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Gall Stone Diseases

Types of GB stones:

• Cholesterol & mixed stones (contain >70%cholesterol monohydrate + admixture of calcium salts, bile acids & bile pigments, etc.) account for 80%;
• Pigment stones (composed primarily of calcium bilirubinate, & <10% cholesterol) comprising the remaining 20%. This occurs more often in Asians & is often associated with infections in the bilirary tree; also seen in pts with chronic hemolysis or alcohlic liver disease.

Predisposing factors for cholesterol & mixed GB stones:
obesity, wieght loss, fasting, prolonged parenteral nutrition, estrogen, ileal disease or resection, aging, pregnancy, drugs as clofibrate, octreotide, high-calorie, high-fat diet, ? diabetes.

Diagnosis of GB stones:
Plain abdominal x-ray, GB ultrasound, oral cholecystogram, Radioisotope GB scans (HIDA, DIDA scan) for confirmation of suspected cholecystitis, useful in dx of acalculous cholecystopathy. ? Abd CT scan?

Symptoms of GB disease:
Biliary colic in the epigastrium or RUQ abd area with frequent radiation to the interscapular are, right scapula, or shoulder; nausea & vomiting, jaundice, fever & chills if infected. Some nonspecific Sx as vague epigastric fullness, dyspepsia, eructation, or flatulence. Sx may be precipitated by eating a fatty meal.

Asymptomatic GB stone in male has the cumulative risk for the development of Sx or complications requiring surgery is relatively low - 10% at 5 yrs, 15% at 10 yrs, 18% at 15 yrs.

Treatment of symptomatic GB stones:

1. ERCP/ Endoscopic sphincterotomy removal of the biliary common duct stone.
2. Cholecystectomy for gall bladder stones
3. Oral Dissolution Therapy
   Oral bile acid Rx is essentially ineffective in dissolving (1) pigmented gallstones, (2) radiopaque or calcified gallstones, (3) gallstones >1.5 cm, (4) gallstones in GB poorly opacified following OCG.
   
   Ursodiol (ursodeoxycholic acid - UDCA) 5-10 mg/kg/day administered orally for six to 12 months results in the dissolution of 60 to 90 percent of susceptible stones. Because this drug is effective only in patients with floating cholesterol stones and a functioning gallbladder, this treatment is limited to perhaps 15 percent of the population with symptomatic stones. Moreover, in patients who can use ursodiol, half the stones recur after therapy ceases (recurrence rate of 30-55% over 3-12 yrs follow-up). Low-dose, long-term therapy with ursodiol may help prevent this recurrence, but such therapy is effective only in patients younger than 50 years. (ref [46]) Chenodiol was the first agent introduced for the dissolution of stones, but ursodiol, which has fewer side effects, has replaced it. Cholesterol stones can be rapidly dissolved using methyl tert-butyl ether (MTBE). (ref [47]) Methyl tert-butyl ether is infused through a transhepatic catheter directly into the gallbladder. The rapid infusion and removal of this ether, which remains liquid at body temperature, results in the dissolution of most cholesterol gallstones within four to 31 hours. Dissolution therapy has limited value except in patients who are poor candidates for surgery.
   
4. Extracorporeal Biliary Lithotripsy
   The administration of ursodiol after fragmentation of stones has been associated with an increase in the percentage of patients who are free of gallbladder stones six months after lithotripsy. Among patients who received 10 to 12 mg/kg of ursodiol daily for six months after lithotripsy, 21 percent were free of gallbladder stones; in contrast, among patients who received a placebo for six months, only nine percent were free of stones. Stone fragments in the common bile duct either may pass spontaneously after endoscopic sphincterotomy or can be extracted with a Dormia basket. Given the widespread availability of laparoscopic cholecystectomy, the usefulness of lithotripsy is limited. The usual criteria for selection of pts include: (1) hx of biliary colic, (2) radiolucent stones, (3) functioning GB with opacification by OCG or normal emptying by cholecystokinin scan, (4) up to a maximum of 3 stones but preferably solitary stones <2cm (success rate 60-70% at 8-12 months), & (5) absence or acute cholecystitis, cholangitis, biliary obstruction, acute pancreatitis, or pregnancy.
   

ACUTE CHOLECYSTITIS
Bacterial inflammation may play a role in 50-85% of acute cholecystitis. These are usually E.Coli, Klebsiella, group D Streptococcus, Staphylococcus species, & Clostridium species.

Symptoms of acute cholecystitis:
Intermittent RUQ colic, may radiate to the interscapular area, right scapula, or shoulder. Peritoneal signs of inflammation may be apparent; anorexia, nausea & vomiting, jaundice, fever & chills; tender RUQ to palpation, an enlarged, tense GB is palpable in 1/4 to 1/2 of pts. Deep inspiration or cough during subcostal palpation of the RUQ usually produces increased pain & inspiratory arrest (Murphy's sign).

Diagnosis of acute cholecystitis:
It is usually made on the basis of a characteristic H&P. The triad of sudden onset of RUQ abdominal tenderness, fever, & leukocytosis is highly suggestive. The serum bilirubin is mildly elevated in 45% of pts, while 25% have modest elevations of ALT. The HIDA biliary scan may be confirmatory if bile duct imaging is seen without visualization of the GB. Ultrasound will demonstrate calculi in 90-95% of cases.

Treatment of acute cholescystitis:
Med. therapy: NPO, NG suction prn, IV fluid & lytes Rx, analgesic as Demerol or pentazocine. IV antibiotic Rx is usually indicated in pts with severe acute cholecystitis. Effective single-agent antibiotics include ampicillin, cephalosporins, ureidopenicillins, or aminoglycosides, but in diabetic or debiliated pts & in those with signs of gram-negative sepsis, combination antibiotic Rx may be preferable. About 75% of pts treated medically have remission of acute Sx within 2-7 days following hospitalization. In 25%, a complication of acute cholecystitis will occur despite conservative Rx. In this setting, prompt surgical intervention (cholecystectomy) is required, esp. there is empyema, emphysematous cholecystitis, or perforation.

Predisposing factors are: serous trauma or burns, postpartum period, vasculitis, GB obstructing adenocarcinoma, DM, torsion of the GB, "unusual" bacterial infections of the GB as Leptospira, Streptococcus, Salmonella, or Vibrio cholerae & prasitic infestation of the GB; also seen in sarcoidosis, TB, syphilis, actinomycosis, & possibly complicate priods of prolonged parenteral hyperalimentation.

Acalculous Cholecystopathy
Disordered motility of the GB can produce recurrent biliary pain in pts without gallstones.

Criteria for the dx of this disorder: (1)a recurrent episodes of typical RUQ biliary pain, (2) abnormal CCK cholescintigraphy demonstrating a GB ejection fraction of <40%), (3) infusion of CCK produces the pt's pain, & (4) prior hx of transient abnormalities in LFT that accompanied episodes of RUQ pain. An additional clue would be the identification of a large GB on ultrasound. Finally, it should be noted that sphincter of Oddi dysfunction also can give rise to recurrent RUQ pain & CCK-scintigraphic abnormalities.

Emphysematous Cholecystitis
It is thought to begin with acute cholecystitis followed by ischemia or gangrene of the GB wall & infection by gas-producing organisms, as the anaerobes Clostridium welchii, or pergringes, & aerobes as E. Coli. It occurs more frequently in elderly men & in pts with DM. The Sx are essentially indistinguishable from those of nongaseous cholecystitis. The sx is usually made on the plain abd film by finding of gas within the GB lumen, dissecting within the GB wall to form a gaseous ring, or in the pericholecystic tissues. The morbidity & mortality rates are considerable. Prompt surgical intervention coupled with appropriate antibiotics is mandatory.

CHRONIC CHOLECYSTITIS
Chronic inflammation of GB is almost always assoc. with gallstones & bacteria was present in the bile in 1/4 of the pts. Appropriate antibiotics intra- & postoperatively are recommended in such pts because colonization with Clostridium organisms may be associated with devastating septic co plications following surgery. Chronic cholecystitis may be asymptomatic for yrs.

Rx: cholecystectomy.

COMPLICATIONS OF CHOLECYSTITIS

1. Empyema & hydrops.
   Empyema of the GB usually results from progression of acute cholecystitis with persistent cystic duct obstruction to superinfection of the stagnant bile with a pus-forming bacterial organism. Sx resemble that of cholangitis with high fever, severe RUQ pain, marked leukocytosis, & often, prostration. It carries a high risk of G-neg sepsis &/or perforation. Emergency surgical intervantion with proper antibiotic coverage is required as soon as the dx is suspected.
   Hydrops or mucocele (mucus) of the GB also may result fromo prolonged obstruction of the cystic duct, usually by a large solitary stone. A visible, easily palpable, nontender mass often extending from the RUQ into the right iliac fossa may be found on physical exam. The pts are usually asymptomatic, although chronic RUQ pain also may occur. Cholecystectomy is indicated.
   
2. Gangrene & perforation of the GB.
   Underlying conditions for gangrene often include marked distentio of the GB, vasculitis, DM, empyema, or torsion resulting in arterial occlusion. Gangrene usually predisposes to perforation of the GB. Localized perforations are usually contained by the omentum or by adhesions produced by recurrent inflammation of the GB. Bacterial superinfection may result in abscess formation. Most pts are best treated with cholecystectomy, but some seriously ill pts may be managed with cholecystostomy & drainage of the abscess. Free perforation is less common but is associated with mortality rate of about 30%. Such pts may experience a sudden transient relief of RUQ pain as the distended GB decompresses; this is followed by signs of generalized peritonitis.
   
3. Fistula formation & gallstone ileus.
   Fistularization into an adjacent organ adherent to the GB wall may result from inflammation & adhesion formation. Fistula into the duodenum are most common, followed in freuqnecy by those involving the hepatic flexure of the colon, stomach or jejunum, abd wall, & renal pelvis. Asymptomatic cholecystoenteric fistulas may sometimes be diagnosed by finding gas in the biliary tree on plain abd films. Barium contrast studies or endoscopy of the upper GI or colon may demonstrate the fistule, but OCG will almost never result in opacification of either the GB or the fistulous tract. Rx usually consists of cholecystectomy, common bile duct exploration, & closure of the fistulous tract.
   Gallstone ileus refers to mechanical intestinal obstruction resulting from the passage of a large gallstone into the bowel lumen. The stone customarily enters the duodenum through a cholecystoenteric fistula. The site of obstruction is usually at the ileocecal valve. Dx may occasionaly be found on the plain abd film or following an upper GI series. Early laparotomy is indicated with enterolithotomy & careful palpation of the more proximal small bowel & Gb to exclude other stones.

POST-CHOLECYSTECTOMY COMPLICATIONS
Early postop complications include atelectasis & other pulm. disorders, abscess formation (often subphrenic), external or internal hemorrhage, biliary-enteric fistula, & bile leaks, or jaundice from common bile duct obstruction or retained calculi or intraductal blood clors, or extrinsic compression.

The most common cause of persistent postcholecystectomy Sx is an overlooked extrabiliary disorder as reflux esophagitis, peptic ulceration, postgastrectomy syndrome, pancreatitis, or irritable bowel syndrome. Some post-cholecystectomy syndromes may be due to (1) biliary strictures, (2) retained biliary calculi, (3) cystic duct stump syndrome, (4) stenosis or dyskinesia of the sphincter of Oddi Dx with ERCP or DIDA scan; Rx with endoscopic or surgical sphincteroplasty), or (5) bile salt-induced diarrhea or gastritis (Rx: cholestyramine?).

Cystic Duct Stump Synd with Sx of biliary colic or cholecystitis have frequently attributed to the disease in a long >1cm cystic duct remnant. But, frequently the complaints are from other causes.

(ref: SAMed 7-95, Harrison's Med Textbook 1994)