hydrogen breath test

What is the hydrogen breath test?

The hydrogen breath test is a test that uses the measurement of hydrogen in the breath to diagnose several conditions that cause gastrointestinal symptoms. In humans, only bacteria – specifically, anaerobic bacteria in the colon – are capable of producing hydrogen. The bacteria produce hydrogen when they are exposed to unabsorbed food, particularly sugars and carbohydrates, not proteins or fats. Although limited hydrogen is produced from the small amounts of unabsorbed food that normally reach the colon, large amounts of hydrogen may be produced when there is a problem with the digestion or absorption of food in the small intestine, that allows more unabsorbed food to reach the colon.

Large amounts of hydrogen also may be produced when the colon bacteria move back into the small intestine, a condition called bacterial overgrowth of the small bowel. In this latter instance, the bacteria are exposed to unabsorbed food that has not had a chance to completely traverse the small intestine to be fully digested and absorbed. Some of the hydrogen produced by the bacteria, whether in the small intestine or the colon, is absorbed into the blood flowing through the wall of the small intestine and colon. The hydrogen-containing blood travels to the lungs where the hydrogen is released and exhaled in the breath where it can be measured.


When is hydrogen breath testing used?

Hydrogen breath testing is used in the diagnosis of three conditions.

  • The first is a condition in which dietary sugars are not digested normally. The most common sugar that is poorly digested is lactose, the sugar in milk. Individuals who are unable to properly digest lactose are referred to as lactose intolerant. Testing also may be used to diagnose problems with the digestion of other sugars such as sucrose, fructose and sorbitol.
  • The second condition for which hydrogen breath testing is used is for diagnosing bacterial overgrowth of the small bowel, a condition in which larger-than-normal numbers of colonic bacteria are present in the small intestine.
  • The third condition for which hydrogen breath testing is used is for diagnosing rapid passage of food through the small intestine. All three of these conditions may cause abdominal pain, abdominal bloating and distention, flatulence (passing gas in large amounts), and diarrhea.
Sphincter of Oddi (SOD)

The sphincter of Oddi is a muscular valve that controls the flow of digestive juices (bile and pancreatic juice) through ducts from the liver and pancreas into the first part of the small intestine (duodenum). Sphincter of Oddi dysfunction (SOD) describes the situation when the sphincter does not relax at the appropriate time (due to scarring or spasm). The back-up of juices causes episodes of severe abdominal pain.

The sphincter of Oddi is a muscular valve that controls the flow of digestive juices (bile and pancreatic juice) through ducts from the liver and pancreas into the first part of the small intestine (duodenum). Sphincter of Oddi dysfunction (SOD) describes the situation when the sphincter does not relax at the appropriate time (due to scarring or spasm). The back-up of juices causes episodes of severe abdominal pain.

Doctors often consider SOD in patients who experience recurrent attacks of pain after surgical removal of the gallbladder (cholecystectomy). More than half a million of these surgeries are performed annually in the United States, and 10–20% of these patients present afterwards with continuing or recurrent pains. SOD is also considered in some patients who suffer from recurrent attacks of unexplained inflammation of the pancreas (pancreatitis).

About half of these patients will have findings on laboratory studies or imaging (blood test, ultrasound, CT scan, or MRCP) to suggest a definite abnormality, such as a stone in the bile duct. MRCP (magnetic resonance cholangiopancreatography) is nowadays a good non-invasive test for checking on the biliary and pancreatic drainage systems.

Based on patients histories, physical examinations, and other clinical data, doctors can categorize these patients as having SOD Types I and II. The categories help guide treatment of the disease. They are based on a system called the Milwaukee criteria.

When symptoms are severe, standard treatment is to perform an endoscopic procedure called ERCP (endoscopic retrograde cholangiopancreatography). ERCP is a procedure for the examination or treatment of the bile duct and pancreatic duct. The procedure carries a risk of serious complications and is done under sedation by experts trained in the technique. It combines the use of x-rays and an endoscope that is passed down to the duodenum, where the bile duct and pancreatic ducts drain, and a dye that is injected into the ducts.

An additional procedure, sphincter of Oddi manometry (SOM), involves passing a catheter into the bile and/or pancreatic duct during ERCP to measure the pressure of the biliary and/or pancreatic sphincter. It is considered the gold standard diagnostic modality for SOD.

Treatment depends on what is found. It may often involve cutting the muscular sphincter (sphincterotomy) to remove any stones or to relieve any scarring or spasm of the sphincter.

As noted above, a very important problem in this context is that these ERCP procedures carry a significant risk of complications. In particular, ERCP (with or without sphincter of Oddi manometry) can cause an attack of pancreatitis in 5–10% of cases. While most of these result in a few days in the hospital, about 1% of patients suffer a major attack, with weeks or months in the hospital. Sphincterotomy also carries a small risk of other severe complications such as bleeding and perforation, and the possibility of delayed narrowing of a duct (stenosis) due to scarring.

Functional SOD

Patients with a similar pain problem, but who have little or no abnormalities on blood tests and standard scans (including MRCP), are categorized as having SOD Type III. The episodes of pain are assumed due to intermittent spasm of the sphincter. It is very difficult to effectively evaluate and manage patients with Type III SOD. Some physicians are skeptical of its existence, or assume that it is a part of a broader problem of a functional digestive disturbance such as irritable bowel syndrome.

Because of the risks of ERCP, patients with suspected SOD III are usually advised to try medical treatments first. Some respond to the use of antispasmodic drugs and/or antidepressants that may help decrease pain.  There have been studies of other medical therapies, such as calcium channel blocking drugs. Despite a few encouraging reports, these methods have not proven to be effective generally, and are not widely used.

Patients who fail these approaches (at least those with severe symptoms) are usually advised to see specialists at referral centers. Further evaluation may involve additional or more specialized tests to help guide treatment options.

Clinical Research Study

The uncertainties in how best to diagnose and to treat “suspected” sphincter of Oddi dysfunction (and the risks involved) mandate further scientific investigation. The National Institutes of Health has recently funded an important study called “EPISOD” in 6 major Gastroenterology centers in USA.

The studies are being conducted at centers located in:

  • Johns Hopkins Hospital, Baltimore, MD
  • University of Alabama at Birmingham, Birmingham, AL
  • Medical University of South Carolina Digestive Disease Center, Charleston, SC
  • Indiana University, Indianapolis, IN
  • Hennepin County Medical Center, Minneapolis, MN
  • Virginia Mason Medical Center, Seattle, WA

Additional details are available at the NIH website at http://clinicaltrials.gov/ by searching: sphincter of Oddi dysfunction III.

IBD versus IBS

Is inflammatory bowel disease (IBD) the same thing as Irritable Bowel Syndrome (IBS)?

No. Inflammatory bowel disease, including UC and CD, is different from irritable bowel syndrome (IBS). Unlike IBD, IBS does not cause inflammation, ulcers or other damage to the bowel. Instead, IBS is a much less serious problem called a functional disorder. This means that the digestive system looks normal but doesn’t work as it should. Symptoms of IBS may include crampy pain, bloating, gas, mucus in the stool, diarrhea and constipation. IBS has also been called spastic colon or spastic bowel

Source: http://www.webmd.com/ibd-crohns-disease/crohns-disease/ibd-versus-ibs


For further information see related separate article Irritable Bowel Syndrome.

Ursodeoxycholic acid
Aust Prescr 1999;22:95-8

Ursofalk (Orphan Australia)
250 mg capsules
Approved indication: chronic cholestasis
Australian Medicines Handbook Section 12

In primary biliary cirrhosis, there is chronic inflammation which destroys the intrahepatic bile ductules. At first, patients may be asymptomatic, but the reduced excretion of bile can cause steatorrhoea. The disease slowly progresses and death can result from hepatic failure or the complications of cirrhosis. Primary biliary cirrhosis is now a common indication for a liver transplant. Although there is no effective drug treatment, some patients will benefit from ursodeoxycholic acid.

Ursodeoxycholic acid is a bile acid which is synthesised from its precursor by intestinal bacteria. Its mechanism of action in primary biliary cirrhosis is uncertain. Ursodeoxycholic acid may have an effect by increasing the flow and altering the composition of bile. It has also been used in the treatment of gallstones.

In clinical trials with at least two years of follow up, patients who took ursodeoxycholic acid had improved liver function tests. This may not always improve the patient’s symptoms or the histology of the liver.

Ursodeoxycholic acid has few known adverse effects. Diarrhoea is the main adverse reaction. Patients can complain of an increase in itching when they begin treatment. This may respond to a reduction in the dose. Ursodeoxycholic acid is contraindicated if there is acute inflammation of the gall bladder or obstruction of the common bile duct.

Ursodeoxycholic acid will probably have a role in delaying the need for liver transplantation. A placebo-controlled study of 145 patients with primary biliary cirrhosis found that the disease progressed more slowly in patients given ursodeoxycholic acid. This group also had a significantly lower probability of transplantation or death during the two-year study.1


. Poupon RE, Poupon R, Balkau B. Ursodiol for the long-term treatment of primary biliary cirrhosis. The UDCA-PBC Study Group. N Engl J Med 1994;330:1342-7.

Aust Prescr 1999;22:147-51

Celebrex (Searle)
100 mg and 200 mg capsules
Approved indication: arthritis
Australian Medicines Handbook Section 15.1

Non-steroidal anti-inflammatory drugs act by inhibiting the enzyme cyclo-oxygenase(COX).1 This enzyme is required for the synthesis of prostaglandins and its activity increases in inflammation. It has two isoforms, COX-1 andCOX-2, both of which are blocked to varying degrees by non-steroidal anti-inflammatory drugs. As COX-1 may produce protective prostaglandins in the stomach, its inhibition could be responsible for some of the adverse effects of the drugs. Celecoxib is much more selective for COX-2, so it may cause fewer adverse effects than the older drugs.

Patients with symptoms of rheumatoid arthritis take celecoxib in two divided doses. A single daily dose may be used in osteoarthritis. The drug is quickly absorbed. Although taking the capsules with food delays absorption, the bioavailability is increased. Celecoxib is metabolised in the liver by cytochrome P450 CYP2C9so there is a potential for interactions with drugs such as fluconazole.

In studies lasting up to 12 weeks, celecoxib has reduced the pain of osteoarthritis more effectively than placebo. Trials, of up to 24 weeks, in patients with rheumatoid arthritis have found the efficacy of celecoxib to be similar to that of naproxen 500 mg twice daily.

The effect of celecoxib on the gut has been assessed by endoscopy. Gastric ulcers were seen significantly less frequently during treatment with celecoxib, than they were in patients taking naproxen or diclofenac. Celecoxib, however, is not free of gastrointestinal adverse effects. Dyspepsia, abdominal pain and diarrhoea occur more frequently than with placebo. In animal studies, COX-2inhibitors retard ulcer healing.1

Most of the enzyme activity in platelets is COX-1, so celecoxib should have little effect on bleeding time. The potential of COX-2 inhibitors to cause fluid retention, renal impairment or hypertension is unknown. In clinical trials peripheral oedema occurred with equal frequency (2.1%) in patients taking celecoxib or naproxen. Celecoxib is not recommended for patients with aspirin-sensitive asthma.

The COX-2 inhibitors have the potential to replace non-steroidal anti-inflammatory drugs for the relief of arthritic symptoms. Whether or not they fulfill this potential will depend on their long-term safety. For example, will they cause fewer gastrointestinal haemorrhages than the non-steroidal anti-inflammatory drugs?


1. Hawkey CJ. COX-2 inhibitors. Lancet 1999;353:307-14.

Postcholecystectomy Syndrome

The laparoscopic cholecystectomy is considered the “gold standard” in chronic calculous cholecystitis treatment. After the gallbladder removal the physiology of gallbladder bile formation is changed.

Absence of the gallbladder leads to development of functional biliary hypertension and dilatation of common bile duct and the common hepatic duct. The dilatation of right and left hepatic ducts may be formed within 3-5 years after cholecystectomy. Functional hypertension in the common bile duct leads to development of functional hypertension in Wirsung’s pancreatic duct accompanied by chronic pancreatitis symptoms.

During this period in some patients this is accompanied by chronic pancreatitis progression, dysfunction of the sphincter of Oddi and duodeno-gastral reflux. Duodeno-gastral reflux causes the development of atrophic (bile-acid-depen­dent) antral gastritis . After cholecystectomy 40% to 60% of patients suffer from dyspeptic disorders, 5% to 40% from pains of different localizations. Up to 70% of patients show symptoms of chronic “bland” intrahepatic cholestasis, chronic cholestatic hepatitis and compensatory bile-acid-dependent apoptosis of hepatocytes. In some of cholecystectomized patients with high concentration of hydrophobic hepatotoxic co-cancerogenic deoxycholic bile acid in serum and/or feces high risk of the colon cancer is found.

Therefore, depending on dysfunction (hyper tonus) or relaxation (hypo tonus) of the sphincter of Oddi, pathology in hepato-biliary-pancreato-duodenal-gastral zone will form after cholecystectomy.

Postcholecystectomy syndrome is a dysfunction of the sphincter of Oddi, caused by noncalculous obstructive disorder, which decrease bile passage and pancreatic juice outflow into the duodenum.

More reading


CDR0000428446_largeGastroparesis, also called delayed gastric emptying, is a disorder in which the stomach takes too long to empty its contents. Normally, the stomach contracts to move food down into the small intestine for digestion. The vagus nerve controls the movement of food from the stomach through the digestive tract. Gastroparesis occurs when the vagus nerve is damaged and the muscles of the stomach and intestines do not work normally. Food then moves slowly or stops moving through the digestive tract.

What causes gastroparesis?

The most common cause of gastroparesis is diabetes. People with diabetes have high blood glucose, also called blood sugar, which in turn causes chemical changes in nerves and damages the blood vessels that carry oxygen and nutrients to the nerves. Over time, high blood glucose can damage the vagus nerve.

Some other causes of gastroparesis are

  • surgery on the stomach or vagus nerve
  • viral infections
  • anorexia nervosa or bulimia
  • medications-anticholinergics and narcotics-that slow contractions in the intestine
  • gastroesophageal reflux disease
  • smooth muscle disorders, such as amyloidosis and scleroderma
  • nervous system diseases, including abdominal migraine and Parkinson’s disease
  • metabolic disorders, including hypothyroidism

Many people have what is called idiopathic gastroparesis, meaning the cause is unknown and cannot be found even after medical tests.

What are the symptoms of gastroparesis?

Signs and symptoms of gastroparesis are

  • heartburn
  • pain in the upper abdomen
  • nausea
  • vomiting of undigested food-sometimes several hours after a meal
  • early feeling of fullness after only a few bites of food
  • weight loss due to poor absorption of nutrients or low calorie intake
  • abdominal bloating
  • high and low blood glucose levels
  • lack of appetite
  • gastroesophageal reflux
  • spasms in the stomach area

Eating solid foods, high-fiber foods such as raw fruits and vegetables, fatty foods, or drinks high in fat or carbonation may contribute to these symptoms.

The symptoms of gastroparesis may be mild or severe, depending on the person. Symptoms can happen frequently in some people and less often in others. Many people with gastroparesis experience a wide range of symptoms, and sometimes the disorder is difficult for the physician to diagnose.

What are the complications of gastroparesis?

If food lingers too long in the stomach, it can cause bacterial overgrowth from the fermentation of food. Also, the food can harden into solid masses called bezoars that may cause nausea, vomiting, and obstruction in the stomach. Bezoars can be dangerous if they block the passage of food into the small intestine.

Gastroparesis can make diabetes worse by making blood glucose control more difficult. When food that has been delayed in the stomach finally enters the small intestine and is absorbed, blood glucose levels rise. Since gastroparesis makes stomach emptying unpredictable, a person’s blood glucose levels can be erratic and difficult to control.

How is gastroparesis diagnosed?

After performing a full physical exam and taking your medical history, your doctor may order several blood tests to check blood counts and chemical and electrolyte levels. To rule out an obstruction or other conditions, the doctor may perform the following tests:

  • Upper endoscopy. After giving you a sedative to help you become drowsy, the doctor passes a long, thin tube called an endoscope through your mouth and gently guides it down the throat, also called the esophagus, into the stomach. Through the endoscope, the doctor can look at the lining of the stomach to check for any abnormalities.
  • Ultrasound. To rule out gallbladder disease and pancreatitis as sources of the problem, you may have an ultrasound test, which uses harmless sound waves to outline and define the shape of the gallbladder and pancreas.
  • Barium x ray. After fasting for 12 hours, you will drink a thick liquid called barium, which coats the stomach, making it show up on the x ray. If you have diabetes, your doctor may have special instructions about fasting. Normally, the stomach will be empty of all food after 12 hours of fasting. Gastroparesis is likely if the x ray shows food in the stomach. Because a person with gastroparesis can sometimes have normal emptying, the doctor may repeat the test another day if gastroparesis is suspected.

Once other causes have been ruled out, the doctor will perform one of the following gastric emptying tests to confirm a diagnosis of gastroparesis.

  • Gastric emptying scintigraphy. This test involves eating a bland meal, such as eggs or egg substitute, that contains a small amount of a radioactive substance, called radioisotope, that shows up on scans. The dose of radiation from the radioisotope is not dangerous. The scan measures the rate of gastric emptying at 1, 2, 3, and 4 hours. When more than 10 percent of the meal is still in the stomach at 4 hours, the diagnosis of gastroparesis is confirmed.
  • Breath test. After ingestion of a meal containing a small amount of isotope, breath samples are taken to measure the presence of the isotope in carbon dioxide, which is expelled when a person exhales. The results reveal how fast the stomach is emptying.
  • SmartPill. Approved by the U.S. Food and Drug Administration (FDA) in 2006, the SmartPill is a small device in capsule form that can be swallowed.The device then moves through the digestive tract and collects information about its progress that is sent to a cell phone-sized receiver worn around your waist or neck. When the capsule is passed from the body with the stool in a couple of days, you take the receiver back to the doctor, who enters the information into a computer.

How is gastroparesis treated?

Treatment of gastroparesis depends on the severity of the symptoms. In most cases, treatment does not cure gastroparesis-it is usually a chronic condition. Treatment helps you manage the condition so you can be as healthy and comfortable as possible.


Several medications are used to treat gastroparesis. Your doctor may try different medications or combinations to find the most effective treatment. Discussing the risk of side effects of any medication with your doctor is important.

  • Metoclopramide (Reglan). This drug stimulates stomach muscle contractions to help emptying. Metoclopramide also helps reduce nausea and vomiting. Metoclopramide is taken 20 to 30 minutes before meals and at bedtime. Side effects of this drug include fatigue, sleepiness, depression, anxiety, and problems with physical movement.
  • Erythromycin. This antibiotic also improves stomach emptying. It works by increasing the contractions that move food through the stomach. Side effects include nausea, vomiting, and abdominal cramps.
  • Domperidone. This drug works like metoclopramide to improve stomach emptying and decrease nausea and vomiting. The FDA is reviewing domperidone, which has been used elsewhere in the world to treat gastroparesis. Use of the drug is restricted in the United States.
  • Other medications. Other medications may be used to treat symptoms and problems related to gastroparesis. For example, an antiemetic can help with nausea and vomiting. Antibiotics will clear up a bacterial infection. If you have a bezoar in the stomach, the doctor may use an endoscope to inject medication into it to dissolve it.

Dietary Changes

Changing your eating habits can help control gastroparesis. Your doctor or dietitian may prescribe six small meals a day instead of three large ones. If less food enters the stomach each time you eat, it may not become overly full. In more severe cases, a liquid or pureed diet may be prescribed.

The doctor may recommend that you avoid high-fat and high-fiber foods. Fat naturally slows digestion-a problem you do not need if you have gastroparesis-and fiber is difficult to digest. Some high-fiber foods like oranges and broccoli contain material that cannot be digested. Avoid these foods because the indigestible part will remain in the stomach too long and possibly form bezoars.

Feeding Tube

If a liquid or pureed diet does not work, you may need surgery to insert a feeding tube. The tube, called a jejunostomy, is inserted through the skin on your abdomen into the small intestine. The feeding tube bypasses the stomach and places nutrients and medication directly into the small intestine. These products are then digested and delivered to your bloodstream quickly. You will receive special liquid food to use with the tube. The jejunostomy is used only when gastroparesis is severe or the tube is necessary to stabilize blood glucose levels in people with diabetes.

Parenteral Nutrition

Parenteral nutrition refers to delivering nutrients directly into the bloodstream, bypassing the digestive system. The doctor places a thin tube called a catheter in a chest vein, leaving an opening to it outside the skin. For feeding, you attach a bag containing liquid nutrients or medication to the catheter. The fluid enters your bloodstream through the vein. Your doctor will tell you what type of liquid nutrition to use.

This approach is an alternative to the jejunostomy tube and is usually a temporary method to get you through a difficult period with gastroparesis. Parenteral nutrition is used only when gastroparesis is severe and is not helped by other methods.

Refractory Gastroparesis

Gastric Electrical Stimulation

Neurostimulator Device

When gastroparesis does not respond to standard medical management including drugs and dietary changes, the condition is said to “refactory”. For patients who have documented delayed gastric emptying with no evidence of abnormal obstruction, a gastric neurostimulator may be implanted to reduce or eliminate nausea and other symptoms.

A gastric neurostimulator is a surgically implanted battery-operated device that releases mild electrical pulses to help control nausea and vomiting associated with gastroparesis. This option is available to people whose nausea and vomiting do not improve with medications. Further studies will help determine who will benefit most from this procedure, which is available in a few centers across the United States.

Implanted neurostimulator device

Gastric electrical stimulation uses a device, surgically implanted in the abdomen, to deliver mild electrical pulses to the nerves and smooth muscle of the lower part of the stomach. This stimulation may reduce chronic nausea and vomiting in patients with gastroparesis resulting from diabetes (diabetic gastropathy) or ideopathic gastroparesis (unknown cause).



If gastroparesis is related to an injury of the vagus nerve, patients may benefit from a procedure called pyloroplasty. This procedure widens and relaxes the valve separating the stomach from the upper part of the small intestine, called the pyloric valve. This permits the stomach to empty more quickly.

In some cases,before deciding to perform the procedure, botulinum toxin (Botox) will be injected at the pyloric valve to temporarily paralyze and relax it. The purpose is to determine if the patient would benefit from a pyloroplasty. While use of botulinum toxin has been associated with improvement in symptoms of gastroparesis in some patients, further research is required to validate its efficacy.

Treatment Goals

The primary treatment goals for gastroparesis related to diabetes are to improve stomach emptying and regain control of blood glucose levels. Treatment includes dietary changes, insulin, oral medications, and, in severe cases, a feeding tube and parenteral nutrition.

Dietary Changes

The doctor will suggest dietary changes such as six smaller meals to help restore your blood glucose to more normal levels before testing you for gastroparesis. In some cases, the doctor or dietitian may suggest you try eating several liquid or pureed meals a day until your blood glucose levels are stable and the symptoms improve. Liquid meals provide all the nutrients found in solid foods, but can pass through the stomach more easily and quickly.

Insulin for Blood Glucose Control

If you have gastroparesis, food is being absorbed more slowly and at unpredictable times. To control blood glucose, you may need to

  • take insulin more often or change the type of insulin you take
  • take your insulin after you eat instead of before
  • check your blood glucose levels frequently after you eat and administer insulin whenever necessary

Your doctor will give you specific instructions for taking insulin based on your particular needs.


Small Intestine Bacterial Overgrowt

Simply put, Small Intestine Bacterial Overgrowth is a chronic bacterial infection of the small intestine.  The infection is of bacteria that normally live in the gastrointestinal tract but have abnormally overgrown in a location not meant for so many bacteria.  

The Problem
The bacteria interfere with our normal digestion and absorption of food and are associated with damage to the lining or membrane of the SI (leaky gut syndrome, which I prefer to call leaky SI in this case). 

  • They consume some of our food which over time leads to deficiencies in their favorite nutrients such as iron and B12, causing anemia.
  • They consume food unable to be absorbed due to SI lining damage, which creates more bacterial overgrowth (a vicious cycle).
  • After eating our food, they produce gas/ expel flatus, within our SI.  The gas causes abdominal bloating, abdominal pain, constipation, diarrhea or both (the symptoms of IBS).  Excess gas can also cause belching and flatulence.
  • They decrease proper fat absorption by deconjugating bile leading to deficiencies of vitamins A & D and fatty stools.
  • Through the damaged lining, larger food particles not able to be fully digested, enter into the body which the immune system reacts to.  This causes food allergies/ sensitivities.
  • Bacteria themselves can also enter the body/bloodstream.  Immune system reaction to bacteria and their cell walls (endotoxin) causes chronic fatigue and body pain and burdens the liver.
  • Finally, the bacteria excrete acids which in high amounts can cause neurological and cognitive symptoms.


What are the other Names for this Condition? (Also known as/Synonyms)


  • Bile Duct Stone
  • Common Bile Duct Stone
  • Gallstone in the Bile Duct


What is Choledocholithiasis? (Definition/Background Information)


  • Choledocholithiasis is the presence of stones (gallstones) in the common bile duct (CBD). The presence of even one stone in the CBD is called Choledocholithiasis
  • The liver is located on the upper right side of the abdomen. Among other functions the liver produces bile, which is important for the digestion of fat
    • The bile comes out of the liver through the common hepatic duct (hollow tube) and enters the gallbladder through the cystic duct
    • The gallbladder is a small sac located under the liver and its main function is to store bile and release it, as and when it is required
    • The cystic duct joins the common hepatic duct to form the common bile duct
    • The common bile duct carries bile into the duodenum (gastrointestinal tract). Bile in the gastrointestinal tract helps in the digestion of fat
  • The gallstones are made up of a mixture of bilirubin, calcium, and cholesterol. There are 4 types of gallstones
    • Cholesterol stones (the most common type)
    • Pigment stones – black: These stones are commonly found in individuals with hemolytic (destruction of red blood cells) anemia
    • Pigment stones – brown: These stones are commonly seen in Asians and are thought to arise due to infection of the bile duct. These type of stones are commonly formed in the common bile duct than in the gallbladder
    • Mixed stones: Contains a mixture of the above stone types
  • The process of gallstone formation in the gallbladder is called cholelithiasis. Some of the stones exit the gallbladder and gets trapped in the CBD to cause Choledocholithiasis (secondary stones). Up to 15% of individuals with gallstones (cholelithiasis) have associated Choledocholithiasis. Uncommonly, stones may be formed within the common bile duct itself (primary stones)
  • Choledocholithiasis may cause no symptoms or cause symptoms such as right upper abdominal pain, jaundice, etc.
  • The treatment options for Choledocholithiasis include the removal of the stones and removal of the gall bladder. The prognosis (outlook) is generally good with prompt diagnosis and early treatment

Who gets Choledocholithiasis? (Age and Sex Distribution)


  • Any individual who has gallstone disease (cholelithiasis) is at risk for Choledocholithiasis (or Gallstone in the Bile Duct). It is more common in the elderly adults, than in children or younger adults
  • Gallstone formation is more common in women than men
  • Cholesterol gallstone formation is more common in certain regions where there is high intake of dietary fat, such as in northern Europe, US, etc. Pigment gallstones-brown type formation is more common in Asia
  • Cholesterol gallstone formation is common in Native Indians than other races or ethnicities
  • Pigment gallstones-black type formation is more common in African-Americans than other races or ethnicities


What are the Risk Factors for Choledocholithiasis? (Predisposing Factors)

The risk factors of Choledocholithiasis include:


  • Individuals who have had their gallbladder removed (cholecystectomy) are at risk to develop Choledocholithiasis
  • Any individual with a history of gallstone disease (cholelithiasis) is also at risk to develop Choledocholithiasis


The following are the risk factors for gallstones formation:


  • Cholesterol gallstones: These gallstones are formed whenever there is too much cholesterol in the bile. The risk factors are:
    • Women gender (due to estrogen)
    • Obesity
    • Diabetes mellitus type 2
    • History of Crohn’s disease
    • Individuals with metabolic syndrome that includes insulin resistance, high blood sugar, obesity, low blood levels of good cholesterol (HDL), and high blood levels of triglycerides
    • Rapid weight loss with extreme calorie and fat restriction
    • Rapid weight loss followed by quick weight gain
    • Gastric bypass surgery performed for weight reduction purposes
    • Organ transplantation
    • High consumption of simple carbohydrates
    • High levels of triglycerides in blood
    • Decreased physical activity (and fitness)
    • Pregnancy
    • Conditions causing stasis of bile in the gallbladder
    • Native Indians are at risk due to LITH genes, which increase fat storage
    • Mutation in ABCG8 gene function increases one’s risk because excess cholesterol is pushed into the bile
    • Use of medications, such as estrogens (oral contraceptive pill), hormone replacement therapy (used in postmenopausal women), clofibrate (used for treating high triglyceride levels), somatostatin, thiazide diuretics, etc.
    • Prolonged intravenous feeding (used when an individual cannot take anything by mouth) increases one’s risk of getting gallstones
  • Individuals with increased red blood cell destruction, such as hemolytic anemias, are at increased risk to get pigment gallstones-black type. Individuals with scarred liver (cirrhosis) are also at risk
  • Individuals of Asian origin along with associated infection of the bile ducts, are at an increased risk to get pigment gallstones-brown type
  • There are other unknown genetic and environmental factors, such as inflammation, infection, etc., which increases one’s risk of gallstones


It is important to note that having a risk factor does not mean that one will get the condition. A risk factor increases ones chances of getting a condition compared to an individual without the risk factors. Some risk factors are more important than others.

Also, not having a risk factor does not mean that an individual will not get the condition. It is always important to discuss the effect of risk factors with your healthcare provider.

What are the Causes of Choledocholithiasis? (Etiology)

Choledocholithiasis occurs due to one of the two mechanisms outlined below:


  • Gallstones formed in the gallbladder move out and get trapped in the common bile duct (CBD)
  • Stones that get formed within the common bile duct itself, which is seen in individuals without a gallbladder (which was surgically removed through a procedure termed cholecystectomy) and in individuals with bile duct infection


There are four types of gallstones. Each type is formed due to various reasons:


  • Cholesterol gallstones are formed when there is too much cholesterol (super-saturation) in the bile. The factors that may increase cholesterol levels in the bile include estrogen (women), obesity, high levels of triglycerides in blood, genetic factors (such as in Native Indians), diabetes mellitus 2, etc.
  • Pigment stones-black type (calcium bilirubinate): Bilirubin, a yellow pigment derived from breakdown of heme (present in red blood cells) tends to form insoluble jet-black pigment stones along with calcium
  • Pigment stones-brown type: Bile is normally sterile, but in some unusual circumstances it may become colonized with bacteria. Bacteria break down lecithin (present in the bile) to release fatty acids which bind with calcium and precipitate to form brown pigment stones
  • Mixed stones are mixture of cholesterol stones and black stones (calcium bilirubinate)


What are the Signs and Symptoms of Choledocholithiasis?

Choledocholithiasis (Gallstones in the Common Bile Duct) and cholelithiasis (with or without infection of the gallbladder) frequently coexist. The signs and symptoms of Choledocholithiasis and cholelithiasis include:


  • Biliary colic: This is characterized by pain in the right upper abdomen (quadrant). The pain usually comes and goes, but sometimes it may be constant. The pain may be cramping or dull in nature. The pain may travel to the right shoulder tip or to the back. The pain may be worsened after having a heavy fatty meal
  • Jaundice
  • Clay-colored stools
  • Nausea and vomiting
  • Loss of appetite
  • Fever with or without chills
  • Tenderness of the right side of upper abdomen
  • Liver enlargement


How is Choledocholithiasis Diagnosed?

The following procedures may be used to diagnose Choledocholithiasis:


  • Thorough evaluation of the individual’s medical history and a thorough physical examination including the abdomen and skin
  • During history-taking the physicians may want to know the following:
    • When the symptoms began and whether they are becoming worse
    • List of prescription and over-the-counter medications currently being taken
    • About one’s personal and family history of gallbladder diseases, diet history, etc.
  • Consultation with a gastroenterologist may be necessary, as they are the experts in dealing with such health conditions
  • Stones in the common bile duct are detected using the following methods:
    • Abdominal ultrasound: It is a noninvasive and inexpensive test that is also safe during pregnancy
    • Endoscopic ultrasound or laparoscopic ultrasound may be used to better characterize the stones and the biliary duct
    • CT scan of the abdomen is useful in diagnostic challenges to characterize complications of gallbladder or bile duct disease
    • Endoscopic retrograde cholangiopancreatography (ERCP) permits radiographic imaging of bile ducts. It is the best test because it can help diagnose and the same time help remove a stone from the common bile duct. It is also helpful to visualize any associated pancreatic disease
    • PTC (percutaneous transhepatic cholangiography) may be the modality of choice when performing ERCP is difficult
    • MRI or MRCP (magnetic resonance cholangiopancreatography) is a good, non-invasive test to detect stones in the biliary tree
    • HIDA scintigraphy is a good test to detect cystic duct obstruction (cystic duct and hepatic duct join to form the common bile duct), and analyze how the bile is flowing through the liver, gallbladder, and biliary tree


  • Other tests that may be required in Choledocholithiasis to rule in or rule out associated diseases. They include:
    • Complete blood count with differential, liver function panel (bilirubin, transaminases [ALT, AST], alkaline phosphatase, protein), blood cultures, amylase, lipase, prothrombin time, etc.

Many clinical conditions may have similar signs and symptoms. Your healthcare provider may perform additional tests to rule out other clinical conditions to arrive at a definitive diagnosis. 


What are the possible Complications of Choledocholithiasis?

The complications of Choledocholithiasis include:


  • Cholangitis: Whenever the bile duct is obstructed the bacteria from the intestine may ascend up and cause infection of the bile ducts and beyond
  • Secondarily biliary cirrhosis: Long-standing obstruction of the common bile duct can cause inflammation, destruction, and scarring of the smaller bile ducts inside the liver and cause liver failure
  • Pancreatitis (inflammation of the pancreas) can occur whenever there is obstruction of the distal part of the common bile duct
  • Gallstones ileus: Sometimes, the gallstone might reach the intestine and cause an obstruction
  • Associated cholelithiasis (stones in the gallbladder) can cause acute cholecystitis (infection of the gallbladder)


How is Choledocholithiasis Treated?

Stones in the Common Bile Duct (Choledocholithiasis) should be removed, even if there are no symptoms. The stones may be removed by one of the following methods:


  • Endoscopic sphincterotomy when an ERCP is performed
  • Simultaneous bile duct exploration when a laparoscopic cholecystectomy (removal of gallbladder) is performed
  • Balloon dilation of sphincter of Oddi, which is the site where the common bile duct attaches to the duodenum. This is usually reserved for individuals who have the tendency to bleed
  • Endoscopic ultrasound-guided drainage along with percutaneous trans-hepatic cholangiography (PTC) is done in individuals, if endoscopic sphincterotomy is not able to remove the stones
  • If the stone is large enough, then procedures such as lithotripsy (shockwaves to destroy stones), cholangioscopy (direct visualization of bile duct), or biliary tract stenting (placement of hollow tube) may be attempted at first
  • If there is an associated bile duct infection, then antibiotics may be given.


How can Choledocholithiasis be Prevented?

The preventative measures of Choledocholithiasis include:


  • Prevention of gallstone formation in the gallbladder through:
    • Low-fat diet
    • Exercise
    • Overweight individuals, if planning to lose weight should decrease their weight gradually, but by meeting appropriate nutritional requirements
    • Replacing saturated fats (animal fat) with monounsaturated fats (example olive oil) or omega-3 fatty acids products (example flaxseed, fish oil)
    • Scientists believe that the consumption of coffee, fruits, vegetables, nuts, and high fiber may prevent gallstone formation


  • Removal of gallstones formed in the gallbladder
    • The gallbladder may be removed (cholecystectomy), if there is associated symptomatic gallbladder disease, or if the gallstones are more than 3 cm in size, or calcification (calcium on the gallbladder wall) is observed. A laparoscopic cholecystectomy is preferred over an open cholecystectomy
    • Ursodeoxycholic acid medication can be used to dissolve the stones in selected individuals who refuse cholecystectomy
  • Treatment of infections affecting the biliary tree (bile carrying ducts)
  • Treatment of associated conditions that trigger gallstone formation

What is the Prognosis of Choledocholithiasis? (Outcomes/Resolutions)


  • With prompt diagnosis and treatment Choledocholithiasis has a favorable diagnosis
  • However, if diagnosis and treatment is delayed, it can cause complications and even lead to life-threatening situations


Additional and Relevant Useful Information for Choledocholithiasis:

Novel procedure Natural Orifice Transluminal Endoscopic Surgery (NOTES) for cholecystectomy is currently under review by the research community.

What are some Useful Resources for Additional Information?

American College of Gastroenterology (ACG)
4900 B South, 31st St. Arlington, VA 22206
Phone: (703) 820-7400
Fax: (703) 931-4520
Website: http://www.acg.gi.org

References and Information Sources used for the Article:

Nlm.nih.gov. Choledocholithiasis: MedlinePlus Medical Encyclopedia. 2015. Available at: http://www.nlm.nih.gov/medlineplus/ency/article/000274.htm. (accessed on 5/5/2015).

Papadakis M, McPhee S, Rabow M. Current Medical Diagnosis & Treatment 2015.; :699-705.

Helpful Peer-Reviewed Medical Articles:

Attasaranya S, Fogel E, Lehman G. Choledocholithiasis, Ascending Cholangitis, and Gallstone Pancreatitis. Medical Clinics of North America. 2008;92(4):925-960. doi:10.1016/j.mcna.2008.03.001.

London: National Institute for Health and Care Excellence (UK). Diagnosis and management of cholelithiasis, cholecystitis and choledocholithiasis. http://wwwncbinlmnihgov/pubmedhealth/. 2014. Available at: http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0070643/pdf/TOC.pdf. Accessed February 5, 2015.

Chandran A, Sivarajan R, Srinivas M, Srinivasan V, Venkataraman J. Risk factors for choledocholithiasis in a south Indian population: A case–control study. Indian Journal of Gastroenterology. 2013;32(6):381-385. doi:10.1007/s12664-013-0354-x.

Reviewed and Approved by a member of the DoveMed Editorial Board
First uploaded: May 28, 2015
Last updated: Aug. 4, 2016

Source: https://www.dovemed.com/diseases-conditions/choledocholithiasis/


Cholelithiasis (Gallstones)

Gallstones are marble-like deposits that form in the gallbladder, due to changes in the concentration of various components of bile. Bile is a fluid that is made by the liver and stored in the gallbladder.

What are the other Names for this Condition? (Also known as/Synonyms)

  • Cholelithiasis
  • Gallbladder Stones
  • Stones in the Gallbladder 

What is Gallstones? (Definition/Background Information)

  • Gallstones are marble-like deposits that form in the gallbladder, due to changes in the concentration of various components of bile. Bile is a fluid that is made by the liver and stored in the gallbladder
  • Gallstones are classified on the basis of their constituent material (what they are composed of). Most commonly these Gallbladder Stones are composed of cholesterol and less commonly are composed of a component of blood called bilirubin
  • The size of these stones can vary from that of a ‘peanut’ to the size of a ‘golf ball’. Majority of the times, Gallstones are found as an incidental finding, when they are not causing any symptoms
  • The symptoms arise when they obstruct the duct of the gallbladder and prevent the gallbladder from draining its fluid into the intestine. The common signs and symptoms of include intermittent pain in the right upper side of abdomen, aggravation of pain by fatty meals, nausea, and vomiting. An ultrasound of abdomen is the diagnostic test of choice
  • Removal of the gallbladder by surgery is the most effective treatment for Gallstones. Once the surgery is performed, the chances of developing the condition is practically nil 


Who gets Gallstones? (Age and Sex Distribution)

  • Women are more commonly affected by Gallstones than men, almost in the ratio of 2:1
  • The affected age group may vary from early 30s to late 50s. The chances of developing Gallstones increase with age
  • Gallstones are less commonly seen in the people of Africa and Asia, but are more common the western world, in North and South America

What are the Risk Factors for Gallstones? (Predisposing Factors)

Risk factors associated with Gallstones include:

  • Female gender
  • Advancing age: The older the age, the higher is the chance of developing Gallstones
  • Obese and overweight individuals
  • Pregnancy is a known condition to be associated with the development of Gallbladder Stones
  • Decreased motility of gallbladder: This occurs in individuals who are on intravenous nutrition for a long period of time
  • Individuals who regularly eat a diet high in fat and cholesterol, but low in fiber
  • The risk increases if family members are affected
  • Post-menopausal women taking hormone replacement
  • Certain conditions affecting the liver can also lead to the development of Gallstones. Conditions, such as liver cirrhosis and infections of the biliary tract, are associated with Gallstone formation
  • Individuals affected by chronic blood disorders, such as sickle cell anemia and thalassemia, are at an increased risk of developing bilirubin-type of Gallstones
  • Those who undergo fat reduction surgeries and those who lose weight very rapidly, while being on a low-calorie diet, also have a greater risk


It is important to note that having a risk factor does not mean that one will get the condition. A risk factor increases ones chances of getting a condition compared to an individual without the risk factors. Some risk factors are more important than others.

Also, not having a risk factor does not mean that an individual will not get the condition. It is always important to discuss the effect of risk factors with your healthcare provider.

What are the Causes of Gallstones? (Etiology)

The exact cause of Gallstone formation is not clear. However, the following factors are known to contribute to their formation:

  • Presence of excess cholesterol in the bile which may precipitate, leading to Gallstone formation
  • Presence of excess bilirubin in the bile, which may occur with certain blood disorders and infections of the biliary tract
  • Improper emptying of the Gallbladder may cause the bile to become concentrated, resulting in stone formation


Gallstones are broadly classified on the basis of their composition. They can be of the following types:

  • Cholesterol stones: These are composed of cholesterol, protein component, and may contain small amounts of calcium and bile pigment. They are the most common types of stones that are present in almost 80% of the patients. The cholesterol level of blood does not affect the development of these stone types
  • Pigment stones: They are seen in up to 20% of the cases presenting with gallbladder disease/condition. The majority of patients have underlying blood disorders that lead to the formation of pigmented Gallstones. The major component of these stone types is bilirubin
  • Mixed type: It is the least common variety of Gallstone. They can contain varied concentration of cholesterol, calcium, bilirubin, and other components

What are the Signs and Symptoms of Gallstones?

Most of the individuals with Gallstones are asymptomatic.

  • The symptoms may develop when a stone is large enough to block the duct draining the bile from the gallbladder to the first part of small intestine, duodenum
  • This leads to increased efforts of the gallbladder to push the bile out, which thus presents as a cramping type of pain in the right upper abdomen
  • This initial pattern presents as intermittent pain that subsides by itself. When it is complicated by some infection or other complication, it presents as continuous pain


The common signs and symptoms of Gallbladder Stones include:

  • Abdominal pain
    • The pain is located in the right upper part of the belly and may radiate to the right shoulder
    • The type of pain may vary from being sharp, dull, or cramping in nature
    • It may be constant or intermittent
    • The pain is typically aggravated by fatty diet
  • Fever and chills:
    • When there is an infection of the gallbladder, the patients may present with fever and chills
    • There may also be associated nausea and vomiting

How are Gallstones Diagnosed?

The diagnosis of Gallstones may involve the following tests and exams:

  • A complete evaluation of medical history along with a thorough physical exam
  • Various modalities of imaging are available to visualize the Gallstones, and these include:
    • Abdominal X-ray: It can only detect up to 10% of the Gallstones, which have high content of calcium and are thus seen on X-ray
    • Abdominal ultrasound: It is a test that uses high-frequency sound waves to detect the presence of Stones in the Gallbladder. It is the test of choice, when a patient presents with symptoms of Gallstones. This test may detect the presence of Gallstones in as many as 80% of the cases
    • HIDA scan: If an abdominal ultrasound does not detect the stones, but the clinical probability is high, then HIDA scans are generally used to confirm their presence. In this test, a dye is injected into the body and the movement of dye is followed through a series of images. This test has a high rate of detection of stones that are not seen on the ultrasound

Other less commonly used modalities in the detection of Gallstones include:

  • CT scan of abdomen: It is a high-resolution scan of the abdomen, which gives better images of the abdomen. It is mainly used for detecting the complications associated with Gallstones, if any
  • Cholangiography: It is a form of test that enables a direct visualization of the bile system. It can be performed by two methods:
    • Endoscopic retrograde cholangiopancreatography (ERCP: It is form of invasive test that serves the dual purpose of diagnosis and treatment
    • Magnetic resonance cholangiopancreatography (MRCP): It is a non-invasive form of test that is excellent to visualise the presence of stones in the biliary system. It is performed in patients who are poor candidates for ERCP

Blood tests to access the liver functions include:

  • Liver function tests:
    • Bilirubin level
    • Liver enzymes, which include aminotransferase and alkaline phosphatase
  • To assess the pancreatic function levels, enzymes secreted by the pancreas are measured that include:
    • Amylase
    • Lipase
  • To assess the blood abnormalities:
    • Complete blood count
    • Coagulation studies
    • Studies to assess hereditary disorders may also be ordered

Many clinical conditions may have similar signs and symptoms. Your healthcare provider may perform additional tests to rule out other clinical conditions to arrive at a definitive diagnosis.

What are the possible Complications of Gallstones?

The complications from Gallstones typically arise when they obstruct the ducts in the biliary system, or when they are associated with infections.

  • Infectious complications:
    • Acute cholecystitis: It occurs when Gallstones block the bile duct and infection occurs in the gallbladder. It is a form of surgical emergency, as the infection is fatal, if timely treatment is not provided
    • Cholangitis: It occurs when the stone leaves the gallbladder and gets stuck in the distal bile duct, and infection of the bile duct taking place. This infection may spread to the liver and can be fatal
  • Complications to obstruction in the biliary system:
    • Choledocholithiasis: When the stone reaches the common bile duct and gets stuck, it results in the obstruction of common bile duct, which may present as jaundice
    • Pancreatitis: It occurs when there is a blockage in the pancreatic ducts. The blockage is typically caused by a stone that leaves the gallbladder and enters the pancreatic system
    • Chronic cholecystitis: With repeated episodes of unresolved acute cholecystitis, a chronic form of the disease may develop. It is associated with decreased functioning of the gallbladder
  • Gallbladder cancer: There is a very small risk of cancer in the gallbladder due to Gallstones, but it is very rare

How are Gallstones Treated?

Only symptomatic patients need treatment for Gallstones. Since most of the asymptomatic Gallstones would not progress to become symptomatic, they may be only monitored.

  • The option to treat symptomatic Gallstones depends on the acuity of presentation
  • Surgery is the first line of treatment
  • If a patient is a poor candidate for surgery, medical management may be undertaken 

A surgical removal of the gallbladder is the treatment of choice. This can be achieved in two ways:

  • Laparoscopic removal (laparoscopic cholecystectomy) is the procedure of choice
    • It offers faster recovery
    • Less pain
    • Less complications
  • Open cholecystectomy, which is rarely performed nowadays, for it involves
    • Bigger incisions
    • More pain
    • Longer hospitalization period

Medical management:

  • It is reserved for the patients who cannot tolerate surgery
  • Medications, such as chenodeoxycholic acid or ursodeoxycholic acid, may be given to dissolve the stones
  • They take a long time to act and have inconsistent effects 


  • For patients who are poor candidates of surgery and who do not respond to medical management
  • It is associated with a high recurrence rate 

How can Gallstones be Prevented?

Prevention of risk factors may be helpful in reducing the risk of Gallstones.

  • Having a healthy diet and proper exercise routine can reduce the chances of developing risk factors for this condition
  • Individuals who want to lose weight should do so progressively slowly and should not lose a considerable amount of weight within a short period of time

What is the Prognosis of Gallstones? (Outcomes/Resolutions)

  • Gallstones may be best treated through a surgery
  • Once the surgery is done the chances of developing the condition again is practically nil

Additional and Relevant Useful Information for Gallstones:

  • The most common indication for performing a laparoscopic cholecystectomy is symptomatic gallstones causing pain (biliary colic)

What are some Useful Resources for Additional Information?

American Gastroenterological Association (AGA)
4930 Del Ray Avenue Bethesda, MD 20814
Phone: (301) 654-2055
Fax: (301) 652-3890
Email: member@gastro.org
Website: http://www.gastro.org

References and Information Sources used for the Article:

http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001318/ (accessed on 07/26/2015)

http://www.nlm.nih.gov/medlineplus/gallstones.html (accessed on 07/26/2015)

Mayo Clinic Gatroenterology and Hepatology Board Review (accessed on 07/26/2015)

Helpful Peer-Reviewed Medical Articles:

Casper, M., &Lammert, F. (2011). [Gallstone disease: basic mechanisms, diagnosis and therapy]. Praxis (Bern 1994), 100(23), 1403-1412. doi: 10.1024/1661-8157/a000721

Chuang, S. C., Hsi, E., & Lee, K. T. (2013).Genetics of gallstone disease.AdvClinChem, 60, 143-185.

Pronio, A., Piroli, S., Caporilli, D., Ciamberlano, B., Coluzzi, M., Castellucci, G., . . .Montesani, C. (2013). Recurrent gallstone ileus: case report and literature review. G Chir, 34(1-2), 35-37.

Ramamurthy, N. K., Rudralingam, V., Martin, D. F., Galloway, S. W., &Sukumar, S. A. (2013). Out of sight but kept in mind: complications and imitations of dropped gallstones. AJR Am J Roentgenol, 200(6), 1244-1253. doi: 10.2214/AJR.12.9430

Svensson, J., & Makin, E. (2012).Gallstone disease in children.SeminPediatrSurg, 21(3), 255-265. doi: 10.1053/j.sempedsurg.2012.05.008

Reviewed and Approved by a member of the DoveMed Editorial Board
First uploaded: Aug. 2, 2015
Last updated: April 8, 2016

Source: https://www.dovemed.com/diseases-conditions/gallstones/




Lithotripsy is the use of high-energy shock waves to fragment and disintegrate kidney stones. The shock wave, created by using a high-voltage spark or an electromagnetic impulse outside of the body, is focused on the stone. The shock wave shatters the stone, allowing the fragments to pass through the urinary system. Since the shock wave is generated outside the body, the procedure is termed extracorporeal shock wave lithotripsy (ESWL). The name is derived from the roots of two Greek words, litho , meaning stone, and trip , meaning to break.


ESWL is used when a kidney stone is too large to pass on its own, or when a stone becomes stuck in a ureter (a tube that carries urine from the kidney to the bladder) and will not pass. Kidney stones are extremely painful and can cause serious medical complications if not removed.


For an unknown reason, the number of persons in the United States developing kidney stones has been increasing over the past 20 years. White people are more prone to develop kidney stones than are persons of color. Although stones occur more frequently in men, the number of women who develop them has been increasing over the past 10 years, causing the ratio to change. Kidney stones strike most people between the ages of 20 and 40. Once persons develop more than one stone, they are more likely to develop others. Lithotripsy is not required for treatment in all cases of kidney stones.


Lithotripsy uses the technique of focused shock waves to fragment a stone in the kidney or the ureter. The affected person is placed in a tub of water or in contact with a water-filled cushion. A sophisticated machine called Lithotripter produces the focused shock waves. A high-voltage electrical discharge is passed through a spark gap under water. The shock waves thus produced are focused on the stone inside the person’s body. The shock waves are created and focused on the stone with the help of a machine called C-Arm Image Intensifier. The wave shatters and fragments the stone. The resulting debris, called gravel, can then pass through the remainder of the ureter, through the bladder, and through the urethra during urination. There is minimal chance of damage to skin or internal organs because biologic tissues are resilient, not brittle, and because the shock waves are not focused on them.

The shock wave is characterized by a very rapid pressure increase in the transmission medium and is quite different from ultrasound. The shock waves are transmitted through a person’s skin and pass harmlessly through soft tissues. The shock wave passes through the
Kidney stones that are too big to pass through the ureter become very painful (B). During lithotripsy, the patient is put in a tub of water, or on a water-filled blanket. Shock waves are used to break up the stone (C). These smaller pieces are able to pass out of the body (D). (Illustration by GGS Inc.)

Kidney stones that are too big to pass through the ureter become very painful (B). During lithotripsy, the patient is put in a tub of water, or on a water-filled blanket. Shock waves are used to break up the stone (C). These smaller pieces are able to pass out of the body (D). (

Illustration by GGS Inc.


kidney and strikes the stone. At the edge of the stone, energy is transferred into the stone, causing small cracks to form on the edge of the stone. The same effect occurs when the shock wave exits the stone. With successive shock waves, the cracks open up. As more cracks form, the size of the stone is reduced. Eventually, the stone is reduced to small particles, which are then flushed out of the kidneys or ureter naturally during urination.


ESWL should not be considered for persons with severe skeletal deformities, people weighing more than 300 lb (136 kg), individuals with abdominal aortic aneurysms, or persons with uncontrollable bleeding disorders. Women who are pregnant should not be treated with ESWL. Individuals with cardiac pacemakers should be evaluated by a cardiologist familiar with ESWL. The cardiologist should be present during the ESWL procedure in the event the pacemaker needs to be overridden.

Prior to the lithotripsy procedure, a complete physical examination is performed, followed by tests to determine the number, location, and size of the stone or stones. A test called an intravenous pyelogram (IVP) is used to locate the stones, which involves injecting a dye into a vein in the arm. This dye, which shows up on x ray, travels through the bloodstream and is excreted by the kidneys. The dye then flows down the ureters and into the bladder. The dye surrounds the stones. In this manner, x rays are used to evaluate the stones and the anatomy of the urinary system. Blood tests are performed to determine if any potential bleeding problems exist. For women of childbearing age, a pregnancy test is done to make sure they are not pregnant. Older persons have an EKG test to make sure that no potential heart problems exist. Some individuals may have a stent placed prior to the lithotripsy procedure. A stent is a plastic tube placed in the ureter that allows the passage of gravel and urine after the ESWL procedure is completed.

The process of lithotripsy generally takes about one hour. During that time, up to 8,000 individual shock waves are administered. Depending on a person’s pain tolerance, there may be some discomfort during the treatment. Analgesicsmay be administered to relieve this pain.


Most persons pass blood in their urine after the ESWL procedure. This is normal and should clear after several days to a week. Lots of fluids should be taken to encourage the flushing of any gravel remaining in the urinary system. Treated persons should follow up with a urologist in about two weeks to make sure that everything is progressing as planned. If a stent has been inserted, it is normally removed at this time.


Abdominal pain is fairly common after ESWL, but it is usually not a cause for worry. However, persistent or severe abdominal pain may imply an unexpected internal injury. Occasionally, stones may not be completely fragmented during the first ESWL treatment and further lithotripsy procedures may be required.

Some people are allergic to the dye material used during an IVP, so it cannot be used. For these people, focused sound waves, called ultrasound, can be used to identify where the stones are located.

Normal results

In most cases, stones are reduced to gravel and passed within a few days. Individuals may return to work whenever they feel able.

Morbidity and mortality rates

Colicky renal pain is very common when gravel is being passed. Other problems may include perirenal hematomas (blood clots near the kidneys) in 66% of the cases; nerve palsies; pancreatitis (inflammation of the pancreas); and obstruction by stone fragments. Death is extremely rare and usually due to an undiagnosed associated or underlying condition that is aggravated by the lithotripsy procedure.


Before the advent of lithotripsy, surgery was used to remove kidney stones. This approach is uncommon today, but occasionally used when other conditions prevent the use of lithotripsy. Attempts are occasionally made to change the pH of urine so as to dissolve kidney stones. This treatment has limited success.




Field, Michael, David Harris, and Carol Pollock. The Renal System. London: Churchill Livingstone, 2001.

Parker, James N. The 2002 Official Patient’s Source Book on Kidney Stones. Logan, UT: ICON Health, 2002.

Tanagho, Emil A., and Jack W. McAninch. Smith’s General Urology, 15th ed. New York: McGraw-Hill, 2000.

Walsh, Patrick C., and Alan B. Retik. Campbell’s Urology, 8th ed. Philadelphia: Saunders, 2002.


Ather, M. H., and M. A. Noor. “Does Size and Site Matter for Renal Stones Up to 30 mm in Size in Children Treated by Extracorporeal Lithotripsy?” Urology 61, no.1 (2003): 212–215.

Downey, P., and D. Tolley. “Contemporary Management of Renal Calculus Disease.” Journal of the Royal College of Surgery (Edinburgh) 47, no.5 (2002): 668–675.

Hochreiter, W. W., H. Danuser, M. Perrig, and U. E. Studer. “Extracorporeal Shock Wave Lithotripsy for Distal Ureteral Calculi.” Journal of Urology 169, no.3 (2003): 878–880.

Rajkumar, P., and G. F. Schmitgen. “Shock Waves Do More Than Just Crush Stones: Extracorporeal Shock Wave Therapy in Plantar Fasciitis.” International Journal of Clinical Practice 56, no.10 (2002): 735–737.


American Foundation for Urologic Disease. 1128 North Charles Street, Baltimore, MD 21201. (800) 242-2383 or (410) 468-1800. http://admin@afud.org. http://www.afud.org .

American Lithotripsy Society. 305 Second Avenue, Suite 200, Waltham, MA 02451.

American Medical Association. 515 N. State Street, Chicago, IL 60610. (312) 464-5000. http://www.ama-assn.org .

American Urological Association. 1120 North Charles Street, Baltimore, MD 21201-5559. (410) 727-1100. http://www.auanet.org/index_hi.cfm .

National Kidney Foundation. 30 East 33rd Street, New York, NY 10016. (800) 622-9010. (781) 895-9098. Fax: (781) 895-9088. E-mail: http://als@lithotripsy.org. http://www.kidney.org .


Case Western Reserve University. [cited March 17, 2003http://www.cwru.edu/artsci/dittrick/artifactspages/b-2lithotripsy.htm .

Global Lithotripsy Services. [cited March 17, 2003] http://www.gls-lithotripsy.com/Howdoes.html .

Lifespan. [cited March 17, 2003] http://www.lifespan.org/mininvasive/revised/patient/gallstones/lithotripsy.htm .

National Institute of Diabetes and Digestive and Kidney Diseases. [cited March 17, 2003] http://www.niddk.nih.gov/health/urolog/pubs/stonadul/stonadul.htm#whogets .

National Library of Medicine. [cited March 17, 2003] http://www.nlm.nih.gov/medlineplus/ency/article/007113.htm .

L. Fleming Fallon, Jr, MD, DrPH


Lithotripsy is performed by a technician or other individual with specialized training under the supervision of a physician. The physician in charge usually has specialized training in urology. Lithotripsy is most often performed as an outpatient procedure in a facility affiliated with a hospital.

Source Read more: http://www.surgeryencyclopedia.com/La-Pa/Lithotripsy.html#ixzz53XzP0D6h

Cystic duct

Cystic duct

The gallbladder stores bile produced in the liver. In order to enter into the duodenum, bile must travel out of the gallbladder, through the cystic duct’s spiral valve, and into the common bile duct. Along with fluid from the pancreas, the bile enters the duodenum through the ampulla of vater.

While there is no other use for the cystic duct, health problems can result when it develops obstructions. If gallstones become lodged in the spiral valve or other parts of the duct, the movement of bile becomes impeded or blocked completely. Should this happen, bile will become trapped within the gallbladder. The bile will build up to the point where the gallbladder will swell. In the worst case scenario, the gallbladder will rupture, leading to a surgical emergency.


Source: https://www.healthline.com/human-body-maps/cystic-duct

Role of Bile Acids In Digestion

Role of Bile Acids In Digestion
Bile is a complex fluid containing water, electrolytes and a battery of organic molecules including bile acids, cholesterol, phospholipids and bilirubin that flows through the biliary tract into the small intestine. There are two fundamentally important functions of bile in all species:

Bile contains bile acids, which are critical for digestion and absorption of fats and fat-soluble vitamins in the small intestine.
Many waste products, including bilirubin, are eliminated from the body by secretion into bile and elimination in feces.
Adult humans produce 400 to 800 ml of bile daily, and other animals proportionately similar amounts. The secretion of bile can be considered to occur in two stages:

Initially, hepatocytes secrete bile into canaliculi, from which it flows into bile ducts. This hepatic bile contains large quantities of bile acids, cholesterol and other organic molecules.
As bile flows through the bile ducts it is modified by addition of a watery, bicarbonate-rich secretion from ductal epithelial cells.
In species with a gallbladder (man and most domestic animals except horses and rats), further modification of bile occurs in that organ. The gall bladder stores and concentrates bile during the fasting state. Typically, bile is concentrated five-fold in the gall bladder by absorption of water and small electrolytes – virtually all of the organic molecules are retained.

Secretion into bile is a major route for eliminating cholesterol. Free cholesterol is virtually insoluble in aqueous solutions, but in bile, it is made soluble by bile acids and lipids like lecithin. Gallstones, most of which are composed predominantly of cholesterol, result from processes that allow cholesterol to precipitate from solution in bile.

Role of Bile Acids in Fat Digestion and Absorption
Bile acids are derivatives of cholesterol synthesized in the hepatocyte. Cholesterol, ingested as part of the diet or derived from hepatic synthesis is converted into the bile acids cholic and chenodeoxycholic acids, which are then conjugated to an amino acid (glycine or taurine) to yield the conjugated form that is actively secreted into cannaliculi.
Bile acids are facial amphipathic, that is, they contain both hydrophobic (lipid soluble) and polar (hydrophilic) faces. The cholesterol-derived portion of a bile acid has one face that is hydrophobic (that with methyl groups) and one that is hydrophilic (that with the hydroxyl groups); the amino acid conjugate is polar and hydrophilic.

Their amphipathic nature enables bile acids to carry out two important functions:

Emulsification of lipid aggregates: Bile acids have detergent action on particles of dietary fat which causes fat globules to break down or be emulsified into minute, microscopic droplets. Emulsification is not digestion per se, but is of importance because it greatly increases the surface area of fat, making it available for digestion by lipases, which cannot access the inside of lipid droplets.
Solubilization and transport of lipids in an aqueous environment: Bile acids are lipid carriers and are able to solubilize many lipids by forming micelles – aggregates of lipids such as fatty acids, cholesterol and monoglycerides – that remain suspended in water. Bile acids are also critical for transport and absorption of the fat-soluble vitamins.
Role of Bile Acids in Cholesterol Homeostasis
Hepatic synthesis of bile acids accounts for the majority of cholesterol breakdown in the body. In humans, roughly 500 mg of cholesterol are converted to bile acids and eliminated in bile every day. This route for elimination of excess cholesterol is probably important in all animals, but particularly in situations of massive cholesterol ingestion.

Interestingly, it has recently been demonstrated that bile acids participate in cholesterol metabolism by functioning as hormones that alter the transcription of the rate-limiting enzyme in cholesterol biosynthesis.

Enterohepatic Recirculation
Large amounts of bile acids are secreted into the intestine every day, but only relatively small quantities are lost from the body. This is because approximately 95% of the bile acids delivered to the duodenum are absorbed back into blood within the ileum.

Venous blood from the ileum goes straight into the portal vein, and hence through the sinusoids of the liver. Hepatocytes extract bile acids very efficiently from sinusoidal blood, and little escapes the healthy liver into systemic circulation. Bile acids are then transported across the hepatocytes to be resecreted into canaliculi. The net effect of this enterohepatic recirculation is that each bile salt molecule is reused about 20 times, often two or three times during a single digestive phase.

It should be noted that liver disease can dramatically alter this pattern of recirculation – for instance, sick hepatocytes have decreased ability to extract bile acids from portal blood and damage to the canalicular system can result in escape of bile acids into the systemic circulation. Assay of systemic levels of bile acids is used clinically as a sensitive indicator of hepatic disease.

Pattern and Control of Bile Secretion
The flow of bile is lowest during fasting, and a majority of that is diverted into the gallbladder for concentration. When chyme from an ingested meal enters the small intestine, acid and partially digested fats and proteins stimulate secretion of cholecystokinin and secretin. As discussed previously, these enteric hormones have important effects on pancreatic exocrine secretion. They are both also important for secretion and flow of bile:

Cholecystokinin: The name of this hormone describes its effect on the biliary system – cholecysto = gallbladder and kinin = movement. The most potent stimulus for release of cholecystokinin is the presence of fat in the duodenum. Once released, it stimulates contractions of the gallbladder and common bile duct, resulting in delivery of bile into the gut.
Secretin: This hormone is secreted in response to acid in the duodenum. Its effect on the biliary system is very similar to what was seen in the pancreas – it simulates biliary duct cells to secrete bicarbonate and water, which expands the volume of bile and increases its flow out into the intestine.


Source:  http://www.vivo.colostate.edu/hbooks/pathphys/digestion/liver/bile.html

Gallstones (expanded)

A male adult pointing to a liver outline and painted gallbladder on his abdomen.

Gallstones facts

  • Gallstones are “stones” that form in the gallbladder or bile ducts.
  • The common types of gallstones are cholesterol, black pigment, and brown pigment.
  • Cholesterol gallstones occur more frequently in several ethnic groups and are associated with female gender, obesity, pregnancy, oral hormonal therapy, rapid loss of weight, elevated blood triglyceride levels, and Crohn’s disease.
  • Black pigment gallstones occur when there is increased destruction of red blood cells, while brown pigment gallstones occur when there is reduced flow and infection of bile.
  • The majority of gallstones do not cause symptoms.
  • The most common symptoms of gallstones are biliary colic and cholecystitis. Gallstones do not cause intolerance to fatty foods, belching, abdominal distention, or gas.
  • Complications of gallstones include cholangitis, gangrene of the gallbladder, jaundice, pancreatitis, sepsis, fistula, and ileus.
  • Gallbladder sludge is associated with symptoms and complications of gallstones; however, like gallstones, sludge usually does not cause problems.
  • The best single test for diagnosing gallstones is transabdominal ultrasonography. Other tests include endoscopic ultrasonography, magnetic resonance cholangio-pancreatography (MRCP), cholescintigraphy (HIDA scan), endoscopic retrograde cholangio-pancreatography(ERCP), liver and pancreatic blood tests, duodenal drainage, oral cholecystogram (OCG), and intravenous cholangiogram (IVC).
  • Gallstones are managed primarily with observation (no treatment) or removal of the gallbladder (cholecystectomy). Less commonly used treatments include sphincterotomy and extraction of gallstones, dissolution with oral medications, and extra-corporeal shock-wave lithotripsy (ESWL). Prevention of cholesterol gallstones also is possible with oral medications.
  • Symptoms of gallstones should stop following cholecystectomy. If they do not, it is likely that gallstones were left in the ducts, there is a second problem within the bile ducts, or there is sphincter of Oddi dysfunction.
  • Many dietary recommendations have been made for the prevention or treatment of gallstones and to prevent their symptoms, but none of them have been shown to be effective.
  • Many home remedies have been suggested for eliminating gallstones, but none have been shown to be effective
  • Continuing research is directed at uncovering the genes that are responsible for the formation of gallstones.
Illustration of the digestive system with gallstones and close up of gallstones in the gallbladder a stone that has also passed in to the cystic duct.

What are gallstones, and how do they form?

Gallstones (often misspelled as gall stones) are stones that form in the gall (bile) within the gallbladder. (The gallbladder is a pear-shaped organ just below the liver that stores bile secreted by the liver.) Gallstones reach a size of between a sixteenth of an inch and several inches.

  • Bile is a watery liquid made by the cells of the liver that is important for digesting food in the intestine, particularly fat, and eliminating toxic substances from the body.
  • Liver cells secrete the bile into small canals within the liver referred to as canaliculi.
  • The bile flows through the canaliculi and into larger collecting ducts within the liver referred to as intrahepatic bile ducts.
  • The bile then flows through merged intrahepatic bile ducts out of the liver as extrahepatic (outside the liver) bile ducts, ( first into the two hepatic bile ducts, then into the single common hepatic duct, and finally, after the common hepatic duct is joined by the cystic duct coming from the gallbladder, into the common bile duct.

From the common bile duct, there are two different directions that bile can flow.

  • The first direction is through the common bile duct and directly into the intestine where the bile mixes with food and promotes digestion of food. At the same time toxic substances that are removed by the liver from the blood are eliminated into the intestine.
  • The second direction is into a off-shoot of the common bile duct, the cystic duct, and from there into the gallbladder.
Illustration showing gallstones in the gallbladder as well as in the distal common bile duct.

What are gallstones and how do they form?

Once in the gallbladder, bile is concentrated by the removal (absorption) of water. During a meal, the muscle that makes up the wall of the gallbladder contracts and squeezes the concentrated bile in the gallbladder back through the cystic duct into the common bile duct and then into the intestine. (Concentrated bile is much more effective for digestion than the un-concentrated bile that goes from the liver straight into the intestine.) The timing of gallbladder contraction – during a meal – allows the concentrated bile from the gallbladder to mix with food.

Gallstones usually form in the gallbladder; however, they also may form anywhere there is bile – in the intrahepatic, hepatic, common bile, and cystic ducts.

Gallstones also may move about in the bile, for example, from the gallbladder into the cystic or the common duct.


What causes gallstones, and who gets them?

Gallstones are common; they occur in approximately 20% of women in the US, Canada and Europe, but there is a large variation in the prevalence among different ethnic groups. For example, gallstones occur 1 ½ to 2 times more commonly in Scandinavians and Mexican-Americans. Among American Indians, gallstone prevalence is more than 80%. These differences probably are accounted for by genetic (hereditary) factors. First-degree relatives (parents, siblings, and children) of individuals with gallstones are 1 ½ times more likely to have gallstones than if they do not have a first-degree relative with gallstones. Further support for a genetic predisposition comes from twin studies. Thus, among non-identical pairs of twins (who share 50% of their genes with one another), both individuals in a pair have gallstones 8% of the time. Among identical pairs of twins (who share 100% of their genes with one another), both individuals have gallstones 23% of the time.

There are several conditions that are associated with the formation of gallstones, and the way in which they cause gallstones can vary. (Please see the section on risks for gallstones in this article.)


Small gallstones made up largely of cholesterol.

What are the types of gallstones?

There are several types of gallstones, and each type has a different cause.

Cholesterol gallstones

Cholesterol gallstones are primarily made up of cholesterol. They are the most common type of gallstone, comprising 80% of gallstones in individuals in Europe and the Americas. Cholesterol is one of the substances (chemicals) that liver cells secrete into bile. Secretion of cholesterol into bile is an important mechanism by which the liver eliminates excess cholesterol from the body.

In order for bile to carry cholesterol, the cholesterol must be dissolved in the bile. Cholesterol is a fat, however, and bile is an aqueous or watery solution; fats do not dissolve in watery solutions. In order to make the cholesterol dissolve in bile, the liver also secretes two detergents, bile acids and lecithin, into the bile. These detergents, just like dish-washing detergents, dissolve the fatty cholesterol so that it can be carried by bile through the ducts. If the liver secretes too much cholesterol for the amount of bile acids and lecithin it secretes, some of the cholesterol does not stay dissolved. Similarly, if the liver does not secrete enough bile acids and lecithin, some of the cholesterol does not stay dissolved. In either case, the undissolved cholesterol sticks together and forms particles of cholesterol that grow in size and eventually become gallstones.

There are two other processes that promote the formation of cholesterol gallstones though neither process is able to cause cholesterol gallstones to form. The first is an abnormally rapid formation and growth of cholesterol particles into gallstones. Thus, with the same concentrations of cholesterol, bile acids and lecithin in the bile, patients with gallstones form particles of cholesterol more rapidly than individuals without gallstones. The second process that promotes the formation and growth of gallstones is reduced contraction and emptying of the gallbladder that allows bile to stay in the gallbladder longer than normally so that there is more time for cholesterol particles to form and grow into gallstones.


A man experiences pain from biliary colic.

What are the symptoms of gallstones?

The majority of people with gallstones have no signs or symptoms and are unaware of their gallstones. (The gallstones are “silent.”) These gallstones often are found as a result of tests (for example, ultrasoundor X-ray examination of the abdomen) performed while evaluating medical conditions other than gallstones. Symptoms can appear later in life, however, after many years without symptoms. Thus, over a period of five years, approximately 10% of people with silent gallstones will develop symptoms. Once symptoms develop, they are likely to continue and often will worsen.

Gallstones are blamed for many symptoms they do not cause. Among the symptoms gallstones do not cause are:

  • dyspepsia (including abdominal bloating and discomfort after eating),
  • intolerance to fatty foods,
  • belching, and
  • flatulence (passing gas or farting).

When signs and symptoms of gallstones occur, they virtually always occur because the gallstones obstruct the bile ducts.

The most common symptom of gallstones is biliary colic. Biliary colic is a very specific type of pain, occurring as the primary or only symptom in 80% of people with gallstones who develop symptoms. Biliary colic occurs when the bile ducts (cystic, hepatic ducts or common bile duct) are suddenly blocked by a gallstone. Slowly-progressing obstruction, as from a tumor, does not cause biliary colic. Behind the obstruction, fluid accumulates and distends the ducts and gallbladder. In the case of hepatic duct or common bile duct obstruction, this is due to continued secretion of bile by the liver. In the case of cystic duct obstruction, the wall of the gallbladder secretes fluid into the gallbladder. It is the distention of the ducts or gallbladder that causes biliary colic.

Characteristically, biliary colic comes on suddenly or builds rapidly to a peak over a few minutes.

  • It is a constant pain; it does not come and go, though it may vary in intensity while it is present. IT is not cramp-like.
  • It lasts for 15 minutes to 4-5 hours. If the pain lasts more than 4-5 hours, it means that a complication – usually cholecystitis – has developed.
  • The pain usually is severe, but movement does not make the pain worse. In fact, patients experiencing biliary colic often walk about or writhe (twist the body in different positions) in bed trying to find a comfortable position.
  • Biliary colic often is accompanied by nausea.
  • Most commonly, biliary colic is felt in the middle of the upper abdomen just below the sternum.
  • The second most common location for pain is the right upper abdomen just below the margin of the ribs.
  • Occasionally, the pain also may be felt in the back at the lower tip of the scapula on the right side.
  • On rare occasions, the pain may be felt beneath the sternum and is mistaken for angina or a heart attack.
  • An episode of biliary colic subsides gradually once the gallstone shifts within the duct so that it is no longer causing obstruction.

Biliary colic is a recurring symptom. Once the first episode occurs, there are likely to be other episodes. Also, there is a pattern of recurrence for each individual, that is, in some individuals the episodes tend to remain frequent while in others they are infrequent. The majority of people who develop biliary colic do not go on to develop cholecystitis or other complications. There is a misconception that contraction of the gallbladder is what causes the obstruction of the ducts and biliary colic. Eating, even fatty foods, does not cause biliary colic; most episodes of biliary colic occur during the night, long after the gallbladder has emptied.


A doctor examining a gallstone patient.

What are the complications of gallstones?

Biliary colic is the most common symptom of gallstones, but, fortunately, it is usually a self-limited symptom. There are, however, more serious complications of gallstones.


Cholecystitis means inflammation of the gallbladder. Like biliary colic, it too is caused by sudden obstruction of the ducts, usually the cystic duct by a gallstone. In fact, cholecystitis may begin with an episode of biliary colic. Obstruction of the cystic duct causes the wall of the gallbladder to begin secreting fluid, but for unclear reasons, inflammation sets in. At first the inflammation is sterile, that is, there is no infection with bacteria; however, over time the bile and gallbladder become infected with bacteria that travel through the bile ducts from the intestine.

With cholecystitis, there is constant pain in the right upper abdomen. Inflammation extends through the wall of the gallbladder, and the right upper abdomen becomes particularly tender when it is pressed or even tapped. Unlike with biliary colic, however, it is painful to move around. Individuals with cholecystitis usually lie still. There is fever, and the white blood cell count is elevated, both signs of inflammation. Cholecystitis usually is treated with antibiotics, and most episodes will resolve over several days. Even without antibiotics, cholecystitis often resolves. As with biliary colic, movement of the gallstone out of the cystic duct and back into the gallbladder relieves the obstruction and allows the inflammation to resolve.


Cholangitis is a condition in which bile in the common, hepatic, and intrahepatic ducts becomes infected. Like cholecystitis, the infection spreads through the ducts from the intestine after the ducts become obstructed by a gallstone. Patients with cholangitis are very sick with high fever and elevated white blood cell counts. Cholangitis may result in an abscess within the liver or sepsis. (See discussion of sepsis that follows.)


Gangrene of the gallbladder is a condition in which the inflammation of cholecystitis cuts off the supply of blood to the gallbladder. Without blood, the tissues forming the wall of the gallbladder die, and this makes the wall very weak. The weakness combined with infection often leads to rupture of the gallbladder. The infection then may spread throughout the abdomen, though often the rupture is confined to a small area around the gallbladder (a confined perforation).

Yellowish eyes are a symptom of jaundice.

What are the complications of gallstones? (Continued)


Jaundice is a condition in which bilirubin accumulates in the body. Bilirubin is brownish-black in color but is yellow when it is not too concentrated. A build-up of bilirubin in the body turns the skin and whites of the eye (sclera) yellow. Jaundice occurs when there is prolonged obstruction of the bile ducts. The obstruction may be due to gallstones, but it also may be due to many other causes, for example, tumors of the bile ducts or surrounding tissues. (Other causes of jaundice are a rapid destruction of red blood cells that overwhelms the ability of the liver to remove bilirubin from the blood or a damaged liver that cannot remove bilirubin from the blood normally.) Jaundice, by itself, generally does not cause problems.


Pancreatitis means inflammation of the pancreas. The two most common causes of pancreatitis are alcoholism and gallstones. The pancreas surrounds the common bile duct as it enters the intestine. The pancreatic duct that drains the digestive juices from the pancreas joins the common bile duct just before it empties into the intestine. If a gallstone obstructs the common bile duct just after the pancreatic duct joins it, the flow of pancreatic juice from the pancreas is blocked. This results in inflammation within the pancreas. Pancreatitis due to gallstones usually is mild, but it may cause serious illness and even death. Fortunately, severe pancreatitis due to gallstones is rare.


Sepsis is a condition in which bacteria from any source within the body, including the gallbladder or bile ducts, enter into the blood stream and spread throughout the body. Although the bacteria usually remain within the blood, they also may spread to distant tissues and lead to the formation of abscesses (localized areas of infection with formation of pus). Sepsis is a feared complication of any infection. The signs of sepsis include high fever, high white blood cell count, and, less frequently, rigors (shaking chills) or a drop in blood pressure.


A fistula is an abnormal tract through which fluid can flow between two hollow organs or between an abscess and a hollow organ or skin. Gallstones cause fistulas when the hard gallstone erodes through the soft wall of the gallbladder or bile ducts. Most commonly, the gallstone erodes into the small intestine, stomach, or common bile duct. This can leave a tract that allows bile to flow from the gallbladder to the small intestine, stomach, or the common bile duct. If the fistula enters the distal part of the small intestine, the concentrated bile can lead to problems such as diarrhea. Rarely, the gallstone erodes into the abdominal cavity. The bile then leaks into the abdominal cavity and causes inflammation of the lining of the abdomen (peritoneum), a condition called bile peritonitis.


Ileus is a condition in which there is an obstruction to the flow of food, gas, and liquid within the intestine. It may be due to a mechanical obstruction, for example, a tumor within the intestine, or a functional obstruction, for example, inflammation of the intestine or surrounding tissues that prevents the muscles of the intestine from working normally and propelling intestinal contents. If a large gallstone erodes through the wall of the gallbladder and into the stomach or small intestine, it will be propelled through the small intestine. The narrowest part of the small intestine is the ileo-cecal valve, which is located at the site where the small intestine joins the colon. If the gallstone is too large to pass through the valve, it can obstruct the small intestine and cause an ileus. Gallstones also may cause ileus if there are other abnormal narrowings in the intestine such as a tumor or scarring.


Cancer of the gallbladder almost always is associated with gallstones, but it is not clear which comes first, that is, whether the gallstones precede the cancer and, therefore, could potentially be the cause of the cancer or the gallstones form because cancer is present. Cancer of the gallbladder arises in less than 1% of individuals with gallstones. Therefore, concern about future development of cancer is by itself not a good reason for removing the gallbladder when gallstones are present.


Longitudinal and axial scans through the gallbladder show layering of sludge (S) in the gallbladder.

What is the relationship of sludge to gallstones?

Sludge is a common term that is applied to an abnormality of bile that is seen with ultrasonography of the gallbladder. Specifically, the bile within the gallbladder is seen to be of two different densities with the denser bile on the bottom. The bile is denser because it contains microscopic particles, usually cholesterol or pigment, embedded in mucus. (The mucus is secreted by the gallbladder.) Over time, sludge may remain in the gallbladder, it may disappear and not return, or it may come and go. As discussed previously, these particles may be precursors of gallstones, and they occur often in some situations in which gallstones frequently appear, for example, rapid weight loss, pregnancy, and prolonged fasting.

Nevertheless, it appears that sludge goes on to become gallstones in only a minority of individuals. Just to make matters more difficult, it is not clear how often – if at all – sludge alone causes problems. Sludge has been blamed for many of the same symptoms as gallstones-biliary colic, cholecystitis, and pancreatitis, but often these symptoms and complications are caused by very small gallstones that are missed by ultrasonography. Thus, there is some uncertainty about the importance of sludge.

It is clear, however, that sludge is not the equivalent of gallstones. The practical implication of this uncertainty is that unless an individual’s symptoms are typical of gallstones, sludge should not be considered as a possible cause of the symptoms.


A female doctor sits next to an ultrasound machine.

What kind of doctor treats gallstones?

Gallstones usually are diagnosed by a gastroenterologist, a medical subspecialist who deals with diseases of the intestine, liver, pancreas and gallbladder. General surgeons also may be involved in the diagnosis of gallstones but usually are the doctors who treat gallstones because the common treatment is surgical removal of the gallbladder.

How are gallstones diagnosed?

Gallstones are diagnosed in one of two situations.

  1. When there are symptoms or signs that suggest the presence of gallstones and the diagnosis of gallstones is being pursued.
  2. Coincidentally while a non-gallstone-related medical problem is being evaluated.

Ultrasonography is the most important means of diagnosing gallstones. Standard computerized tomography (CT or CAT scan) and magnetic resonance imaging (MRI) may occasionally demonstrate gallstones; however, they are not as useful compared to ultrasonography because they miss gallstones.


Ultrasonography is a radiological technique that uses high-frequency sound waves to produce images of the organs and structures of the body. The sound waves are emitted from a device called a transducer and are sent through the body’s tissues. The sound waves are reflected by the surfaces and interiors of internal organs and structures as “echoes.” These echoes return to the transducer and are transmitted onto a viewing monitor. On the monitor, the outline of organs and structures can be determined as well as their consistency, for example, liquid or solid.

There are two types of ultrasonographic techniques that can be used for diagnosing gallstones: transabdominal ultrasonography and endoscopic ultrasonography.

Transabdominal ultrasonography

For transabdominal ultrasonography, the transducer is placed directly on the skin of the abdomen. The sound waves travel through the skin and then into the abdominal organs. Transabdominal ultrasonography is painless, inexpensive, and without risk to the patient. In addition to identifying 97% of gallstones in the gallbladder, abdominal ultrasonography can identify many other abnormalities related to gallstones. It can identify:

  • A thickened wall of the gallbladder when there is cholecystiti and inflammation has thickened the wall
  • Enlarged gallbladder and bile duct due to obstruction by gallstones
  • Pancreatitis
  • Fluid surrounding the gallbladder (a possible sign of inflammation) sludge

Transabdominal ultrasonography also may identify diseases not related to gallstones that may be the cause of the patient’s problem, for example, appendicitis. The limitations of transabdominal ultrasonography are that it can only identify gallstones larger than 4-5 millimeters in size, and it is poor at identifying gallstones in the bile ducts.

MRCP image showing stones in the common bile duct: (a) Gallbladder with stones (b) Stone in bile duct (c) Pancreatic duct (d) Duodenum.

How are gallstones diagnosed? (Part 2)

Endoscopic ultrasonography (EUS)

For endoscopic ultrasonography, a long flexible tube – the endoscope – is swallowed by the patient after he or she has been sedated with intravenous medication. The tip of the endoscope is fitted with an ultrasound transducer. The transducer is advanced into the duodenum where ultrasonographic images are obtained.

Endoscopic ultrasonography can identify gallstones and the same abnormalities as transabdominal ultrasonography; however, since the transducer is much closer to the structures of interest – the gallbladder, bile ducts, and pancreas – better images are obtained than with transabdominal ultrasonography. Thus, it is possible to visualize smaller gallstones with EUS than transabdominal ultrasonography. EUS also is better in identifying gallstones in the common bile duct.

Although endoscopic ultrasonography is in many ways better than transabdominal ultrasonography, it is expensive, not available everywhere, and carries a small risk of complications such as those associated with the use of intravenous sedation, and intestinal perforation by the endoscope. Fortunately, transabdominal ultrasonography usually gives most of the information that is necessary, and endoscopic ultrasonography is needed only infrequently. Endoscopic ultrasonography also is a better way than transabdominal ultrasonography to evaluate the pancreas for pancreatitis or its complications.

Magnetic resonance cholangio-pancreatography (MRCP)

Magnetic resonance cholangio-pancreatography or MRCP is a modification of magnetic resonance imaging (MRI) that allows the bile and pancreatic ducts to be examined.

  • For MRCP, the patient is placed in a strong magnetic field that through its energy-carrying radio waves aligns (magnetizes) the protons in the molecules of water in the tissues. (Protons are parts of the atoms that make up water molecules. All tissues in the body contain water though they contain different amounts of water.)
  • Energy-carrying radio waves are passed through the tissues, and the energy is absorbed by the water’s protons.
  • The radio waves are turned off, and the protons release the energy they had absorbed.
  • The released energy is used to form an image of the tissues and organs of the body.
  • The MRI separates tissues and organs based on their concentration of water. Since different tissues contain different amounts of water, MRCP is very good at providing images of organs and tissues.
  • Since bile is mostly water, MRCP gives an excellent image of bile within the gallbladder and bile ducts. The pancreatic duct, which, like the bile ducts, is filled with a watery fluid, also is seen well.
  • Often an intravenous injection of a dye is used to better delineate the bile and pancreatic ducts.

The procedure is called cholangio- (referring to the bile ducts) pancreatography (referring to the pancreatic duct) because it can demonstrate the bile and pancreatic ducts.

MRCP has in many instances replaced other procedures such as cholescintigraphy (HIDA scan) and endoscopic retrograde cholangiopancreatography (ERCP) for evaluating the bile ducts. It can identify gallstones in the bile ducts, obstruction of the ducts, and leaks of bile. There are no risks to the patient with MRCP except for very rare reactions to the injected dye.


Normal hepatobiliary scan (HIDA scan) showing a series of scans done over time to see where bile is excreted and/or accumulated.

How are gallstones diagnosed? (Part 3)

Cholescintigraphy (HIDA scan)

Cholescintigraphy is a procedure done by nuclear medicine physicians. It also is referred to as a HIDA scan or a gallbladder scan.

  • For a HIDA scan, a radioactive chemical is injected intravenously into a patient.
  • The radioactive chemical is removed from the blood by the liver and secreted into the bile.
  • The chemical then disperses everywhere that the bile goes-into the bile ducts, the gallbladder, the intestine, and any place else that bile goes.
  • A camera that senses radioactivity (like a Geiger counter) is then placed over the patient’s abdomen and a “picture” of the liver, bile ducts, and gallbladder is obtained which corresponds to where the radioactive chemical has traveled within, or outside of the bile-filled bile ducts, and gallbladder.

HIDA scans are used to identify obstruction of the bile ducts, for example, by a gallstone. They also may identify bile leaks and fistulas. There are no risks to the patient with HIDA scans.

Cholescintigraphy also is used to study the emptying of the gallbladder. Some patients with gallstones have had gallbladder inflammation due to recognized or unrecognized episodes of cholecystitis. (There also are uncommon, non-gallstone-related causes of inflammation of the gallbladder.) The inflammation can result in scarring of the gallbladder’s wall and muscle, which reduces the ability of the gallbladder to contract. As a result, the gallbladder does not empty normally. During cholescintigraphy, a synthetic hormone related to cholecystokinin (the hormone the body produces and releases during a meal to cause the gallbladder to contract) can be injected intravenously to cause the gallbladder to contract and squeeze out its bile and radioactivity into the intestine. If the gallbladder does not empty the bile and radioactivity normally, it is assumed that the gallbladder is diseased as a result of gallstones or non-gallstone related inflammation.

The problem with interpreting a gallbladder emptying study is that many people with normal gallbladders have abnormal emptying of the gallbladder. Therefore, it is hazardous to base a diagnosis of a diseased gallbladder on abnormal gallbladder emptying alone.

Doctor performs an endoscopic retrograde cholangio-pancreatography (ERCP) on a woman for gallstones.

How are gallstones diagnosed? (Part 4)

Endoscopic retrograde cholangio-pancreatography (ERCP)

ERCP is a combined endoscope and X-ray procedure performed to examine the duodenum (the first portion of the small intestine), the papilla of Vater (a small nipple-like structure where the common bile and pancreatic ducts enter the duodenum), the bile ducts, the gallbladder and the pancreatic duct.

The procedure is performed by using a long, flexible, side viewing instrument (a duodenoscope, a type of endoscope) about the diameter of a fountain pen. The duodenoscope is flexible and can be directed and moved around the many bends of the stomach and intestine. The video-endoscope is the most common type of duodenoscope, and uses chip at the tip of the instrument to transmit video images to a TV screen.

  • First the patient is sedated with intravenous drugs.
  • The duodenoscope is inserted through the mouth, to the back of the throat, down the food pipe (esophagus), through the stomach and into the first portion of the small intestine (duodenum).
  • Once the papilla of Vater is identified, a small plastic catheter (cannula) is passed through a channel in the duodenoscope into the papilla of Vater, and into the bile ducts and the pancreatic duct.
  • Contrast material (dye) is injected, and x-rays are taken of the bile ducts, gallbladder and/or the pancreatic duct.

ERCP can identify; 1) gallstones in the gallbladder (though it is not particularly good at this) and 2) blockage of the bile ducts, for example, by gallstones, and 3) bile leaks. ERCP also may identify diseases not related to gallstones that may be the cause of the patient’s problem, for example, pancreatitis or pancreatic cancer.

An important advantage of ERCP is that instruments can be passed through the same channel as the cannula used to inject the dye to extract gallstones stuck in the common and hepatic ducts. This can save the patient from having an operation. ERCP has several risks associated with it, including the drugs used for sedation, perforation of the duodenum by the duodenoscope, and pancreatitis (due to damage to the pancreas). If gallstones are extracted, bleeding also may occur as a complication.

A doctor holding an anatomical model of the human liver and pointing to a gallstone.

How are gallstones diagnosed? (Part 5)

Liver and pancreatic blood tests

When the liver or pancreas becomes inflamed or their ducts become obstructed and enlarged, the cells of the liver and pancreas release some of their enzymes into the blood. The most commonly-measured liver enzymes in blood are aspartate aminotransferase (AST) and alanine aminotransferase (ALT). The most commonly-measured pancreatic enzymes in blood are amylase and lipase. Many medical conditions that affect the liver or pancreas cause these blood tests to become abnormal, so these abnormalities alone cannot be used to diagnose gallstones. Nevertheless, abnormalities of these tests suggest there is a problem with the liver, bile ducts, or pancreas, and gallstones are a common cause of such abnormal tests, particularly during sudden obstruction of the bile ducts or pancreatic ducts. Thus, abnormal liver and pancreatic blood tests direct attention to the possibility that gallstones may be causing the acute problem.

Duodenal biliary drainage

Duodenal biliary drainage is a procedure that occasionally can be useful in diagnosing gallstones; however, it is not often used. As previously discussed, gallstones begin as microscopic particles of cholesterol or pigment that grow in size. It is clear that some people who develop biliary colic, cholecystitis, or pancreatitis have only these particles in their gallbladders, yet the particles are too small to obstruct the ducts. There are two potential explanations for how obstruction might occur in this situation. The first is that a small gallstone initially caused an obstruction before passing through the bile ducts into the intestine. The second is that particles passing through the bile ducts can “irritate” the ducts, causing spasm of the muscle within the walls of the ducts (which obstructs the flow of bile) or inflammation of the duct that causes the wall of the duct to swell (and also obstructs the duct).

  • For duodenal drainage, a thin plastic or rubber tube with several holes at its tip is passed through a patient’s anesthetized nostril, down the back of the throat, through the esophagus and stomach, and into the duodenum where the bile and pancreatic ducts enter the small intestine. This is done with the help of x-ray (fluoroscopy).
  • Once the tube is in place, a synthetic hormone related to cholecystokinin, the hormone that is normally released after a meal to cause the gallbladder, is injected intravenously. As a result, the gallbladder contracts and squeezes out its concentrated bile into the duodenum.
  • The bile is sucked through the tube in the duodenum and examined for the presence of small cholesterol and pigment particles under a microscope.

The risks to the patient of duodenal drainage are minimal. (There have been no reports of reactions to the synthetic hormone.) Nevertheless, duodenal drainage is uncomfortable.

A modification of duodenal drainage involves collection of bile through an endoscope at the time of an upper gastrointestinal endoscopy-either esophago-gastro-duodenoscopy (EGD) or ERCP.

Oral cholecystogram (OCG)

The oral cholecystogram or OCG is a radiologic (X-ray) procedure for diagnosing gallstones.

  • The patient takes iodine-containing tablets for one or two nights in a row and then has an X-ray of the abdomen.
  • The iodine is absorbed from the intestine into the blood, removed from the blood by the liver, and excreted into bile.
  • In the gallbladder, the iodine becomes concentrated along with the bile.
  • On the X-ray, the iodine, which is dense and stops X-rays, fills the gallbladder and outlines the gallstones which are not dense, and allow X-rays to pass through them. The ducts cannot be seen on the x-ray because the iodine is not concentrated in the ducts.

The OCG is an excellent procedure for diagnosing gallstones; it finds 95% of them. The OCG has been replaced, however, by ultrasonography because ultrasonography is slightly better at finding gallstones and can be done immediately without waiting one or two days for the iodine to be absorbed, excreted, and concentrated.

Unlike ultrasonography, the OCG also cannot give information about the presence of non-gallstone related diseases. As would be expected, ultrasonography sometimes finds gallstones that are missed by the OCG. Less frequently, the OCG finds gallstones that are missed by ultrasonography. For this reason, if there is a strong suspicion that gallstones are present but ultrasonography does not show them, it is reasonable to consider doing an OCG; however, EUS has mostly replaced the OCG in this situation. An OCG should not be done in individuals who are allergic to iodine.

Intravenous cholangiogram (IVC)

The intravenous cholangiogram or IVC is a radiologic (X-ray) procedure that is used primarily for looking at the larger intrahepatic and the extrahepatic bile ducts. It can be used to locate gallstones within these ducts.

An iodine-containing dye is injected intravenously into the blood. The dye is removed from blood by the liver and excreted into bile. Unlike the iodine used in the OCG, the iodine in the IVC is concentrated sufficiently enough in the bile ducts to outline the ducts and any gallstones within them. The IVC is rarely used because it has been replaced by MRI cholangiography and endoscopic ultrasound. Moreover, occasional serious reactions to the iodine-containing dye can occur, which rarely may result in the death of the patient.

A senior male patient and doctor.

What are the potential pitfalls of diagnosing gallstones?

Usually, it is not difficult to diagnose gallstones. Problems arise, however, because of the high prevalence of silent gallstones and the occasional gallstone that is difficult to diagnose.

If a patient has symptoms that are typical for gallstones, for example, biliary colic, cholecystitis, or pancreatitis, and has gallstones on ultrasonography, little else usually needs to be done to demonstrate that the gallstones are causing the symptoms unless the patient has other complicating medical issues.

If symptoms are not typical for gallstones there is a possibility that the gallstones are innocent bystanders (silent), and most importantly, removing the gallbladder surgically will resolve the patient’s problem or prevent further symptoms. In addition, the real cause of the symptoms will not be pursued. In such a situation, there is a need to obtain further evidence, other than their mere presence, that the gallstones are causing the problem. Such evidence can be obtained during an acute episode or shortly thereafter.

If ultrasonography can be done during an acute episode of pain or inflammation caused by gallstones, it may be possible to demonstrate an enlarged gallbladder or bile duct caused by obstruction of the ducts by the gallstone. This is likely to require ultrasonography again after the episode has resolved in order to demonstrate that the gallbladder indeed was larger during the episode than before or after the episode. It is easier to obtain the necessary ultrasonography if the episode lasts several hours, but it is much more difficult to obtain ultrasonography rapidly enough if the episode lasts only 15 minutes.

Another approach is to test the blood for abnormal liver and pancreatic enzymes. The advantage here is that the enzymes, though not always elevated, can be elevated during an acute attack and for several hours after an episode of gallstone-related pain or inflammation, so they may be abnormal even after the episode has subsided. It is important to remember, however, that the enzymes are not specific for gallstones, and it is necessary to exclude other liver and pancreatic causes for abnormal enzymes.

Sometimes, episodes of pain or inflammation may be more or less typical of gallstones, but transabdominal ultrasonography may not demonstrate either gallstones or another cause of the episodes. In this situation, it is necessary to decide whether suspicion is high or low for gallstones as a cause of the episodes. If suspicion is low because of lack of typical symptoms, it may be reasonable only to repeat the ultrasonography, obtain an OCG, and/or test for abnormalities of liver or pancreatic enzymes. If suspicion is high because of more typical symptoms, it is reasonable to investigate even further with endoscopic ultrasonography, ERCP, and duodenal drainage. Prior to these “invasive” procedures, some physicians recommend MRCP.


X-Ray during laparoscopic cholecystectomy.

How are gallstones treated?


Most gallstones are silent, and do not need treatment.

  • If silent gallstones are discovered in an individual at age 65 (or older), the chance of developing symptoms from the gallstones is only 20% (or less) assuming a life span of 75 years. In this instance, it is reasonable not to treat the individual.
  • In younger individuals, no treatment also may be appropriate if the individuals have serious, life-threatening diseases, for example, serious heart disease, that are likely to shorten their life span.
  • On the other hand, in healthy young individuals, treatment should be considered even for silent gallstones because the individuals’ chances of developing symptoms from the gallstones over a lifetime will be higher. Once symptoms begin, treatment should be recommended since further symptoms are likely and more serious complications can be prevented.


Cholecystectomy (removal of the gallbladder surgically) is the standard treatment for gallstones in the gallbladder. Surgery may be done through a large abdominal incision, laparoscopically or robotically through small punctures in the abdominal wall. Laparoscopic surgery results in less pain and a faster recovery. Robot-assisted laparoscopic surgery has 3D visualization. Cholecystectomy has a low rate of complications, but serious complications such as damage to the bile ducts and leakage of bile occasionally occur. There also is risk associated with the general anesthesia that is necessary for either type of surgery. Problems following removal of the gallbladder are few. Digestion of food is not affected, and no change in diet is necessary. Nevertheless, chronic diarrhea occurs in approximately 10% of patients.

Sphincterotomy and extraction of gallstones

Sometimes a gallstone may be stuck in the hepatic or common bile ducts. In such situations, there usually are gallstones in the gallbladder as well, and cholecystectomy is necessary. It may be possible to remove the gallstone stuck in the duct at the time of surgery, but this may not always be possible. An alternative means for removing gallstones in the duct before or after cholecystectomy is with sphincterotomy followed by extraction of the gallstone.

Sphincterotomy involves cutting the muscle of the common bile duct (sphincter of Oddi) at the junction of the common bile duct and the duodenum in order to allow easier access to the common bile duct. The cutting is done with an electrosurgical instrument passed through the same type of endoscope that is used for ERCP. After the sphincter is cut, instruments may be passed through the endoscope and into the hepatic and common bile ducts to grab and pull out the gallstone or to crush the gallstone. It also is possible to pass a lithotripsy instrument that uses high frequency sound waves to break up the gallstone. Complications of sphincterotomy and extraction of gallstones include risks associated with general anesthesia, perforation of the bile ducts or duodenum, bleeding, and pancreatitis.

Oral dissolution therapy

It is possible to dissolve some cholesterol gallstones with medication taken orally. The medication is a naturally-occurring bile acid called ursodeoxycholic acid or ursodiol (Actigall, Urso). Bile acids are one of the detergents that the liver secretes into bile to dissolve cholesterol. Although one might expect therapy with ursodiol to work by increasing the amount of bile acids in bile and thereby cause the cholesterol in gallstones to dissolve, the mechanism of ursodiol’s action actually is different. Ursodiol reduces the amount of cholesterol secreted in bile. The bile then has less cholesterol and becomes capable of dissolving the cholesterol in the gallstones.

There are important limitations to the use of ursodiol:

  • It is only effective for cholesterol gallstones and not pigment gallstones.
  • It works only for small gallstones, less than 1-1.5 cm in diameter.
  • It takes one to two years for the gallstones to dissolve, and many of the gallstones reform following cessation of treatment.

Due to these limitations, ursodiol generally is used only in individuals with smaller gallstones that are likely to have a very high cholesterol content and who are at high risk for surgery because of ill health. It also is reasonable to use ursodiol in individuals whose gallstones were perhaps formed because of a transient event, for example, rapid loss of weight, since the gallstones would not be expected to recur following successful dissolution. Another use of ursodiol is to prevent the formation of gallstones in patients who will lose weight rapidly.

Extracorporeal shock-wave lithotripsy

Extracorporeal shock-wave lithotripsy (ESWL) is an infrequently used method for treating gallstones, particularly those lodged in bile ducts. ESWL generators produce shock waves outside of the body that are then focused on the gallstone. The shock waves shatter the gallstone, and the resulting pieces of the gallstone either drain into the intestine on their own or are extracted endoscopically. Shock waves also can be used to break up gallstones via special catheters passed through an endoscope at the time of ERCP.


A doctor discusses gallstone prevention and possible after effects of removal with a patient in the hospital.

Can gallstones be prevented?

Ideally, it would be better if gallstones could be prevented rather than treated. Prevention of cholesterol gallstones is feasible since ursodiol, the bile acid medication that dissolves some cholesterol gallstones, also prevents them from forming. The difficulty is to identify individuals who are at a high risk for developing cholesterol gallstones over a relatively short period of time so that the duration of preventive treatment can be limited. One such group is obese individuals losing weight rapidly with very low calorie diets or with surgery. The risk of gallstones in this group is as high as 40% to 60%. In fact, ursodiol has been shown in several studies to be very effective at preventing gallstones in these individuals. It is important to stress that no dietary changes have been shown to treat or prevent gallstones.

Can symptoms continue after gallstones are removed?

Removal of the gallbladder (cholecystectomy) should eliminate all gallstone-related symptoms except in three situations:

  1. gallstones were left in the ducts,
  2. there were problems with the bile ducts in addition to gallstones, and
  3. gallstones were not the cause of the symptoms.

The possibility of gallstones in the ducts can be pursued with MRCP, endoscopic ultrasound, and ERCP. Rarely, gallstone-like symptoms can be caused by a condition called sphincter of Oddi dysfunction, discussed below.

The common bile duct has a muscular wall. The last several centimeters of the common bile duct’s muscle immediately before the duct joins the duodenum comprise the sphincter of Oddi. The sphincter of Oddi controls the flow of bile. Since the pancreatic duct usually joins the common bile duct shortly before it enters the duodenum, the sphincter also controls the flow of fluid from the pancreatic duct. When the muscle of the sphincter tightens, it shuts off the flow of bile and pancreatic fluid. When it relaxes, bile and pancreatic fluid again flow into the duodenum, for example, after a meal. The sphincter may become scarred, and the duct is narrowed by the scarring. (The cause of the scarring is unknown.) The sphincter also may go into spasm intermittently. In either case, the flow of bile and pancreatic fluid may intermittently stop abruptly, mimicking the effects of a gallstone causing biliary colic and pancreatitis.

The diagnosis of sphincter of Oddi dysfunction can be difficult to make. The best diagnostic test requires an endoscopic procedure with the same type of endoscope as ERCP. Instead of filling the ducts with dye, however, the pressure within the sphincter is measured. If the pressure is abnormally high, scarring or spasm of the sphincter are likely. The treatment for sphincter of Oddi dysfunction is sphincterotomy (described previously). The measurement of liver and pancreatic enzymes in the blood also may be useful in diagnosing sphincter dysfunction.

Bandages cover a patient's laparoscopic gallstone surgery scars.

What’s new with gallstones?

It is clear that genetic factors are important in determining who develops gallstones. Current scientific studies are directed at uncovering the specific genes that are responsible for gallstones. To date, 8-10 genes have been identified as being associated with cholesterol gallstones, at least in animals that develop cholesterol gallstones. Not surprisingly, the products of many of these genes control the production and secretion (by the liver) of cholesterol, bile acids, and lecithin. The long-term goal is to be able to identify individuals who are genetically at very high risk for cholesterol gallstones and to offer them preventive treatment. An understanding of the exact mechanism(s) of gallstone formation also may result in new therapies for treatment and prevention.

Surgery for gallstones has undergone a major transition from requiring large abdominal incisions to requiring only tiny incisions for laparoscopic instruments (laparoscopic cholecystectomy). It is possible that there will be another transition. Surgeons are experimenting with a technique called natural orifice transluminal endoscopic surgery (NOTES). NOTES is a new technique for accomplishing standard intraabdominal surgery, but access to the abdomen is through a natural orifice – the mouth, anus or vagina.

For NOTES, a flexible endoscopic instrument is similar to the flexible endoscopes presently being used widely is introduced through the chosen orifice, through an incision somewhere inside the orifice (for example, the stomach), and into the abdominal cavity. Thus, the only incision is within the body and not visible on the body’s surface. There are potential advantages to this type of surgery, but it is in the early stages of development, and it is unclear what the future role of NOTES will be in gallbladder surgery. Nevertheless, several series of patients have already been described who have had their gallbladders removed via NOTES primarily through the vagina.


Source: https://www.medicinenet.com/gallstones/article.htm


  • Medical Author: Jay W. Marks, MD
  • Medical Editor: Bhupinder S. Anand, MBBS, MD, DPHIL (OXON)



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gallstone is a solid crystal deposit that forms in the gallbladder, which is a pear-shaped organ that stores bile salts untilthey are needed to help digest fatty foods. Gallstones can migrate to other parts of the digestive tract and cause severepain with life-threatening complications.


Gallstones vary in size and chemical structure. A gallstone may be as tiny as a grain of sand or as large as a golf ball.Eighty percent of gallstones are composed of cholesterol. They are formed when the liver produces more cholesterol thandigestive juices can liquefy. The remaining 20% of gallstones are composed of calcium and an orange-yellow wasteproduct called bilirubin. Bilirubin gives urine its characteristic color and sometimes causes jaundice.
Gallstones are the most common of all gallbladder problems. They are responsible for 90% of gallbladder and bile ductdisease, and are the fifth most common reason for hospitalization of adults in the United States. Gallstones usuallydevelop in adults between the ages of 20 and 50; about 20% of patients with gallstones are over 40. The risk ofdeveloping gallstones increases with age-at least 20% of people over 60 have a single large stone or as many as severalthousand smaller ones. The gender ratio of gallstone patients changes with age. Young women are between two and sixtimes more likely to develop gallstones than men in the same age group. In patients over 50, the condition affects menand women with equal frequency. Native Americans develop gallstones more often than any other segment of thepopulation; Mexican-Americans have the second-highest incidence of this disease.


Gallstones can cause several different disorders. Cholelithiasis is defined as the presence of gallstones within thegallbladder itself. Choledocholithiasis is the presence of gallstones within the common bile duct that leads into the firstportion of the small intestine (the duodenum). The stones in the duct may have been formed inside it or carried there fromthe gallbladder. These gallstones prevent bile from flowing into the duodenum. Ten percent of patients with gallstoneshave choledocholithiasis, which is sometimes called common-duct stones. Patients who don’t develop infection usuallyrecover completely from this disorder.
Cholecystitis is a disorder marked by inflammation of the gallbladder. It is usually caused by the passage of a stone fromthe gallbladder into the cystic duct, which is a tube that connects the gallbladder to the common bile duct. In 5-10% ofcases, however, cholecystitis develops in the absence of gallstones. This form of the disorder is called acalculouscholecystitis. Cholecystitis causes painful enlargement of the gallbladder and is responsible for 10-25% of all gallbladdersurgery. Chronic cholecystitis is most common in the elderly. The acute form is most likely to occur in middle-aged adults.
Cholesterolosis or cholesterol polyps is characterized by deposits of cholesterol crystals in the lining of the gallbladder.This condition may be caused by high levels of cholesterol or inadequate quantities of bile salts, and is usually treated bysurgery.
Gallstone ileuswhich results from a gallstone’s blocking the entrance to the large intestine, is most common in elderlypeople. Surgery usually cures this condition.
Narrowing (stricture) of the common bile duct develops in as many as 5% of patients whose gallbladders have beensurgically removed. This condition is characterized by inability to digest fatty foods and by abdominal pain, whichsometimes occurs in spasms. Patients with stricture of the common bile duct are likely to recover after appropriatesurgical treatment.

Causes and symptoms

Gallstones are caused by an alteration in the chemical composition of bile. Bile is a digestive fluid that helps the bodyabsorb fat. Gallstones tend to run in families. In addition, high levels of estrogen, insulin, or cholesterol can increase aperson’s risk of developing them.
Pregnancy or the use of birth control pills can slow down gallbladder activity and increase the risk of gallstones. So candiabetes, pancreatitisand celiac diseaseOther factors influencing gallstone formation are:
  • infection
  • obesity
  • intestinal disorders
  • coronary artery disease or other recent illness
  • multiple pregnancies
  • high-fat, low-fiber diet
  • smoking
  • heavy drinking
  • rapid weight loss
Gallbladder attacks usually follow a meal of rich, high-fat foods. The attacks often occur in the middle of the night,sometimes waking the patient with intense pain that ends in a visit to the emergency room. The pain of a gallbladderattack begins in the abdomen and may radiate to the chest, back, or the area between the shoulders. Other symptoms ofgallstones include:
  • inability to digest fatty foods
  • low-grade fever
  • chills and sweating
  • nausea and vomiting
  • indigestion
  • gas
  • belching.
  • clay-colored bowel movements


Gallstones may be diagnosed by a family doctor, a specialist in digestive problems (a gastroenterologist), or a specialist ininternal medicine. The doctor will first examine the patient’s skin for signs of jaundice and feel (palpate) the abdomen forsoreness or swelling. After the basic physical examinationthe doctor will order blood counts or blood chemistry tests todetect evidence of bile duct obstruction and to rule out other illnesses that cause fever and pain, including stomachulcers, appendicitisand heart attacks.
More sophisticated procedures used to diagnose gallstones include:
  • Ultrasound imaging. Ultrasound has an accuracy rate of 96%.
  • Cholecystography (cholecystogram, gallbladder series, gallbladder x ray). This type of study shows how thegallbladder contracts after the patient has eaten a high-fat meal.
  • Fluoroscopy. This imaging technique allows the doctor to distinguish between jaundice caused by pancreatic cancerand jaundice caused by gallbladder or bile duct disorders.
Gallstones form in the gallbladder but can migrate to other parts of the body via the bileduct.

(Illustration by Argosy Inc.)
  • Endoscopy (ERCP). ERCP uses a special dye to outline the pancreatic and common bile ducts and locate the positionof the gallstones.
  • Radioisotopic scan. This technique reveals blockage of the cystic duct.


Watchful waiting

One-third of all patients with gallstones never experience a second attack. For this reason many doctors advise watchfulwaiting after the first episode. Reducing the amount of fat in the diet or following a sensible plan of gradual weight lossmay be the only treatments required for occasional mild attacks. A patient diagnosed with gallstones may be able tomanage more troublesome episodes by:
  • applying heat to the affected area
  • resting and taking occasional sips of water
  • using non-prescription forms of acetaminophen (Tylenol or Anacin-3)
doctor should be notified if pain intensifies or lasts for more than three hours; if the patient’s fever rises above 101 °F(38.3 °C); or if the skin or whites of the eyes turn yellow.


Surgical removal of the gallbladder (cholecystectomy) is the most common conventional treatment for recurrent attacks.Laparoscopic surgery, the technique most widely used, is a safe, effective procedure that involves less pain and a shorterrecovery period than traditional open surgery. In this technique, the doctor makes a small cut (incision) in the patient’sabdomen and removes the gallbladder through a long tube called a laparoscope.

Nonsurgical approaches

LITHOTRIPSYShock wave therapy (lithotripsyuses high-frequency sound waves to break up the gallstones. Thepatient can then take bile salts to dissolve the fragments. Bile salt tablets are sometimes prescribed without lithotripsy todissolve stones composed of cholesterol by raising the level of bile acids in the gallbladder. This approach requires long-term treatment, since it may take months or years for this method to dissolve a sizeable stone.
CONTACT DISSOLUTION. Contact dissolution can destroy gallstones in a matter of hours. This minimally invasiveprocedure involves using a tube (catheter) inserted into the abdomen to inject medication directly into the gallbladder.

Alternative treatment

Alternative therapies, like non-surgical treatments, may provide temporary relief of gallstone symptoms. Alternativeapproaches to the symptoms of gallbladder disorders include homeopathy, Chinese traditional herbal medicine, and acupunctureDietary changes may also help relieve the symptoms of gallstones. Since gallstones seem to develop moreoften in people who are obese, eating a balanced diet, exercising, and losing weight may help keep gallstones fromforming.


Forty percent of all patients with gallstones have “silent gallstones” that produce no symptoms. Silent stones, discoveredonly when their presence is indicated by tests performed to diagnose other symptoms, do not require treatment.
Gallstone problems that require treatment can be surgically corrected. Although most patients recover, some developinfections that must be treated with antibiotics.
In rare instances, severe inflammation can cause the gallbladder to burst. The resulting infection can be fatal.


The best way to prevent gallstones is to minimize risk factors. In addition, a 1998 study suggests that vigorous exercise may lower a man’s risk of developing gallstones by as much as 28%. The researchers have not yet determined whetherphysical activity benefits women to the same extent.

Key terms

Acalculous cholecystitis — Inflammation of the gallbladder that occurs without the presence of gallstones.
Bilirubin — A reddish-yellow waste product produced by the liver that colors urine and is involved in the formation ofsome gallstones.
Celiac disease — Inability to digest wheat protein (gluten), which causes weight loss, lack of energy, and pale, foul-smelling stools.
Cholecystectomy — Surgical removal of the gallbladder.
Cholecystitis — Inflammation of the gallbladder.
Choledocholithiasis — The presence of gallstones within the common bile duct.
Cholelithiasis — The presence of gallstones within the gallbladder.
Cholesterolosis — Cholesterol crystals or deposits in the lining of the gallbladder.
Common bile duct — The passage through which bile travels from the cystic duct to the small intestine.
Gallstone ileus — Obstruction of the large intestine caused by a gallstone that has blocked the intestinal opening.
Lithotripsy — A nonsurgical technique for removing gallstones by breaking them apart with high-frequency sound waves.



National Digestive Diseases Clearinghouse (NDDIC). 2 Information Way.
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). Building 31, Room 9A04, 31 Center Drive,MSC 2560, Bethesda, MD 208792-2560. (301) 496-3583. http://www.niddk.nih.gov.
Gale Encyclopedia of Medicine. Copyright 2008 The Gale Group, Inc. All rights reserved.


Round, oval or faceted masses of cholesterol, chalk (calcium carbonate), calcium bilirubinate, or amixture of these. Gallstones vary in size, from less than a millimetre to several centimetres, and are often present butunsuspected. They are commoner in women than in men and are more likely if the composition of the bile is abnormal orthere is infection or blockage of outflow of bile. They tend to cause inflammation of the gall bladder (cholecystitis) and can befragmented by LITHOTRIPSY.

Collins Dictionary of Medicine © Robert M. Youngson 2004, 2005