Definition
A.Cholecystitis is the acute or chronic inflammation of the gallbladder. Acute cholecystitis is associated with stone formation (cholelithiasis) in 90% of all cases, causing obstruction and inflammation. Biliary sludge is a feature of chronic cholecystitis.
B.Following a cholecystectomy, stones may recur in the bile duct.
Incidence
A.Gallbladder disease afflicts more than 20 million people (10%–20% of adults) in the United States. Most patients have asymptomatic gallbladder disease, however 20% progress to experiencing acute biliary symptoms. Once acute symptoms develop, there is a 30% chance of persistent recurrences and therefore acute cholecystectomy is the recommended treatment for symptomatic patients. Mortality related to acute cholecystitis is 5% to 10%, with the highest risk for patients older than age 60. The most common complication of acute cholecystitis is the development of gall-bladder gangrene (20%) with the potential for subsequent perforation (2%). Gangrenous cholecystitis is most common in older patients, diabetics, or patients who delay treatment.
Pathogenesis
A.Cholecystitis occurs subsequent to bile stasis, bacterial infection, ischemia, or cystic obstruction by a gallstone. Acute cholecystitis is related to the impaction of a calculus in the neck of the gallbladder in approximately 90% of cases. Spontaneous resolution may occur after the reestablishment of cystic duct patency.
B.Escherichia coli is the primary microorganism in 80% of cholecystitis infections. Other pathogens include Enterobacter, Enterococcus, and Klebsiella. Positive culture rates range from 22% to 46%.
C.Estrogen-induced alteration in bile salts may favor stone formation. Stones occur when cholesterol supersaturates the bile in the gallbladder and precipitates out of the bile. Cholesterol stones are the most common type of gallstones in the United States.
D.Pigment stones occur when free bilirubin combines with calcium. Pigment stones are found in patients with cirrhosis, hemolysis, and infections in the biliary tree.
E.Acalculous cholecystitis is associated with infection and local inflammation. Formation of gallstones is not necessary for the obstruction of the bile duct.
Predisposing Factors
A.Female gender.
B.Sudden starvation/prolonged fasting.
C.Medications:
1.Cholesterol-lowering drugs: Stone formation increases in users of cholesterol-lowering drugs, which are known to increase biliary cholesterol saturation.
2.Thiazide diuretics.
3.Ceftriaxone.
4.Cyclosporine.
5.Opiate narcotic analgesics.
6.Estrogen usage (oral contraceptives [OCPs] and hormone therapy [HT]): Stone formation increases in users of contraceptives and estrogens, which are known to increase biliary cholesterol saturation.
7.Octreotide.
D.Bile acid malabsorption.
E.Genetic predisposition: Native Americans and those of Chinese or Japanese descent have a high incidence.
F.Total parenteral nutrition (TPN).
G.Obesity.
H.Status post–bariatric surgery. (Patients who have had either the Roux-en-Y or laparoscopic banding surgeries are at increased risk for gallstones.)
I.Pregnancy secondary to elevated progesterone.
J.Increasing age.
K.Hemolytic anemia.
L.Diabetes.
M.Hepatic cirrhosis.
N.Biliary tree infections.
Common Complaints
A.Abrupt, severe abdominal pain lasting greater than 6 hours
B.Constant aching pain or gnawing pain in the right upper quadrant (RUQ), right subcostal region, with radiation to the back and right shoulder.
C.Nausea and vomiting.
Other Signs and Symptoms
A.Anorexia.
B.Heartburn.
C.Upper abdominal fullness.
D.Biliary colic: Sudden onset of severe pain in the epigastrium or right hypochondrium that subsides relatively slowly. Tenderness may remain for days.
E.Fat intolerance.
F.Fever (low-grade).
G.Mild jaundice (20%).
H.Complicated disease such as an abscess or perforation; symptoms includes more severe localized persistent pain, tenderness, fever, chills, and leukocytosis.
I.Chronic diarrhea (4 to 10 bowel movements [BMs] every day for at least 3 months).
Subjective Data
A.Review the onset, location, duration, course, and quality of pain.
B.Use a pain-rating scale, such as a 10-point pain scale, with 0 being no pain and 10 being equivalent to the worst pain the patient has ever felt. Determine progression of the pain as well.
C.Review any alleviating factors, such as antacids, and any worsening factors, such as deep inspiration.
D.Review any pain radiating to the jaw, neck, shoulder, or arm.
E.Review onset of pain in relation to last meal and foods ingested.
F.Ask the patient about recurrent history of epigastric pain.
G.Obtain history and demographic data that may indicate the risk factors for biliary disease.
H.Review the date of the patient’s last menstrual period (LMP), and if she is pregnant, establish gestational age.
Physical Examination
A.Check temperature, pulse, respirations, and blood pressure (BP). Tachycardia, increased fever, and elevated white blood cell (WBC) are markers of inflammatory disease.
B.Inspect:
1.Observe general appearance, walking, and facial expressions such as grimacing during the examination. Overall appearance is generally unremarkable between attacks; ill appearance occurs during acute attack.
2.Observe skin turgor and color (15% have jaundice).
3.Patients generally remain still during exam due to peritoneal inflammation, which aggravates pain with movement.
C.Auscultate:
1.Heart.
2.Lung fields.
3.Abdomen for bowel sounds.
D.Percuss abdomen.
E.Palpate:
1.Palpate the abdomen; check for tenderness in the RUQ, especially with inspiration; assess for guarding and rebound tenderness.
2.Check Murphy’s sign. Positive Murphy’s sign is inspiratory arrest secondary to extreme tenderness when subhepatic area is palpated during deep inspiration.
F.Perform rectal exam, if indicated.
Diagnostic Tests
A.Laboratory tests:
1.Complete blood count (CBC) with differential.
2.Amylase.
3.Alkaline phosphate.
4.Bilirubin.
5.Aspartate transaminase (AST).
6.Alanine transaminase (ALT).
7.Urinalysis to rule out pyelonephritis and renal calculi.
8.Pregnancy test if childbearing age.
9.Stool for occult blood to rule out bleeding.
B.Radiography:
1.Ultrasonography: Study of choice and can often establish the diagnosis. Assess for presence of gallstones, gallbladder wall thickening (>4–6 mm), and sonographic Murphy’s sign.
2.Cholescintigraphy (hepatobiliary iminodiacetic acid [HIDA]) scan is indicated if the diagnosis is uncertain after an ultrasound.
3.Magnetic resonance (MR) cholangiography—sensitive for stone in cystic duct.
4.CT scan.
5.Endoscopic retrograde cholangiopancreatography (ERCP) and percutaneous transhepatic cholangiography (PTC).
6.Chest radiography to rule out pneumonia.
C.ECG to rule out myocardial infarction (MI).
Differential Diagnoses
A.Acute cholecystitis.
B.Biliary colic: Caused by contraction of the gallbladder after a fatty meal pressing a stone toward the orifice of the cystic duct. Distinguishing features of biliary colic include pain that peaks after several hours and then totally resolves (<4–6 hours). No associated fever, nausea, vomiting, or leukocytosis. Usually patients with acute cholecystitis have experienced episodes of biliary colic in the past, which can complicate diagnosis.
C.Acute pancreatitis.
D.Appendicitis.
E.Peptic ulcer disease (PUD)/perforation.
F.Acute hepatitis.
G.Pneumonia or pleurisy.
H.MI.
I.Renal calculi or other pathology associated with the right kidney.
J.Gastroesophageal reflux disease (GERD).
K.Pregnancy: Urolithiasis, pyelonephritis.
L.Functional bowel disorders including nonulcerative dyspepsia, irritable bowel syndrome (IBS)—pain predominant, functional gallbladder disorder.
M.Sphincter of Oddi dysfunction.
N.Intraabdominal abscess.
O.Fitz-Hugh–Curtis syndrome—perihepatitis caused by gonococcal infection.
Plan
A.General interventions: Patients with a single episode of biliary colic (pain <4–6 hours with full resolution) are reasonable candidates for expectant management, as long as they continue to be free of recurrent pain.
B.Patient teaching:
1.No activity restriction is required.
2.Treatment depends on acuteness, severity, and frequency of attack(s). Heat may be used as needed for pain. If pain continues to worsen, have the patient contact his or her healthcare provider. Hospitalization and/or surgery may be required depending on the severity of the attack.
C.Dietary management:
1.Counsel the patient to avoid fatty foods.
2.Encourage the patient to avoid fasting and starvation diets, which make the bile even more lithogenic.
D.Surgical management:
1.Cholecystectomy is recommended for symptomatic patients with positive findings on imaging. The standard of care is the laparoscopic cholecystectomy. Conversion from a laparoscopic procedure to an open surgical procedure is approximately 5%.
2.Patients are admitted to the hospital for intravenous (IV) fluid replacement, pain control, and antibiotics. Interventional therapy depends on patient’s risk factors for surgery and severity of symptoms.
3.Conservative treatment includes IV antibiotics, bowel rest, and an interventional cholecystectomy 6 to 8 weeks later.
4.A WBC count above 15,000 cells/μL indicates a non-resolving inflammation and is a predictor of treatment failure after 24 to 48 hours of conservative observation. Other predictive factors of failed conservative treatment include the following:
a.Age greater than 70 years.
b.Diabetes.
c.Distended gallbladder.
5.Percutaneous drainage (cholecystostomy) is reserved for patients who fail conservative treatment, or as a salvage procedure for high-risk patients.
6.Extracorporeal shockwave lithotripsy.
E.Pharmaceutical therapy:
1.Nonsteroidal anti-inflammatory drugs (NSAIDs) are recommended for pain control.
2.Anticholinergics are not helpful.
3.Oral bile acid therapy decreases the amount of cholesterol produced by the liver and absorbed by the intestines. This therapy is reserved for poor surgical candidates who are at high risk for developing recurrent gallstones. Bile acid is not prescribed for calcified radio-opaque or radiolucent bile pigment stones or those with urgent need for surgery:
a.Actigall (Ursodiol):
i.Dissolution of stones: 8 to 10 mg/kg/d in two to three divided doses.
ii.Prevention therapy 300 mg twice a day.
b.Urso (Ursodiol) 250 mg tablets also available as Urso Forte 500 mg tablets:
i.13 to 15 mg/kg/d in two to four divided doses.
Follow-Up
A.See the patient at next pain attack to reevaluate.
B.Surgical follow-up in 2 weeks.
C.Patients on oral bile acid therapy should follow up with serial ultrasound at 6 and 12 months, and 1 to 3 months after dissolution of the stone. AST and ALT should be measured at the start of therapy and every 6 months thereafter.