Biliary Tract Disease
Benjamin Braslow
I. Acute Cholecystitis
Acute cholecystitis is a syndrome of right upper quadrant (RUQ) pain, fever, and leukocytosis associated with an acute inflammation of the gallbladder. Ninety percent of cholecystitis is calculous in origin resulting from persistent obstruction of the gallbladder outlet by an impacted stone. This obstruction results in gallbladder distension, sub-serosal edema, mucosal sloughing, venous and lymphatic congestion, and localized ischemia. The natural history of acute cholecystitis depends on relief of the obstruction, development and extent of secondary bacterial invasion, age of the patient, and comorbidities. Most attacks resolve spontaneously without surgery or other specific therapy. Some progress to free perforation with local abscess formation or generalized peritonitis. Other complications include sepsis, empyema (suppurative cholecystitis), gallstone ileus, and cholecystic–enteric fistula. Repeated episodes of acute inflammation lead to chronic cholecystitis where the gallbladder wall becomes thick, fibrotic, and often contracted.
The cause of acute cholecystitis is speculative; most result from stagnation of bile secondary to stone impaction and subsequent infection. The edema and inflammation can play a role in elevating the gallbladder wall away from the impacted stone, thus resulting in disimpaction and spontaneous drainage. Failure of spontaneous disimpaction results in continued cystic duct obstruction, gallbladder ischemia, and increased inflammatory that necessitates operative intervention.
Clinical presentation
Acute cholecystitis presents with severe pain below the right costal margin. The pain frequently radiates to the back, the right scapula, or the right clavicular area. Majority of patients will recount a previous attack of biliary colic at first indistinguishable from the present illness. This new pain, however, does not mitigate and in fact worsens with time and is often associated with nausea, emesis, anorexia, or low grade fever (38 to 38.5°C). Mild icterus is present in about 10% of cases. High fever with chills is uncommon and suggests the possibility of cholangitis. Likewise, severe jaundice suggests the presence of common bile duct (CBD) stones, cholangitis, or obstruction of the common hepatic duct by severe pericholecystic inflammation associated with an impacted large stone in Hartmann’s pouch, which mechanically obstructs the bile duct (Mirizzi’s syndrome).
Physical examination reveals RUQ tenderness to palpation. A RUQ mass is palpable in one-third of patients. Murphy’s sign is accentuated tenderness and pain with a deep breath during palpation in the right subcostal region.
The white blood cell count (WBC) is usually elevated to 12,000 to 15,000/mm3 but normal counts are not uncommon. A high WBC (>20,000/mm3) should suggest further complications of cholecystitis such as gangrene, perforation, or cholangitis. A mild elevation of the serum bilirubin (2 to 4 mg/dL) is common presumably a result of secondary inflammation of the CBD; higher values usually indicate the presence of CBD stones. Mild elevations in alkaline phosphatase, transaminases, amylase, or lipase may also be present. However, dramatic elevations in any of these laboratory values suggest the presence of complications.
Imaging
Ultrasound is the initial diagnostic modality to identify cholecystitis with ∼95% specificity and sensitivity. Ultrasound findings most suggestive of acute
cholecystitis include gallbladder distension, gallbladder wall thickening (>4 mm), pericholecystic fluid, an impacted stone, biliary sludge, or positive sonographic Murphy’s sign. Comorbid factors (e.g., ascites) decrease the specificity of this test.
When ultrasound is equivocal, technically not possible, or negative in a patient with high clinical suspicion for cholecystitis, the patency of the cystic duct can be assessed with cholescintigraphy. Intravenous administration of gamma-emitting Tc-labeled hydroxyl iminodiacetic acid (HIDA) or diisopropyl iminodiacetic acid (DISIDA), is rapidly taken up by hepatocytes and secreted into the bile.
The scan is considered normal when radionucleotide is detected in the gallbladder, CBD, and small bowel within 30 to 60 minutes.
An abnormal or “positive scan” is defined as the non-visualization of the gallbladder with preserved excretion into the CBD or small bowel. HIDA scanning has a high sensitivity and specificity (100% and 95%, respectively), and a diagnostic accuracy rate approaching 98% in patients with clinical evidence of acute calculous cholecystitis.
A false-positive scan, defined as the absence of isotope in the gallbladder, is seen in patients who have fasted for more than 5 days, that is, critically ill patients or those receiving total parenteral nutrition (TPN). In this population, false-positive rates are high. Augmentation with morphine (which increases sphincter of Oddi and common duct pressure) is used if the gallbladder has not visualized after 60 minutes to decrease false-positive scans.
In most cases, the use of computed tomography (CT) in uncomplicated acute cholecystitis is limited unless other abdominal pathology is suspected or concern for gallbladder perforation, abscess, or enteric fistula. CT is less sensitive than US in the detection of gallstones.
Magnetic resonance imaging (MRI), although accurate in detection of cholecystitis, has a limited role in acute cases. Magnetic resonance cholangiopancreatography (MRCP) is an excellent modality for detection of CBD stones that complicate acute cholecystitis (see later).
Management
Patients with acute cholecystitis should be admitted. Initial therapy includes intravenous hydration, pain relief, and correction of any electrolyte disorders.
The need for antibiotic treatment in uncomplicated acute cholecystitis remains unproven, yet the practice in the United States has been to provide patients with antibiotic prophylaxis. Despite the low incidence of positive bile cultures assayed from patients with acute cholecystitis, broad spectrum intravenous antibiotics are given to most patients for an episode of cholecystitis.
The most common pathogens include Escherichia coli, Enterococcus, Klebsiella, and Enterobacter. Suggested regimens of antibiotics include: (1) Metronidazole plus a third generation cephalosporin or a fluoroquinolone or aztreonam, (2) piperacillin/tazobactam, (3) ampicillin/sulbactam, (4) ticarcillin–clavulanate, or (5) imipenem.
Patients with elevated liver function test results (specifically serum total bilirubin or alkaline phosphatase) or dilated bile ducts (>6 mm) on ultrasound should be further evaluated for the presence of CBD stones (see section later).
The definitive therapy for acute cholecystitis is cholecystectomy. Cholecystectomy (open or laparoscopic) has low complication rates: <0.2% mortality, <5% major morbidity, and a bile duct injury rate of ∼0.4%. Laparoscopic cholecystectomy has become the preferred operation in most patients; reduces hospital LOS and hastens recovery time and return to normal activity.
Conversion to open cholecystectomy is an important option to ensure patient safety. In laparoscopic cases with extensive inflammation, adhesions or bleeding that can make dissection of Calot’s triangle and recognition of the biliary anatomy hazardous, conversion to an open cholecystectomy or tube cholecystectomy is recommended.
Conversion is also advocated for persistent bleeding or intraoperative injury to a duct (other than the cystic duct) or bowel. Conversion should not be considered a complication or failure of laparoscopic surgery, rather a judicious
surgical decision in a complicated case to avoid further problems. Predictors of conversion include male gender, history of biliary disease, delay in surgery of more than 48 hours, marked leukocytosis (>18,000/mm3), obesity, adhesions, and inability to demonstrate the biliary anatomy.
The timing of cholecystectomy is variable. Ten to twenty percent of patients require immediate operation (for hemodynamic instability or generalized peritonitis). These findings suggest gangrene and perforation of the gallbladder; delays in operation increase morbidity and mortality. In the remaining 80% to 90%, the timing of operation remains controversial. In the past, delayed cholecystectomy, 6 to 12 weeks after resolution of symptoms, was preferred for acute cholecystitis. Current practice is early cholecystectomy for acute cholecystitis. Early cholecystectomy (within 72 hours) whether performed laparoscopically or open, results in reduced overall hospital LOS, decreased costs and no difference in complications. More importantly, 23% of people awaiting delayed cholecystectomy require urgent operation because of recurrent or worsening symptoms.
Emergent cholecystectomy in high-risk patients with acute cholecystitis, (severe comorbid conditions, i.e., advanced cardiopulmonary disease) carries mortality near 50%. Percutaneous gallbladder drainage (cholecystostomy) is the treatment of choice. The procedure is routinely performed by interventional techniques using fluoroscopic or ultrasound guidance. The preferred route for tube insertion is transhepatic, which takes advantage of a stabilized gallbladder during insertion and decreases peritoneal leakage. The transhepatic route is also preferred over the transperitoneal route in the setting of ascites to promote tract maturation. The procedure is well tolerated with less than 5% morbidity (i.e., catheter dislodgement, bleeding, liver hematoma, bile leakage, etc.). If the percutaneous method is not available, a small right subcostal incision permitting visualization of the fundus is made under local anesthesia. The gallbladder is then aspirated, decompressed, and a mushroom tip-catheter inserted and secured with a purse string suture. The catheter is exteriorized away from the costal margin, and secured to the skin.
The optimal timing of removal of tube cholecystostomy is debated. In the majority of patients with a transhepatic cholecystostomy, a 2-week period was sufficient for the tract to mature, while a minimum of 3 weeks were needed for the transperitoneal route. Tube cholecystography should be performed after resolution of the cholecystitis. If contrast flows into the duodenum and no stones are identified the cholecystostomy tube can be removed. Patients with gallstones should undergo an interval cholecystectomy after recovery from their acute illness as approximately 80% will have recurrent symptoms or further complications. The laparoscopic approach to interval cholecystectomy is successful in the majority of patients.
Complications
Complications of acute cholecystitis are common and often require surgical intervention. These include empyema, emphysematous cholecystitis, perforation and cholecystenteric fistula.
Empyema of the gallbladder (suppurative cholecystitis), describes an inflamed and infected gallbladder containing frank pus. The patient is septic and toxic, with high fever (39 to 40°C), chills, and an elevated WBC (15,000/mm3 or greater). Severe sepsis with hemodynamic instability and multi-system organ failure may be present or develop rapidly without prompt diagnosis and treatment. Treatment consists of fluid resuscitation, administration of broad-spectrum antibiotics (including anaerobic coverage), and emergent cholecystectomy or cholecystostomy.
Emphysematous cholecystitis is characterized by bubbles of gas from anaerobic infection appearing in the gallbladder lumen, its wall, the pericholecystic space, and, on occasion, the bile ducts. Clostridia species are the most common identified organism, but other potential gas forming anaerobes require antibiotic coverage as well. Males outnumber females (3:1) and 20% of patients are diabetic. The disease is often not associated with gallstones.
Patients present with severe pain, are toxic in appearance, with high fever and a significant leukocytosis. Abdominal x-rays or CT usually demonstrate air within gallbladder. Broad-spectrum antibiotics, including an anti-clostridial agent are given; fluid resuscitation and emergent cholecystectomy are indicated. Cholecystostomy can be used in unstable patients.
Perforation occurs when gallbladder wall ischemia progresses to gangrene. Perforation may occur early (within 3 days) or late (2 weeks or later) after the onset of acute cholecystitis. This occurs in <10% of cases and may be localized or free perforation. Localized perforation results in the formation of a pericholecystic abscesses as the omentum walls off the contamination limiting it to the RUQ. In these cases, cholecystectomy (open or laparoscopic) with abscess drainage can be performed safely after resuscitation and antibiotic therapy. Again, in those critically ill patients, cholecystostomy or percutaneous abscess drainage can be used to temporize the situation.
Cholecystenteric fistula occurs in 1% to 2% of patients with acute cholecystitis. The inflamed gallbladder becomes adherent to a neighboring hollow viscus and as necrosis develops, penetration into the adjacent lumen occurs and fistula formation follows. The duodenum (∼20%) and the hepatic flexure of the colon (∼80%) are the most common sites, but fistulas to the stomach are also reported. After the fistula forms, the episode of acute cholecystitis resolves as the gallbladder spontaneously decompresses. Rarely, patients vomit gallstones or develop steatorrhea, but in most cases the acute attack subsides and the cholecystenteric fistula remains clinically undetected. If a large gallstone passes into the small intestine, a mechanical bowel obstruction may result, which is termed gallstone ileus. This occurs in 10% to 15% of patients; patients present with signs and symptoms of small bowel obstruction. The pain may be episodic as the stone temporarily impacts at one site in the intestinal lumen then dislodges and is carried distally by peristalsis where it obstructs again. The terminal ileum is the usual final site of stone impaction. Often abdominal plain films will show dilated small bowel loops with air–fluid levels, pneumobilia and a calcified gallstone in the right lower quadrant.
The initial management of gallstone ileus includes removal of the obstructing stone, via a proximal enterotomy in a segment of non-edematous small bowel.
There is no debate over the need to emergently relieve the obstruction. However, if and when the cholecystenteric fistula should be addressed is debated. The traditional approach favored treating only the obstruction at the urgent operation and if symptomatic, the gallbladder removed after an interval of recovery. This may still be the safest approach. The cholecystenteric fistula does not require definitive treatment at exploration for small bowel obstruction. This approach is based on evidence that the majority of cholecystenteric fistula will close spontaneously with a less than 5% recurrence rate of gallstone ileus. Recently, several studies suggest a one-stage procedure consisting of enterolithotomy, cholecystectomy, and fistula excision, either with open or a laparoscopic approach.
II. Acute Acalculous Cholecystitis
Acute acalculous cholecystitis accounts for 5% to 10% of patients with acute cholecystitis. The disease often has a more fulminant course than acute calculous cholecystitis, often progressing to empyema, or gangrene with perforation. There is a strong association with clinical illnesses and conditions including recent non-biliary surgery, major trauma or burns, sepsis/shock, immunosuppression, TPN, diabetes mellitus, prolonged mechanical ventilation, narcotic administration, or multiple connective tissue/rheumatologic disorders.Related posts:
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