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Gallstones Are the Most Commonest Biliary Pathology - Essay Example

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The paper "Gallstones Are the Most Commonest Biliary Pathology" states that gallstones are a common disorder and often cause no symptoms. However, they can produce severe pain and complications, which require prompt treatment. An ultrasound exam provides a simple, quick method of diagnosis…
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Gallstones Are the Most Commonest Biliary Pathology
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Introduction Gallstones are the commonest biliary pathology, more prevalent in western countries. Although it is asymptomatic in the majority, it can cause significant morbidity and mortality if left untreated. A variety of imaging modalities are performed to accurately diagnose the condition. There are a variety of both surgical and medical methods of treatment. The purpose of this study was to explore the typical conditions of this disorder, the various investigations and treatment modalities, as well as to review the complications and prognosis of the condition. Prevalence In general, gallstones are about two times more common in women than in men. Most study series show a prevalence of gall stones in women between the age of 20-55 years (5-20%) and after the age of 50 years, the prevalence for men is about half as that for women in a given age group (Sleisenger, 2002). Ethnic And Genetic predisposition The first degree relatives of patients with gall stones are 4.5 times more likely to develop the same condition as compared to age and gender matched controls (Sarin, 1995). High-risk populations include Pima Indians in Arizona, where 70% of women older than 25 years have gallstones. About 50 % of Scandinavians develop the condition by 50 years of age. Other high-risk populations comprise the American Indian groups in Alaska, Canada, Bolivia and Chile (Egbert, 1991). The populations at the lowest risk are those in Sub-Saharan Africa and Asia (Su CH, 1992) Age Bile becomes more lithogenic with increasing age because the cholesterol secretion into bile increases with age, whereas the bile acid formation may decrease (Sleisenger, 2002). Obesity Obesity is a well-known risk factor and individuals with BMI > 45kg/w2 are at a seven-fold higher risk for the development of gallstones in comparison with controls (Stampfer MJ, 1992). Cholesterol hypersecretion into bile and increased cholesterol secretion have been implicated. Rapid weight loss contributes to gallstone disease. About 25% of obese patients on strict dietary restriction and 50% of patients who have gastric bypass develop gallstones, 6 months following the surgery (Shiffman ML et al., 1986.) Other factors Foetal parenteral nutrition and drugs like clofibrate, oral contraceptives, estrogens, progesterone, ceftriaxone and octreotide are causative agents. Pregnancy is a potentially lithogenic condition due to increased cholesterol secretion and supersaturation of bile, occurring due to increased estrogen levels (Lynn J, 1973). In many studies, fecundity has been implicated in the increased prevalence of gallstone (Tsimoyiannis, 1994 & Miquel JF, 1998.) Pathogenesis According to their chemical composition, gallstones can be classified into cholesterol stones, mixed stones, and pigment stones. Cholesterol stones, which comprise 6 % , consist entirely of cholesterol and are often solitary. Mixed stones occur in about 90% of the population in western countries, with cholesterol as the major component. Other components include calcium phosphate, calcium bilirubinate, calcium carbonate , calcium palmitate and proteins. Pigment stones are more common in the Far East, and are almost entirely composed of calcium bilirubinate. They may be black or brown-pigmented stones (Mann CV, Russell RCG, 1991.) Supersaturation of bile with cholesterol, nucleation of cholesterol monohydrate crystals and gall bladder hypomotility are three major factors, which are implicated in cholesterol stone formation (Harrison, 2005). The major predisposing factor in the formation of black pigment stone is the hypersecretion of bilirubin conjugate into bile (Wolff BG, 1995). Thus, the associated conditions are those with chronic haemolysis (beta thalassemia, hereditary spherocytosis, sickle cell disease), cirrhosis and pancreatitis (Trotman BW, 1991). Brown pigment stone formation recurs secondary to anaerobic infections of the bile (Leung JW, 1989.) Relationship of sludge to gallstones The term sludge is applied to an abnormality of bile seen with gallbladder ultrasonography. Inside the gallbladder, the bile is denser because it contains microscopic particles, usually cholesterol or pigment, embedded in mucus. Thus it is seen to be of two different densities with the denser bile on the bottom. This sludge may either remain as such in the gallbladder, may disappear, or it may come and go. The particles in sludge may ultimately be the precursors of gallstones, and it has been observed that in certain situations like rapid weight loss, pregnancy, and with prolonged fasting, they occur more often. However, there is still some uncertainty on whether sludge progresses to become gallstones. Practically, this implies that sludge should not be considered the cause of the symptoms, unless an individuals symptoms are typical of gallstones. (MedicineNet, 2006.) Clinical Features Gallstones may remain asymptomatic in upto 75% of patients. A gallstone becomes symptomatic by two mechanisms: obstruction to the cystic duct or common bile duct (Traverso LW, 1993.) Biliary colic- this is the most characteristic symptom, which begins suddenly and persists between 30 minutes to 5 hours with a severe intensity, and may be a poorly localised epigastric or right upper quadrant visceral pain. It is due to the intermittent obstruction of the cystic duct. Nausea and vomiting may accompany the pain. Complaints of vague fullness, eructation and flatulence are not specific for biliary calculi and should not be confused for biliary pain. Mild to moderate gall bladder tenderness may often be present. Acute cholecystitis- an impacted stone in the cystic duct may result in acute inflammation of the gall bladder mucosa and cause visceral epigastric pain , which progresses to severe localised right upper quadrant pain , lasting more than 6 hours (Raine PAM, 1975). Fever, less than 102oF is usually present in 20 % of the patients and the serum bilirubin is usually < 4mg/dl (Dumont AE, 1976). Murphy’s sign is a relatively specific finding in acute cholecystitis (Raine PAM, 1975). The gall bladder may be palpable in 1/3rd of the cases. The resolution of pain occurs in 7-10 days ( Edlund Y, 1961). Choledocholithiasis- this is due to the intermittent obstruction of the common bile duct. This condition is often asymptomatic. Acute obstruction causes biliary colic and jaundice, but gradually progressive obstruction developing over months may present as pruritis or jaundice alone (Way LW, 1973). Findings on physical examination may range from normal to the presence of jaundice. The gall bladder is usually not palpable. Cholangitis-when bacterial superinfection occurs in stagnant bile (secondary to impacted stone in the CBD), cholangitis occurs. This manifests as Charcot’s triad of right upper quadrant pain, fever, and jaundice, which is seen in about 70 % of the cases (Pitt HA, 1987). When superimposed with hypotension and confusion, gram-negative sepsis should be suspected. Atypical clinical features Acute cholecystitis with high toxicity may be a pointer towards emphysematous cholecystitis. Features of small bowel obstruction may occur when the gallstone exceeds 25 mm in diameter and causes obstruction in the iliocaecal area (Clavier PA, 1990) Investigations The following tests are routinely performed: 1. Haemogram, including total and differential counts. 2. Liver function test (serum bilirubin, aminotransferase and alkaline phosphatase). 3. Blood culture. 4. Serum amylase. 5. Imaging studies. These include plain abdominal radiography, which however, lacks specificity and sensitivity. About 50 % of pigment stones and 20 % of cholesterol stones are visible on plain abdominal X-rays. They have utility in assessing unusual complications like emphysematous cholecystitis, cholecystoenteric fistula. Ultrasonography is the gold standard for the diagnosis of gall bladder stones. It requires no special patient preparation, does not involve ionising radiation, is simple t perform, gives anatomically accurate information, it is portable, and thus available at the bedside of sick patients (Bortoff GA, 2000). The procedure is done after 8 hours of fasting. The picture consists of echogenic objects within the lumen, producing acoustic shadows, aggregating in the dependent portion of the gallbladder. The sensitivity is more than 95% for stones > 2mm in diameter (Shea JA, 1994). It is less useful in the detection of CBD stones due to interference from bowel gas shadows. The finding of a dilated CBD may suggest an obstructing CBD stone. Acute cholecystitis shows pericholecystic fluid in the absence of ascites, and ultrasonographic Murphy’s sign. 6. Oral Cholecystography. It is used as a secondary means of identifying gallstones, and useful when ultrasound is unable to demonstrate gallbladder when it is contracted with stones. 7. Computed Tomographic Cholangiography and Magnetic Resonance. These are useful to detect gallstone complications like pericholecystic fluid in acute cholecystitis, gas in the gall bladder wall, perforation and abscess formation. Sophisticated computer analysis of raw CT or MRI data can help in the 3D reconstruction of CBD and detection of CBD stones (Fulcher AS, 1999). This correlates well with ERCP results. These procedures are reserved for patients with low probability of having CBD stones. 8. ERCP. This is the gold standard for the diagnosis of Choledocholithiasis (Ott DJ, 1992). The overall sensitivity in detecting stones in CBD is 95%, as is the specificity. The additional advantage is the therapeutic application of CBD stone removal. 9. Endoscopic ultrasonography. This has the advantage of being able to visualise CBD and thus confirm or exclude cholelithiasis. It has a positive predictive value of 98% and a negative predictive value of 88 % for the diagnosis of CBD stones (Praf F, 1996). The procedure is comparable with ERCP with regards to accuracy, is safer and less expensive. However, the disadvantages are that it cannot be used as a therapeutic modality for gallstone removal, unlike ERCP, and is more invasive and expensive than traditional ultrasound. 10. Cholescintigraphy (Hepatobiliary Scintigraphy). The greatest utility of this technique is in the evaluation of acute cholecystitis (Prevot N, 1999). After IV administration of Tc99 labelled hydroxy-imini-diacetic acid (HIDA) and di-isopropyl-imino-diacetic acid (DISIDA) they are rapidly taken up by the liver and excreted in the bile, and serial scans after injection show radiolucency in the gall bladder, CBD and small bowel within 30-60 minutes. An abnormal or positive scan result is defined as the non-visualisation of the gall bladder with preserved excretion into he CBD or small bowel, indicating an obstruction of the cystic duct (sensitivity is approximately 95% and specificity 90%). Management of Gallstone Disease: Broadly, they can be considered under surgical and non-surgical methods. Surgery- the indications for cholecystectomy (open cholecystectomy or laparoscopic cholecystectomy) are: 1. Biliary colic-surgery is performed to relieve symptoms and prevent complications. 2. Acute cholecystitis. 3. Emphysematous cholecystitis. 4. Gallstone pancreatitis. 5. Mirizzi syndrome. 6. Childhood gallstone disease. 7. Incidental cholecystectomy-in large (72.5 cm) gallstones and those with calcification of gall bladder wall (porcelain gall bladder), the higher risk of developing gallbladder carcinoma and acute cholecystitis warrants incidental cholecystectomy. Results of cholecystectomy: about 90-95% of patients are cured of the symptoms. The mortality rate due to cholecystectomy is less than 1 %. The major complication of the procedure includes: bile leak, bile duct injury causing biliary stricture and acute pancreatitis. Compared to open cholecystectomy, laparoscopic cholecystectomy is minimally invasive, has less scarring, and the patient can have a faster rehabilitation. Non-surgical management of gallstone disease: 1. Oral bile acid dissolution therapy-the mechanism of action is by reversal of the supersaturation of bile with cholesterol (Paum Gartner G, 1991). Ursodeoxycholic acid removes cholesterol from the gallstones by the formation of liquid crystalline phase. The dose is 10-15 mg/kg/day. Bedtime administration enhances bile acid secretion during the night. Chenodeoxycholic acid aids in cholesterol removal by micellar solubilisation. The dose is 14-16 mg/kg/day. The side effects are diarrhoea, rise in aminotransferase, and rise in serum cholesterol. These side effects can be avoided by combining low dose (5mg/kg) each of UDCA and chenodeoxycholic acid. The criteria for patient selection for oral bile acid dissolution therapy, includes the following: symptomatic patients without complications of gallstone disease, patent cystic duct, radiolucent stones, and stones with a diameter < 5mm. 2. Extra Corporeal Shock Wave Lithotripsy (ESWL). This is used as an adjunct to oral bile acid dissolution therapy. It increases the surface to volume ratio of gallstones and enhances the cholesterol stone dissolution. Small stone fragments are created, which can pass into the intestine and increases the clearance of stone material (Paum Gartner G, 1991). The selection criteria for this procedure includes: symptomatic patients without complications, patent cystic duct, gall bladder emptying >60% of fasting volume, radiolucent stones with diameter Mann CV, Russell RCG, 1991. Gallstones. Bailey & Love’s Short Practice Of Surgery. 21st edition. ELBS. 1059. NIH Publication, 1994. Digestive diseases in the United States: Epidemiology and Impact, NIDDK. No. 94-1447. Ott DJ (1992). Interventional endoscopy of biliary and pancreatic ducts-Current Medications and Methods. Am J Roentgenol, 1992. 158: 243. Pitt HA (1987). Acute Cholangitis. Surgery of gall bladder and bile ducts. WB Saunders, 1987. 295. Praf F (1996). Prospective controlled study of endoscopic ultrasound and ERCP in patients with suspected common bile duct stones. Lancet, 1996. 347: 75. Paum Gartner G (1991). Gallstones: Pathogenesis. Lancet, 1991. 338:1117. Raine PAM (1975). Acute cholecystitis. Br J Surgery, 1975. 62:697. Sarin Sk et al (1995). High familial prevalence of gallstones in first-degree relatives of gallstone patients. Hepatology 22: 138, 1995. Sackman M et al (1991). Munich Gall bladder lithotripsy study: Results of first 5 years with 711 Patients. Ann Intern Med, 1991. 114:290. Shiffman ML et al (1986). Gallstone formation after rapid weight loss. Am J Gastroenterol, 1991. 86:1000. Shea JA et al (1994). Revised estimates of diagnostic test sensitivity & specificity in suspected biliary tract disease. Am J Gastroenterol, 1994. 56:789. Su CA (1992). Relative prevalence of gallstone diseases in Taiwan: A nationwide cooperative study. DigbDis Sci, 1992. 37:764. Sleisenger (2002). Gastrointestinal and Liver Disease. 7th Ed. Vol 1. Saunders. Stampfer MJ (1992). Risk of symptomatic gallstones in women with severe obesity. Am J Clinic Nutr, 1992. 55:652. Tsuchiya Y(1995). Repeated piezoelectric lithotripsy for gallstones with and without Ursodeoxycholic acid dissolution. J Gastroenterol, 1995. 30:768. Tsimoyiannis EC, 1994. Cholelithiasis during pregnancy & lactation: prospective study. Eur J Surg, 1994. 160:627 Trotman BW (1991). Pigment gallstones. Gastroenterol Clin North Am, 1995. 20:111. Traverso LW (1993). Clinical manifestations and impact of gallstone disease. Am J Surg, 1993. 27:915. Way LW (1973). Retained common duct stones. Surg Clin North Am, 1973. 53:1139-1973. Wolff BG (1995). Current status of incidental surgery. Dis Colon Rectum, 1995. 38: 431-441. Read More
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