbladder pathologic findings. Small vessel occlusion, on the basis of low splanchnic flow or intravascular coagulation, may be a fundamental element in the pathogenesis of acute acalculous cholecystitis.

Acalculous candida cholecystitis: a complication of critical surgical illness.Am Surg. 1991 Dec;57(12):825-9.

Four patients with underlying diseases including multiple trauma, aortic graft infection, and complex fistulae developed acute acalculous cholecystitis with bile cultures positive only for Candida albicans. The primary site of the candida infection included urinary tract, gastrointestinal tract, and an aortic graft in one patient each and was undetermined in the trauma victim. All had received broad-spectrum antibiotics; three of the four were in the intensive care unit (ICU) with organ failure. Ultrasonography showed a thickened gallbladder wall in three patients and sludge in one. Hepato-iminodiacetic acid scans were nonvisualizing in these three patients. Operative findings included gangrenous cholecystitis in two patients and edematous cholecystitis in one. The fourth patient was treated with percutaneous cholecystostomy and interval cholecystectomy. The interval from the onset of symptoms to recognition of the need for operation was an average of 7 days. Two of the four patients died of ongoing sepsis. Candida cholecystitis is a life-threatening complication of critical surgical illness. Risk factors are similar to those for candida infection elsewhere and include antibacterial therapy, complex fistulae, disseminated malignancy, immunosuppression, and prolonged ICU stay. A high index of suspicion for this fungal pathogen and aggressive surgical therapy offer the only chance for a favorable outcome.

Cholecystokinin cholescintigraphy: detection of abnormal gallbladder motor function in patients with chronic acalculous gallbladder disease. J Nucl Med. 1991 Sep;32(9):1695-9.

CCK cholescintigrams were performed in 374 patients with recurrent postprandial right upper quadrant pain, biliary colic, and a normal gallbladder sonogram and/or cholecystogram. The results of these examinations were correlated with the patients' final medical/surgical diagnoses. Twenty-seven patients recruited as control volunteers without objective clinical evidence of biliary disease also underwent CCK cholescintigraphy to determine if the degree of gallbladder contraction post-CCK differs in symptomatic versus asymptomatic subjects. Decreased gallbladder motor function was identified (maximal gallbladder ejection fraction response to CCK less than 35%) in 94% of patients with histopathologically confirmed chronic acalculous cholecystitis or the cystic duct syndrome and in 88% of patients clinically believed to have chronic acalculous biliary disease. Decreased gallbladder motor function does not distinguish symptomatic from asymptomatic gallbladder disease.