The solubility of cholesterol in bile is determined by:
Pure cholesterol stones are uncommon and account for < 10% of all stones. They usually occur as single large stones 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. Colors range from whitish yellow and green to black. Most cholesterol stones are radiolucent; < 10% are radiopaque. Whether pure or of mixed nature, the common primary event in the formation of cholesterol stones is supersaturation of bile with cholesterol. Therefore, high bile cholesterol levels and cholesterol gallstones are considered one disease. Cholesterol is highly nonpolar and insoluble in water and bile. Cholesterol solubility depends on the relative concentration of cholesterol, bile salts, and lecithin (the main phospholipid in bile). Supersaturation almost always is caused by cholesterol hypersecretion rather than by a reduced secretion of phospholipid or bile salts.
Acute cholecystitis is considered:
Obstruction of the cystic duct by a gallstone is the initiating event that leads to gallbladder distention, inflammation, and edema of the gallbladder wall. Why inflammation develops only occasionally with cystic duct obstruction is unknown. It is probably related to the duration of obstruction of the cystic duct. Initially, acute cholecystitis is an inflammatory process, probably mediated by the mucosal toxin lysolecithin, a product oflecithin, as well as bile salts and platelet -activating factor. Increase in prostaglandin synthesis amplifies the inflammatory response. Secondary bacterial contamination is documented in 15 to 30% of patients undergoing cholecystectomy for acute uncomplicated cholecystitis. In acute cholecystitis, the gallbladder wall becomes grossly thickened and reddish with subserosa! hemorrhages. Pericholecystic fluid often is present. The mucosa may show hyperemia and patchy necrosis. In severe cases, about 5 to 10%, the inflammatory process progresses and leads to ischemia and necrosis of the gallbladder wall. More frequently, the gallstone is dislodged and the inflammation resolves.
A 54-year-old otherwise healthy woman presents to the emergency department with abdominal pain, fever, chills, and confusion. Blood pressure is 95/50, heart rate 1 10, and temperature 39°C. Laboratory tests demonstrate a white blood cell count of 15,000, normal hematocrit and platelets, as well as a direct bilirubin of 7.2. Initial management should be:
The initial treatment of patients with cholangitis includes intravenous (IV) antibiotics and fluid resuscitation. These patients may require intensive care unit monitoring and vasopressor support. Most patients will respond to these measures. However, the obstructed bile duct must be drained as soon as the patient has been stabilized. About 15% of patients will not respond to antibiotics and fluid resuscitation, and an emergency biliary decompression may be required. Biliary decompression may be accomplished endoscopically, via the percutaneous transhepatic route, or surgically. The selection of procedure should be based on the level and the nature of the biliary obstruction. Patients with choledocholithiasis or periampullary malignancies are best approached endoscopically, with sphincterotomy and stone removal, or by placement of an endoscopic biliary stent. In patients in whom the obstruction is more proximal or perihilar, or when a stricture in a biliaryenteric anastomosis is the cause or the endoscopic route has failed, percutaneous transhepatic drainage is used. When neither ERCP nor percutaneous transhepatic cholangiography (PTC) is available, an emergent operation for decompression of the common bile duct with a T tube may be necessary and lifesaving. Definitive operative therapy should be deferred until the cholangitis has been treated and the proper diagnosis established. Patients with indwelling stents and cholangitis usually require repeated imaging and exchange of the stent over a guidewire.
Risk factors for acalculous cholecystitis include:
Acute inflammation of the gallbladder can occur without gallstones. Acalculous cholecystitis typically develops in critically ill patients in the intensive care unit. Patients on parenteral nutrition with extensive burns, sepsis, major operations, multiple trauma, or prolonged illness with multiple organ system failure are at risk for developing acalculous cholecystitis. The cause is unknown, but gallbladder distention with bile stasis and ischemia has been implicated as causative factors. Pathologic examination of the gallbladder wall reveals edema of the serosa and muscular layers, with patchy thrombosis of arterioles and venules. US is the diagnostic test of choice. Percutaneous US or CT-guided cholecystostomy is typically the intervention of choice, as they are often unfit for surgery. After recovery from the systemic disease, cholecystectomy may be indicated.
Appropriate management of a patient with cirrhosis secondary to sclerosing cholangitis includes:
Sclerosing cholangitis (primary or secondary) is an uncommon disease characterized by inflammatory strictures involving the intrahepatic and extrahepatic biliary tree. It is a progressive disease which can lead to biliary cirrhosis. Medical therapy has long been attempted with immunosuppressants, antibiotics, steroids, and ursodeoxycholic acid, and has been disappointing. Surgical management with resection of the extrahepatic biliary tree and hepaticojejunostomy has produced reasonable results in patients with extrahepatic and bifurcation strictures, but without cirrhosis or significant hepatic fibrosis. In patients with sclerosing cholangitis and advanced liver disease, liver transplantation is the only option. It offers excellent results, with overall 5-year survival as high as 85%. Primary sclerosing cholangitis recurs in 10 to 20% of patients and may require retransplantation.
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