Spontaneous Type 1 Gallbladder Perforation in an Elderly Patient Presenting with Acute Generalised Peritonitis: a Case Report
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Gallbladder (GB) perforation is a rare phenomenon, but a known complication of acute cholecystitis. It can be seen after acalculous cholecystitis too. The incidence of GB perforation in patients with cholecystitis has been reported to be from 2 to 11%, but Derici et al. reported it to be 4.8% in their study . Spontaneous GB perforations are further rare and are mainly idiopathic. It is believed that the continuously rising pressure inside the GB leads to ischemia and inflammation leading to the GB perforation. This usually occurs at the fundus and presents with the features of a generalised peritonitis in the acute setting, but subacute and chronic perforations are also seen with pericholecystic fluid collections and cholecystoenteric and cholecystobiliary fistulae, respectively. It is seen in older age or immunocompromised people having comorbid medical ailments. Thus, it has gotten high morbidity and mortality, which is further compounded by delayed diagnosis and treatment. The mortality rate of GB perforation ranges between 0.8 and 11% . Cholecystectomy with peritoneal toileting and drainage is the treatment of choice.
Gallbladder (GB) perforation is a rare phenomenon seen in patients with cholecystitis. It is usually seen in the old, immunocompromised people or in people having diabetes mellitus, atherosclerosis, malignancies or organ failures. Although acute cholecystitis is seen more frequently in females, GB perforations are seen more commonly in males. The incidence of GB perforation after acute cholecystitis ranges between 0.8 and 11% . It is not so common to see GB perforations in people with acalculous cholecystitis . The site of perforation is the fundus of the GB in about 60% of the cases . This is the most distal part of the GB and thus, it has gotten a compromised blood supply. The GB distension leads to decreased venous and lymphatic return which ultimately leads to ischemia and necrosis of the GB wall. Neimeier classified the GB perforation into three types in 1934 . Type 1 perforations are acute perforations presenting with the features of acute generalised peritonitis. Type 2 perforations are subacute in nature and present with pericholecystic fluid collections or abscesses. Type 3 perforations are chronic and present with cholecystoenteric fistulae. Further, type 4 has been introduced by Andersen et al. in 1987, associated with cholecystobiliary fistula . The GB perforations are further classified as spontaneous, traumatic and iatrogenic in nature. The spontaneous group has been further subdivided into idiopathic and secondary due to causes like infection, gallstones or congenital causes . Spontaneous GB perforation is further rare. This condition presents with features similar to those of acute cholecystitis, and since most of the times these patients are old and immunocompromised, the clinical signs and symptoms are further suppressed; thus, the diagnosis is delayed and is associated with high morbidity and mortality. Ultrasonogram of the abdomen is the initial preferred investigation. Although GB wall thickening, oedematous GB wall, pericholecystic fluid and abscesses may be seen in GB perforation, the demonstration of sonographic hole sign is most consistent with GB wall perforation . Other direct evidence of GB perforation is the presence of free gallstones outside the gallbladder. The sentinel clot sign within and around the GB on CECT of the abdomen should raise the suspicion of GB perforation . CECT of the abdomen will show GB wall discontinuity along with haemobilia. There may be pericholecystic fluid collection, abscess or biloma formation with free extraluminal gallstones in it. Apart from this GB oedema, intramural gas, GB wall thickness, wall enhancement, intramural haemorrhage, GB stones, bile duct stones and cystic duct stones can be demonstrated by CECT. The CT of the abdomen has gotten 88% sensitivity for the detection of GB perforations; thus, it is the investigation of choice for pre-operative diagnosis of GB perforation [4, 8]. Type 1 perforations are usually present with acute generalised peritonitis in patients of less than 50 years of age. Thus, they will require urgent laparotomy where cholecystectomy is done along with peritoneal toileting and drainage. In type 2 patients, the fluid collections or abscesses are drained usually under radiological guidance, sepsis is controlled and once the patient is stabilised cholecystectomy is done. They are also usually less than 50 years of age. Type 3 and type 4 patients are difficult to treat, as they are usually older than 80 years of age and have long-standing gallstone disease and other comorbid conditions like diabetes mellitus and atherosclerotic heart disease. Type 3 GB perforations require repair of the cholecystoenteric fistula along with cholecystectomy. Type 4 fistulae require cholecystectomy and choldocholithotomy. The duct can be repaired primarily over T Tube or sometimes duct enterotomy may be required. Our patient was a 77-year-old female who did not have any gallstones, had no known comorbid conditions, and had type 1 GB perforation. She was most likely suffering from acalculous cholecystitis. The mortality was as high as 42%  around 60 years ago but has now come down to 12–16% [1, 10] these days, thanks to newer radiological advances, quick sepsis control, better anaesthesia techniques, and improved intensive care management [1, 4].
Spontaneous perforations of the GB in females of more than 50 years of age are a rare phenomenon. These patients are very frail. The typical features of generalised peritonitis are usually not seen. Further, the diagnosis is confused with acute cholecystitis. The diagnosis of GB perforation is not always possible pre-operatively. Thus, a high index of suspicion for the condition and a good clinical knowledge supported by radiological investigation can help to avoid delay in the diagnosis and treatment of a patient having biliary peritonitis with GB perforation.
RC contributed substantially to the conception, design, acquisition of data, analysis and interpretation of data, drafting the article, critical revision of the article and final approval of the version to be published. NG contributed substantially to the conception and design, acquisition of data, critical revision of the article and final approval of the version to be published. RKA contributed substantially to the conception and design of the article and final approval of the version to be published. MMA contributed substantially to the conception and design, acquisition of data, critical revision of the article and final approval of the version to be published. SS contributed to the acquisition of data, critical revision of the article and final approval of the version to be published. SK contributed substantially to the conception and design, acquisition of data, critical revision of the article and final approval of the version to be published.
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Conflict of Interest
The authors declare that they have no conflict of interest.
This was a case report and the patient identity was totally concealed; hence, the ethical approval was not taken.
Written informed consent was obtained from the patient for publication of this case report and any accompanying images. A copy of the written consent is available for review by the editor-in-chief of this journal.
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