Title: coronary angioplasty performed in 2012. Physical examination:


Consequences of gallbladder inflammation: Spontaneous
cholecystocutaneous fistula-A case report

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One of the most unusual
complications in gall bladder disease is spontaneous cholecystocutaneous
fistula (SCF), which has only been reported a few times in the literature. We
report the case of a 67-year-old man who presented with a right hypochondrium discharge
sinus. Identification
of a cholecystocutaneous fistula was made by computed tomography with contrast
media, followed by MRCP. This confirmed the presence of a fistulous pathway
between the gallbladder and the skin. The patient underwent subtotal cholecystectomy
surgery and open laparotomy with en block aponeurotic muscle, skin
and fistula orifice excision.



Spontaneous cholecystocutaneous fistula (SCF) is an exceptionally uncommon complication of gall
bladder disease. Thilesus first described the condition in 1670, and since 2007
there have only been 28 cases published. 1 Due to availability of increasingly sophisticated medical imagining
techniques and higher standards of public health in general, the incidence of
such cases is expected to have markedly declined. Wider acceptance of laparoscopic
has brought about a revolution in management of the cholelithiasis.
Nonetheless, occasionally in neglected, compromised, elderly, cholelithiasis
patients with long standing disease, such rare complication can occur. We
report a case of 67-year-old patient who presented with a discharging sinus in
right upper quadrant /hypochondrium and suspected SCF.


Initial presentation and history:

We present a case of 67-year-old man presenting to the
emergency department of our hospital with chief complaints of pain and swelling
over the right upper abdomen for 30 days, and discharge from right upper
abdomen for 25 days. There was no history of fever. The patient reported having
the cholelithiasis for at least 10 years. He had episodes of abdomen pain 4
years earlier which subsided after taking medication. The patient had past
history of head injury, craniotomy and convulsions 20 years earlier
and he was
on antiepileptics
and  antihypertensive. He also had
ischemic heart disease and had previously undergone percutaneous transluminal
coronary angioplasty performed in 2012.

Physical examination:

The patient was severely hypertensive (at 180/100mmHg)
and presented with pallor. On per abdomen examination approximately 10cm x
soft to firm mass in right hypochondrium, mild tenderness, and sinus opening with serous like discharge. Surrounding skin was indurated
but non-tender and local temperature was not raised.

Laboratory examination and radiological study:

Blood test revealed haemoglobin 7mg/dl, white blood cell count was 18,000/ microliter , C-Reactive protein was 80 mg/L, International normalization ratio was 4, Liver
Function Test unremarkable except raised Alkaline Phosphatase . Contrast Enhanced Computed Tomography(CECT) revealed   a thick-walled gall bladder and thick walled enhancing fistulous tract
extending from gall bladder to anterior upper abdominal wall. Magnetic
resonance cholangiopancreatography (MRCP) revealed a track running from base of the gall bladder to anterior upper abdominal
wall and not communicating with common bile duct, duodenum, colon, stomach and confirmed with gadolinium sinogram. And a single
calculus was noted as a well-defined defect in gall bladder.Figure1  Also, 2D-Echocardiography showed 45% Ejection Fraction with Grade 3 Left
Ventricle dysfunction


Treatment and outcome:

Patient was started on broad spectrum intravenous
antibiotics and anti-hypertensive. Fresh-frozen plasma transfusion  transfusion done for deranged INR. Blood
transfusion done for anaemia. After initial stabilization patient planned for
surgery on the second day after diagnosis. The patient underwent elective
subtotal cholecystectomy performed through subcostal incision and single large
gall bladder stone (6cm) retrieved,
en-block aponeurotic muscle skin and fistula orifice excision, with drain
placement. During surgery common bile duct, colon, jejunum, stomach inspected
carefully for any communication. In post-operative period patient was shifted
to Intensive Care Unit . On post operative day 2 (POD2), the patient had
delirium but serum electrolytes were normal. So, in view of hepatic
encephalopathy serum ammonia levels were done, that were raised (65µmol/L). Syrup lactulose was given. On POD 4, the patient become stable and shifted to ward and started orally.
Drain removed on POD
6. and patient
discharged on POD
8. Histopathology
reports confirmed the Acute on chronic cholecystitis, without any evidence of malignancy.


The pathophysiology
of the condition
involves increased pressure in the gallbladder,
secondary to cystic duct obstruction, either caused by a calculus or neoplasia. 2 Predisposing factors are cholelithiasis, infections, malignancy,
diabetes, atherosclerosis, prolonged high dose steroids associated
disease like polyarteritis nodusa. 3,4 Fundus most distant from cystic artery and physiologically least
vascularised therefore most susceptible to ischemia hence is the most common site
of perforation
.5,6 The
increase in intraluminal pressure compromises the venous and lymphatic drainage
of gallbladder resulting in necrosis and finally gallbladder perforation. 7 Spontaneous biliary
fistula can be either internal or external with the majority internal. 8  Internal fistula connections occur
at the duodenum 77%, colon 15%, stomach, jejunum, Common bile duct.  9 Generally, fistula or
abscess present in right upper quadrant, although other locations such as
epigastrium, umbilical, right groin, even the gluteal
region, right breast have also been described. 3,10,11. Rare cases of biliary fistulas joined to
regions such as the renal pelvis, uterus, vagina, ovary, urinary bladder,
hepatic artery, portal vein, pericardium, and bronchial tree have also been
reported. 12,13, 14  Perforation of
the gallbladder with cholecystohepatic communication is a rare cause of liver
abscess 15  Niemeier in the 1930s, proposed a classification of
gallbladder perforation: Type I – acute free perforation into peritoneal cavity,
without protective adhesions; Type II – subacute perforation with
pericholecystic abscess; and Type III – chronic perforation with
cholecystoenteric fistula. 3,16  A fourth type is suggested by Andersen et al
type IV: cholecystobiliary fistula formation 17.  Roslyn et al 18 reported in their study that type I and type II
gallbladder perforations are mostly seen in young patients (