TOC | GI
Gall Stone Diseases
Types of GB stones:
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:
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
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.
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.
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 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.
COMPLICATIONS OF CHOLECYSTITIS
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)