Understanding Acalculous Cholecystitis: A Gallbladder Disorder

Acalculous cholecystitis involves hypokinetic gallbladder emptying.

October 2023
Goals :

Review the epidemiology and identify some risk factors associated with the development of AC.

Explain the pathophysiology of AC.

Describe treatment considerations for patients with AC.

Describe the importance of a communicative interprofessional team with extensive experience in the recognition and management of patients with AC.

 Acalculous cholecystitis (AC) is a life-threatening disorder that has a high risk of perforation and necrosis compared to the more typical calculous disease.

Introduction

CA is a form of cholecystitis caused by gallbladder emptying dysfunction or hypokinesia . The most common condition of AC is caused by mechanical blockage of the gallbladder’s outlet into the cystic duct, usually by a gallstone. Although it can present acutely, CA usually presents more insidiously. The condition is most common in patients admitted to the intensive care unit (ICU). CA is a life -threatening disorder that has a high risk of perforation and necrosis compared to the more typical calculous disease.

Etiology

Many different factors can cause gallbladder dysfunction. Its incidence may increase due to long periods of fasting, total parenteral nutrition, and drastic weight loss. Often the etiology is due to other, more serious conditions. Patients admitted to the ICU or recovering from major surgeries or other serious ailments, such as stroke, heart attack, sepsis, severe burns, and extensive trauma, are at increased risk of developing AC.

Gallbladder stasis secondary to lack of stimulation of the gallbladder leads to concentration of bile salts with increased pressure within the gallbladder. This leads to ischemia, pressure necrosis and finally perforation. This static condition also increases the seeding and growth of enteric pathogens such as Escherichia coli , Klebsiella , Bacteroides , Proteus , Pseudomonas and Enterococcus faecalis .

People with chronic AC may have decreased gallbladder emptying function, hypokinetic biliary dyskinesia. This can be due to a variety of factors, such as those related to hormones, vasculitis, and decreased nerve innervation from conditions such as diabetes. The exact etiology of chronic AC is often unknown.

Epidemiology

AC accounts for 10% of all cases of acute cholecystitis and 5-10% of all cases of cholecystitis. The predisposition is the same in both sexes. However, men are more likely to develop acute CA after surgery.

Rates increase in patients with HIV and other immunosuppressed conditions. These individuals are more susceptible to certain opportunistic infections such as microsporidia, Cytomegalovirus (CMV), and Cryptosporidium, which can seed and flourish in the bile within the gallbladder.

Carriers of Giardia lamblia , Helicobacter pylori and Salmonella typhi are also associated with a higher risk of developing cholecystitis.

Pathophysiology

Gallbladder stasis results in the buildup of intraluminal pressure, leading to ischemia and inflammation of the gallbladder wall.

This stasis can also lead to bacterial colonization which contributes to the inflammatory response. If the pressure is not relieved, the gallbladder wall will become progressively ischemic, eventually leading to gangrene and perforation, leading to sepsis and shock. These findings make up the picture of acute cholecystitis.

Chronic AC usually presents in a more insidious manner. Symptoms last longer and may be less severe. They may also be more intermittent and vague, although patients may present with signs of acute biliary colic.

Histopathology

AC presents with varying degrees of inflammation. The findings are similar to those of gallstone cholecystitis, only with the absence of gallstones. The wall of the gallbladder will be thickened to varying degrees and there may be adhesions to the serosal surface. Signs of smooth muscle hypertrophy are found, especially in chronic conditions.

Sometimes bile sludge or very viscous bile is observed. These findings are common precursors to gallstones that form from increased bile salts or stasis. The bacterial species that may be present in 11% to 30% of cases are several.

Rokitansky-Aschoff sinuses are found in 90% of cholecystitis specimens. This is a herniation of the intraluminal sinuses due to increased pressure, possibly associated with the Luschka ducts.

The mucosa presents various degrees of inflammation, from mild to ulcerations with gangrenous changes. Extreme situations may show total gangrenous lesions of the gallbladder with perforation.

Toxicokinetics

Generally, in mild cases of CA, only the symptoms of biliary colic are treated. Cases of acute cholecystitis can cause sepsis and shock. Pressurized intraluminal gallbladder bile may be susceptible to bacterial seeding.

Antibiotics are often ineffective due to increased intraluminal pressure and compromised intraluminal blood supply.

The occurrence of a perforation will cause biliary peritonitis and contribute to the production of shock. The release of inflammatory byproducts also contributes to shock and susceptibility to sepsis.

History and physical examination

Mild CA may present similarly to calculous cholecystitis. Patients may have abdominal pain in the right upper quadrant, reproduced with deep palpation (Murphy sign). Nausea, food intolerances, bloating, and belching may also occur. Signs of acute acalculous cholecystitis show a sudden onset of symptoms of severe pain in the right upper quadrant.

The gallbladder may be distended and palpable. These patients present very ill, possibly septic, and are admitted to the ICU. Leukocytosis is usually present, but not always. They have often been in the hospital for other major illnesses or are recovering from major surgery.

Assessment

The test of choice for chronic CA is radionuclide biliary scintigraphy with administration of cholecystokinin.

This study examines the function of the gallbladder. After the radionuclide is administered, cholecystokinin is administered to stimulate emptying of the gallbladder. A calculated ejection fraction ≤35% may be indicative of hypokinetic gallbladder function. Ultrasound of the gallbladder may also be helpful. If the gallbladder wall is thickened >3.5 mm, it may be due to cholecystitis. The blood test is not diagnostic, but will reveal leukocytosis and abnormal liver function tests.

The diagnosis of acute CA can often be made with an abdominal ultrasound which will show a significantly thickened wall with edema and possible pericholecystic fluid. This diagnosis can also be made using a CT scan. If there are still diagnostic doubts, a nuclear scintigraphy can be performed. Acute cholecystitis prevents filling of the gallbladder with contrast radionuclide.

Treatment and management

Patients with AC have a very poor general condition and need to be stabilized before any procedure can be performed. In unstable patients, placement of a drainage tube in the gallbladder may be considered, percutaneously or with the intervention of the radiologist. Another option is the placement of a stent through retrograde cholangiiopancreatography, in order to decompress the gallbladder.

Chronic AC is treated the same as stone cholecystitis. The treatment of choice is laparoscopic cholecystectomy . An open cholecystectomy can also be performed , when there is a contraindication to laparoscopic surgery. Acute cholecystitis must be addressed quite urgently, otherwise progression and deterioration can quickly occur. The best definitive therapy is cholecystectomy , either laparoscopic or open. If the patient is too unstable to undergo major surgery, percutaneous drainage is needed with possible definitive cholecystectomy at a later date.

Broad-spectrum antibiotics are routinely administered but are generally not effective as they do not penetrate the pressurized gallbladder, but will help treat any systemic bacteremia .

Differential diagnosis

Cholangitis

Acute cholecystitis

Pancreatitis

Hepatitis

Forecast

AC is a serious disease that presents a high morbidity and mortality, which varies between 30% and 50% depending on the age of the patient. Even those who survive have a long recovery that can take months.

Complications

Perforation of the gallbladder

Gallbladder gangrene

Sepsis

Postoperative care and during rehabilitation

Most patients remain on bowel rest until the clinical condition has improved. Therefore, intravenous hydration is necessary.

Optimizing Healthcare Team Outcomes

CA is a life-threatening disorder that can quickly prove fatal.

Most patients are elderly, frail and have many comorbidities. Due to the complexity of management, the condition improves with the participation of a multidisciplinary team that includes:

Surveillance in the ICU of patients with AC, who are very deteriorated patients. Nurses caring for these patients should have a high index of suspicion for the disorder because the signs and symptoms of sepsis are often vague. Fluid intake and output should be monitored along with respiratory status .

These patients require deep vein thrombosis and peptic ulcer prophylaxis and incentive spirometry.

Because patients are maintained without oral nutrition, a dietary consultation should be requested to determine the need for intravenous nutrition.

The radiologist must be aware of the patient’s admission since percutaneous drainage of the gallbladder may be urgent. The gastroenterologist may need to perform an endoscopy to place a stent in the ampulla of Vater to decompress the gallbladder.

Because patients are frail, bedside physical therapy is needed to regain muscle strength and function.

Finally, the general surgeon may need to perform an urgent cholecystectomy in patients with gangrene.

Results

The outcome of patients with AC is reserved. Over the years, mortality has decreased but remains around 10% despite optimal treatment. These patients usually develop fulminant sepsis, acute respiratory distress syndrome, and multiple organ failure. They also have a high incidence of adverse cerebrovascular events.

Most case reports indicate poor outcomes, and even patients who survive have a prolonged recovery period and never achieve full functional recovery.