case stydy on cholithiasis

7/30/2019 Case Stydy on Cholithiasis

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Post RN BScN 1st

Semester

Advance Concept of Nursing

Clinical Port Folio - I

Case Study on

Typhoid Fever


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Table of Content

S.No Index Page #

1 Clinal case Sanerio 01

2 Clinical Objectives

3 Patient History

Demographic data

Presenting complain

History of present illness

Past medical and surgical history

Medication

Family History

Social history

4 Functional Health Pattern

Health perception management

Active exercise pattern

Cognitive perceptual pattern

Value belief pattern

Sleep rest pattern

Nutrition metabolic pattern

Urinary elimination pattern Coping/Stress tolerance pattern

Role relationship pattern

Sexually reproductive pattern

Self perception pattern

Self concept pattern

5 Review of System

General appearance

Skin, nails, hairs

Face ( Ear, Nose, Throat, Mouth )

Neck

Chest

Breast

Heart

Abdomen


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Extremities

Genitals

6 Treatment Modalities

Ultrasound

Lab Investigations Medications

7 Disease process

8 Nursing Care Plans

9 Drug Card

10 Reflections

11 References

12 Articles


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Cholelithiasis

BackgroundCholelithiasis is the medical term for gallstone disease. Gallstones are concretions that form in the biliary

tract, usually in the gallbladder (see the image below).

Cholelithiasis. A gallbladder filled with gallstones (examined extracorporally afterlaparoscopic cholecystectomy [LC]).Gallstones develop insidiously, and they may remain asymptomatic for decades. Migration of a a

gallstone into the opening of the cystic duct may block the outflow of bile during gallbladder contraction.The resulting increase in gallbladder wall tension produces a characteristic type of pain (biliary colic).Cystic duct obstruction, if it persists for more than a few hours, may lead to acute gallbladderinflammation (acute cholecystitis).

Choledocholithiasisrefers to the presence of one or more gallstones in the common bile duct. Usually,this occurs when a gallstone passes from the gallbladder into the common bile duct (see the imagebelow).

Common bile duct stone (choledocholithiasis). The sensitivity of transabdominalultrasonography for choledocholithiasis is approximately 75% in the presence of dilated ducts and 50% for nondilated ducts.Image courtesy of DT Schwartz.A gallstone in the common bile duct may impact distally in the ampulla of Vater, the point where thecommon bile duct and pancreatic duct join before opening into the duodenum. Obstruction of bile flow bya stone at this critical point may lead to abdominal pain and jaundice. Stagnant bile above an obstructingbile duct stone often becomes infected, and bacteria can spread rapidly back up the ductal system intothe liver to produce a life-threatening infection called ascending cholangitis. Obstruction of the pancreaticduct by a gallstone in the ampulla of Vater also can trigger activation of pancreatic digestive enzymes

within the pancreas itself, leading toacute pancreatitis.

[1, 2]

Chronically, gallstones in the gallbladder may cause progressive fibrosis and loss of function of thegallbladder, a condition known as chronic cholecystitis. Chronic cholecystitis predisposes togallbladdercancer.

Ultrasonography is the initial diagnostic procedure of choice in most cases of suspected gallbladder orbiliary tract disease (see Workup).
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The treatment of gallstones depends upon the stage of disease. Asymptomatic gallstones may bemanaged expectantly. Once gallstones become symptomatic, definitive surgical intervention with excisionof the gallbladder (cholecystectomy) is usually indicated. Cholecystectomy is among the most frequentlyperformed abdominal surgical procedures (see Treatment). Complications of gallstone disease mayrequire specialized management to relieve obstruction and infection.

Go toPediatric Cholelithiasisfor complete information on this topic.

PathophysiologyGallstone formation occurs because certain substances in bile are present in concentrations thatapproach the limits of their solubility. When bile is concentrated in the gallbladder, it can becomesupersaturated with these substances, which then precipitate from solution as microscopic crystals. Thecrystals are trapped in gallbladder mucus, producing gallbladder sludge. Over time, the crystals grow,aggregate, and fuse to form macroscopic stones. Occlusion of the ducts by sludge and/or stonesproduces the complications of gallstone disease.

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. Livercells secrete cholesterol into bile along with phospholipid (lecithin) in the form of small sphericalmembranous bubbles, termed unilamellar vesicles. Liver cells also secrete bile salts, which are powerfuldetergents required for digestion and absorption of dietary fats.

Bile salts in bile dissolve the unilamellar vesicles to form soluble aggregates called mixed micelles. Thishappens 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 3molecules of lecithin). If bile contains a relatively high proportion of cholesterol to begin with, then as bileis concentrated, progressive dissolution of vesicles may lead to a state in which the cholesterol-carryingcapacity 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 ofcholesterol secreted by liver cells, relative to lecithin and bile salts, and (2) the degree of concentrationand 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 livercells. Most of the bilirubin in bile is in the form of glucuronide conjugates, which are quite water solubleand stable, but a small proportion consists of unconjugated bilirubin. Unconjugated bilirubin, like fattyacids, phosphate, carbonate, and other anions, tends to form insoluble precipitates with calcium. Calciumenters bile passively along with other electrolytes.

In situations of high heme turnover, such as chronic hemolysis or cirrhosis, unconjugated bilirubin may bepresent in bile at higher than normal concentrations. Calcium bilirubinate may then crystallize fromsolution and eventually form stones. Over time, various oxidations cause the bilirubin precipitates to takeon a jet-black color, and stones formed in this manner are termed black pigment gallstones. Blackpigment 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 becomecolonized with bacteria. The bacteria hydrolyze conjugated bilirubin, and the resulting increase inunconjugated bilirubin may lead to precipitation of calcium bilirubinate crystals.
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Bacteria also hydrolyze lecithin to release fatty acids, which also may bind calcium and precipitate fromsolution. The resulting concretions have a claylike consistency and are termed brown pigment stones.Unlike cholesterol or black pigment gallstones, which form almost exclusively in the gallbladder, brownpigment gallstones often form de novo in the bile ducts. Brown pigment gallstones are unusual in theUnited States but are fairly common in some parts of Southeast Asia, possibly related to liver flukeinfestation.

Mixed gallstones

Cholesterol gallstones may become colonized with bacteria and can elicit gallbladder mucosalinflammation. 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 bilirubinateand other calcium salts, producing mixed gallstones. Large stones may develop a surface rim of calciumresembling an eggshell that may be visible on plain x-ray films.

EtiologyCholesterol 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, andincreasing age. Other risk factors include the following:

Obesity

Pregnancy

Gallbladder stasis

Drugs

HeredityThe metabolic syndrome of truncal obesity, insulin resistance, type II diabetes mellitus, hypertension, andhyperlipidemia 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 majorcontributing factor is thought to be the high progesterone levels of pregnancy. Progesterone reducesgallbladder 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 cordinjuries, prolonged fasting with total parenteral nutrition, and rapid weight loss associated with severecaloric and fat restriction (eg, diet, gastric bypass surgery).

A number of medications are associated with formation of cholesterol gallstones. Estrogens administeredfor contraception or for treatment of prostate cancer increase the risk of cholesterol gallstones byincreasing biliary cholesterol secretion. Clofibrate and other fibrate hypolipidemic drugs increase hepaticelimination 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 fromstudies of identical and fraternal twins. At least a dozen genes may contribute to the risk.[3]A raresyndrome of low phospholipidassociated cholelithiasis occurs in individuals with a hereditary deficiencyof the biliary transport protein required for lecithin secretion.[4]


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Black and brown pigment gallstones

Black pigment gallstones occur disproportionately in individuals with high heme turnover. Disorders ofhemolysis associated with pigment gallstones includesickle cell anemia,hereditary spherocytosis,andbeta-thalassemia. Incirrhosis,portal hypertensionleads tosplenomegaly. This, in turn, causes redcell sequestration, leading to a modest increase in hemoglobin turnover. About half of all cirrhotic patientshave pigment gallstones.

Prerequisites for formation of brown pigment gallstones include intraductal stasis and chronic colonizationof bile with bacteria. In the United States, this combination is most often encountered in patientswithpostsurgical biliary stricturesorcholedochal cysts.

In rice-growing regions of East Asia, infestation with biliary flukes may produce biliary strictures andpredispose to formation of brown pigment stones throughout intrahepatic and extrahepatic bile ducts. Thiscondition, termed hepatolithiasis, causes recurrent cholangitis and predisposes to biliary cirrhosisandcholangiocarcinoma.

Other comorbidities

Crohn disease, ileal resection, or other diseases of the ileum decrease bile salt reabsorption and increasethe risk of gallstone formation.

Other illnesses or states that predispose to gallstone formation include burns, use of total parenteralnutrition, paralysis, ICU care, and major trauma. This is due, in general, to decreased enteral stimulationof the gallbladder with resultant biliary stasis and stone formation.

EpidemiologyThe prevalence of cholelithiasis is affected by many factors, including ethnicity, gender, comorbidities,and genetics.

United States statistics

In the United States, about 20 million people (10-20% of adults) have gallstones. Every year 1-3% ofpeople develop gallstones and about 1-3% of people become symptomatic. Each year, in the UnitedStates, approximately 500,000 people develop symptoms or complications of gallstones requiringcholecystectomy.

Gallstone disease is responsible for about 10,000 deaths per year in the United States. About 7000deaths are attributable to acute gallstone complications, such as acute pancreatitis. About 2000-3000deaths are caused by gallbladder cancers (80% of which occur in the setting of gallstone disease withchronic cholecystitis). Although gallstone surgery is relatively safe, cholecystectomy is a very commonprocedure, and its rare complications result in several hundred deaths each year.

International statistics

The prevalence of cholesterol cholelithiasis in other Western cultures is similar to that in the United

States, but it appears to be somewhat lower in Asia and Africa.

A Swedish epidemiologic study found that the incidence of gallstones was 1.39 per 100 person-years.[5] Inan Italian study, 20% of women had stones, and 14% of men had stones. In a Danish study, gallstoneprevalence in persons aged 30 years was 1.8% for men and 4.8% for women; gallstone prevalence inpersons aged 60 years was 12.9% for men and 22.4% for women.

The prevalence of choledocholithiasis is higher internationally than in the United States, mainly becauseof the additional problem of primary common bile duct stones caused by parasitic infestation with liverflukes such as Clonorchis sinensis.
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Race-, sex-, and age-related demographics

Prevalence of gallstones is highest in people of northern European descent, and in Hispanic populationsand Native American populations.[6] Prevalence of gallstones is lower in Asians and African Americans.

Women are more likely to develop cholesterol gallstones than men, especially during their reproductiveyears, when the incidence of gallstones in women is 2-3 times that in men. The difference appears to be

attributable mainly to estrogen, which increases biliary cholesterol secretion.[7]

Risk of developing gallstones increases with age. Gallstones are uncommon in children in the absence ofcongenital anomalies or hemolytic disorders. Beginning at puberty, the concentration of cholesterol in bileincreases. After age 15 years, the prevalence of gallstones in US women increases by about 1% peryear; in men, the rate is less, about 0.5% per year. Gallstones continue to form throughout adult life, andthe prevalence is greatest at advanced age. The incidence in women falls with menopause, but newstone formation in men and women continues at a rate of about 0.4% per year until late in life.

Among individuals undergoing cholecystectomy for symptomatic cholelithiasis, 8-15% of patients youngerthan 60 years have common bile duct stones, compared with 15-60% of patients older than 60 years.

PrognosisLess than half of patients with gallstones become symptomatic. The mortality rate for an electivecholecystectomy is 0.5% with less than 10% morbidity. The mortality rate for an emergentcholecystectomy is 3-5% with 30-50% morbidity.

Following cholecystectomy, stones may recur in the bile duct.

Approximately 10-15% of patients have an associated choledocholithiasis. The prognosis in patients withcholedocholithiasis depends on the presence and severity of complications. Of all patients who refusesurgery or are unfit to undergo surgery, 45% remain asymptomatic from choledocholithiasis, while 55%experience varying degrees of complications.

Patient EducationPatients with asymptomatic gallstones should be educated to recognize and report the symptoms ofbiliary colic and acute pancreatitis. Alarm symptoms include persistent epigastric pain lasting for greaterthan 20 minutes, especially if accompanied by nausea, vomiting, or fever. If pain is severe or persists formore than an hour, the patient should seek immediate medical attention.

For patient education information, see theLiver, Gallbladder, and Pancreas CenterandCholesterolCenter, as well asGallstones.

History

Gallstone disease may be thought of as having the following 4 stages:

1. The lithogenic state, in which conditions favor gallstone formation2. Asymptomatic gallstones3. Symptomatic gallstones, characterized by episodes of biliary colic4. Complicated cholelithiasis

Symptoms and complications of gallstone disease result from effects occurring within the gallbladder orfrom stones that escape the gallbladder to lodge in the common bile duct.
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Asymptomatic gallstones

Gallstones may be present in the gallbladder for decades without causing symptoms or complications. Inpatients with asymptomatic gallstones discovered incidentally, the likelihood of developing symptoms orcomplications is 1-2% per year. In most cases, asymptomatic gallstones do not require any treatment.

Because they are common, gallstones often coexist with other gastrointestinal conditions. There is little

evidence to support a causal association between gallstones and chronic abdominal pain, heartburn,postprandial distress, bloating, flatulence, constipation, or diarrhea.

Dyspepsia that occurs reproducibly following ingestion of fatty foods is often wrongly attributed togallstones, whenirritable bowel syndromeorgastroesophageal refluxis the true culprit. Gallstonesdiscovered during an evaluation for nonspecific symptoms are usually innocent bystanders, and treatmentdirected at the gallstones is unlikely to relieve these symptoms.

Biliary colic

Pain termed biliary colic occurs when gallstones or sludge fortuitously impact in the cystic duct during agallbladder contraction, increasing gallbladder wall tension. In most cases, the pain resolves over 30 to90 minutes as the gallbladder relaxes and the obstruction is relieved.

Episodes of biliary colic are sporadic and unpredictable. The patient localizes the pain to the epigastriumor right upper quadrant and may describe radiation to the right scapular tip (Collins sign [8] ). The painbegins postprandially (usually within an hour after a fatty meal), is often described as intense and dull,and may last from 1-5 hours. From onset, the pain increases steadily over about 10 to 20 minutes andthen gradually wanes when the gallbladder stops contracting and the stone falls back into the gallbladder.The pain is constant in nature and is not relieved by emesis, antacids, defecation, flatus, or positionalchanges. It may be accompanied by diaphoresis, nausea, and vomiting.

Other symptoms, often associated with cholelithiasis, include indigestion, dyspepsia, belching, bloating,and fat intolerance. However, these are very nonspecific and occur in similar frequencies in individualswith and without gallstones; cholecystectomy has not been shown to improve these symptoms.

Most patients develop symptoms prior to complications. Once symptoms of biliary colic occur, severesymptoms develop in 3-9% of patients, with complications in 1-3% per year and a cholecystectomy rate of

3-8% per year. Therefore, in people with mild symptoms, 50% have complications after 20 years.

Zollinger performed studies in the 1930s in which the gallbladder wall or common bile duct was distendedwith a balloon; pain was elicited in the epigastric region. Only if the distended gallbladder touched theperitoneum did the patient experience right upper quadrant pain. Associated symptoms of nausea,vomiting, or referred pain were present in distention of the common bile duct (CBD) but not of thegallbladder.

Physical ExaminationPatients with the lithogenic state or asymptomatic gallstones have no abnormal findings on physicalexamination.

Distinguishing uncomplicated biliary colic from acute cholecystitis or other complications is important.Both often present with the same constellation of symptoms, and physical examination may help todifferentiate the two.

Since the gallbladder is not inflamed in uncomplicated biliary colic, the pain is poorly localized andvisceral in origin; the patient has an essentially benign abdominal examination without rebound orguarding. Fever is absent.

In acute cholecystitis, inflammation of the gallbladder with resultant peritoneal irritation leads to well-localized pain in the right upper quadrant, usually with rebound and guarding. Although nonspecific, a
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positive Murphy sign (inspiratory arrest on deep palpation of the right upper quadrant during deepinspiration) is highly suggestive of cholecystitis. Fever is often present, but it may lag behind other signsor symptoms.

Although voluntary guarding may be present, no peritoneal signs are present. Tachycardia anddiaphoresis may be present as a consequence of pain. These should resolve with appropriate painmanagement.

The presence of fever, persistent tachycardia, hypotension, or jaundice necessitate a search forcomplications of cholelithiasis, including cholecystitis, cholangitis, pancreatitis, or other systemic causes.

In severe cases of acute cholecystitis, ascending cholangitis, or acute pancreatitis, bowel sounds areoften absent or hypoactive.

Choledocholithiasis with obstruction of the common bile duct produces cutaneous and scleral icterus thatevolves over hours to days as bilirubin accumulates.

The Charcot triad of severe right upper quadrant tenderness with jaundice and fever is characteristic ofascending cholangitis.

Acute gallstone pancreatitis is often characterized by epigastric tenderness. In severe cases,

retroperitoneal hemorrhage may produce ecchymoses of the flanks and periumbilical ecchymoses (Cullensign and Grey-Turner sign).

Complications of gallbladder stones

Acute cholecystitis occurs when persistent stone impaction in the cystic duct causes the gallbladder tobecome distended and progressively inflamed. Patients experience the pain of biliary colic, but, instead ofresolving spontaneously, the pain persists and worsens.

Overgrowth of colonizing bacteria in the gallbladder often occurs, and, in severe cases, accumulation ofpus in the gallbladder, termedgallbladder empyema, occurs. The gallbladder wall may become necrotic,resulting in perforation and pericholecystic abscess. Acute cholecystitis is considered a surgicalemergency, although pain and inflammation may subside with conservative measures, such as hydrationand antibiotics.

Chronically, gallstones may cause progressive fibrosis of the gallbladder wall and loss of gallbladderfunction, termed chronic cholecystitis. The pathogenesis of this complication is not completelyunderstood. Repeated attacks of acute cholecystitis may play a role, as may localized ischemia producedby pressure of stones against the gallbladder wall. The chronically fibrotic gallbladder may becomeshrunken and adherent to adjacent viscera.

Gallbladder adenocarcinoma is an uncommon cancer that usually develops in the setting of gallstonesand chronic cholecystitis.Gallbladder cancerscommonly invade the adjacent liver and common bile duct,producing jaundice. The prognosis is poor unless the cancer is localized to the gallbladder, in which casecholecystectomy may be curative.

Occasionally, a large stone may erode through the wall of the gallbladder into an adjacent viscus(typically the duodenum), producing a cholecystoenteric fistula. The stone, if sufficiently large, may

obstruct the small intestine, usually at the level of the ileum, a phenomenon termed gallstone ileus.

Complications of stones in the common bile duct

Gallstones are initially retained in the gallbladder by the spiral valves of the cystic duct. Followingepisodes of gallstone impaction in the cystic duct, these valves may become obliterated and stones maypass into the common bile duct. Patients who have passed one stone tend to pass more stones over thesubsequent months.


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Stones in the common bile duct may be asymptomatic, but, more commonly, they impact distally in theampulla of Vater. This may produce biliary colic indistinguishable from that caused by cystic duct stones.Because impaction of common bile duct stones occludes the flow of bile from the liver to the intestine,pressure rises in the intrahepatic bile ducts, leading to increased liver enzymes and jaundice.

Bacterial overgrowth in stagnant bile above an obstructing common duct stone produces purulentinflammation of the liver and biliary tree, termed ascending cholangitis. Characteristic features include the

Charcot triad of fever, jaundice, and right upper quadrant pain. Patients may rapidly develop septic shockunless ductal obstruction is relieved.

A stone impacted in the ampulla of Vater may transiently obstruct the pancreatic duct, leading to in situactivation of pancreatic proteases and triggering an attack of acute pancreatitis. Pancreatic pain isdifferent from biliary pain. The pain is located in the epigastric and midabdominal areas and is sharp,severe, continuous, and radiates to the back. Nausea and vomiting are frequently present, and a similarprevious episode is reported by approximately 15% patients.

Stone impaction in the distal common bile duct is often relieved spontaneously within hours to days bypassage of the stone into the intestine.

Other complications

Inflammation from chronic cholelithiasis may result in fusion of the gallbladder to the extrahepatic biliarytree, causing Mirizzi syndrome. Alternatively, a fistula into the intestinal tract may form, causing gallstoneileus.[9]

Cholelithiasis Workup

Diagnostic ConsiderationsConsider that both intra-abdominal and extra-abdominal pathology can present as upper abdominal pain,and that these conditions often coexist with cholelithiasis. Among the different entities to considerarepeptic ulcer disease,pancreatitis(acute or chronic), hepatitis, dyspepsia, gastroesophageal refluxdisease (GERD), irritable bowel syndrome, esophageal spasm, pneumonia, cardiac chest pain,

anddiabetic ketoacidosis. A careful history and physical examination should guide further workup.

Differential Diagnoses Appendicitis

Bile Duct Strictures

Bile Duct Tumors

Cholangiocarcinoma

Cholecystitis

Gallbladder Cancer

Gastritis and Peptic Ulcer Disease

Gastroenteritis

Pancreatic Cancer

Pancreatitis, Acute

Approach ConsiderationsPatients with uncomplicated cholelithiasis or simple biliary colic typically have normal laboratory testresults. Laboratory testing is generally not necessary unless cholecystitis is a concern.[10]

Asymptomatic gallstones are often found incidentally on plain radiographs, abdominal sonograms, or CTscan for workup of other processes. Plain radiographs have little role in the diagnosis of gallstones or
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gallbladder disease. Cholesterol and pigment stones are radiopaque and visible on radiographs in only10-30% of instances, depending on their extent of calcification.

Blood StudiesIn patients with suspected gallstone complications, blood tests should include a complete blood cell(CBC) count with differential, liver function panel, and amylase and lipase.

Acute cholecystitis is associated with polymorphonuclear leukocytosis. However, up to one third of thepatients with cholecystitis may not manifest leukocytosis.

In severe cases, mild elevations of liver enzymes may be caused by inflammatory injury of the adjacentliver.

Patients with cholangitis and pancreatitis have abnormal laboratory test values. Importantly, a singleabnormal laboratory value does not confirm the diagnosis of choledocholithiasis, cholangitis, orpancreatitis; rather, a coherent set of laboratory studies leads to the correct diagnosis.

Choledocholithiasis with acute common bile duct (CBD) obstruction initially produces an acute increase inthe level of liver transaminases (alanine and aspartate aminotransferases), followed within hours by arising serum bilirubin level. The higher the bilirubin level, the greater the predictive value for CBD

obstruction. CBD stones are present in approximately 60% of patients with serum bilirubin levels greaterthan 3 mg/dL.

If obstruction persists, a progressive decline in the level of transaminases with rising alkalinephosphatase and bilirubin levels may be noted over several days. Prothrombin time may be elevated inpatients with prolonged CBD obstruction, secondary to depletion of vitamin K (the absorption of which isbile-dependent).Concurrent obstruction of the pancreatic duct by a stone in the ampulla of Vater may beaccompanied by increases in serum lipase and amylase levels.

Repeated testing over hours to days may be useful in evaluating patients with gallstone complications.Improvement of the levels of bilirubin and liver enzymes may indicate spontaneous passage of anobstructing stone. Conversely, rising levels of bilirubin and transaminases with progression ofleukocytosis in the face of antibiotic therapy may indicate ascending cholangitis with need for urgentintervention. Blood culture results are positive in 30-60% of patients with cholangitis.

Abdominal RadiographyUpright and supine abdominal radiographs are occasionally helpful in establishing a diagnosis ofgallstone disease.

Black pigment or mixed gallstones may contain sufficient calcium to appear radiopaque on plain films.The finding of air in the bile ducts on plain films may indicate development of a choledochoenteric fistulaor ascending cholangitis with gas-forming organisms. Calcification in the gallbladder wall (the so-calledporcelain gallbladder) is indicative of severe chronic cholecystitis.

The main role of plain films in evaluating patients with suspected gallstone disease is to exclude othercauses of acute abdominal pain, such as intestinal obstruction, visceral perforation, renal stones, orchronic calcific pancreatitis.

Go toImaging of Cholelithiasisfor complete information on this topic.

UltrasonographyUltrasonography is the procedure of choice in suspected gallbladder or biliary disease; it is the mostsensitive, specific, noninvasive, and inexpensive test for the detection of gallstones. Moreover, it is
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simple, rapid, and safe in pregnancy, and it does not expose the patient to harmful radiation orintravenous contrast. An added advantage is that it can be performed by skilled practitioners at thebedside. The American College of Radiology (ACR) in its Appropriateness Criteria right upper quadrantpain, published in 2010, supports this conclusion.[11]

Sensitivity is variable and dependent upon operator proficiency, but in general, it is highly sensitive andspecific for gallstones greater than 2 mm. It is less so for microlithiasis or biliary sludge.

Ultrasonography is very useful for diagnosing uncomplicated acute cholecystitis. The sonographicfeatures of acute cholecystitis include gallbladder wall thickening (>5 mm), pericholecystic fluid,gallbladder distention (>5 cm), and a sonographic Murphy sign. The presence of multiple criteriaincreases its diagnostic accuracy.

Gallstones appear as echogenic foci in the gallbladder. They move freely with positional changes andcast an acoustic shadow. (See the image below.)

Cholecystitis with small stones in the gallbladder neck. Classic acoustic shadowingis seen beneath the gallstones. The gallbladder wall is greater than 4 mm. Image courtesy of DT Schwartz. Ultrasonography is also helpful in cases of suspected acute cholecystitis to exclude hepatic abscessesand other liver parenchymal processes.

When the gallbladder is completely filled with gallstones, the stones may not be visible on ultrasound.However, closely spaced double echogenic lines (one from the gallbladder wall and one from the stones)with acoustic shadowing may be evident. (See the images below.)

The WES (wall echogenic shadow) sign, long axis of the gallbladder. The arrowhead points to the gallbladder wall. The second hyperechoic line represents the edge of the congregated gallstones.Acoustic shadowing (AS) is readily seen. The common bile duct can be seen just above the portal vein (PV). Image courtesy

of Stephen Menlove. WES sign, short axis view of the gallbladder. Image courtesy of Stephen Menlove.
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Common bile duct (CBD) stones are missed frequently on transabdominal ultrasonography (sensitivity,15-40%). The detection of CBD stones is impeded by the presence of gas in the duodenum, possiblereflection and refraction of the sound beam by curvature of the duct, and the location of the duct beyondthe optimal focal point of the transducer.

On the other hand, dilatation of the CBD on ultrasonographic images is an indirect indicator of CBDobstruction. CBD dilatation is identified accurately, with up to 90% accuracy. However, this finding may be

absent if the obstruction is of recent onset. The usefulness of ultrasonography findings as a predictor ofCBD stones is at best 15-20%.


Endoscopic ultrasound

Endoscopic ultrasound (EUS) is also an accurate and relatively noninvasive technique to identify stonesin the distal common bile duct. Sensitivity and specificity of CBD stone detection are reported in range of85-100%.[12]

Laparoscopic ultrasound

Laparoscopic ultrasound has shown some promise as a primary method for bile duct imaging during

laparoscopic cholecystectomy.

[13]

Yao et al were able to evaluate the common bile duct with laparoscopicultrasound during laparoscopic cholecystectomy in 112 of 115 patients (97.4%) with cholelithiasis.

In patients who were categorized preoperatively as having a low probability of bile duct stones, theoccurrence rate of stones was found to be 7%; in those who were preoperatively assessed as having anintermediate probability of such stones, the occurrence rate was 36.4%; and in those who were rated withthe highest probability of bile duct stones, the occurrence rate was 78.9%. [13]

The investigators suggested that as experience increases with laparoscopic ultrasound, this method maybecome routine for evaluating the bile duct during laparoscopic cholecystectomy. In addition, Yao et aladvised mandatory aggressive preoperative evaluation of the common bile duct in those who aresuspected to have an intermediate or high risk of having choledocholithiasis

Computed TomographyComputed tomography (CT) scanning is more expensive and less sensitive than ultrasonography for thedetection of gallbladder stones. CT scanning is often used in the workup of abdominal pain, as it providesexcellent images of all the abdominal viscera. CT scanning is superior to ultrasonography for thedemonstration of gallstones in the distal common bile duct.

Gallstones are often found incidentally on CT. Findings on CT for acute cholecystitis are similar to thosefound on sonograms. Although not the initial study of choice in biliary colic, CT can be used in diagnosticchallenges or to further characterize complications of gallbladder disease. CT is particularly useful for thedetection of intrahepatic stones or recurrent pyogenic cholangitis.


Magnetic Resonance ImagingMagnetic resonance imaging (MRI) with magnetic resonance cholangiopancreatography (MRCP) hasemerged as an excellent imaging study for noninvasive identification of gallstones anywhere in the biliarytract, including the common bile duct (see the image below). Because of its cost and the need forsophisticated equipment and software, it is usually reserved for cases in which choledocholithiasis issuspected. The 2010 ACR guidelines recommend MRI as a secondary imaging study if ultrasoundimages do not result in a clear diagnosis of acute cholecystitis or gallstones .[11]


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Magnetic resonance cholangiopancreatography (MRCP) showing 5 gallstones inthe common bile duct (arrows). In this image, bile in the duct appears white; stones appear as dark-filling defects. Similarimages can be obtained by taking plain radiographs after injection of radiocontrast material in the common bile duct, eitherendoscopically (endoscopic retrograde cholangiography) or percutaneously under fluoroscopic guidance (percutaneoustranshepatic cholangiography), but these approaches are more invasive.Go toImaging of Cholelithiasisfor complete information on this topic.

ScintigraphyTechnetium-99m (99m Tc) hepatoiminodiacetic acid (HIDA) scintigraphy is occasionally useful in thedifferential diagnosis of acute abdominal pain. Scintigraphy gives little information about nonobstructingcholelithiasis and cannot detect other pathologic states, but it is highly accurate for the diagnosis of cysticduct obstruction.

HIDA is normally taken up by the liver and excreted into bile, where it fills the gallbladder and can bedetected with a gamma camera. Failure of HIDA to fill the gallbladder, while flowing freely into theduodenum, is indicative of cystic duct obstruction. A nonvisualizing gallbladder on a HIDA scan in apatient with abdominal pain supports a diagnosis of acute cholecystitis.

A meta-analysis by Mahid et al found that patients without gallstones who have right upper quadrant painand a positive HIDA scan result are more likely to experience symptom relief if they undergocholecystectomy than if they are treated medically.[14]

Endoscopic Retrograde CholangiopancreatographyEndoscopic retrograde cholangiopancreatography (ERCP) permits radiographic imaging of the bile ducts.In this procedure, an endoscope is passed into the duodenum and the papilla of Vater is cannulated.Radiopaque liquid contrast is injected into the biliary ducts, providing excellent contrast on radiographicimages. Stones in bile appear as filling defects in the opacified ducts. Currently, ERCP is usuallyperformed in conjunction with endoscopic retrograde sphincterotomy and gallstone extraction. [15]

Percutaneous Transhepatic CholangiographyPercutaneous transhepatic cholangiography (PTC) may be the modality of choice in patients in whomERCP is difficult (eg, those with previous gastric surgery or distal obstructing CBD stone), in the absenceof an experienced endoscopist, and in patients with extensive intrahepatic stone disease and

cholangiohepatitis. A long large-bore needle is advanced percutaneously and transhepatically into anintrahepatic duct, and cholangiography is performed. A catheter can be placed in the biliary tree over aguidewire.

Uncorrected coagulopathy is a contraindication for PTC, and the normal size of the intrahepatic ductsmakes the procedure difficult. Prophylactic antibiotics are recommended to reduce the risk of cholangitis.
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Cholelithiasis Treatment & Management

Approach ConsiderationsThe treatment of gallstones depends upon the stage of disease. Ideally, interventions in the lithogenicstate could prevent gallstone formation, although, currently, this option is limited to a few specialcircumstances. Asymptomatic gallstones may be managed expectantly.

Once gallstones become symptomatic, definitive surgical intervention with cholecystectomy is usuallyindicated, although, in some cases, medical dissolution may be considered. In uncomplicatedcholelithiasis with biliary colic, medical management may be a useful alternative to cholecystectomy inselected patients, particularly those for whom surgery would pose high risk. Medical treatment, beyondpain control, is not initiated in the emergency department.

Medical treatments for gallstones, used alone or in combination, include the following:

Oral bile salt therapy (ursodeoxycholic acid)

Contact dissolution

Extracorporeal shockwave lithotripsyMedical management is more effective in patients with good gallbladder function who have small stones

(< 1 cm) with a high cholesterol content. Bile salt therapy may be required for more than 6 months andhas a success rate less than 50%

Treatment of Asymptomatic GallstonesSurgical treatment of asymptomatic gallstones without medically complicating diseases is discouraged.The risk of complications arising from interventions is higher than the risk of symptomatic disease.Approximately 25% of patients with asymptomatic gallstones develop symptoms within 10 years.

Persons with diabetes and women who are pregnant should have close follow-up to determine if theybecome symptomatic or develop complications.

However, cholecystectomy for asymptomatic gallstones may be indicated in the following patients:

Patients with large gallstones greater than 2 cm in diameter

Patients with nonfunctional or calcified (porcelain) gallbladder observed on imaging studies and who areat high risk of gallbladder carcinoma

Patients with spinal cord injuries or sensory neuropathies affecting the abdomen

Patients with sickle cell anemia in whom the distinction between painful crisis and cholecystitis may bedifficult

Patients with risk factors for complications of gallstones may be offered elective cholecystectomy, even ifthey have asymptomatic gallstones. These groups include persons with the following conditions anddemographics:

Cirrhosis

Portal hypertension Children

Transplant candidates

Diabetes with minor symptomsPatients with a calcified or porcelain gallbladder should consider elective cholecystectomy due to thepossibly increased risk of carcinoma (25%). Refer to a surgeon for removal as an outpatient procedure.


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Medical dissolution of gallstones

Ursodeoxycholic acid (ursodiol) is a gallstone dissolution agent. In humans, long-term administration ofursodeoxycholic acid reduces cholesterol saturation of bile, both by reducing liver cholesterol secretionand by reducing the detergent effect of bile salts in the gallbladder (thereby preserving vesicles that havea high cholesterol carrying capacity). Desaturation of bile prevents crystals from forming and, in fact, mayallow gradual extraction of cholesterol from existing stones.

In patients with established cholesterol gallstones, treatment with ursodeoxycholic acid at a dose of 8-10mg/kg/d PO divided bid/tid may result in gradual gallstone dissolution. This intervention typically requires6-18 months and is successful only with small, purely cholesterol stones. Patients remain at risk forgallstone complications until dissolution is completed. The recurrence rate is 50% within 5 years.Moreover, after discontinuation of treatment, most patients form new gallstones over the subsequent 5-10years.

Treatment of Patient with Symptomatic GallstonesIn patients with symptomatic gallstones, discuss the options for surgical and nonsurgical intervention;emergency physicians should refer patients to their primary care provider and surgical consultant foroutpatient follow-up.

Cholecystectomy

Removal of the gallbladder (cholecystectomy) is generally indicated in patients who have experiencedsymptoms or complications of gallstones, unless the patient's age and general health make the risk ofsurgery prohibitive. In some cases of gallbladder empyema, temporary drainage of pus from thegallbladder (cholecystostomy) may be preferred to allow stabilization and to permit later cholecystectomyunder elective circumstances.

In patients with gallbladder stones who are suspected to have concurrent common bile duct stones, thesurgeon can perform intraoperative cholangiography at the time of cholecystectomy. The common bileduct can be explored using a choledochoscope. If common duct stones are found, they can usually beextracted intraoperatively. Alternatively, the surgeon can create a fistula between the distal bile duct andthe adjacent duodenum (choledochoduodenostomy), allowing stones to pass harmlessly into theintestine.

Open versus laparoscopic cholecystectomy

The first cholecystectomy was performed in the late 1800s. The open approach pioneered byLangenbuch remained the standard until the late 1980s, when laparoscopic cholecystectomy wasintroduced.[16, 17] Laparoscopic cholecystectomy was the vanguard of the minimally invasive revolution,which has affected all areas of modern surgical practice. Currently, open cholecystectomy is mainlyreserved for special situations.

The traditional open approach to cholecystectomy employed a large, right subcostal incision. In contrast,laparoscopic cholecystectomy employs 4 very small incisions. Recovery time and postoperative pain arediminished markedly by the laparoscopic approach.

Currently, laparoscopic cholecystectomy is commonly performed in an outpatient setting. By reducinginpatient stay and time lost from work, the laparoscopic approach has also reduced the cost ofcholecystectomy.[18]

In its 2010 guidelines for the clinical application of laparoscopic biliary tract surgery, the Society ofAmerican Gastrointestinal and Endoscopic Surgeons (SAGES) states that patients with symptomaticcholelithiasis are eligible for laparoscopic surgery. Cholelithiasis patients whose laparoscopiccholecystectomy was uncomplicated may be sent home the same day if postoperative pain and nauseaare well controlled. Patients older than 50 years may be at greater risk of readmission.[19]


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During laparoscopic cholecystectomy, a surgeon must retrieve stones that might escape through aperforated gallbladder. Conversion to an open procedure might be required in certain cases.

In patients in whom gallstones have been lost in the peritoneal cavity, the current recommendation isfollow-up with ultrasonographic examinations for 12 months. Most of the complications (usually, abscessformation around the stone) occur within this time frame.

The most dreaded and morbid complication of cholecystectomy is damage to the common bile duct. Bileduct injuriesincreased in incidence with the advent of laparoscopic cholecystectomy, but the incidence ofthis complication has since declined as experience and training in minimally invasive surgery haveimproved.[20]

Routine cholangiography is only of minimal help in preventing common bile duct injury. However, goodevidence indicates that it leads to intraoperative detection of such injuries.

Cholecystostomy

In patients who are critically ill with gallbladder empyema and sepsis, cholecystectomy can betreacherous. In this circumstance, the surgeon may elect to perform cholecystostomy, a minimalprocedure involving placement of a drainage tube in the gallbladder. This usually results in clinicalimprovement. Once the patient stabilizes, definitive cholecystectomy can be performed under elective

circumstances.

Cholecystostomy also can be performed in some cases by invasive radiologists under CT-scan guidance.This approach eliminates the need for anesthesia and is especially appealing in a patient who is clinicallyunstable.

Endoscopic sphincterotomy

If surgical removal of common bile duct stones is not immediately feasible, endoscopic retrogradesphincterotomy can be used. In this procedure, the endoscopist cannulates the bile duct via the papilla ofVater. Using an electrocautery sphincterotome, the endoscopist makes an incision measuringapproximately 1 cm through the sphincter of Oddi and the intraduodenal portion of the common bile duct,creating an opening through which stones can be extracted.

Endoscopic retrograde sphincterotomy is especially useful in patients who are critically ill with ascendingcholangitis caused by impaction of a gallstone in the ampulla of Vater. Other indications for the procedureare as follows:

Removal of common bile duct stones inadvertently left behind during previous cholecystectomy

Preoperative clearing of stones from the common bile duct to eliminate the need for intraoperativecommon bile duct exploration, especially in situations where the surgeon's expertise in laparoscopic bileduct exploration is limited or the patient's anesthesia risk is high

Preventing recurrence of acute gallstone pancreatitis or other complications of choledocholithiasis inpatients who are too sick at present to undergo elective cholecystectomy or whose long-term prognosisis poor

Intraoperative endoscopic sphincterotomy (IOES) during laparoscopic cholecystectomy has beensuggested as an alternative treatment to preoperative endoscopic sphincterotomy (POES) followed bylaparoscopic cholecystectomy; this is because IOES is as effective and safe as POES and results in a

significantly shorter hospital stay

Prevention of GallstonesUrsodeoxycholic acid treatment can prevent gallstone formation. This has been demonstrated in thesetting of rapid weight loss caused by very low-calorie diets or by bariatric surgery, which are associatedwith a high risk of new cholesterol gallstones (20-30% within 4 mo). Administration of ursodeoxycholicacid at a dose of 600 mg daily for 16 weeks reduces the incidence of gallstones by 80% in this setting.
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Recommending dietary changes of decreased fat intake is prudent; this may decrease the incidence ofbiliary colic attacks. However, it has not been shown to cause dissolution of stones.

Diet and ActivityLittle evidence suggests that dietary composition affects the natural history of gallstone disease inhumans. Obese patients who undertake aggressive weight-loss programs or undergo bariatric surgeryare at risk to develop gallstones; short-term prophylaxis with ursodeoxycholic acid should be considered.

Regular exercise may reduce the frequency of cholecystectomy.

ConsultationsPatients who have experienced an episode of typical biliary colic or a complication of gallstones shouldbe referred to a general surgeon with experience in laparoscopic cholecystectomy.

If symptoms are atypical, consultation with a general gastroenterologist may be appropriate. Agastroenterologist specializing in biliary endoscopy should be consulted if endoscopic retrogradesphincterotomy may be required.

Long-Term MonitoringFollowing cholecystectomy, about 5-10% of patients develop chronic diarrhea. This is usually attributed tobile salts. The frequency of enterohepatic circulation of bile salts increases after the gallbladder isremoved, resulting in more bile salt reaching the colon. In the colon, bile salts stimulate mucosal secretionof salt and water.

Postcholecystectomy diarrhea is usually mild and can be managed with occasional use of over-the-counter antidiarrheal agents, such as loperamide. More frequent diarrhea can be treated with dailyadministration of a bile acid-binding resin (eg, colestipol, cholestyramine, colesevelam).

Following cholecystectomy, a few individuals experience recurrent pain resembling biliary colic. The termpostcholecystectomy syndrome is sometimes used for this condition.

Many patients with postcholecystectomy syndrome have long-term functional pain that was originallymisdiagnosed as being of biliary origin.[22] Persistence of symptoms following cholecystectomy isunsurprising. Diagnostic and therapeutic efforts should be directed at the true cause.

Some individuals with postcholecystectomy syndrome have an underlying motility disorder of thesphincter of Oddi, termed biliary dyskinesia, in which the sphincter fails to relax normally followingingestion of a meal. The diagnosis can be established in specialized centers by endoscopic biliarymanometry. In established cases of biliary dyskinesia, endoscopic retrograde sphincterotomy is usuallyeffective in relieving the symptoms.

Cholelithiasis Medication

Medication SummaryMedical dissolution of gallstones may be attempted with administration of ursodiol.


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Gallstone Dissolution AgentsClass Summary

These agents suppress hepatic cholesterol synthesis and secretion, and inhibit intestinal absorption ofcholesterol. Ursodiol is the most common drug used. It solubilizes cholesterol in micelles and acts bydispersing cholesterol in aqueous media.

View full drug information

Ursodiol (Actigall, URSO, URSO Forte)

Ursodiol (ursodeoxycholic acid) is indicated for radiolucent noncalcified gallbladder stones smaller than20 mm in diameter when conditions preclude cholecystectomy. Ursodiol suppresses hepatic cholesterolsynthesis and secretion and inhibits intestinal absorption. It appears to have little inhibitory effect on thesynthesis and secretion into bile of endogenous bile acids and does not appear to affect secretion ofphospholipids into bile. After repeated doses, the drug reaches steady-state bile concentrations in about 3weeks. Cholesterol is insoluble in aqueous media, but it can be solubilized in at least 2 different ways inthe presence of dihydroxy bile acids. In addition to solubilizing cholesterol in micelles, ursodiol acts bydispersing cholesterol as liquid crystals in aqueous media. The overall effect of ursodiol is to increase theconcentration level at which saturation of cholesterol occurs.

The various actions of ursodiol combine to change the bile of patients with gallstones from cholesterol-precipitating to cholesterol-solubilizing bile, thus resulting in bile conducive to cholesterol stonesdissolution.

Gallstone Dissolution

8-10 mg/kg/d PO divided q8-12hr PO; not to exceed 300 mg/dose

Maintenance: 250 mg PO HS x6 months

capsules

300mg

tablets

250mg

500mg

Primary Biliary Cirrhosis

13-15 mg/kg/d PO divided PO with food

Cystic Fibrosis Liver Disease (Orphan)

Indicated for treatment of cystic fibrosis liver disease

Contraindic ated (0)

Serious - Use A lternative (0)

Signif icant - Monito r Closely (6)

aluminum hydroxide

calcium carbonate

crofelemer

ethinylestradiol

sodium bicarbonate

sodium citrate/citric acidMinor (4)

cholestyramine

colesevelam
http://reference.medscape.com/drug/actigall-urso-forte-ursodiol-342072http://reference.medscape.com/drug/actigall-urso-forte-ursodiol-342072http://reference.medscape.com/drug/actigall-urso-forte-ursodiol-342072http://reference.medscape.com/drug/actigall-urso-forte-ursodiol-342072http://opencalc%28%27/calculator/dosing/weight-dosing','Gallstone%20Dissolution','Adult','8-10%20mg/kg/d%20PO%20divided%20q8-12hr%20PO;%20not%20to%20exceed%20300%20mg/dose');http://opencalc%28%27/calculator/dosing/weight-dosing','Primary%20Biliary%20Cirrhosis','Adult','13-15%20mg/kg/d%20PO%20divided%20PO%20with%20food');http://opencalc%28%27/calculator/dosing/weight-dosing','Primary%20Biliary%20Cirrhosis','Adult','13-15%20mg/kg/d%20PO%20divided%20PO%20with%20food');http://opencalc%28%27/calculator/dosing/weight-dosing','Gallstone%20Dissolution','Adult','8-10%20mg/kg/d%20PO%20divided%20q8-12hr%20PO;%20not%20to%20exceed%20300%20mg/dose');http://reference.medscape.com/drug/actigall-urso-forte-ursodiol-342072http://reference.medscape.com/drug/actigall-urso-forte-ursodiol-342072


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colestipol

mestranol

Adverse Effects>10%

Headache

Dizziness

Diarrhea

Dyspepsia

Nausea/vomiting

Back pain

Upper respiratory tract infection

1-10%

Alopecia

Rash

Hyperglycemia

Flatulence

Peptic ulcer

Urinary tract infection

Leukopenia

Thrombocytopenia

Cholecystitis

>1%

Fatigue

Abdominal pain

Thrombocytopenia

Pruritus

Angioedema

Peripheral edema

Biliary pain

Postmarketing Reports

Hepatobiliary disorders: Jaundice (or aggravation of pre-existing jaundice)


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Abnormal laboratory tests: Increased ALT, AST, alkaline phosphatase, bil irubin, gamma-GT

Contraindications & CautionsContraindications

Hypersensitivity

Gallstone complication requiring surgery

Known hepatocyte or bile ductal abnormalities, inflammatory bowel disease

Calcified gallstones, bile acid allergy, chronic hepatic disease

Billiary gastrointestinal fistula

Patients requiring cholecystectomy

Cautions

Only use in radiolucent, non calcified, high cholesterol content gallstoneChronic liver disease

Liver function tests (gamma-GT, alkaline phosphatase, AST, ALT) and bilirubin levels should bemonitored q3months x3 months after start of therapy, and q6months thereafter

Gallbladder stone dissolution may take several months

50% of cases have stone recurrence in 5 yr

Pregnancy & Lactation

Pregnancy Category: B

Lactation: unknown if excreted in breast milk; use caution

A:Generally acceptable. Controlled studies in pregnant women show no evidence of fetal risk.

B:May be acceptable. Either animal studies show no risk but human studies not available or animalstudies showed minor risks and human studies done and showed no risk.

C:Use with caution if benefits outweigh risks. Animal studies show risk and human studies not availableor neither animal nor human studies done.

D:Use in LIFE-THREATENING emergencies when no safer drug available. Positive evidence of human

fetal risk.

X:Do not use in pregnancy. Risks involved outweigh potential benefits. Safer alternatives exist.

NA: Information not available.


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PharmacologyMechanism of Action

Naturally-occurring bile acid; reduces cholesterol secretion from the liver; reduces the fractionalreabsorption of cholesterol by the intestines.

AbsorptionBioavailability: 90%

Onset: Initial response for gallstone dissolution is 3-6 months

Distribution

Protein Bound: 70%

Metabolism

Taken up rapidly by the liver, conjugated with glycine or taurine, and excreted in the bile

Nonabsorbed ursodiol passes into the colon where it is 7-dehydroxylated to lithocholic acid (anintermediary compound, sometimes formed, is called chenodiol); chenodiol is then dehydroxylated tolithocholic acid

Metabolites: Glyco-ursodeoxycholic acid, tauro-ursodeoxycholic acid, 7-keto-lithocholic acid (inactive);lithocholic acid (inactive) is formed from the 7-hydroxylation of ursodiol and chenodiol; a small portion ismetabolized to sulfated lithocholic acid conjugates which are excreted in bile & eliminated in feces

Elimination

Excretion: Mainly in feces

mages

BRAND FORM. PILL IMAGE

Actigall 300mgcapsule


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ursodiol 250mgtablet


ursodiol 300mgcapsule


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Patient Handout

Patient Education

ursodiol OralIMPORTANT: HOW TO USE THIS INFORMATION: This is a summary and does NOT have all possibleinformation about this product. This information does not assure that this product is safe, effective, orappropriate for you. This information is not individual medical advice and does not substitute for theadvice of your health care professional. Always ask your health care professional for completeinformation about this product and your specific health needs.

URSODIOL - ORAL

(UR-soe-DYE-ol)

COMMON BRAND NAME(S): Actigall, Urso

USES:Ursodiol is used to dissolve certain types of gallstones, to prevent gallstones from forming in obesepatients who are losing weight rapidly, and to treat a certain type of liver disease (primary biliarycirrhosis). Ursodiol is a bile acid.

HOW TO USE:Take this medication exactly as directed by your doctor.

Dosage is based on your medical condition and response to therapy.

Do not increase your dose or take this medication more often without your doctor's approval. Yourcondition will not improve any faster, and the risk of serious side effects may be increased.

Use this medication regularly to get the most benefit from it. To help you remember, take it at the sametimes each day.

SIDE EFFECTS:Stomach upset, nausea, diarrhea, dizziness, back pain, hair loss, or cough may occur. If any of theseeffects persist or worsen, tell your doctor or pharmacist promptly.

Remember that your doctor has prescribed this medication because he or she has judged that the benefitto you is greater than the risk of side effects. Many people using this medication do not have serious sideeffects.

Tell your doctor immediately if any of these unlikely but serious side effects occur: weakness, swelling ofthe ankles/feet, increased thirst/urination, signs of infection (e.g., fever, persistent sore throat), easybleeding/bruising.


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A very serious allergic reaction to this drug is rare. However, seek immediate medical attention if younotice any symptoms of a serious allergic reaction, including: rash, itching/swelling (especially of theface/tongue/throat), severe dizziness, trouble breathing.

This is not a complete list of possible side effects. If you notice other effects not listed above, contact yourdoctor or pharmacist.

In the US -

Call your doctor for medical advice about side effects. You may report side effects to FDA at 1-800-FDA-1088.

In Canada - Call your doctor for medical advice about side effects. You may report side effects to HealthCanada at 1-866-234-2345.

PRECAUTIONS:Before taking ursodiol, tell your doctor or pharmacist if you are allergic to it; or to other bile acids; or if youhave any other allergies. This product may contain inactive ingredients, which can cause allergicreactions or other problems. Talk to your pharmacist for more details.

This medication should not be used if you have certain medical conditions. Before using this medicine,

consult your doctor or pharmacist if you have: certain gallbladder/bile duct problems (e.g., acutecholecystitis, cholangitis, biliary obstruction, gallstone pancreatitis, biliary-gastrointestinal fistula).

Before using this medication, tell your doctor or pharmacist your medical history, especially of: liverdisease (e.g., ascites, variceal bleeding, hepatic encephalopathy).

This drug may make you dizzy. Do not drive, use machinery, or do any activity that requires alertnessuntil you are sure you can perform such activities safely. Limit alcoholic beverages.

During pregnancy, this medication should be used only when clearly needed. Discuss the risks andbenefits with your doctor.

It is not known whether this drug passes into breast milk. Consult your doctor before breast-feeding.

DRUG INTERACTIONS:Your doctor or pharmacist may already be aware of any possible drug interactions and may be monitoringyou for them. Do not start, stop, or change the dosage of any medicine before checking with your doctoror pharmacist first.

Before using this medication, tell your doctor or pharmacist of all prescription and nonprescription/herbalproducts you may use, especially of: aluminum-containing antacids, birth control pills, cholesterolmedications (e.g., cholestyramine, clofibrate, colestipol), estrogen.

This document does not contain all possible interactions. Therefore, before using this product, tell yourdoctor or pharmacist of all the products you use. Keep a list of all your medications with you, and sharethe list with your doctor and pharmacist.

OVERDOSE:

If overdose is suspected, contact a poison control center or emergency room immediately. US residentscan call their local poison control center at 1-800-222-1222. Canada residents can call a provincial poisoncontrol center. Symptoms of overdose may include: severe diarrhea.

NOTES:Do not share this medication with others.

Laboratory and/or medical tests (e.g., liver function tests, bilirubin level) should be performed periodicallyto monitor your progress or check for side effects. Consult your doctor for more details.


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MISSED DOSE:If you miss a dose, take it as soon as you remember. If it is near the time of the next dose, skip themissed dose and resume your usual dosing schedule. Do not double the dose to catch up.

STORAGE:Store at room temperature away from light and moisture. Different brands/strengths of this medicationmay have different storage requirements. Read the package labeling or ask your pharmacist for the

storage requirements for the product you are using. Do not store in the bathroom. Keep all medicinesaway from children and pets.

Do not flush medications down the toilet or pour them into a drain unless instructed to do so. Properlydiscard this product when it is expired or no longer needed. Consult your pharmacist or local wastedisposal company for more details about how to safely discard your product.

Information last revised June 2013. Copyright(c) 2013 First Databank, Inc.

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