Chapter 16 Laparoscopic Cholecystectomy for Acute Cholecystitis

Wan Yee Lau, Eric C.H. Lai, Stephanie Hiu Yan Lau

The videos associated with this chapter are listed in the Video Contents and can be found on the accompanying DVDs and on Expertconsult.com.

Although laparoscopic cholecystectomy is now the gold standard operation for symptomatic gallstones, its role in the management of acute cholecystitis has only been accepted in the past one to two decades. It is still considered a relative contraindication for some patients and for surgeons who are not experienced in laparoscopic surgery.

In acute calculous cholecystitis, acute inflammation can result in considerable distortion of the biliary and vascular anatomy, putting the common bile duct and the hepatic artery at a higher risk for injury. This distortion is especially prominent around the triangle of Calot, where a stone is usually impacted at the cystic duct, causing distention and thickening of the gallbladder. Edema, as a consequence of inflammation, makes the dissection of the triangle of Calot difficult. The cystic duct might become so edematous and thickened that it cannot be secured with the standard clips used for elective laparoscopic cholecystectomy. Also, if the inflammation resolves rapidly after gallbladder removal, the clips might loosen and become dislodged. Therefore, alternative methods like using an Endoloop (Ethicon Biosurgery, Cincinnati, Ohio), suturing, or a linear stapler may have to be considered in these situations. In severe cases, the cystic duct and the cystic artery may not be visualized. The greater omentum and sometimes the adjacent organs such as the duodenum and the colon become adherent to the inflamed gallbladder. These structures are highly friable because of the inflammation and can be easily injured if handled without care. The inflamed gallbladder often proves difficult to grasp and maneuver because the tissues are too edematous and friable, or the gallbladder may simply be too distended to allow the grasping forceps to obtain an adequate grip. The acutely inflamed gallbladder is also more easily torn, resulting in bile or stone spillage.

Bleeding is a common reason for conversion from laparoscopic to open surgery, either because the laparoscopic view is obscured or because the bleeding cannot be stopped laparoscopically. There are many potential sources of intraoperative bleeding. Torn mesenteric or omental vessels may occur during dissection of inflammatory adhesions away from the gallbladder and ductal structures. Bleeding can also arise from an injured or torn cystic artery because of the difficult dissection. Often, the most difficult to avoid is bleeding from the gallbladder fossa. These injuries occur because it is difficult to dissect the posterior wall of the inflamed gallbladder from the gallbladder fossa and to adequately coagulate the small vessels within the liver bed. Bile leaks may also occur in the gallbladder fossa if the dissection has been carried out too deeply into the liver. Finally, extraction of the gallbladder specimen from the peritoneal cavity can be difficult because of the thickened gallbladder wall.

The pathophysiology in the initiation of acute calculous cholecystitis is believed to be due to obstruction to the cystic duct by a stone. This causes distention of the gallbladder and stretching of the gallbladder wall. This stimulates the synthesis of prostaglandins I₂ and E₂, which mediate the inflammatory response, resulting in chemical cholecystitis with inflammation and edema. Secondary bacterial infection with enteric organisms (most commonly Escherichia coli, Klebsiella species, and Streptococcus faecalis) sets in usually after 2 to 3 days if the attack of acute cholecystitis is not resolved. This can further progress to gangrenous changes and perforation of the gallbladder. The omentum usually adheres to the gangrenous or perforated site, and the infection is confined. At times, when the omentum fails to contain the gangrenous and perforated site, bile peritonitis follows. If untreated, the patient develops septicemia.

The pathogenesis of acute acalculous cholecystitis is a paradigm of complexity. Ischemia and reperfusion injury, or the effects of eicosanoid proinflammatory mediators, appear to be the central mechanisms. Bile stasis, gallbladder distention due to prolonged fasting, total parenteral nutrition, opioid therapy, and positive-pressure ventilation have all been implicated. Patients who are hypotensive, old, or diabetic and those who are immunocompromised are especially prone to developing this condition.

Operative indications

Diagnosis of Acute Calculous Cholecystitis

The presumptive diagnosis of acute calculous cholecystitis is based mainly on clinical grounds, with fever, persistent right upper quadrant abdominal pain, tenderness, and guarding in the right upper abdomen and a positive Murphy sign. These patients should be admitted to a hospital and investigated further. Routine blood tests show leukocytosis with a white cell count usually greater than 10,000/mm³. Liver function tests usually show normal bilirubin and alkaline phosphatase. Abdominal ultrasound should be a routine investigation carried out soon after hospital admission. The sensitivity and specificity of ultrasound are 85% and 95%, respectively, for diagnosing acute cholecystitis, and normal liver function tests and a normal common bile duct on ultrasonographic examination would effectively rule out choledocholithiasis. An ultrasound diagnosis of acute cholecystitis is made with the following findings:

• Presence of gallstones with a distended gallbladder

• Thickened gallbladder wall

• Pericholecystic fluid (double-wall sign)

• Positive ultrasonic Murphy’s sign

Note that these ultrasonic signs should be interpreted carefully and should be taken together and interpreted with the clinical presentations of the patient. The presence of gallbladder stones alone without the other ultrasonic and clinical features of acute cholecystitis might suggest that the patient is suffering from an attack of biliary colic. The presence of gallbladder sludge is nonspecific and may be observed during prolonged fasting and during parenteral nutrition. Gallbladder distention may be present in the setting of prolonged fasting, parenteral nutrition, prior vagotomy, or distal common bile duct obstruction. It may not be present when prior inflammation and fibrosis limit the distensibility of the gallbladder. The finding of pericholecystic fluid alone is not sensitive in diagnosing acute cholecystitis, and it may even be absent in the early stages of inflammation. It is also nonspecific and may occur in patients with pancreatitis, ascites, or peritonitis. A positive sonographic Murphy’s sign is very specific for acute cholecystitis, but it can still be masked by the heavy use of narcotics. A combined use of the clinical features, ultrasound, and laboratory testing would give an accuracy rate of more than 95% in diagnosing acute cholecystitis.

In case of doubt, computed tomography (CT) can be added to improve the diagnostic accuracy. The CT features of acute cholecystitis include a distended gallbladder with thickened wall, pericholecystic inflammatory changes, and fluid. Gallstones may or may not be visualized. Transient hepatic attenuation difference in the adjacent liver, especially with the use of intravenous contrast, may be detected because of the hyperemia caused by the adjacent inflammation. Biliary scintigraphy can also be used to enhance the accuracy rate of acute cholecystitis.

The finding of common bile stones in patients with acute cholecystitis is extremely uncommon. Patients who have a strong suspicion of associated choledocholithiasis, including patients with dilated common bile duct on ultrasonography, abnormal liver function with elevated bilirubin and/or alkaline phosphatase, and elevated pancreatic enzymes (i.e., amylase or lipase) should be further investigated with magnetic resonance cholangiopancreatography or endoscopic retrograde cholangiopancreatography (ERCP). The management of patients with associated choledocholithiasis is beyond the scope of this chapter.

Diagnosis of Acute Acalculous Cholecystitis

Acute acalculous cholecystitis accounts for 5% to 14% of all cases of acute cholecystitis. It develops in critically ill, aged patients or patients who have severe multitrauma. However, the development of acute acalculous cholecystitis is not limited to severely ill patients or patients who are treated in the intensive care unit. There is an association between acute acalculous cholecystitis and patients with diabetes, malignant disease, abdominal vasculitis, congestive heart failure, atherosclerotic disease, shock, and cardiac arrest. In children, it is associated with a postviral attack. The mortality rate approaches 50%, and death is due to delay in diagnosis in a poor-risk patient. The clinical diagnosis can be difficult in severely ill patients. Ultrasonographic diagnosis of acute acalculous cholecystitis in critically ill patients is controversial, and there is evidence that ultrasound may not be a reliable routine screening tool for acute acalculous cholecystitis. The role of laparoscopic surgery is also controversial. In a high surgical risk patient, however, early diagnosis with rapid intervention is crucial in managing this disease if outcomes are to be improved. Percutaneous cholecystostomy appears to be a logical treatment for those patients who have no evidence of gallbladder perforation and bile peritonitis. If the diagnosis is made late with bile peritonitis, open cholecystectomy may be the preferred treatment for critically ill patients.

The remainder of this chapter concentrates only on laparoscopic cholecystectomy for acute calculous cholecystitis.

Preoperative evaluation, testing, and preparation

The patient is well hydrated, and any electrolyte imbalances are corrected. Broad-spectrum antibiotics (usually a second-generation cephalosporin) are administered, the pain is alleviated, and the patient is kept NPO. A nasogastric tube is used if there is evidence of ileus; otherwise, a nasogastric tube is inserted during surgery after induction of general anesthesia. Cardiopulmonary workup is carried out in those patients who have a past history of heart or lung diseases, and correction of associated morbidities (e.g., diabetes and hypertension) is done. A thorough explanation of the diagnosis and the various therapeutic alternatives are discussed with the patient.

Choice of therapies

The gold standard of treatment for a low-risk patient with acute cholecystitis is cholecystectomy, either early or delayed. However, for patients who are critically ill and those who are too frail or too old for cholecystectomy, ultrasound- or CT-guided percutaneous cholecystostomy is an effective treatment, without any evidence of gallbladder perforation and bile peritonitis. Percutaneous cholecystostomy can be used as a definitive treatment or as a temporizing measure in critically ill patients, allowing for delayed definitive surgical treatment when the patient’s condition improves.

Laparoscopic versus Open Cholecystectomy for Acute Cholecystitis

Studies have shown that laparoscopic cholecystectomy, carried out in experienced hands, offers significant advantages compared with open cholecystectomy in terms of morbidity, hospital stay, and return to normal activity. The quality of life after laparoscopic cholecystectomy is excellent, which includes physical activities and social function.

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