GB torsion is rare, with less than 400 reported cases in the literature and few treated laparoscopically.1,2,3
The youngest reported patient was 2 y old, with the peak incidence in the pediatric population occurring between the ages of 6 and 13 y with a 4:1 male-to-female preponderance.4
Specific clinical signs or symptoms are typically absent, and laboratory data may reveal nonspecific inflammatory changes. The challenge therefore is to correctly identify this unusual cause of abdominal pain that is commonly misdiagnosed. Levard et al.5
describe 2 of 9 patients in whom the diagnosis was missed and who subsequently died. Even with early diagnosis and surgical intervention, the mortality rate is estimated to be 5%.5
The differential diagnoses that should be considered for right upper quadrant abdominal pain include acute cholecystitis, peptic ulcer, intussusception, intestinal volvulus, and high retrocecal appendicitis as well as GB torsion.6
Although there have been reports in the literature that suggest conventional imaging modalities, such as ultrasound (US) and CT, are useful in the preoperative diagnosis of GB torsion, most cases are diagnosed intraoperatively.7
These reports suggest that radiographic features of GB torsion on abdominal CT scan include a fluid collection in the GB fossa, an unusual GB location with marked dilation of the GB, a well-enhanced cystic duct located on the right side of the GB, and inflammatory changes, such as edema with GB wall thickening.6,8
In this case, even in retrospect, the GB was distended, but not necessarily pathologic appearing on abdominal CT scan, highlighting the difficulty in diagnostic specificity. A preoperative US was not obtained because findings such as GB wall thickening or even an emphysematous gallbladder wall were not identified by abdominal CT scan. The pathologic evaluation identified full-thickness wall ischemia with impending necrosis with no evidence for perforation.
Multiple hypotheses have been proposed as the mechanism of GB torsion. From an anatomic perspective, torsion of the GB in children may be related to perturbation of the embryological migration of the GB, which leaves the organ abnormally mobile on a stalk consisting only of the cystic duct and artery.6
Two anatomic variants have been described: (1) a torsion-prone mesentery and (2) a mesentery supporting only the cystic duct allowing a completely peritonealized GB to hang free.9
In conjunction with an anomalous anatomic configuration, an inciting may even occur to initiate torsion of the cystic duct and artery pedicle.10
It has been suggested that events, such as violent peristaltic movements of neighboring organs, sudden body movements, or abdominal trauma may play a role in precipitating GB torsion. Carter et al.4
described 2 types of torsion: (1) incomplete torsion (rotation < 180 degrees) with gradual onset and (2) complete torsion (rotation > 180 degrees), with acute onset. Further, cholelithiasis is an infrequent cause of GB torsion, because one large study of 245 patients found gallstones in 24.4%.11
Torsion of the gallbladder leads to occlusive obstruction of biliary drainage and blood flow with subsequent ischemia and gangrenous changes.