Role of Indocyanine Green (ICG) in the Management of Acute Gangrenous Cholecystitis Secondary to Gall bladder Empyema in Mirizzi's Syndrome: A Case Report

Introduction

Mirizzi’s syndrome is a complication of chronic gallstone disease, named after the Argentinian surgeon, Pablo Louis Mirizzi, who first described the condition in 1948.^1,2 A stone impacted in the Hartman’s pouch or cystic duct causing extrinsic compression of the bile ducts is implied as the underlying mechanism.² Constant pressure, chronic inflammation, ulceration and superadded infection lead to critical surgical emergencies namely, cholecystobiliary or cholecystoenteric fistulae, gallbladder (GB) empyema, gangrene or perforation of gallbladder and sepsis.^4,5

Over the years, various classification systems have been proposed for this syndrome. All types clinically represent evolving stages in disease progression.² Csendes classification is a rather simple way which classifies Mirizzi’s syndrome into 4 types (Table 1).⁵

There are 2 forms of the disease; acute and chronic. Acute form is most commonly encountered.5 Lack of specific signs and symptoms make it difficult to diagnose early with a preoperative diagnosis rate ranging from 8% to 62.5%.^2,5 Clinical presentation ranges from asymptomatic to nonspecific symptoms as obstructive jaundice (27.8%-100%), pain right upper abdominal quadrant (16.7%-100%) and fever.³ On rare occasions, it may present as gallstone ileus.³

Treatment of Mirizzi’s syndrome is surgical, tailored according to the type, patient condition and surgeon’s experience. Cholecystectomy is performed in all settings, usually staged in type II. Laparoscopic approach in a known case of Mirizzi’s syndrome can be disastrous as it may lead to bile duct injuries because of distorted anatomy and severe inflammation.^1,5 This approach is associated with a high conversion rate.³

Case Presentation

A 48-year-old male who was a known case of choledocholithiasis presented to the outpatient department (OPD) with complaints of pain in the right hypochondrium for 7 days and yellowish discolouration of skin and sclera with high-coloured urine for 5 days. Patient denied any history of fever or vomiting. Patient's past medical history was insignificant.

Patient had similar complaints 6 months back for which he was evaluated elsewhere and was diagnosed to have choledocholithiasis for which endoscopic retrograde cholangiopancreatography (ERCP) was done but the procedure had failed to clear the common bile duct (CBD) due to altered periampullary and biliary anatomy.

Per abdominal examination revealed palpable mass in the right hypochondrium with associated tenderness. Murphy's Sign was positive. Patient was icteric but afebrile. The remaining clinical examinations were unremarkable. Initial biochemical investigations revealed a total leukocyte count (TLC) of 13,000/mm³ , total bilirubin of 5.2 mg/dL, indirect component being 2.61 mg/dL and direct bilirubin being 2.59 mg/dL. Alkaline Phosphatase (ALP) (420 IU/L) and Gamma-Glutamyl Transferase (GGT) (156 IU/L) were also raised. Serum amylase and lipase were within normal limits. Patient had incidentally raised International Normalized Ratio (INR) for which preoperatively patient was started on intravenous (IV) vitamin K injections. By clinic-biochemical correlation, the differential diagnosis was narrowed down to jaundice of surgical importance.

For further correlation, radiological investigations were done. Ultrasound (USG) abdomen revealed pathological contracted GB with multiple calculi and oedematous wall with mild dilatation of the intrahepatic and extrahepatic biliary radicles. Further magnetic resonance cholangiopancreatography (MRCP) was done to delineate biliary anatomy, which revealed the picture of acute calculous cholecystitis with irregularity and thinning of GB wall probably suggestive of localised perforation, with a 2.5 cm calculus impacted at GB neck/ cystic duct causing extrinsic compression over the common hepatic duct with mild dilatation of bilateral intrahepatic biliary radicles, concluding it as a Type I Mirizzi Syndrome (Figure 1).

Discussion

Mirizzi's syndrome can be challenging to diagnose because it often presents with delayed symptoms. While rare, it primarily affects women and can occur at any age. It's important to report cases of Mirizzi's syndrome because it can be easily overlooked by doctors, leading to serious consequences. Our patient, for example, developed empyema of the GB, and localized perforation. Further delays could have resulted in biliary peritonitis and sepsis. While ultrasound can be operator-dependent, confirming the diagnosis with ERCP or MRCP is recommended. Although there is controversy surrounding the use of laparoscopic procedures for this condition, in skilled hands, it is generally safe and offers the advantages of shorter hospital stays, faster recovery, and lesser postoperative pain. In our case, we opted for a laparoscopic approach, aspirated the empyema, opened the gallbladder wall, extracted the stone, and performed a subtotal cholecystectomy

Table 1: Classification of Mirizzi syndrome, according to Csendes et al.⁽⁴⁾