ACALCULOUS.html
Acalculous cholecystitis presenting in an out-patient with no risk factors
M Goodier, MB ChB
S Mulira, MB ChB
S Andronikou, MB BCh, FCRad, FRCR (Lond), PhD
Department of Radiology, University of the Witwatersrand, Johannesburg
Corresponding author: M Goodier (goodiermatt@gmail.com)
Abstract
Acute
acalculous cholecystitis (AAC) is recognised to occur in patients with
serious co-morbid illnesses such as after major surgery, severe trauma,
burns, multi-organ failure, systemic sepsis and prolonged intravenous
hyperalimentation. The development of AAC in outpatients with none of
the traditional risk factors appears to be increasing. The incidence of
this form of AAC in South Africa has not yet been established. Prompt
recognition of this condition and appropriate surgical management is
necessary to minimise morbidity and mortality. This report describes a
52-year-old man who developed AAC in the absence of the usual risk
factors.
Background
Acute acalculous cholecystitis (AAC) is acute
inflammation of the gallbladder in the absence of gallstones. The
condition has previously been regarded as occurring in the context of
the intensive care unit in patients who are post major surgery or who
have major systemic illnesses. According to international reports, the
incidence of AAC developing in outpatients with none of the traditional
risk factors appears to be increasing.1 To date, there have been no reports from South Africa regarding the local incidence of this form of AAC.
Case report
We present the case of a 52-year-old man
presenting from home with right upper quadrant pain. He had a history
of hypertension and was on hydrochlorothiazide 12.5 mg daily. He was
otherwise well with no history of diabetes mellitus, auto-immune
disease or any other significant illness.
On examination, the patient was pyrexial and
tachycardic. There was tenderness and peritonism localised to the right
upper quadrant. There was laboratory evidence of a systemic
inflammatory process, with a white cell count of 20.4x109
cells/l and a C-reactive protein (CRP) of 231.7 mg/l. Electrolytes and
liver enzymes were within normal limits. He tested HIV-negative.
Plain films of the abdomen were considered
non-specific at the time. Ultrasound of the abdomen failed to
demonstrate the gallbladder with prominent gas shadowing in the
gallbladder fossa. The sonographic Murphy’s sign was positive. A
computed tomogram (CT) of the abdomen performed on admission showed a
thickened gallbladder wall with surrounding inflammatory fatty
stranding. The gallbladder lumen was noted to contain a significant
amount of gas suggestive of a complicated cholecystitis (Fig. 1).
An open cholecystectomy was performed on day
2 post admission. The gallbladder appeared inflamed, gangrenous and
necrotic (Fig. 2a). No gallbladder calculi were noted at operation.
Pathological examination of the resected specimen showed features of an
acute gangrenous cholecystitis (Fig. 2b).
Postoperative recovery was complicated with a
repeat CT done on day 10 showing a small subhepatic collection that was
treated conservatively. The patient was discharged on day 25.
Discussion
Acalculous cholecystitis has traditionally been
recognised to occur in patients with serious co-morbid illnesses
especially after major surgery, severe trauma, burns, multi-organ
failure, systemic sepsis and prolonged intravenous hyperalimentation.2
Diabetes and auto-immune conditions are also known risk factors.
Patients with acquired immune deficiency syndrome (AIDS) may develop a
cholecystitis secondary to opportunistic infection of the gallbladder. 3
However, there have recently been an increasing number of reports in
the literature of the occurrence of AAC in patients with none of the
established risk factors. Two recent series suggest that, in some
settings, a significant number of patients with acalculous
cholecystitis present from home with no evidence of predisposing
illness or trauma. This group of patients may comprise up to 14% of all
outpatients with acute cholecystitis4 and as many as 77% of all patients finally diagnosed with AAC.5
The development of gallbladder inflammation in AAC is traditionally believed to be secondary to ischaemia.6
The cystic artery is an end artery with no significant source of
collateral supply to the gallbladder. Ischaemia of the gallbladder in
critically ill patients is often multifactorial, with dehydration,
sepsis, gallbladder stasis with the accumulation of sludge and multiple
transfusions being possible predisposing factors. The pathogenetic
mechanisms of AAC in patients with no risk factors is as yet unclear;
however, as many as 72% of these patients have evidence of
atherosclerotic vascular disease.5
These patients are also commonly hypertensive (as was our patient),
further suggesting that vascular disease may play a role in the
pathogenesis of this condition.5
Acalculous cholecystitis had been considered to
have a poor prognosis, but this most probably reflects the severity of
the underlying condition. In patients with no major systemic illness,
an increased incidence of gangrenous cholecystitis (as much as 59%) has
been reported, but this is possibly owing to diagnostic uncertainty and
delay in performing surgery in this group of patients.4
With prompt and appropriate treatment, the outcome in the group of
patents with no underlying systemic illness appears to be similar to
patients with calculous cholecystitis.7
Conclusion
Although acalculous cholecystitis often occurs in
the context of the intensive care unit in patients with major
underlying illnesses, it should be recognised that a significant
proportion of patients with this condition present as outpatients with
no underlying risk factors. The incidence of this form of AAC in South
Africa has not been established. Prompt recognition of this condition
and surgical management is necessary to minimise the associated
morbidity and mortality.
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acalculous cholecystitis in young patients without predisposing
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Fig. 1. Axial computed tomogram demonstrating
the thick-walled gallbladder (arrow) which contains air. There is
stranding in the surrounding mesenteric fat.
Fig. 2a. Intraoperative image demonstrating the inflamed gallbladder.
Fig. 2b. Gross pathological specimen showing necrosis and gangrene of
the gallbladder wall. No calculi were present within the gallbladder.