Sie sind auf Seite 1von 47

Introduction

Background
Gallbladder disease is one of the most common gastrointestinal disorders in the United States. The spectrum of gallbladder disease ranges from asymptomatic cholelithiasis to gallbladder (or biliary) colic, cholecystitis, choledocholithiasis, and cholangitis. Further complications of gallbladder disease include gallstone pancreatitis, gallstone ileus, biliary cirrhosis, and gallbladder cancer. Cholelithiasis is the presence of gallstones in the gallbladder. Biliary colic is pain caused by a stone temporarily obstructing the cystic duct. Cholecystitis is inflammation of the gallbladder from obstruction of the cystic duct. Choledocholithiasis is the presence of a stone in the common bile duct.

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.

Cholangitis occurs when a gallstone obstructs the biliary or hepatic ducts, causing inflammation and infection. This article focuses on the pathophysiology and epidemiology of gallstones and biliary colic. Cholecystitis, cholangitis, and gallstone pancreatitis are covered in other articles.

Pathophysiology
Gallstones are rocklike collections of material that form inside the gallbladder. Different types exist, and they are categorized by their primary composition; cholesterol stones are most common (75-80% in the United States) followed by pigment, then mixed stones. The stones form when there is an imbalance or change in the composition of bile. Normally, bile acids, lecithin, and phospholipids help to maintain cholesterol solubility in bile. When the ratio of cholesterol to biles acids or phospholipids is increased, bile becomes supersaturated with cholesterol; it crystallizes and forms a nidus for stone formation. Calcium and pigment also may be incorporated in the stone. Impaired gallbladder motility, biliary stasis, and bile content predispose people to the formation of gallstones. Gallbladder sludge is crystallization within bile without stone formation. Sludge may be a step in the formation of stones, or it may occur independently. 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.

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

Pigment stones, which comprise 15% of gallstones, are formed by the crystallization of calcium bilirubinate. Diseases that lead to increased destruction of red blood cells (hemolysis), abnormal metabolism of hemoglobin (cirrhosis), or infections (including parasitic) predispose people to pigment stones. Black stones and brown stones exist. Black stones are found in people with hemolytic disorders. Brown stones are found in the intrahepatic or extrahepatic duct. They are associated with infection in the gallbladder and commonly are found in people of Asian descent. Gallstone differentiation is an important consideration in management; cholesterol stones are more likely to respond to nonsurgical management than are pigment or mixed stones.

Frequency
United States

Prevalence of cholelithiasis is affected by many factors including ethnicity, gender, comorbidities, and genetics. In the United States, about 20 million people (10-20% of adults) have gallstones. Every year 13% of people develop gallstones and about 1-3% of people become symptomatic.
International

In an Italian study, 20% of women had stones, and 14% of men had stones. In a Danish study, gallstone prevalence in persons aged 30 years was 1.8% for men and 4.8% for women; gallstone prevalence in persons aged 60 years was 12.9% for men and 22.4% for women.

Mortality/Morbidity
Every year, 1-3% of people develop gallstones and about the same number develop symptoms of gallstones. Asymptomatic gallstones are not associated with fatalities. Morbidity and fatalities are associated with symptomatic cholelithiasis, cholecystitis, or cholangitis.

Race
Prevalence of gallstones is highest in fair-skinned people of northern European descent and in Hispanic populations and Native American populations. Prevalence of gallstones is low in Asians and African Americans; however, African Americans with sickle cell disease have gallstones early in life secondary to associated hemolysis.

Sex

Gallstones are more common in women than in men. It is postulated that estrogens cause increased cholesterol secretion and progesterone promotes biliary stasis.1 Women who are pregnant are more likely to experience symptomatic gallstones due to the hormonal influences and decreased gut motility. Whether women who are pregnant are more likely to form stones is uncertain; however, women with multiple pregnancies are more likely to have stones.

Age
Risk of developing gallstones increases with age. Incidence of gallstones increases by 1-3% per year. It is uncommon for children to form gallstones. Children with gallstones are more likely to have congenital anomalies, biliary malformation and disease, or hemolytic pigment stones. Other risk factors for gallstones include exogenous estrogen intake, obesity, frequent fasting, rapid weight loss, lack of physical activity, diabetes mellitus, diseases associated with increased hemolysis (eg, sickle cell disease), cirrhosis, and certain medications (eg, octreotide, estrogens, fibrates).

Clinical
History
The clinical stages of cholelithiasis are asymptomatic (the presence of gallstones without symptoms), symptomatic (biliary colic), and complicated (eg, cholecystitis, choledocholithiasis, cholangitis). Most gallstones (60-80%) are asymptomatic. Classically, biliary colic is described as episodic pain in the right upper quadrant, that may radiate to the right shoulder or back (Collins's sign). 2 It begins postprandially (usually within an hour) and may last from 1-5 hours. It is caused by contraction of the gallbladder (in response to a fatty meal) against an obstructing gallstone (or sludge) in the cystic duct. This leads to increased pressure within the gallbladder and pain. The pain is often described as intense and dull and typically subsides after several hours, when the gallbladder stops contracting and the stone falls back into the gallbladder. Associated symptoms may include diaphoresis, nausea, and vomiting. These symptoms can be nonspecific and insensitive. The pain may be more prominent in the midepigastrium, wake the patient from sleep, and be unrelated to meals. The pain of biliary colic is not characteristically positional, pleuritic, or relieved by bowel movement or flatus. 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 individuals with 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, severe symptoms 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 distended with a balloon; pain was elicited in the epigastric region. Only if the distended gallbladder touched the peritoneum 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 the gallbladder. o In classic cases, pain is in the right upper quadrant; however, visceral pain and gallbladder wall distention may be only in the epigastric area. o Once the peritoneum is irritated, pain localizes into the right upper quadrant. Small stones are more likely to be symptomatic than large stones.

Physical
Physical findings vary along the spectrum of gallbladder disease. Vital signs and physical examination findings in asymptomatic cholelithiasis are normal. These are generally patients with an incidental finding of gallstones. Findings in between acute biliary colic attacks are generally also normal, though some mild residual upper abdominal pain with little or no tenderness may persist shortly after an attack. During an acute attack of biliary colic, the patient may complain of severe, poorly localized upper abdominal pain, but is non-toxic and has a benign abdominal exam with little or no tenderness. Any prolonged pain episode lasting more than 5-6 hours should dictate a search for obstructed stone(s) or complications from cholelithiasis. o Although voluntary guarding may be present, no peritoneal signs are present. o Tachycardia and diaphoresis may be present as a consequence of pain. These should resolve with appropriate pain management. Nausea and vomiting are commonly present as well, although rarely to the extent of electrolyte imbalance. Intravenous fluids may be necessary to restore intravascular volume. 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 to differentiate the two. o Since the gallbladder is not inflamed in uncomplicated biliary colic, the pain is poorly localized and visceral in origin; the patient has an essentially benign abdominal examination without rebound or guarding. Fever is absent. o 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 positive Murphy sign (inspiratory arrest on deep palpation of the right upper quadrant during deep inspiration) is highly suggestive of cholecystitis. Fever is often present, but it may lag behind other signs or symptoms. The presence of fever, persistent tachycardia, hypotension, or jaundice necessitate a search for complications of cholelithiasis, including cholecystitis, cholangitis, pancreatitis, or other systemic causes. Consider that both intra-abdominal and extra-abdominal pathology can present with upper abdominal pain, and often coexist with cholelithiasis. Among the different entities to consider are peptic ulcer disease, pancreatitis (acute or chronic), hepatitis, dyspepsia, gastroesophageal reflux disease (GERD), irritable bowel syndrome, esophageal spasm, pneumonia, cardiac chest pain, and diabetic ketoacidosis. A careful history and physical examination should guide further workup.

Causes
Ethnicity, gender, age, genetics, dietary considerations, and presence of certain comorbidities are major risk factors in the development of cholelithiasis and associated complications.

Ethnicity: Prevalence rates of cholelithiasis are highest among western Caucasian, Hispanic, and Native American populations. Eastern European, African American, and Asian populations are less afflicted. Age: Advancing age is a major risk factor for gallbladder disease; gallstones are exceedingly rare in children. Gender: The prevalence rate of cholelithiasis is higher in women of all age groups. The difference is attributed to increased levels of estrogens and progesterone, which ultimately promote the formation of gallstones. Estrogens increase cholesterol formation, which supersaturate the bile, leading to precipitation of cholesterol stones; progesterone inhibits gallbladder motility leading to biliary stasis and stone formation. Pregnancy contributes to the female preponderance in prevalence due to increases in circulating sex steroids in the gravid state. High-fat diet: Historically, but not statistically, high-fat diet is associated with the formation of gallstones and symptoms associated with gallstones. Estrogen therapy, in similar fashion, is associated with higher risk of cholelithiasis. Genetics: Studies in family history suggest that genetics have a significant role in development of gallstones. Dietary considerations: Obesity, high-fat diet, and hypertriglyceridemia are strongly associated with the formation of gallstones and arising complications. Additional dietary risk factors include decreased oral intake, rapid weight loss, and use of parenteral nutrition. Diosgenin-rich beans, particularly associated with a South American diet, increase cholesterol secretion and gallstone formation. Bariatric surgery: More than one third of the 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 Comorbidities o 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. o Crohn disease, ileal resection, or other diseases of the ileum decrease bile salt reabsorption and increase the risk of gallstone formation. o Hemolytic diseases, including sickle cell disease and spherocytosis, promote the formation of pigmented stones. o Bacterial or parasitic infections from organisms that contain B -glucuronidase, an enzyme that deconjugates bilirubin glucuronide, increase the risk for pigmented stones. o 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. o Other illnesses or states that predispose to gallstone formation include the following: burns, use of total parenteral nutrition, paralysis, ICU care, or major trauma. o This is due, in general, to decreased enteral stimulation of the gallbladder with resultant biliary stasis and stone formation.

Related literature

Single-port-access (SPA) cholecystectomy: a multi-institutional report of the first 297 cases.


Surg Endosc 2010,Aug,01;24(8):1854-60; (PMID: 20135180) Publication Type: Journal Article, Research Support, Non-U.S. Gov't Surgical endoscopy Curcillo, Paul G ; Wu, Andrew S ; Podolsky, Erica R ; Graybeal, Casey ; Katkhouda, Namir ; Saenz, Alex ; Dunham, Robert ;Fendley, Steven ; Neff, Marc ; Copper, Chad ; Bessler, Marc ; Gumbs, Andrew A ; Norton, Michael ; Iannelli, Antonio ; Mason, Rodney ; Moazzez, Ashkan ; Cohen, Larry ; Mouhlas, Angela ; Poor, Alex;

Department of Surgery, Drexel University College of Medicine, 219 North Broad Street, Philadelphia, PA 19107, USA. paul.curcillo@drexelmed.edu

article abstract
BACKGROUND: An important aspect of a new surgical technique is whether it can be performed by other surgeons in other institutions. The authors report the first 297 cases in a multi-institutional and multinational review of laparoscopic cholecystectomy performed via a single portal of entry. METHODS: Data were collected retrospectively for the initial patientsundergoing single-port cholecystectomy by 13 surgeons who performed these procedures in their institutions after training by the authors. The review included operative time, blood loss, incision length, length of hospital stay (LOS), necessary additional trocars, and other parameters important to cholecystectomy. A database of all the single-port-access (SPA) surgeries performed by the surgeons included demographic and procedural details, LOS, complications, and initial follow-up data.RESULTS: To date, 297 single-port cholecystectomies have been performed for a variety of diagnoses, primarily cholelithiasis.The average operative time was 71 min, and the average LOS was 1-2 days. The average blood loss was minimal. The use of additional port sites outside the umbilicus occurred in 34 of the cases. Of the 35 intraoperative cholangiograms performed, 34 were successful. No significant complications occurred except for seromas and minor postoperative wound infections. These results are comparable with those for standard multiport cholecystectomy. In addition, no access site hernias (ASH) occurred.CONCLUSIONS: The findings demonstrate that SPA surgery is an alternative to multiport laparoscopy with fewer scars and better cosmesis. One factor affecting the rate for adoption of SPA surgery among other surgeons is the reproducibility of this new procedure. Although this study had insufficient data to determine fully the benefits of SPA surgery, the feasibility of this procedure with safe, acceptable results was demonstrated in this initial large series across multinational institutions.

L
Laboratory Studies
Laboratory study results are normal in the asymptomatic patient and patients with uncomplicated biliary colic. They are generally not necessary unless cholecystitis is a concern. An elevated lipase is indicative of pancreatitis, the most common causes of which are alcohol and gallstones.

Imaging Studies
Asymptomatic gallstones are often found incidentally on plain radiographs, abdominal sonograms, or CT scan for workup of other processes. Radiography: Cholesterol and pigment stones are radiopaque and visible on radiographs in only 10-30% of instances, depending on their extent of calcification, and have little role in the diagnosis of gallstones or gallbladder disease.

Ultrasonography: The procedure of choice in suspected gallbladder or biliary disease, it is a simple, rapid test that is safe in pregnancy and does not expose the patient to harmful radiation or intravenous contrast. An added advantage is that it can be performed by skilled practitioners at the bedside. o Sensitivity is variable and dependent upon operator proficiency, but in general, it is highly sensitive and specific for gallstones greater than 2 mm. It is less so for microlithiasis or biliary sludge. o Ultrasonography is very useful for diagnosing uncomplicated acute cholecystitis. The sonographic features of acute cholecystitis include gallbladder wall thickening (>5 mm), pericholecystic fluid, gallbladder distention (>5 cm), and a sonographic Murphy sign. The presence of multiple criteria increases its diagnostic accuracy. o 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.

The WES (wall echogenic shadow) sign, long axis of the gallbladder. The arrow head 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.

Cholecystitis with small stones in the gallbladder neck. Classic acoustic shadowing is seen beneath the gallstones. The gallbladder wall is greater than 4 mm. Image courtesy of DT Schwartz.

Computerized tomography: Gallstones are often found incidentally on CT. Findings on CT for acute cholecystitis are similar to those found on sonograms. Although not the initial study of choice in biliary colic, CT can be used in diagnostic challenges or to further characterize complications of gallbladder disease. CT is particularly useful for the detection of intrahepatic stones or recurrent pyogenic cholangitis. Biliary scintigraphy (HIDA scan): Scintigraphy gives little information about nonobstructing cholelithiasis and cannot detect other pathologic states, although it is highly accurate for the diagnosis of cystic duct obstruction.

Treatment
Emergency Department Care
Gallstones found incidentally may be followed until they become symptomatic. Surgical 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. In patients with symptomatic gallstones, discuss the options for surgical and nonsurgical intervention and refer the patient to their primary care provider and surgical consultant for outpatient follow-up. Persons with diabetes and women who are pregnant should have close follow-up to determine if they become symptomatic or develop complications. Patients with risk factors for complications of gallstones may be offered elective cholecystectomy, even with asymptomatic gallstones. These groups include persons with the following conditions and demographics: o Cirrhosis o Portal hypertension o Sickle cell disease o Children o Transplant candidates o Diabetes with minor symptoms Patients with a calcified or porcelain gallbladder should consider elective cholecystectomy due to the increased risk of carcinoma (25%). Refer to a surgeon for removal as an outpatient procedure.

If cholecystitis or other infectious complication is suspected, emergent consultation with a general surgeon should be obtained. See related eMedicine articles, Cholecystectomy, Laparoscopic; Cholecystectomy, Open; andCholecystectomy, Single Port.

Consultations
In patients with symptomatic gallstones, discuss the options of medical management or elective surgery with the patient and refer for follow-up to the primary care provider and general surgeon. Use of a single-step procedure of laparoscopic cholecystectomy (LC) and intraoperative endoscopic retrograde cholangiopancreatography (LC+IO-ERCP) and endoscopic sphincterotomy (ES) has shown promising results on patients with gallbladder stones and with confirmed or suspected common bile duct stones.5 Refer patients with a calcified or porcelain gallbladder to a surgeon for removal on an outpatient basis. Emergency consultation with a general surgeon should be sought if cholecystitis is strongly suspected or diagnosed.

Medication
For asymptomatic gallstones, medical therapies are rarely used because they require long-term therapy, may have adverse reactions or complications, and recurrence of gallstones is relatively common (25% within 5 years). In patients who present with an acute attack of biliary colic, pain can be controlled with oral or parenteral opioids. Elective cholecystectomy is the treatment of choice for symptomatic cholelithiasis. 6,7 In uncomplicated cholelithiasis with biliary colic, medical management may be a useful alternative to cholecystectomy in selected patients, particularly in patients with high surgical risk. Medical treatment, beyond pain control, however, is not initiated in the emergency department, and patients should be referred to their primary care provider for further medical management. Medical management of gallstones, used alone or in combination, include the following: oral bile salt therapy (ursodeoxycholic acid, chenodeoxycholic acid), contact dissolution, and extracorporeal shockwave lithotripsy. Medical management is more efficacious in patients with small stones (<1 cm), high cholesterol content, and good gallbladder function. Bile salt therapy may be required for greater than 6 months of therapy, with a success rate less than 50%. Complicated cholelithiasis that cannot tolerate surgery should be considered for ERCP or percutaneous lithotomy.

Follow-up
Further Outpatient Care
Refer patients with asymptomatic gallstones to their primary care physician. It may be difficult to determine if nonspecific presenting symptoms are due to cholelithiasis. Dyspepsia, bloating, and flatulence are nonspecific and usually are not due to gallstones; these symptoms are not likely to be cured by cholecystectomy.

Deterrence/Prevention
Recommending dietary changes of decreased fat intake is prudent; this may decrease the incidence of biliary colic attacks; however, it has not been shown to cause dissolution of stones.

Complications
Complications of cholelithiasis may include the following: Biliary colic8 Cholecystitis (acute or chronic) Choledocholithiasis Cholangitis Sepsis Gallstone pancreatitis9 Gallstone ileus9

Prognosis
Less than half of patients with gallstones become symptomatic. The mortality rate for an elective cholecystectomy is 0.5% with less than 10% morbidity. The mortality rate for an emergent cholecystectomy is 3-5% with 30-50% morbidity. Approximately 10-15% of patients have an associated choledocholithiasis. Following cholecystectomy, stones may recur in the bile duct.

Patient Education
Instruct patients about symptoms of gallstones and the stress the importance of return for signs or symptoms of complications. Discuss the importance of follow-up care with their primary care giver for long-term management and treatment options. A low-fat diet is advisable though not proven to be preventative. For excellent patient education resources, see eMedicine's Liver, Gallbladder, and Pancreas Center andCholesterol Center. Also, visit eMedicine's patient education article Gallstones.

Miscellaneous
Medicolegal Pitfalls
Failure to recognize life-threatening complications of gallbladder disease (cholecystitis, cholangitis, others). Failure to recognize obstructed choledocholithiasis. Failure to consider other causes of upper abdominal pain, such as myocardial infarct, pneumonia, peptic ulcer disease, pancreatitis, diabetic ketoacidosis, and others. Failure to provide adequate instructions for the patients to return back to the emergency department.

Multimedia

Media file 1: The pathology in the accompanying ultrasound image was found incidentally in a person without abdominal complaints. One to 3% of gallstones become symptomatic each year. Image courtesy of DT Schwartz.

(Enlarge Image)

Media file 2: Sludge in the gallbladder. Note the lack of shadowing. Image courtesy of DT Schwartz.

(Enlarge Image)

Media file 3: Cholecystitis with small stones in the gallbladder neck. Classic acoustic shadowing is seen beneath the gallstones. The gallbladder wall is greater than 4 mm. Image courtesy of DT Schwartz.

(Enlarge Image)

Media file 4: 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.

(Enlarge Image)

Media file 5: WES sign, short axis view of the gallbladder. Image courtesy of Stephen Menlove.

(Enlarge Image)

Media file 6: The WES (wall echogenic shadow) sign, long axis of the gallbladder. The arrow head 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.

(Enlarge Image)

Definition
By Mayo Clinic staff

Gallstones

Gallstones are hardened deposits of digestive fluid that can form in your gallbladder. Your gallbladder is a small, pear-shaped organ on the right side of your abdomen, just beneath your liver. The gallbladder holds a digestive fluid called bile that's released into your small intestine.

Gallstones range in size from as small as a grain of sand to as large as a golf ball. Some people develop just one gallstone, while others develop many gallstones at the same time. Gallstones are common in the United States. People who experience symptoms from their gallstones usually require gallbladder removal surgery. Gallstones that don't cause any signs and symptoms typically don't need treatment.

Symptoms
By Mayo Clinic staff
Gallstones may cause no signs or symptoms. If a gallstone lodges in a duct and causes a blockage, signs and symptoms may result, such as:

Sudden and rapidly intensifying pain in the upper right portion of your abdomen Sudden and rapidly intensifying pain in the center of your abdomen, just below your breastbone Back pain between your shoulder blades Pain in your right shoulder Gallstone pain may last several minutes to a few hours. When to see a doctor Make an appointment with your doctor if you have any signs or symptoms that worry you. Seek immediate care if you develop signs and symptoms of a serious gallstone complication, such as:

Abdominal pain so intense that you can't sit still or find a comfortable position Yellowing of your skin and the whites of your eyes High fever with chills

Causes
By Mayo Clinic staff

Gallstones

It's not clear what causes gallstones to form. Doctors think gallstones may result when:

Your bile contains too much cholesterol. Normally, your bile contains enough chemicals to dissolve the cholesterol excreted by your liver. But if your bile contains more cholesterol than can be

dissolved, the cholesterol may form into crystals and eventually into stones. Cholesterol in your bile has no relation to the levels of cholesterol in your blood.

Your bile contains too much bilirubin. Bilirubin is a chemical that's produced when your body breaks down red blood cells. Certain conditions cause your liver to make too much bilirubin, including liver cirrhosis, biliary tract infections and certain blood disorders. Your gallbladder doesn't empty correctly. If your gallbladder doesn't empty completely or often enough, bile may become very concentrated and this contributes to the formation of gallstones. Types of gallstones Types of gallstones that can form in the gallbladder include:

Cholesterol gallstones. The most common type of gallstones, called cholesterol gallstones, often appears yellow in color. These gallstones are composed mainly of undissolved cholesterol, although they can also have other components. Pigment gallstones. These dark brown or black stones form when your bile contains too much bilirubin.

Risk factors
By Mayo Clinic staff
Factors that may increase your risk of gallstones include:

Being female Being age 60 or older Being an American Indian Being a Mexican-American Being overweight or obese Being pregnant Eating a high-fat diet Eating a high-cholesterol diet Eating a low-fiber diet Having a family history of gallstones Having diabetes Losing weight very quickly Taking cholesterol-lowering medications Taking medications that contain estrogen, such as hormone therapy drugs

Complications
By Mayo Clinic staff

Pancreatitis caused by gallstones

Gallbladder cancer

Complications of gallstones may include:

Inflammation of the gallbladder. A gallstone that becomes lodged in the neck of the gallbladder can cause inflammation of the gallbladder (cholecystitis). Cholecystitis can cause severe pain and fever. Blockage of the common bile duct. Gallstones can block the tubes (ducts) through which bile flows from your gallbladder or liver to your small intestine. Jaundice and bile duct infection (cholangitis) can result. Blockage of the pancreatic duct. The pancreatic duct is a tube that runs from the pancreas to the common bile duct. Pancreatic juices, which aid in digestion, flow through the pancreatic duct. A gallstone can cause a blockage in the pancreatic duct, which can lead to inflammation of the pancreas (pancreatitis). Pancreatitis causes intense, constant abdominal pain and usually requires hospitalization. Gallbladder cancer. People with a history of gallstones have an increased risk of gallbladder cancer. But gallbladder cancer is very rare, so even though the risk of cancer is elevated, the likelihood of gallbladder cancer is still very small.

Definition Symptoms Causes Risk factors Complications Preparing for your appointment Tests and diagnosis Treatments and drugs Alternative medicine Prevention

Mayo Clinic Health Manager


Get free personalized health guidance for you and your family.
GET STARTED

Free E-Newsletters

Subscribe to receive the latest updates on health topics.About our newsletters

Housecall Alzheimer's caregiving Living with cancer


Enter e-mail

Subscribe

close window

About our e-newsletters


Free e-newsletters Mayo Clinic expertise We do not share your e-mail address Housecall, our weekly general-interest e-newsletter, keeps you up to date on a wide variety of health topics with timely, reliable, practical information, recipes, blogs, questions and answers with Mayo Clinic experts and more. Our biweekly topic-specific e-newsletters also include blogs, questions and answers with Mayo Clinic experts, and other useful information that will help you manage your health.

Housecall Archives

RSS Feeds

close window

Mayo Clinic Housecall


What you get

Free weekly e-newsletter Mayo Clinic expertise Recipes, tools and other helpful information We do not share your e-mail address Sign up View past issues

Stay up to date on the latest health information.

Preparing for your appointment


By Mayo Clinic staff
You're likely to start by seeing your family doctor or a general practitioner. If your doctor suspects you may have gallstones, you may be referred to a doctor who specializes in the digestive system (gastroenterologist) or to a surgeon. Because appointments can be brief, and because there's often a lot of ground to cover, it's a good idea to be well prepared for your appointment. Here's some information to help you get ready for your appointment, and what to expect from your doctor. What you can do

Be aware of any pre-appointment restrictions. At the time you make the appointment, be sure to ask if there's anything you need to do in advance, such as restrict your diet.

Write down any symptoms you're experiencing, including any that may seem unrelated to the reason for which you scheduled the appointment. Write down key personal information, including any major stresses or recent life changes. Make a list of all medications, as well as any vitamins or supplements, that you're taking. Take a family member or friend along, if possible. Sometimes it can be difficult to absorb all the information provided during an appointment. Someone who accompanies you may remember something that you missed or forgot. Write down questions to ask your doctor. Your time with your doctor is limited, so preparing a list of questions will help you make the most of your time together. List your questions from most important to least important in case time runs out. For gallstones, some basic questions to ask your doctor include:

Are gallstones the likely cause of my abdominal pain? What are other possible causes for my symptoms? What kinds of tests do I need? Is there a chance that my gallstones will go away without treatment? Do I need gallbladder removal surgery? What are the risks of surgery? How long does it take to recover from gallbladder surgery? Are there other treatment options for gallstones? Should I see a specialist? What will that cost, and will my insurance cover it? Are there any brochures or other printed material that I can take with me? What Web sites do you recommend? In addition to the questions that you've prepared to ask your doctor, don't hesitate to ask questions during your appointment at any time that you don't understand something. What to expect from your doctor Your doctor is likely to ask you a number of questions. Being ready to answer them may allow more time to cover other points you want to address. Your doctor may ask:

When did you first begin experiencing symptoms? Have your symptoms been continuous, or occasional? How severe are your symptoms? What, if anything, seems to improve your symptoms? What, if anything, appears to worsen your symptoms?

Tests and diagnosis


By Mayo Clinic staff

ERCP procedure

Tests and procedures used to diagnose gallstones include:

Tests to create pictures of your gallbladder. Your doctor may recommend an abdominal ultrasound or a computerized tomography (CT) scan to create pictures of your gallbladder. These images can be analyzed to look for signs of gallstones. Tests to check your bile ducts for gallstones. A test that uses a special dye to highlight your bile ducts on images may help your doctor determine whether a gallstone is causing a blockage. Tests may include a hepatobiliary iminodiacetic acid (HIDA) scan, magnetic resonance imaging (MRI) or endoscopic retrograde cholangiopancreatography (ERCP). Gallstones discovered using ERCP can be removed during the procedure. Blood tests to look for complications. Blood tests may reveal an infection, jaundice, pancreatitis or other complications caused by gallstones.

Treatments and drugs


By Mayo Clinic staff

Laparoscopic cholecystectomy

Gallstones that don't cause signs and symptoms Gallstones that don't cause signs and symptoms, such as those detected during an ultrasound or CT scan done for some other condition, typically don't require treatment. Your doctor may recommend you be alert for symptoms of gallstone complications, such as intensifying pain in your upper right abdomen. If gallstone signs and symptoms occur in the future, you can have treatment. But most people with gallstones that don't cause symptoms will never need treatment. Treatment for gallstones that cause signs and symptoms Treatment options for gallstones include:

Surgery to remove the gallbladder (cholecystectomy). Your doctor may recommend surgery to remove your gallbladder, since gallstones frequently recur. Once your gallbladder is removed, bile flows directly from your liver into your small intestine, rather than being stored in your gallbladder. You don't need your gallbladder to live, and gallbladder removal doesn't affect your ability to digest food, but it can cause diarrhea.

Medications to dissolve gallstones. Medications you take by mouth may help dissolve gallstones. But it may take months or years of treatment to dissolve your gallstones in this way. An experimental treatment to inject gallstone medications directly into the gallbladder may dissolve gallstones more quickly. Tests are ongoing to determine whether this procedure is safe and effective. Medications for gallstones aren't commonly used and are reserved for people who can't undergo surgery.

Alternative medicine
By Mayo Clinic staff
Remedies to prevent gallstones from causing complications If you have gallstones that aren't causing signs or symptoms, you may worry that you'll experience pain or other symptoms of gallstones in the future. For this reason, some people turn to complementary and alternative medicine for gallstone cures. No alternative therapies have been proved to cure or dissolve gallstones. Some alternative therapies may help reduce your risk of gallstone complications, though. Ask your doctor about which therapies may be safe for you to try. Options might include:

Eating a high-fiber diet that includes healthy fats. Choose a diet that's full of a variety of fruits and vegetables. These high-fiber foods may help prevent additional gallstones from forming. Also include healthy, unsaturated fats in your diet. Foods that contain unsaturated fats include fish and nuts. Taking vitamin supplements. People who don't get enough vitamin C, vitamin E or calcium may have an increased risk of gallstones. There isn't enough evidence to suggest that supplements containing these vitamins can prevent gallstones.


Ask your doctor about the benefits and risks of vitamin supplements. The safest way to get more vitamins is to choose foods that contain them.

Prevention
You can reduce your risk of gallstones if you:

Don't skip meals. Try to stick to your usual meal times each day. Skipping meals or fasting can increase the risk of gallstones. Exercise most days of the week. Being inactive may increase the risk of gallstones, so incorporate physical activity into your day. If you haven't been active lately, start slowly and work your way up to 30 minutes of activity on most days of the week. Lose weight slowly. If you need to lose weight, go slow. Rapid weight loss can increase the risk of gallstones. Aim to lose 1 or 2 pounds (0.5 to about 1 kg) a week. Maintain a healthy weight. Obesity and overweight increase the risk of gallstones. Work to achieve a healthy weight by reducing the number of calories you eat and increasing the amount of physical activity you get. Once you achieve a healthy weight, work to maintain that weight by continuing your healthy diet and continuing to exercise.

CHOLECYSTECTOMY

Definition
By Mayo Clinic staff

Gallbladder and bile duct

Cholecystectomy (ko-lay-sis-TEK-tuh-me) is a surgical procedure to remove your gallbladder a pear-shaped organ that sits just below your liver on the upper right side of your abdomen. Your gallbladder collects and stores bile a digestive fluid produced in your liver. Cholecystectomy may be necessary if you experience pain from gallstones that block the flow of bile. Cholecystectomy is a common surgery, and it carries only a small risk of complications. In most cases, you can go home the same day of your cholecystectomy. Cholecystectomy is most commonly performed using a tiny video camera to see inside your abdomen and special surgical tools to remove the gallbladder. Doctors call this laparoscopic

Why it's done


By Mayo Clinic staff

Gastrointestinal tract

Cholecystectomy is used to treat gallstones and the complications they cause. Your doctor may recommend cholecystectomy if you have:

Gallstones in the gallbladder (cholelithiasis) Gallstones in the bile duct (choledocholithiasis) Gallbladder inflammation (cholecystitis) Pancreas inflammation (pancreatitis)

Risks
By Mayo Clinic staff
Cholecystectomy carries a small risk of complications including:

Bile leak Bleeding Blood clots Death Heart problems Infection Injury to nearby structures, such as the bile duct, liver and small intestine Pancreatitis Pneumonia Your risk of complications depends on your overall health and the reason for your cholecystectomy. Emergency cholecystectomy carries a higher risk of complications than does a planned cholecystectomy.

How you prepare


By Mayo Clinic staff
To prepare for cholecystectomy, your surgeon may ask you to:

Drink a solution to clean out your intestines. In the days before your procedure you may be given a prescription solution that flushes stool out of your intestines. Eat nothing the night before your surgery. You may drink a sip of water with your medications, but avoid eating and drinking at least four hours before your surgery. Stop taking certain medications and supplements. Tell your doctor about all the medications and supplements you take. Continue taking most medications as prescribed. Your doctor may ask you to stop taking certain medications and supplements because they may increase your risk of bleeding. Shower using a special soap. Your doctor may give you a special antibacterial soap to use before your surgery. Prepare for your recovery Plan ahead for your recovery after surgery. For instance:

Plan for a hospital stay. Most people go home the same day of their cholecystectomy, but complications can occur that require one or more nights in the hospital. If the surgeon needs to make a long incision in your abdomen to remove your gallbladder, you may need to stay in the hospital longer. It's not always possible to know ahead of time what procedure will be used. Plan ahead in case you need to stay in the hospital by bringing personal items, such as your toothbrush, comfortable clothing and books or magazines to pass the time. Find someone to drive you home and stay with you. Ask a friend or family member to drive you home and stay close the first night after surgery.

What you can expect


By Mayo Clinic staff

Gallbladder and bile duct

Laparoscopic cholecystectomy

During your cholecystectomy Cholecystectomy is performed using general anesthesia, so you won't be aware during the procedure. Anesthesia drugs are given through a vein in your arm. Once the drugs take affect, your health care team will insert a tube down your throat to help you breathe. Your surgeon then performs the cholecystectomy using either a laparoscopic or open procedure. Minimally invasive (laparoscopic) cholecystectomy During laparoscopic cholecystectomy, the surgeon makes four small incisions in your abdomen. A tube with a tiny video camera is inserted into your abdomen through one of the incisions. Your surgeon watches the picture on a monitor in the operating room as special surgical tools are inserted through the other incisions in your abdomen and your gallbladder is removed. Next you'll undergo cholangiography, a special X-ray to check your bile duct for abnormalities. If your surgeon finds gallstones or other problems in your bile duct, those may be remedied. Then your incisions are sutured, and you're taken to a recovery area. Laparoscopic cholecystectomy takes one or two hours. Laparoscopic cholecystectomy isn't appropriate for everyone. In some cases your surgeon may begin with a laparoscopic approach and find it necessary to make a larger incision because of scar tissue from previous operations or complications. Traditional (open) cholecystectomy During open cholecystectomy your surgeon makes a 6-inch (about 15 cm) incision in your abdomen below your ribs on your right side. The muscle and tissue are pulled back to reveal your liver and gallbladder. Your surgeon then removes the gallbladder. The incision is sutured, and you're taken to a recovery area. Open cholecystectomy takes one or two hours. After cholecystectomy You'll be taken to a recovery area as the anesthesia drugs wear off. Then you'll be taken to a hospital room to continue recovery. Recovery varies depending on your procedure:

Laparoscopic cholecystectomy. People are often allowed to go home the same day as their surgery, though sometimes a one-night stay in the hospital is needed. In general, you can expect to go home once you're able to eat and drink without pain and are able to walk unaided. It takes about a week to fully recover. Open cholecystectomy. Expect to spend two or three days in the hospital recovering. Once at home, it may take four to six weeks to fully recover.

Results
By Mayo Clinic staff
Cholecystectomy can relieve the pain and discomfort of gallstones. Conservative treatments, such as dietary modifications, usually can't stop gallstones from recurring. Cholecystectomy is the only way to prevent gallstones. Some people experience mild diarrhea after cholecystectomy, though this usually goes away with time. Most people won't experience digestive problems after cholecystectomy. Your gallbladder isn't essential to healthy digestion. How quickly you can return to normal activities after cholecystectomy depends on which procedure your surgeon uses and your overall health. People undergoing laparoscopic cholecystectomy may be able to go back to work in a matter of days. Those undergoing open cholecystectomy may need a week or more to recover enough to return to work.

ACKNOWLEGDEMENT Without the knowledge that was been shared to us, our case may not be possible. Despite of the mistakes that have been done, we appreciated the time and support given to us by those people who helped us to be successful within this case study. The group would like to thank the following persons for their support and cooperation in the completion of this case study: To Batangas Regional Hospital who gives their place to the nursing students likes us. To the staff nurses in Station IV. To the groups Clinical Instructor, Mr. Mharlon Melo for guiding and teaching us the right actions to do. For giving information and additional knowledge to each of the member. For telling to us that NURSING must be taken seriously because our job is not a game because we are handling a ones life. For inspiring us to be better NURSES someday. To our co-students, friends, and loved ones who lifts us when were down. To the patient and relatives for being approachable and cooperative to make our case study successful. To our parents for supporting our expenses to make this case study successful. For their unconditional love and support in every trial we have. Above all, Almighty God for giving us enough wisdom and strength. For giving a powerful hand in treating our patients.For guiding us and leading to the right one. For everyday support. THANKYOU VERY MUCH!!!GOD BLESS YOU ALL!!

Objectives of the Study I. General Objectives This study aims to develop the knowledge, skills and attitudes of student nurses through effective utilization of nursing process in dealing with the course treatment of patient with Cholelithiasis

Cholelithiasis is the fifth leading cause of hospitalization among adults. The disease may also be occurring in persons who are obese, who have high cholesterol, or who are on cholesterol lowering drugs. 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. Diseases of the gallbladder and biliary tract are common and painful conditions that may be life threatening and mostly require surgery. They are generally associated with deposition of calculi and inflammation. 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. Cholangitis, infection of the bile duct, is commonly associated with choledocholithiasis. Predisposing factors may include bacterial or metabolic alteration of bile acids. Cholecystitis, acute or chronic inflammation of the gallbladder is usually associated with a gallstone impacted in the cystic duct that may cause painful distention of the gallbladder. Postcholecystectomy syndrome commonly results from residual gal1stones or stricture of the common bile duct. It may be occurs in 1 % to 5 % of all patients whose gallbladders have been surgical1y removed and may produce right upper quadrant abdominal pain, biliary colic, dyspepsia and indigestion. Gallstones develop in many people without causing symptoms. The chance of symptoms or complications resulting from cholelithiasis is about 20%. With current surgical approaches, the outcome is excellent with no recurrence of symptoms in over 99% of individuals. We have chosen this case not only because it is only the choice but somehow, we observed and noticed that during our ages, 20-60,we can have this. And for further knowledge to control the number of the case, that will start on us even though we are just student nurses

C. DRUG STUDY Name of Drug: Ceftriaxone Phil. Brand: Rocephin, Patrixon Therapeutic Class: Anti-infective Indication: Treatment of susceptible infections including chancroid, gastroenteritis (invasive salmonellosis, shegilosis), lyme disease, meningitis (including meningococcal magnetism prophylaxis), syphilis, typhoid fever, whipples disease. Pre-operative prophylaxis to reduce chance of post-operative surgical infections. Dosage: Adult usual dosage 1g/day in a single injection and up to 2g/day once daily according to the infection severity and the patients body weight. Contraindication: Ceftriaxone is contraindicated in patients with hypersensitivity to cephalosporins and penicillins, lidocaine or any other local anesthetic product of the amide type. Adverse Reaction: Pain, induration, phlebitis after IV administration, rash, diarrhea, eosinophilia, casts in urine, thrombocytosis and leukopenia Nursing Responsibilities: Use with caution in patients with history of gastrointestinal disease Name of Drug: Ketorolac Phil. Brand: Acular, Kortezor, Toradol Therapeutic Class: Analgesic Indication: Short term management of moderate to severe acute post operative pain Dosage: IM injection adult less than 35 yrs: 60mg, greater than 35 yrs:30mg. IV injection - adult less than 65 yrs: 30mg. Adults more than 65 yrs: 15mg

Contraindication: Active peptic ulcer disease, recent gastrointestinal bleeding or perforatin, moderate to severe renal impairment, hypovolemia or dehydration Adverse Reaction: Gastrointestinal ulceration, bleeding and perforation, postoperative bleeding. Hypertension, pruritus, rash, GI disturbances, nausea, dyspepsia, diarrhea, headache, drowsiness, dizziness, sweating, edema Nursing Responsibilities: Check if the client takes the medication. Check for the doctors order and if it is the right patient. Observe for any effect and if any side effects occur inform physician TRAMADOL Phil. Brand: Dolotral, Milador, Peptrad, Sivedol, Tradonal, Tramal Therapeutic Class: Analgesic Indication: Used for moderate to severe pain Dosage: Usual dose by mouth are 50 to 100 mg every 4-6 hrs. Total daily dosage by mouth should not exceed 400 mg. Contraindication: Hypersensitivity.Acute intoxication with alcohol, hypnotics, centrally acting analgesics, opioids, or psychotropic agents. Adverse Reaction: Vasodilation; dizziness/vertigo, headache, somnolence,

stimulation, anxiety, confusion, coordination disturbances, euphoria, nervousness, sleep disorder, seizures. Nursing Responsibilities: Give with antiemetic for nausea, vomiting. Administer when pain is beginning to return; determine dosage interval by patient response Name of Drug: Ranitidine Phil. Brand: Ceranid, Cygran, Drug Makers Biotech Ranitidine, Incid, Pharex Ranitidine, Ramadine, Raxide, Ulcin, Zantac/Zantac FR Zantac 75/Zantac Ampule Therapeutic Class: Gastrointestinal Drug Indication: Used in the management of various gastrointestinal disorders such as dyspepsia, gastro-esophageal reflux disease (GERD), peptic ulcer, and Zollinger-Ellison syndrome. Dosage: Tablet/Fast-release (FR) tablet: Adult duodenal/gastric ulcer 150mg twice a day or 300mg at bedtime for 4 wks. Maintenance 150mg

at bedtime. NSAID-associated peptic ulcer 150mg twice a day or 300mg at bedtime for 8-12 wks. For children, 2-4mg/kg 3x a day. Route: Oral; may be given with or without meals. Give antacids 1hr before or 1hr after this drug. IV: give by direct IV after diluting 50mg/20mL of 0.9% D5W, NaCl over 5 mins or more Contraindication: Hypersensitivity. History of acute porphyria. Long-term therapy. Adverse Reaction: Cardiac arrhytmias, bradycardia. Headache, somnolence, fatigue, dizziness, hallucinations, depression, insomnia. Nursing Responsibilities: Advice patient to not take any new medication during therapy without consulting a physician. Allow 1hr between any other antacids and ranitidine.

Ursodiol
From Wikipedia, the free encyclopedia
(Redirected from Ursodeoxycholic acid)

This article needs additional citations for verification.


Please help improve this article by adding reliable references. Unsourced material may be challenged and removed.(January 2009)

Ursodiol, also known as ursodeoxycholic acid and the abbreviation UDCA, is one of the secondary bile acids, which are metabolic byproducts of intestinal bacteria.

Ursodiol

Systematic (IUPAC) name

3,7-dihydroxy-5-cholan-24-oic acid OR (R)-4-((3R,5S,7S,8R,9S,10S,13R,14S,17R)-3,7-dihydroxy10,13-dimethylhexadecahydro1H-cyclopenta[a]phenanthren-17-yl)pentanoic acid

Identifiers

CAS number

128-13-2

ATC code

A05AA02

Chemical data

Formula

C24H40O4

Mol. mass

392.56 g/mol

SMILES

eMolecules & PubChem

Synonyms

ursodeoxycholic acid, Actigall, Ursosan, Urso, Urso Forte

Physical data

Melt. point

203 C (397 F)

Therapeutic considerations

Pregnancy cat.

Legal status

(what is this?) (verify)

Contents
[hide]

1 Endogenous effects 2 As a pharmaceutical 3 Production 4 References 5 External links

[edit]Endogenous

effects

Primary bile acids are produced by the liver and stored in the gall bladder. When secreted into the colon, primary bile acids can be metabolized into secondary bile acids by intestinal bacteria. Primary and secondary bile acids help the body digestfats. Ursodeoxycholic acid helps regulate cholesterol by reducing the rate at which the intestine absorbs cholesterol molecules while breaking up micelles containing cholesterol. Because of this property, ursodeoxycholic acid is used to treat (cholesterol) gallstones non-surgically. While some bile acids are known to be colon tumor promoters (e.g. deoxycholic acid), others such as ursodeoxycholic acid are thought to be chemopreventive, perhaps by inducing cellular differentiation and/or cellular senescence in colon epithelial cells.[1] It is believed to inhibit apoptosis.[2] Ursodeoxycholic acid has also been shown experimentally to suppress immune response such as immune cell phagocytosis. Prolonged exposure and/or increased quantities of systemic (throughout the body, not just in the digestive system) ursodeoxycholic acid can be toxic.[3]

[edit]As

a pharmaceutical

Ursodeoxycholic acid goes by the trade names Actigall, Ursosan, Ursofalk, Urso, and Urso Forte. In Italy and Switzerland, it is marketed under the name Deursil. Ursodeoxycholic acid can be chemically synthesized and was brought to market by the Montreal-based Axcan Pharma in 1998,[citation needed] which continues to market the drug. The drug reduces cholesterol absorption and is used to dissolve (cholesterol)gallstones in patients who want an alternative to surgery. The drug is very expensive, however, and if the patient stops taking it, the gallstones tend to recur if the condition that gave rise to their formation does not change. For these reasons, it has not supplanted surgical treatment by cholecystectomy.

It is the only FDA approved drug to treat primary biliary cirrhosis.[4][5] A Cochrane review to evaluate if ursodeoxycholic acid has any beneficial effect in primary biliary cirrhosis patients included 16 randomized clinical trials with a total of 1447 patients. The primary outcome measures were mortality and mortality or liver transplantation. Although treatment with ursodeoxycholic acid showed a reduction in liver biochemistry, jaundice, and ascites, it did not decrease mortality or liver transplantation.[6] In children, its use is not licensed, as its safety and effectiveness are not established. [7][8][9] In double the recommended daily dose ursodeoxycholic acid reduces elevated liver enzyme levels in patients with primary sclerosing cholangitis, but its use was associated with an increased risk of serious adverse events (the development of cirrhosis, varices, death or liver transplantation) in patients who received ursodeoxycholic acid compared with those who received placebo). After adjustment for baseline stratification characteristics, the risk was 2.1 times greater for death,transplantation, or minimal listing criteria in patients on ursodeoxycholic acid than for those on placebo (P = 0.038). Serious adverse events, were more common in the ursodeoxycholic acid group than the placebo group (63% versus 37% [P < 0.01])).[10]

[edit]Production
The drug is generally not derived from animals. However, it is believed more than 12,000 bile bears are kept on farms in China, Vietnam and South Korea for the purpose of harvesting ursodeoxycholic acid.[11] Ursodeoxycholic acid is found in large quantities in bear bile.

Anatomy and Function of the Gastrointestinal Tract


We want anyone considering gastric bypass surgery to have a basic understanding of gastrointestinal (GI) anatomy and physiology. The GI tract is the pathway food takes from the mouth, through the esophagus, stomach, small and large intestine within where the nutrients are extracted for the needs of the body. The residue then passes to the rectum where it is evacuated. The first part of the pathway is the esophagus, which is a conduit that guides food from the mouth, where it is prepared by chewing, down to the stomach where it is stored. The stomach is both a storage space, holding as much as a quart and a half of ingested food, and a secretory organ that produces the gastric acid necessary for digestion. However, the stomach does not absorb food. When food enters the stomach from the esophagus it remains for a short period while it is mixed with gastric acid. The stomach then by involuntary muscle contractions (peristalsis) empties the food gradually into the duodenum, the first part of the small intestine. The small intestine consists of three parts: the duodenum, the jejunum and the ileum. In these three parts, certain digestive secretions are mixed with food, and the nutrients are absorbed into the blood stream. The duodenum treats the food it receives with bile from the liver and enzymes from the pancreas. It also adds liquid duodenal fluid that comes from the wall of the duodenum itself. The food, bile, enzymes and liquids brought together in the duodenum are then passed into the jejunum. The jejunum or second portion of the small intestine is approximately 10 feet long. It lies immediately behind the duodenum and continues the process of digestion, breaking down food into essential elements. The ileum or third portion of the small intestine, like the jejunum, is about 10 feet long. It is here that a major part of the absorption of food products and liquids occurs. Waste products of the digestive process are passed from the small intestine or terminal ileum, into the large intestine, also known as the colon. The beginning of the colon is in the right lower quadrant of the abdomen, near the appendix. The colon moves waste products through about four feet by the continuing process of undulating motions or peristalsis, which is common to all parts of the gastrointestinal tract. The primary function of the colon is to store waste products of digestion prior to evacuation. The colon absorbs small amounts of water and electrolytes.

Jejunal perforation in gallstone ileus a case series

Louise E Browning1 , Jeremy D Taylor2 , Sue K Clark3 and Nariman D Karanjia4 1 Department of Surgery, University Hospital Lewisham, Lewisham, UK 2 Department of Radiology, St. George's Hospital, London, UK 3 Department of Surgery, St Mark's Hospital, Harrow, UK 4 Department of Surgery, Royal Surrey County Hospital, Surrey, UK author email corresponding author email Journal of Medical Case Reports 2007, 1:157doi:10.1186/1752-19471-157 The electronic version of this article is the complete one and can be found online at:http://www.jmedicalcasereports.com/content/1/1/157 Received: Accepted: 12 August 2007 28 November 2007

Published: 28 November 2007 2007 Browning et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract
Introduction

Gallstone ileus is an uncommon complication of cholelithiasis but an established cause of mechanical bowel obstruction in the elderly. Perforation of the small intestine proximal to the obstructing gallstone is rare, and only a handful of cases have been reported. We present two cases of perforation of the jejunum in gallstone ileus, and remarkably in one case, the gallstone ileus caused perforation of a jejunal diverticulum and is to the best of our knowledge the first such case to be described.

Case presentations
Case 1 A 69 year old man presented with two days of vomiting and central abdominal pain. He underwent laparotomy for small bowel obstruction and was found to have a gallstone obstructing the mid-ileum. There was a 2 mm perforation in the anti-mesenteric border of the dilated proximal jejunum. The gallstone was removed and the perforated segment of jejunum was resected. Case 2 A 68 year old man presented with a four day history of vomiting and central abdominal pain. Chest and abdominal radiography were unremarkable however a subsequent CT scan of the abdomen showed aerobilia. At laparotomy his distal ileum was found to be obstructed by an impacted gallstone and there was a perforated diverticulum on the mesenteric surface of the mid-jejunum. An enterolithotomy and resection of the perforated small bowel was performed.

Conclusion
Gallstone ileus remains a diagnostic challenge despite advances in imaging techniques, and pre-operative diagnosis is often delayed. Partly due to the elderly population it affects, gallstone ileus continues to have both high morbidity and mortality rates. On reviewing the literature, the most appropriate surgical intervention remains unclear. Jejunal perforation in gallstone ileus is extremely rare. The cases described illustrate two quite different causes of perforation complicating gallstone ileus. In the first case, perforation was probably due to pressure necrosis caused by the gallstone. The second case was complicated by the presence of a perforated jejunal diverticulum, which was likely to have been secondary to the increased intra-luminal pressure proximal to the obstructing gallstone. These cases should raise awareness of the complications associated with both gallstone ileus, and small bowel diverticula.

Introduction
Gallstone ileus is an uncommon surgical emergency that occurs almost exclusively in the elderly, with a peak incidence between 65 and 75 years of age. However, it is of increasing significance with the current demographic shift towards an elderly population. Perforation of the small intestine proximal to the obstructing gallstone is rare with less than 10 cases ever having been

described. We present two cases of perforation of the jejunum in gallstone ileus, and remarkably in one case, the gallstone ileus caused perforation of a jejunal diverticulum and is to the best of our knowledge the first such case to be described. The main objective of this review is to critically evaluate the known difficulties associated with the diagnosis and treatment of gallstone ileus, and report a rare complication, thus increasing the awareness of jejunal perforation and small bowel diverticula.

Case presentation
Case 1
A 69 year old man presented with two days of vomiting and central abdominal pain. He suffered with hypertension and gastro-oesphageal reflux disease but had never undergone surgery. His bilirubin was 28 mmoll-1, otherwise liver function tests were normal. An abdominal radiograph showed dilated loops of small bowel. He underwent a laparotomy at which a gallstone was found obstructing the mid-ileum. There was a 2 mm perforation in the anti-mesenteric border of the dilated proximal jejunum. The gallstone was removed via enterolithotomy and the perforated segment of jejunum was resected. He made an uneventful recovery.

Case 2
A 68 year old man presented with a four day history of vomiting and central abdominal pain. He was hypertensive and had no history of previous abdominal surgery. Chest and abdominal radiography were unremarkable. A subsequent CT

scan of the abdomen showed aerobilia (Figure 1) and small bowel dilatation to the distal ileum with accompanying free intra-abdominal fluid (Figure 2). At laparotomy his distal ileum was found to be obstructed by an impacted gallstone and there was a perforated diverticulum on the mesenteric surface of the mid-jejunum. In retrospect, the CT also showed a small pocket of air within the mesentery and later these findings were later confirmed on histology. The gallstone was removed via enterolithotomy and the perforated segment of jejunum was resected. He made an uneventful recovery.

Figure 1. CT scan showing aerobilia (arrow) consistent with a cholecysto-enteric fistula and free fluid within the abdomen.

Figure 2. CT scan showing multiple dilated loops of small bowel with free fluid and air seen on the mesenteric border of the mid jejunum (arrow) suggesting perforation of the small bowel.

Discussion
In both of the above cases, the patients presented with small bowel obstruction with a preceding history of several days of abdominal pain and vomiting. This protracted history is the classical presentation of gallstone ileus, with the majority of patients suffering with abdominal pain and vomiting for at least three days prior to presentation [1]. This is caused by the gallstone moving down the intestine and intermittently

obstructing before becoming impacted, so called 'tumbling obstruction'. Apart from small bowel obstruction, the abdominal radiographs showed none of the three radiological signs of gallstone ileus, namely aerobilia, aberrantly located gallstone or a change in location of a previous gallstone. This is often the case, as two from these three signs are present in only 4050 per cent of patients with gallstone ileus. It is well recognized that gallstone ileus is a difficult clinical and radiological diagnosis [2] and only a decade ago, correct pre-operative diagnosis was as low as 20%. However, recent advances in ultrasonography and computerised tomography can show the presence and location of gallstones, fistulae and aerobilia. Unreserved use of these imaging techniques, in combination with plain abdominal radiographs, can expedite the correct diagnosis in over 50% of cases and decrease preoperative delay [1]. The mainstay of surgical treatment for gallstone ileus is prompt relief of the small bowel obstruction by removing the gallstone by open enterolithotomy. However, to date, controversy reigns over both the most appropriate approach, and the proper extent of surgery. There are two well recognised surgical procedures; the one stage procedure combines enterolithotomy, cholecystectomy and fistula repair, whereas the two stage procedure consists of enterolithotomy alone and biliary surgery at a later stage if indicated. Whether it is preferable to perform the more complex one stage operation, or the simpler enterolithotomy, continues to be actively debated.

Support for enterolithotomy alone, results from it being the minimalist surgery possible in order to relieve bowel obstruction in the emergency situation. It is safe in both low and high-risk patients, requires a shorter operating time than the one stage procedure, and is technically less demanding [3]. It can be combined with an elective laparoscopic cholecystectomy at a later date if biliary symptoms persist, but in most cases enterolithotomy alone is adequate treatment in the elderly patient and subsequent cholecystectomy is not mandatory [2]. It is argued that the one stage procedure significantly decreases mortality because removing the gallbladder and biliary-enteric fistula prevents future recurrence of gallstone ileus, and recurrent biliary symptoms with their associated morbidity and mortality [4]. It also obviates the need for a second operation. The largest review to date, of 1001 reported case of gallstone ileus found the one-stage procedure carried an associated mortality of 16.9%, compared to 11.7% for simple enterolithotomy. Also, interestingly the recurrence rate of gallstone ileus was less than 5 per cent, and only 10 per cent of patients required re-operation for continued symptoms related to the biliary tract [5]. A more recent study reported similar mortality rates, and concluded that urgent fistula repair is associated with a high rate of complications having found the morbidity rate for the one stage group to be twice that of enterolithotomy alone [3].

Despite great advances in peri-operative care over the past few years, mortality rates for gallstone ileus remain high, in the region of 15 18% [3-5]. This is partly due to the elderly patient population having multiple medical co-morbidities and one study showed 86% to have an ASA grade of 3 or 4 at the time of surgery. This subset of patients could potentially benefit from a minimally-invasive technique. Thus, several laparoscopic approaches have been reported including laparoscopic-assisted enterolithotomy [6], laparoscopic enterolithotomy alone, and in combination with staged laparoscopic cholecystectomy and fistula closure. In the laparoscopic-assisted procedure, diagnostic laparoscopy is used to identify the exact location of the gallstone in the small bowel. A small, targeted incision can then be made directly over the stone and routine enterolithotomy performed. Other than the obvious benefits of expedious discharge, it offers the opportunity of diagnostic laparoscopy alone and the chance to perform the enterolithotomy laparoscopically, when clinically appropriate and the expertise is available [7]. In several reported cases, diagnostic laparoscopy has presented the opportunity for simple disimpaction of the gallstone into the large bowel [8]. As with open surgery, controversy exists as to the indication of timing and surgical approach to laparoscopic cholecystectomy and fistula repair. In both of the presented cases, at the time of surgery the patients were both high risk (ASA 3) and required the minimalist surgery possible. Simple enterolithotomy alone was performed to remove the gallstone, combined with mandatory

small bowel resection to excise the perforated jejunum. Diagnostic laparoscopy would have been possible in both cases and indeed would have aided the diagnosis and allowed for a targeted incision. Of note however, is although the jejunal perforation in the first case may have been easily visible, the jejunal diverticular perforation was between the mesenteric folds and may have been concealed. Perforation of the jejunum in gallstone ileus is very rare indeed. A review of 458 cases of gallstone ileus reported only two cases of jejunal perforation [9]. The perforation occurs either at the site of impaction, or at previous sites of obstruction, as the gallstone tumbles down the intestine, and is thought to be the result of the gallstone causing pressure necrosis of the jejunal wall. This is the likely cause of the anti-mesenteric jejunal perforation described in the first case. Jejunal diverticula have a prevalence of approximately 1% in the general population and account for 80% of all small bowel diverticula. Of note, they affect a similar age group to gallstone ileus as the prevalence increases with age and peaks at the six and seventh decades [10]. Jejunal diverticula are acquired and thought to be pulsation lesions or 'false' diverticula in contrast to 'true' congenitaldiverticula, such as, Meckelian diverticula. They arise from the mesenteric border of the bowel and are formed by the herniation of mucosa and submucosa through the muscular layer at a point of weakness where arteries enter the bowel wall. Fortunately, most remain asymptomatic and the diagnosis is frequently made incidentally by radiological investigation or at laparotomy. The reported complications of

jejunal diverticula include perforation, inflammation, abscess formation and intestinal obstruction, and occur in approximately 610% of patients. Perforation is less common than that of large bowel diverticula perhaps, because the intraluminal pressure is less. In the second of our cases we believe that the presence of a gallstone obstructing the lumen of the ileum caused a rise in the intra-luminal pressure of the proximal jejunum and was responsible for the perforation of a diverticulum arising from the mesenteric aspect. At operation the diagnosis may be difficult as most diverticula form between the two folds of mesentery, resulting more often in a mesenteric abscess rather than free perforation.

Conclusion
Gallstone ileus accounts for one to four per cent of mechanical intestinal obstruction and particularly occurs in the 65 to 75 year age group. However, perforation of the small intestine proximal to the obstructing gallstone is very rare. The cases described illustrate two quite different causes of perforation complicating gallstone ileus, and highlights the difficulties associated with pre-operative diagnosis and subsequent management. The cases should also raise awareness of small bowel diverticula.

Introduction
Cholelithiasis is an uncommon condition during childhood representing only 1% of total cases (1,2). In neonates and infants cholelithiasis has been reported only rarely (3). Among various predisposing conditions described, hemolytic conditions like hereditary spherocytosis & sickle cell disease are the commonest (4-5). Biliary pain and obstructive jaundice are the most common presentations, but a large number of cases remain asymptomatic (6).Phototherapy which is widely used in the neonatal ICU has been identified as a risk factor for cholelithiasis by many authors (7-10). Laproscopic cholecystectomy is the routine treatment of choice in symptomatic cases(11-12), but spontaneous resolution of gall stones in infants are being increasingly reported(13-14).We report a 40 day old infant with cholelithiasis.

Case Report
A male term intrauterine growth retarded (IUGR) baby with a birth weight of 1.9 kg was delivered by cesarean section for fetal distress. Baby was admitted in the neonatal intensive care unit (NICU) on 3rd day of life with symptomatic hypoglycemia & hyperbilirubinemia. Baby was treated with phototherapy for 72 hours, was not given any antibiotics & was discharged after 7 days of hospital stay. There was no respiratory distress, prolonged fasting or total parenteral nutrition. Antenatal period was uneventful with a normal antenatal ultrasonogram. Mother noticed yellowish discoloration of sclera & urine on 40thday of life &was admitted in our hospital for evaluation. Stool was clay colored intermittently & there was deep staining of the diapers. On examination the baby was active, alert & icterus was present. There was no facial dysmorphism, microcephaly, failure to thrive or ocular cataract. Liver was palpable 3.5 cm below the right costal margin with a firm consistency & the span was 6cm. On investigation total bilirubin was 11 mg% with a conjugate fraction of 8 mg%., ALT & AST were 330 and 512 IU/L respectively. Alkaline phosphatase was 603 IU/L & random blood sugar was 76mg%. Thyroid function was normal. TORCH screening, HIV, serum markers for hepatitis A, B & C were negative. Urine for reducing substances were also negative. Peripheral smear was normal with no evidence of hemolysis. Reticulocyte count was 1.2% & direct coomb's test was negative. Blood culture, urine culture & C-reactive protein were negative. X- Ray abdomen did not show any radio opaque shadows. With these data, a diagnosis of neonatal hepatitis was considered and an ultrasonography of abdomen was done. It showed 6.5 cm sized liver with normal echogenicity, distended gall bladder and multiple gall stones in the gall bladder with largest measuring 8 mm size. Hepatobiliary scintigraphy was not done as the gall bladder was seen distended and extrahepatic biliary atresia was not considered as a possibility. Liver biopsy was suggested but the parents were not willing. As cystic fibrosis is uncommon in our locality, we have planned to evaluate for the same, if symptomatic on follow up. Baby was treated conservatively and was closely followed up. One month later urine color became normal & jaundice disappeared. Bilirubin became 1.5mg% with conjugate fraction 0.5mg% ALT & AST reduced to 85 & 95 IU/L respectively. Repeat Ultrasonography showed disappearance of many small stones & regression of largest calculi to 6mm size. On follow up after 2 months liver was not palpable, bilirubin was 0.5 mg/% and ALT & AST were 42 & 47IU/L respectively.

Discussion
Cholelithiasis in children occurs secondary to various predisposing conditions. In children, >70% of gall stones are of pigment type, 15-20% are cholesterol stones & remaining are a mixture of cholesterol, organic matrix and calcium bicarbonate (17). In infants brown pigments are common which is due to biliary tract infections & are radiolucent. The common predisposing conditions are

hemolytic anemias, prolonged fasting, total parenteral nutrition, ileal resection, sepsis & cystic fibrosis. Others include drugs like Ceftriaxone & frusemide (10), prematurity (15), phototherapy (78), gastrointestinal dysfunctions (16), necrotizing enterocolitis, disturbances of enterohepatic circulation of bile acids & biliary dyskinesia. Recently bronchopulmonary dysplasia & gastroesophageal reflux are also reported as risk factors for cholelithiasis (10,15).Among hemolytic disorders sickle cell disease (12%) and hereditary spherocytosis (4-63%) are the commonest conditions. No predisposing causes are found in upto 42.8% of infants (14,19).Biliary sludging can be detected in >40% of infants receiving ceftriaxone for >10 days. It forms calcium ceftriaxone salts (pseudocholelithiasis) (17). Most common presentations of cholelithiasis are biliary pain and obstructive jaundice. Jaundice is more commonly seen in infants and young children (18). Twenty nine percent cases present with obstructive jaundice. Other presentations are pancreatitis (1%), intolerance for fatty foods etc. Acute cholecystitis could be the first symptom. But 67% of gall stones remain asymptomatic and they are detected during routine ultrasonography (18). So all newborn babies with any risk factors can be screened for gall stones during early infancy. Phototherapy was the only risk factor identified in our case. Laproscopic cholecystectomy is generally the treatment of choice in symptomatic cases of cholelithiasis. In asymptomatic cases it may take decades to develop symptoms & many develop complications also. So management in asymptomatic cases poses problems and depends on the risk factors (18). Spontaneous resolution of symptomatic & asymptomatic cases are being increasingly reported (10,14,19,20). In our case surgical management was not tried as the baby showed signs of resolution early. Our case presented with obstructive jaundice & gall stones were detected during evaluation. Many authors suggests that gall stones can be included among the causes of obstructive jaundice in infants (14,20).

Das könnte Ihnen auch gefallen