Bijan Eghtesad and John Fung (eds.)Surgical Procedures on the Cirrhotic Patient10.1007/978-3-319-52396-5_10

10. Cholecystitis, Cholelithiasis, and Cholecystectomy in Cirrhotic Patients

Kenneth D. Chavin¹, Gabriel R. Chedister², Vinayak S. Rohan² and Arun P. Palanisamy¹

(1)

Department of Surgery, Case Western Reserve University, Cleveland, OH, USA

(2)

Medical University of South Carolina, Charleston, SC CSB409, USA

Kenneth D. Chavin (Corresponding author)

Email: Kenneth.chavin@uhhospitals.org

Gabriel R. Chedister

Email: chediste@musc.edu

Vinayak S. Rohan

Email: rohanv@musc.edu

Arun P. Palanisamy

Email: arun.palanisamy@case.edu

Keywords

CirrhosisCholelithiasisCholecystitisCholecystectomy

Introduction

Like many other ailments that can be attributed to or worsened by liver cirrhosis, disease of the gallbladder has been shown to be more common in patients with cirrhosis. While gallstones are found in approximately 10–15% of the general population in developed countries, prevalence of gallstones in cirrhotic patients can be as high as 25–30%, twice the rate [1–4]. The reason for increased prevalence of gallstones in cirrhotic patients is multifactorial, with some factors associated with the causes of the cirrhotic liver disease and some the sequelae. These gallstones can cause further complications in patients with an already morbid illness. Due to many patient factors and associated comorbidities, management of gallbladder disease in cirrhotic patients requires careful consideration in determining the best course for each individual patient. The care of these patients may include both nonoperative as well as operative interventions, where an evolution of surgical technique has proven that laparoscopic cholecystectomy, previously thought to be contraindicated in cirrhotic patients, can be of benefit.

Pathogenesis of Gallstones in the Cirrhotic Patient

There are many factors that lead to the increased prevalence of gallstones in cirrhotic patients. The same conditions that can lead to cirrhosis have been linked to gallstone development. Chronic Hepatitis C viral infections (HCV), alcohol abuse, as well as nonalcoholic fatty liver disease (NAFLD), each of which can lead to cirrhosis, are risk factors for gallstones with increased risk associated with advanced stages of each disease. Like the general population, the prevalence of gallstones increases with age in cirrhotic patients, but cirrhotic patients have a more even distribution between the sexes. The rate of symptomatic versus asymptomatic gallstones is similar for cirrhotic patients and noncirrhotic patients, with the majority of gallstones being asymptomatic [5]. Cirrhotic patients who are female, of advanced age, have a family history of gallstones, or have cirrhosis due to viral infection, however, have been shown to have greater rates of symptomatic gallbladder disease [1].

While cholesterol stones are predominant in the general population, they represent only about 15% of stones in cirrhotic patients, with black pigmented stones making up the majority [1]. The black pigmented stones develop due to a number of factors associated with the cirrhotic pathophysiology. Portal hypertension, commonly associated with cirrhosis, often results in hypersplenism, which in turn leads to increased hemolysis [5]. This, coupled with impaired bile acid synthesis by the liver, leads to the supersaturation of calcium bilirubinate in the bile. This supersaturation is further compounded by induced enterohepatic cycling of unconjugated bilirubin due to the reduced bile salt concentrations as well as alcoholic abuse and low-protein diets, leading to precipitation of the black pigmented stones.

Reductions of gallbladder motility and decreased emptying in the setting of supersaturation also play a significant role in lithogenesis. Patients with cirrhosis have larger fasting gallbladder volumes and hypomotility as a result of liver disease [1]. Edema in the wall of the gallbladder from venous congestion, secondary to portal hypertension, and decreased serum albumin are thought to play a role in decreased gallbladder contractability. Impaired hepatic metabolic functions resulting in increased plasma levels of estrogen, progesterone, and other intestinal peptide hormones (vasoactive intestinal peptide, somatostatin, glucagon, pancreatic polypeptide) also result in hypomotility through inhibition of gallbladder smooth muscle [1, 6]. This decreased motility results in longer retention of contents in the gallbladder and greater opportunity for precipitation of stones.

Cholelithiasis in the Cirrhotic

Patient Presentation

While the prevalence of gallstones is increased in cirrhotics, many do not report any symptoms from the stones. Symptomatic gallbladder disease can present in the cirrhotic patient much as it does in patients without liver disease. Signs and symptoms of symptomatic gallbladder disease need to be approached with care in cirrhotic patients, as liver disease adds additional considerations to the differential diagnosis. Postprandial right upper quadrant pain, nausea, and emesis are common symptoms associated with both gallbladder and chronic liver diseases. Spontaneous bacterial peritonitis in patients with ascites can also present with symptoms similar to gallbladder disease [7]. This necessitates the need to carefully consider the diagnosis in cirrhotic patients.

Assessment and Work–Up

Work-up for a patient presenting with symptomatic gallbladder disease should include a thorough history and physical focusing on both gallbladder and liver disease. Vitals should be examined with added concern for patients with fever and other signs of systemic inflammatory response syndrome. A right upper quadrant ultrasound to evaluate for the presence of stones, signs of acute cholecystitis, obstruction of the common bile duct, and other related pathologies is warranted. Laboratory values including complete blood count, basic metabolic panel, liver function tests, and prothrombin time are also needed [6]. It is not only important to make the diagnosis of gallbladder disease but also to determine the extent of liver disease in the cirrhotic patient, as this plays a key role in the treatment decisions for the patient and also the overall prognosis.

Determination of Child-Turcotte-Pugh (CTP) score as well as Model for End-stage Liver Disease (MELD) is important to help determine the appropriate course of care. While there is some debate as to which is a better predictor of outcome for surgery in chronic liver patients, the CTP score (total bilirubin, serum albumin, prothrombin time, ascites, hepatic encephalopathy) and MELD (total bilirubin, serum creatinine, INR) are both good adjuncts to help decide if a patient is appropriate for surgical intervention. Surgical intervention should be considered for patients with CTP class A and B or with MELD scores of <8 [5]. Mortality rates for patients undergoing surgery have been shown to be 0.5% for patients in CTP class A and 3% for patients in CTP class B. MELD similarly shows increasing risk with increasing scores—mortality rates of 0% for patients with a score <8% and 6% for scores >8. A MELD score of 14 or greater was found to be a better predictor of poor outcome than CTP class C, for which surgical intervention for gallbladder disease is unwise with reported mortality of 23–50% and morbidity as high as 75% after cholecystectomy [8, 9].

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