cholelithiasis etiology and features.pptx

presentation on cholelithiasis

1. Gallstones donot cause symptoms in upto 80% of carriers. Within 5 years, 10% to 20% became symptomatic. The risk of further symptoms is approximately 2% per year with an overall risk of biliary complications-(acute pancreatitis and symptomatic choledocholithiasis) in asymptomatic patients of 0.3% per year. Half of the patients with symptoms develop a second attack within a year. Based on study of Venneman et al, 2005, there was no clear cost benefit and no life-years were gained from prophylactic cholecystectomy, indicating no clear-cut advantages of prophylactic cholecystectomy in asymptomatic cholelithiasis.

2. Causes of gall stones I. Metabolic : Cholesterol is synthesised in liver. Its solubility is determined by relative concentration of cholesterol, bile salts and lecithin. Altered levels of cholesterol, lecithin, and bile salts in bile reduces the micelle concentration in the bile leading to precipitation of insoluble cholesterol, hence, the stone formation (Lithogenic bile). Normal ratio of bile salt + lecithin to cholesterol is 25:1. Ratio below 13:1 leads to precipitation of cholesterol. . If cholesterol component increases, bile gets supersaturated and inadequate micelle makes insoluble cholesterol to undergo crystallisation and cholesterol monohydrate stone formation

3. II. Infections and Infestations : Bacteria like E. coli, Salmonella Parasites like Clonorchis sinensis and Ascaris lumbricoides are often associated. III. Bile stasis : Occurs due to estrogen therapy, pregnancy, vagotomy and in patients who are on long-term intravenous fluids or TPN. IV. Increased bilirubin production Due to any of the causes of haemolysis as in hereditary spherocytosis, sickle cell anaemia, thalassaemia, malaria, cirrhosis. Here pigment stones are common.

4. TYPES OF GALLSTONES: Cholesterol Stones: Pure cholesterol stones are uncommon and account for <10% of all stones. They usually occur as single large stone with smooth surfaces. Most other cholesterol stones contain variable amounts of bile pigments and calcium, but are always >70% cholesterol by weight. These stones are usually multiple, of variable size, and may be hard and faceted or irregular, mulberry-shaped, and soft. Colours range from whitish yellow and green to black. Most cholesterol stones are radiolucent; <10% are radiopaque.

5. Pigment Stones: Black Pigment Stones: These are usually small, brittle, and sometimes speculated. These are formed by supersaturation of Calcium bilirubinate , carbonate, and phosphate, most often secondary to haemolytic disorders such as hereditary spherocytosis and sickle cell disease, and in those with cirrhosis. In Asian countries such as Japan, black stones account for a much higher percentage of gallstones than in Western hemisphere.

6. Brown Pigment Stones : They may form either in the gallbladder or in bile ducts, usually secondary to bacterial infection called by bile stasis. Precipitated calcium bilirubinate and bacterial cell bodies compose the major part of the stone. Bacteria such as E.coli secrete beta-glucuronidase that enzymatically cleaves bilirubin glucuronide to produce the insoluble unconjugated bilirubin. It precipitates with calcium, and along with dead bacterial cell bodies,

7. RISK FACTORS FOR GALLSTONES DEVELOPMENT: AGE: The incidence of gallstones increases with age across all ethnic groups, and it is very low among infants and children. Some specific populations such as Pima Indians have an increased incidence of gallstones ( upto 70%) by 30 years of age. This implies hereditary metabolic factors in the causation of gallstones.

8. GENDER: Female genders are at a greater risk of developing gallstones by a factor 0f 2:1. Pregnancy is associated with upto 30% risk of developing biliary sludge.

9. GENETICS: Studies indicate upto 30% genetic component in the development of gallstone disease. Genes controlling hepatic cholesterol metabolism have been implicated in the pathogenesis of gallstone formation in knockout mouse models and in humans.

10. EFFECTS OF GALLSTONES In the Gallbladder: Silent asymptomatic stones occur in 10% males and 20% females Biliary colic with periodicity. Biliary colic is spasmodic pain often severe in right upper quadrant and epigastrium radiating to chest and right shoulder. Acute cholecystitis.

11. Chronic cholecystitis. Empyema gallbladder. Mucocele of gallbladder. Perforation causing biliary peritonitis or pericholecystic abscess. Carcinoma of gallbladder.

12. In the Common bile duct. Secondary CBD stones. Cholangitis. Pancreatitis. In the intestine Cholecystoduodenal fistula causing gallstone ileus and so intestinal obstruction

13. ACUTE CHOLECYSTITIS Commonly, it occurs in a patient with pre-existing chronic cholecystitis but often also can occur as a first presentation. Usual cause is impacted gallstone in the Hartmann’s pouch, obstructing cystic duct. Classification Acute calculous cholecystitis . Acute acalculous cholecystitis (10%).

14. Pathogenesis of Acute Cholecystitis Stone causes obstruction at Hartmann’s pouch or in cystic duct. Obstruction causes stasis, oedema of the wall, bacterial infection, acute cholecystitis and its effects. Impacted stone also causes mucosal erosion allowing bile salts to act over the submucosal tissues as bile is toxic to these tissues. It leads into necrosis, further infection and often perforation of the gallbladder usually at Hartmann’s pouch.

15. Complications of Acute Cholecystitis Acute cholecystitis can lead to: Perforation—5–10% which usually occurs in the fundus or in the neck (Hartmann’s). It can cause cholecystoduodenal , cholecystointestinal or cholecystobiliary fistula, Mirrrizi's syndrome. Peritonitis. Pericholecystitic abscess. Cholangitis and septicaemia. Empyema gallbladder, gangrenous gallbladder

16. Clinical Features Sudden onset of pain in the right hypochondrium, with tenderness, guarding, and rigidity. Palpable, tender, smooth, soft gallbladder. Area of hyperaesthesia between 9th and 11th ribs posteriorly on the right side ( Boas’s sign). Jaundice may be present. Fever, nausea, palpable tender mass in GB region (25%). Tachycardia and toxic features. Murphy’s sign may be positive (mid-inspiratory arrest

17. Ultrasound abdomen—very useful, reveals presence or absence of gallstones; and thickening of gallbladder wall. Sonographic Murphy’s sign may be positive. Plain X-ray abdomen—10% of gallstones are radio-opaque; also rules out other causes of acute pain abdomen. Gas is seen in emphysematous GB. Total count shows neutrophilia. LFT is important. Increased serum bilirubin often signifies cholangitis or stone in the CBD. Plain X-ray abdomen is not very relevant but is often important to rule out duodenal ulcer perforation, peritonitis. Only 10% of gallstones are radio-opaque.

18. Treatment Advised hospitalisation. Initially (nonoperative) conservative treatment (95%): Nasogastric aspiration. IV fluids. Analgesics and antispasmodics. Broad spectrum antibiotics ( cefoperazone , ceftazidime, ceftriaxone, cefotaxime + amikacin, tobramycin + metronidazole {antimicrobial}). Observation. Follow-up U/S scan.

19. Indications for Laparoscopic Cholecystectomy Symptomatic cholelithiasis. Biliary colic Acute cholecystitis (within 48 to 72 hours). Acalculous cholecystitis. Gallstone pancreatitis.

20. Asymptomatic cholelithiasis Total parenteral nutrition Children with haemoglobinopathies (Sickle cell disease, spherocystosis , thalassemia) Chronic immunosuppression

21. ACUTE ACALCULOUS CHOLECYSTITIS (5%) It is not an uncommon entity, but can be commonly missed. It is common in patients who have undergone major surgeries, trauma, burns, or any other stress . Common in ICU patients—in critically-ill patients. It is due to bile stasis and ischaemia . Common in AIDs, elderly males, diabetics, patients who have undergone major non biliary surgery, patients who are on TPN, atherosclerotics . Exact cause is not known..

22. Pathology is oedema and necrosis of the gallbladder wall with features of acute inflammation. Presentation is usually acute. Gangrene, perforation, empyema are very common (70%). Treatment: Cholecystectomy. Percutaneous US-guided/CT-guided or open cholecystostomy initially, later cholecystectomy is the treatment of choice

23. MIRIZZI SYNDROME In Mirizzi syndrome, gallstone impacts in the gallbladder wall and compresses it causing pressure necrosis which further gets adherent to CHD/CBD wall. It eventually causes compression and later occasionally leads into cholecystocholedochal fistula. It occurs either from Hartmann’s pouch into CHD/CBD (common) or from fundus of gallbladder into the CBD.

24. Mirizzi syndrome is suspected on CT scan, but usually identified on table. X Partial cholecystectomy with primary closure of CHD/CBD is done with a T-tube insertion through a separate choledochotomy in type 2 or RouX-en-Y hepaticojejunostomy

25. CHOLEDOCHOLITHIASIS Classification Primary—Rare—brown pigment stones. Secondary—Common—black pigment stones/cholesterol stones. It is seen in 15% of gallstone disease; 75% are cholesterol stones, 15% are pigment stones.

26. Primary stones They are formed in CBD and biliary tree itself, and are multiple, often sludge like, commonly pigment or mixed type, extends into hepatic ducts (Brown pigment stones). Causes: Defective pathophysiology of biliary tree causing stasis , biliary dyskinesia, benign biliary stricture, sclerosing cholangitis, biliary dilatation, choledochal cyst. Congenital conditions like Caroli’s disease, choledochal cyst. Infections and infestations like clonorchiasis , ascariasis.

27. Secondary biliary stones They are from gallbladder (gallstones) pass through cystic duct to CBD. Here CBD and biliary tree are otherwise normal. Secondary stones are better and easier to manage than primary stones. Commonly gallstones get impacted in supraduodenal portion of CBD

28. Clinical Features Incidental CBD stones along with jaundice/without jaundice. Pain: It may be biliary colic; nonspecific abdominal pain; pain of ascending cholangitis, pain of pancreatitis. Jaundice—most common clinical manifestation. Fever with chills and rigors (Cholangitis) Charcots triad – intermittent pain ,fever, jaundice Reynold’s pentad – septic shock + altered mental status

29. Investigations US abdomen may show gallstones, dilated CBD >8 mm which suggests biliary obstruction. Sensitivity for CBD stones is only 65%.  If a strong suspicion still exists based on history, physical, and laboratory findings in the face of a negative ultrasound, then a magnetic resonance cholangiopancreatography (MRCP) can be ordered. 92% sensitivity and a specificity of 100% MRCP is noninvasive investigation which delineates biliary tree anatomy and pathology clearly; but it is not therapeutic. Blood investigations Serum amylase and lipase should be done to rule out associated pancreatitis. ERCP- Diagnostic + Therapeutic

30. A sphincterotomy with a balloon sweep is done and stones are extracted, with a less than 5% to 8% complication rate. (bleeding, perforation, pancreatitis) Indications for preoperative ERCP include cholangitis, biliary pancreatitis, and patients with multiple comorbidities. However, some studies have suggested higher risk of surgical site infection in patients who receive preoperative ERCP before cholecystectomy.

31. Treatment ERCP – sphincterotomy + stone extraction , lap cholecystectomy before discharging patient Lap / open cholecystectomy followed by intra-op cholangiogram – if cbd stone found-------lap cbd exploration or send patient for ERCP Large stones (usually more than 2.5 cm), altered gastric or duodenal anatomy such as Roux-en-Y, impacted stones, intrahepatic stones, or multiple stones, are the most common causes of failure of ERCP After CBD exploration , bile duct is closed over a T-tube, t-tube cholangiogram done after 2 weeks No filling defects- remove T-tube, else do ERCP