Background

Gallstones are concretions that form in the biliary tract, usually in the gallbladder. Cholelithiasis is the presence of gallstones in the gallbladder (see the image below).

Cholelithiasis. A gallbladder filled with gallstones (examined extracorporally after laparoscopic cholecystectomy [LC]).

Gallstones develop insidiously, and they may remain asymptomatic for decades. Migration of gallstones may lead to obstruction of the cystic duct (biliary colic), with subsequent inflammation (acute cholecystitis). Cholangitis occurs when a gallstone obstructs the biliary or hepatic ducts, causing inflammation and infection. Obstruction of pancreatic duct can cause acute pancreatitis.[1, 2] Choledocholithiasis is the presence of a gallstone in the common bile duct (see the image below). Choledocholithiasis complicates the workup and management of cholelithiasis, necessitates additional diagnostic and therapeutic procedures, and adds to the morbidity and mortality of gallstone disease.

Common bile duct stone (choledocholithiasis). The sensitivity of transabdominal ultrasonography for choledocholithiasis is approximately 75% in the presence of dilated ducts and 50% for nondilated ducts. Image courtesy of DT Schwartz.

Chronic gallstone disease may lead to fibrosis and loss of function of the gallbladder, and it predisposes to gallbladder cancer. Ultrasonography is the procedure of choice in suspected gallbladder or biliary disease (see Workup). The treatment of gallstones depends upon the stage of disease. Asymptomatic gallstones may be managed expectantly. Once gallstones become symptomatic, definitive surgical intervention with excision of the gallbladder (cholecystectomy) is usually indicated. Cholecystectomy is among the most frequently performed abdominal surgical procedures. In some cases, however, medical dissolution may be considered (see Treatment and Management) Go to Pediatric Cholelithiasis for complete information on this topic.

Pathophysiology
Gallstone formation occurs because certain substances in bile are present in concentrations that approach the limits of their solubility. When bile is concentrated in the gallbladder, it can become supersaturated with these substances, which then precipitate from solution as microscopic crystals. The crystals are trapped in gallbladder mucus, producing gallbladder sludge (see the image below). Over

time, the crystals grow, aggregate, and fuse to form macroscopic stones. Occlusion of the ducts by sludge and/or stones produces the complications of gallstone disease.

Sludge in the gallbladder. Note the lack of shadowing. Image courtesy of DT Schwartz.

Although sludge may be a step in the formation of stones, it may also cause disease in itself. Five to fifteen percent of patients with acute cholecystitis present without stones (acalculous cholecystitis). This typically occurs in patients with prolonged illness, such as those with major trauma or with prolonged ICU stays. The 2 main substances involved in gallstone formation are cholesterol and calcium bilirubinate.

Cholesterol gallstones
More than 80% of gallstones in the United States contain cholesterol as their major component. Liver cells secrete cholesterol into bile along with phospholipid (lecithin) in the form of small spherical membranous bubbles, termed unilamellar vesicles. Liver cells also secrete bile salts, which are powerful detergents required for digestion and absorption of dietary fats. Bile salts in bile dissolve the unilamellar vesicles to form soluble aggregates called mixed micelles. This happens mainly in the gallbladder, where bile is concentrated by reabsorption of electrolytes and water. Compared with vesicles (which can hold up to 1 molecule of cholesterol for every molecule of lecithin), mixed micelles have a lower carrying capacity for cholesterol (about 1 molecule of cholesterol for every 3 molecules of lecithin). If bile contains a relatively high proportion of cholesterol to begin with, then as bile is concentrated, progressive dissolution of vesicles may lead to a state in which the cholesterol-carrying capacity of the micelles and residual vesicles is exceeded. At this point, bile is supersaturated with cholesterol, and cholesterol monohydrate crystals may form. Thus, the main factors that determine whether cholesterol gallstones will form are (1) the amount of cholesterol secreted by liver cells, relative to lecithin and bile salts, and (2) the degree of concentration and extent of stasis of bile in the gallbladder.

Calcium, bilirubin, and pigment gallstones

Bilirubin, a yellow pigment derived from the breakdown of heme, is actively secreted into bile by liver cells. Most of the bilirubin in bile is in the form of glucuronide conjugates, which are quite water soluble and stable, but a small proportion consists of unconjugated bilirubin. Unconjugated bilirubin, like fatty acids, phosphate, carbonate, and other anions, tends to form insoluble precipitates with calcium. Calcium enters bile passively along with other electrolytes. In situations of high heme turnover, such as chronic hemolysis or cirrhosis, unconjugated bilirubin may be present in bile at higher than normal concentrations. Calcium bilirubinate may then crystallize from solution and eventually form stones. Over time, various oxidations cause the bilirubin precipitates to take on a jet-black color, and stones formed in this manner are termed black pigment stones. Black pigment stones represent 10-20% of gallstones in the United States.

Bile is normally sterile, but in some unusual circumstances (eg, above a biliary stricture), it may become colonized with bacteria. The bacteria hydrolyze conjugated bilirubin, and the resulting increase in unconjugated bilirubin may lead to precipitation of calcium bilirubinate crystals. Bacterial hydrolysis of lecithin leads to the release of fatty acids, which complex with calcium and precipitate from solution. The resulting concretions have a claylike consistency and are termed brown pigment stones. Unlike cholesterol or black pigment stones, which form almost exclusively in the gallbladder, brown pigment stones often form de novo in the bile ducts. Brown pigment stones are unusual in the United States but are fairly common in some parts of Southeast Asia, possibly related to liver fluke infestation.

Mixed gallstones
Cholesterol gallstones may become colonized with bacteria and can elicit gallbladder mucosal inflammation. Lytic enzymes from bacteria and leukocytes hydrolyze bilirubin conjugates and fatty acids. As a result, over time, cholesterol stones may accumulate a substantial proportion of calcium bilirubinate and other calcium salts, producing mixed gallstones. Large stones may develop a surface rim of calcium resembling an eggshell that may be visible on plain x-ray films.

Common bile duct stones

Choledocholithiasis occurs as a result of either the primary formation of stones in the common bile duct (CBD) or the passage of gallstones from the gallbladder through the cystic duct into the CBD. (Images of CBD stones are shown below.) Obstruction of the CBD by gallstones leads to symptoms and complications that include pain, jaundice, cholangitis, pancreatitis, and sepsis.

Intraoperative cholangiogram demonstrating a distal common bile duct stone with

dilatation. without

Intraoperative cholangiogram demonstrating a distal common bile duct stone

Etiology
Cholesterol gallstones, black pigment gallstones, and brown pigment gallstones have different pathogeneses and different risk factors.

Cholesterol gallstones
Cholesterol gallstones are associated with female sex, European or Native American ancestry, and increasing age. Other risk factors include the following: Obesity Pregnancy Gallbladder stasis Drugs Heredity The metabolic syndrome of truncal obesity, insulin resistance, type II diabetes mellitus, hypertension, and hyperlipidemia is associated with increased hepatic cholesterol secretion and is a major risk factor for the development of cholesterol gallstones. Cholesterol gallstones are more common in women who have experienced multiple pregnancies. A major contributing factor is thought to be the high progesterone levels of pregnancy. Progesterone reduces gallbladder contractility, leading to prolonged retention and greater concentration of bile in the gallbladder. Other causes of gallbladder stasis associated with increased risk of gallstones include high spinal cord injuries, prolonged fasting with total parenteral nutrition, and rapid weight loss associated with severe caloric and fat restriction (eg, diet, gastric bypass surgery). More than one third of patients develop gallstones after bariatric surgery. Weight loss greater than 25% is the best predictor for the gallstone formation. Rapid weight loss mobilizes tissue cholesterol stores and increases the saturation of bile.[3] Obesity, a high-fat diet, and hypertriglyceridemia are strongly associated with the formation of gallstones. Diosgenin-rich beans, particularly associated with a South American diet, increase cholesterol secretion and gallstone formation. Estrogens administered for contraception or for treatment of prostate cancer increase the risk of cholesterol gallstones. Clofibrate and other fibrate hypolipidemic drugs increase hepatic elimination of cholesterol via biliary secretion and appear to increase the risk of cholesterol gallstones. Somatostatin analogues appear to predispose to gallstones by decreasing gallbladder emptying. About 25% of the predisposition to cholesterol gallstones appears to be hereditary, as judged from studies of identical and fraternal twins. At least a dozen genes may contribute to the risk. [4] A rare syndrome of low phospholipidassociated cholelithiasis occurs in individuals with a hereditary deficiency of the biliary transport protein required for lecithin secretion.

Black pigment gallstones

Black pigment gallstones occur disproportionately in individuals with high heme turnover. In most cases, however, no risk factor can be identified. Disorders of hemolysis associated with pigment gallstones include sickle cell anemia, hereditary spherocytosis, and beta-thalassemia. In cirrhosis, portal hypertension leads to splenomegaly. This, in turn, causes red cell sequestration, leading to a modest increase in hemoglobin turnover. About half of all cirrhotic patients have pigment gallstones. Prerequisites for formation of brown pigment gallstones include colonization of bile with bacteria and intraductal stasis. In the United States, this combination is most often encountered in patients with postsurgical biliary strictures or choledochal cysts.

In hepatolithiasis, a condition encountered mainly in rice-growing regions of East Asia, intraductal formation of brown pigment stones accompanies multiple strictures throughout intrahepatic and extrahepatic bile ducts. This condition causes recurrent cholangitis and predisposes to biliary cirrhosis and cholangiocarcinoma. The etiology is unknown, but liver flukes have been implicated.

Other comorbidities
Diabetes mellitus is associated with an increased risk of gallstone, though the mechanism is unclear; once symptomatic, patients with diabetes are prone to more severe complications. Crohn disease, ileal resection, or other diseases of the ileum decrease bile salt reabsorption and increase the risk of gallstone formation. Bacterial or parasitic infections from organisms that contain B -glucuronidase, an enzyme that deconjugates bilirubin glucuronide, increase the risk for pigmented stones. Cirrhosis carries major multifactorial risks for gallstone formation and gallbladder disease. Reduced hepatic synthesis and transport of bile salts, hyperestrogenemia, impaired gallbladder contraction, and increased biliary stasis, among other factors, contribute to the formation of gallstones (typically pigment stones) in cirrhosis. Other illnesses or states that predispose to gallstone formation include burns, use of total parenteral nutrition, paralysis, ICU care, and major trauma. This is due, in general, to decreased enteral stimulation of the gallbladder with resultant biliary stasis and stone formation.

Bile duct stones

Primary common bile duct stones are caused by conditions leading to bile stasis and chronic bactibilia. Up to 90% of patients with brown pigment CBD stones have bile culture results positive for bacteria. In Western populations, biliary stasis is secondary to factors such as sphincter of Oddi dysfunction, benign biliary strictures, sclerosing cholangitis, and cystic dilatation of the bile ducts. Bile stasis promotes growth of bacteria, which produce phospholipase A1, thus releasing fatty acids from biliary phospholipids. The duct epithelium and/or bacteria (eg, Escherichia coli) produce beta-glucuronidase in amounts sufficient to deconjugate bilirubin diglucuronide. The presence of free fatty acids, deconjugated bilirubin, and bile acids leads to the formation of insoluble calcium bilirubinate particles. With the loss of bile acids, cholesterol becomes insoluble, resulting in the formation of biliary sludge. The sludge also contains mucin and bacterial cytoskeletons, which further aid in stone formation. In Asian populations, infestation with Ascaris lumbricoides and Clonorchis sinensis may promote stasis by either blocking the biliary ducts or by damaging the duct walls, resulting in stricture formation. Bactibilia is also common in these instances, probably secondary to episodic portal bacteremia. Some authors have suggested that the stones are formed because of the bactibilia alone and that the parasites' presence is just a coincidence.

Gallstones

Gallstones are hard, pebble-like deposits that form inside the gallbladder. Gallstones may be as small as a grain of sand or as large as a golf ball. See also:

 Causes

Acute cholecystitis Choledocholithiasis

The cause of gallstones varies. There are two main types of gallstones: Stones made out of cholesterol. Gallstones made out of cholesterol are by far the most common type. Cholesterol gallstones have nothing to do with the cholesterol levels in the blood. Stones made from too much bilirubin in the bile. Bile is a liquid made in the liver that helps the body digest fats. Bile is made up of water, cholesterol, bile salts, and other chemicals, such as bilirubin. Such stones are called pigment stones.

Gallstones are more common in women, Native Americans and other ethnic groups, and people over age 40. Gallstones may also run in families. The following also make you more likely to develop gallstones: Failure of the gallbladder to empty bile properly (this is more likely to happen during pregnancy) Medical conditions that cause the liver to make too much bilirubin, such as chronic hemolytic anemia, including sickle cell anemia Liver cirrhosis and biliary tract infections (pigmented stones) Diabetes Bone marrow or solid organ transplant Rapid weight loss, particularly eating a very low-calorie diet Receiving nutrition through a vein for a long period of time (intravenous feedings)

Symptoms Many people with gallstones have never had any symptoms. The gallstones are often discovered when having a routine x-ray, abdominal surgery, or other medical procedure. However, if a large stone blocks either the cystic duct or common bile duct (called choledocholithiasis), you may have a cramping pain in the middle to right upper abdomen. This is known as biliary colic. The pain goes away if the stone passes into the first part of the small intestine (the duodenum). Symptoms that may occur include: Pain in the right upper or middle upper abdomen: o May go away and come back o May be sharp, cramping, or dull o May spread to the back or below the right shoulder blade o Occurs within minutes of a meal Fever Yellowing of skin and whites of the eyes (jaundice)

Additional symptoms that may occur with this disease include:

Abdominal fullness Clay-colored stools Nausea and vomiting

It is important to see a doctor if you have symptoms of gallstones. Gallstones are found in many people with gallbladder cancer. Exams and Tests Tests used to detect gallstones or gallbladder inflammation include: Abdominal ultrasound Abdominal CT scan Endoscopic retrograde cholangiopancreatography (ERCP) Gallbladder radionuclide scan Endoscopic ultrasound Magnetic resonance cholangiopancreatography (MRCP) Percutaneous transhepatic cholangiogram (PTCA)

Your doctor may order the following blood tests: Bilirubin Liver function tests Pancreatic enzymes

Treatment SURGERY Some people have gallstones and have never had any symptoms. The gallstones may not be found until an ultrasound is done for another reason. Surgery may not be needed unless symptoms begin. In general, patients who have symptoms will need surgery either right away, or after a short period of time. In the past, open cholecystectomy (gallbladder removal) was the usual procedure for uncomplicated cases. However, this is done less often now. A technique called laparoscopic cholecystectomy is most commonly used now. This procedure uses smaller surgical cuts, which allow for a faster recovery. Patients are often sent home from the hospital on the same day as surgery, or the next morning.

Endoscopic retrograde cholangiopancreatography (ERCP) and a procedure called a sphincterotomy may be done to locate or treat gallstones in the common bile duct. MEDICATION

Medicines called chenodeoxycholic acids (CDCA) or ursodeoxycholic acid (UDCA, ursodiol) may be given in pill form to dissolve cholesterol gallstones. However, they may take 2 years or longer to work, and the stones may return after treatment ends. Rarely, chemicals are passed into the gallbladder through a catheter. The chemical rapidly dissolves cholesterol stones. This treatment is not used very often, because it is difficult to perform, the chemicals can be toxic, and the gallstones may return. LITHOTRIPSY Electrohydraulic shock wave lithotripsy (ESWL) of the gallbladder has also been used for selected patients who cannot have surgery. Because gallstones often come back in many patients, this treatment is not used very often anymore. Outlook (Prognosis) Gallstones develop in many people without causing symptoms. The chance of symptoms or complications from gallstones is low. Nearly all patients who have gallbladder surgery do not have their symptoms return (if the symptoms were actually caused by gallstones). Possible Complications Blockage of the cystic duct or common bile duct by gallstones may cause the following problems: Acute cholecystitis Cholangitis Cholecystitis - chronic Choledocholithiasis Pancreatitis

When to Contact a Medical Professional Call for an appointment with your health care provider if you have: Pain in the right upper part of your abdomen Yellowing of the skin or whites of the eyes

Prevention There is no known way to prevent gallstones. If you have gallstone symptoms, eating a low-fat diet and losing weight may help you control symptoms. Alternative Names Cholelithiasis; Gallbladder attack; Biliary colic; Gallstone attack; Bile calculus; Biliary calculus

Cholelithiasis - Causes, Symptoms And Treatment

Diseases of the gallbladder and biliary tract are common and, in many cases, painful conditions that may be life threatening and usually require surgery. They are generally associated with deposition of calculi and inflammation. Cholelithiasis is the fifth leading cause of hospitalization among adults and accounts for 90% of all gallbladder and duct diseases. Women have two to three times the incidence as men of developing cholelithiasis. The disease may also be more prevalent in persons who are obese, who have high cholesterol, or who are on cholesterol lowering drugs. The prognosis is usually good with treatment unless infection occurs, in which case prognosis depends on its severity and response to antibiotics. In most cases, gallbladder and bile duct diseases occur during middle age. Between ages 20 and 50, they're six times more common in women, but incidence in men and women becomes equal after age 50. Incidence rises with each succeeding decade. Causes of Cholelithiasis Cholelithiasis stones or calculi (gallstones) in the gallbladder. results from changes in bile components. Gallstones are made of cholesterol, caldurn bilirubinate, or a mixture of cholesterol and bilirubin pigment. They arise during periods of sluggishness in the gallbladder due to pregnancy. hormonal contraceptives. diabetes mellitus. celiac disease, cirrhosis of the liver, and pancreatitis. One out of every 10 patients with gallstones develops Cholelithiasis, or gallstones in the common bile duct (sometimes called common duct stones). This condition occurs when stones pass out of the gallbladder and lodge in the hepatic and common bile ducts. obstructing the flow of bile into the duodenum. Prognosis is good unless infection occurs. Cholangitis, infection of the bile duct, is commonly associated with choledocholithiasis and may follow percutaneous transhepatic cholangiography or occlusion of endoscopicstents. Predisposing factors may include bacterial or metabolic alteration of bile acids. Widespread inflammation may cause fibrosis and stenosis of the common bile duct. The prognosis for this rare condition is poor without stenting or surgery.

Cholecystitis. acute or chronic inflammation of the gallbladder. is usually associated with a gallstone impacted in the cystic duct, causing painful distention of the gallbladder. Cholecystitis accounts for 10% to 25% of all patients requiring gallbladder surgery. The acute form is most common during middle age; the chronic form occurs most commonly among the elderly. The prognosis is good with treatment. Cholesterolosis. polyps or crystal deposits of cholesterol in the gallbladder's submucosa, may result from bile secretions containing high concentrations of cholesterol and insufficient bile salts. The polyps may be localized or speckle the entire gallbladder. Cholesterolosis the most common pseudotumor. isn't related to widespread inflammation of the mucosa or lining of the gallbladder. The prognosis is good with surgery. Biliary cirrhosis. ascending infection of the biliary system, sometimes follows viral destruction of liver and duct cells. but the primary cause is unknown. This condition usually leads to obstructive jaundice and involves the portal and periportal spaces of the liver. It's nine times more common among women ages 40 to 60 than among men. The prognosis is poor without liver transplantation. Gallstone ileus results from a gallstone lodging at the terminal ileum; it's more common in the elderly. The prognosis is good with surgery. Postcholecystectomy syndrome commonly results from residual gal1stones or stricture of the common bile duct. It occurs in 1 % to 5 % of all patients whose gallbladders have been surgical1y removed and may produce right upper quadrant abdominal pain, biliary colic, fatty food intolerance, dyspepsia. and indigestion. The prognosis is good with selected radiologic procedures, endoscopic procedures, or surgery. Acalculous cholecystitis is more common in critical1y ill patients, accounting for about 5% of cholecystitis cases. It may result from primary infection with such organisms as Salmollella typhi. Escherichia coli, or Clostridium or from obstruction of the cystic duct due to lymphadenopathy or a tumor. It appears that ischemia usually related to a low cardiac output. also has a role in the pathophysiology of this disease. Signs and symptoms of acalculous cholecystitis include unexplained sepsis, right upper quadrant pain, fever, leukocytosis, and a palpable gallbladder. Cholelithiasis Symptoms and Signs Although gallbladder disease may produceno symptoms. acute cholelithiasis, acute cholecystitis, choledocholithiasis. and cholesterolosis produce the

symptoms of a classic gallbladder attack. Attacks commonly follow meals rich in fats or may occur at night. suddenly awakening the patient. They begin with acute abdominal pain in the right upper quadrant that may radiate to the back. between the shoulders. or to the front of the chest; the pain may be so severe that the patient seeks emergency department care. Other features may include recurring fat intolerance. biliary colic. belching. flatulence, indigestion. diaphoresis. nausea. vomiting. chills. low-grade fever. jaundice (if a stone obstructs the common bile duct). and clay-colored stools (with choledocholithiasis). Clinical features of cholangitis include a rise in eosinophils, jaundice, abdominal pain. high fever. and chills; biliary drrhosis may produce jaundice, related itching, weakness, fatigue. slight weight loss. and abdominal pain. Gallstone ileus produces signs and symptoms of small bowel obstruction nausea. vomiting, abdominal distention, and absent bowel sounds if the bowel is completely obstructed. Its most telling symptom is intermittent recurrence of colicky pain over several days. Each of these disorders produces its own set of complications.
Diagnosis and testing information

Differential diagnosis is essential in gallbladder and biliary tract disease because gallbladder disease can mimic other diseases (myocardial infarction. angina. pancreatitis. pancreatic head cancer. pneumonia, peptic ulcer, hiatal henda, esophagitis. and gastritis). Serum amylase distinguishes gallbladder disease from pancreatitis. With suspected heart disease. serial cardiac enzyme tests and electrocardiogram should precede gallbladder and upper GI diagnostic tests. Tests used to diagnose gallbladder and biliary tract disease include:

Ultrasound reflects stones in the gallbladder with 96% accuracy. It's also considered the primary tool for diagnosing cholelithiasis. Percutaneous trashepatic cholangiography. done under fluoroscopic control. distinguishes between gallbladder or bile duct disease and cancer of the pancreatic head in patients with jaundice. Endoscopic retrograde cholangiopancreatography (ERCP) visualizes the biliary tree after insertion of an endoscope down the esophagus into the duodenum, cannulation of the common bile and pancreatic ducts, and injection of contrast medium. HIDA scan of the gallbladder detects obstruction of the cystic duct. Computed tomography scan, although not used routinely, helps distinguish between obstructive and non obstructive jaundice. Flat plate of the abdomen identifies calcified, but not cholesterol. stones with 15% accuracy.

Oral cholecystography, which is rarely used, shows stones in the gallbladder and biliary duct obstruction.

Elevated icteric index, total bilirubin, urine bilirubin, and alkaline phosphatase support the diagnosis. White blood cell count is slightly elevated during a cholecystitis attack. Cholelithiasis treatment Surgery, usually elective, is the treatment of choice for gallbladder and biliary tract diseases and may include open or laparoscopic cholecystectomy, cholecystectomy with operative cholangiography and, possibly, exploration of the common bile duct. Other treatments include a low-fat diet to prevent attacks and vitamin K for itching, jaundice, and bleeding tendendes due to vitamin K deficiency. Treatment during an acute attack may include insertion of a nasogastric tube and an I.V.line and, possibly, antibiotic and analgesic administration. A non surgical treatment for choledocholithiasis involves placement of a catheter through the percutaneous transhepatic cholangiographic route. Guided by fluoroscopy, the catheter is directed toward the stone. A basket is threaded through the catheter,opened, twirled to entrap the stone, closed, and withdrawn. This procedure can be performed endoscopically. Ursodiol (Actigall), which dissolves radiolucent stones, provides an alternative for patients who are poor surgical risks or who refuse surgery. however, use of urdodiol is limited by the need for prolonged treatment, the high incidence of adverse effects, and the frequency of stone formation after the treatment ends. Extra corporeal shock wave lithotrillsy (ESWL) has also been adapted for the treatment of gallstones. ESWL Is a non surgical procedure used to ('rush stones inside the gallbladder. A lithotripsy machine focuses sound waves against the gallstones to break Them into smaller pieces that can pass out of the gallbladder through the cystic duct and common bile duct into the small intestine. ........................................................................................................... .....................
SPECIAL NEEDS

Lithotripsy is contraindicated in pregnant women and those who have a pacemaker or serious heart problems.

........................................................................................................... ..................... Special considerations or prevention Patient care for gallbladder and biliary tract diseases focuses on supportive care and close postoperative observation:

Before surgery, teach the patient to deep-breathe, cough, expectorate, and perform leg exercises that are necessary after surgery. Also teach splinting, repositioning, and ambulation techniques. Explain the procedures that will be performed before, during, and after surgery to help ease the patient's anxiety and help ensure cooperation. After surgery, monitor vital signs for signs of bleeding, infection, or at electasis. Evaluate the indsion site for bleeding. Serosanguineous drainage is common during the first 24 to 48 hours if the patient has a wound drain. If, after a choledochostomy, a T-tube drain is placed in the duct and attached to a drainage bag, make sure that the drainage tube has no kinks. Also check that the connecting tubing from the T tube is well secured to the patient to prevent dislodgment. Measure and record T-tube drainage daily. (200 to 300 ml is normal.) Teach patients who will be discharged with a T tube how to perform dressing changes and routine skin care. Monitor intake and output. Allow the patient nothing by mouth for 24 to 48 hours or until bowel sounds return and nausea and vomiting cease. (Postoperative nausea may indicate a full bladder.) If the patient doesn't void within 8 hours (or if the amount voided is inadequate based on I.V. fluid intake), percuss over the symphysis pubis for bladder distention (especially in patients receiving anticholinergics). Patients who have had a laparoscopic cholecystectomy may be discharged the same day or within 24 hours after surgery. These patients should have minimal pain, be able to tolerate a regular diet within 24 hours after surgery, and be able to return to normal activity within a few days to 1 week. Encourage deep-breathing and leg exercises every hour. The patient should ambulate after surgery. Provide antiembolism stockings to support leg muscles and promote venous blood flow, thus preventing stasis and clot formation. Evaluate the location, duration, and character of any pain. Administer adequate medication to relieve pain, especially before such activities as deep breathing and ambulation, which increase pain. At discharge, advise the patient against heavy lifting or straining for 6 weeks. Urge her to walk daily. Tell her that food restrictions are Unnecessary unless she has an intolerance to a specific food or some underlying condition (such as diabetes, atherosclerosis, or obesity) that requires such restriction. Instruct the patient to notify the surgeon if she has pain for more than 24 hours, notices jaundice, anorexia, nausea or vomiting, fever, or tenderness

in the abdominal area because these may indicate a biliary tract injury from cholecystectomy that requires immediate attention.