Biliary Colic



Richard K Gilroy, MBBS, FRACP, Associate Professor, Medical Director of Liver Transplantation and Hepatology, Department of Internal Medicine, Kansas University Medical Center

Nothing to disclose.


Jean Frederick Botha, MBBCh, FCS(SA), Assistant Professor of Surgery, Transplant Surgeon, Department of Surgery, University of Nebraska Medical Center

Nothing to disclose.

Sandeep Mukherjee, MB, BCh, MPH, FRCPC, Associate Professor, Department of Internal Medicine, Section of Gastroenterology and Hepatology, University of Nebraska Medical Center; Consulting Staff, Section of Gastroenterology and Hepatology, Veteran Affairs Medical Center

Nothing to disclose.

Specialty Editor(s)

Alex J Mechaber, MD, FACP, Associate Dean for Undergraduate Medical Education, Associate Professor of Medicine, University of Miami Miller School of Medicine

Nothing to disclose.

Anil Minocha, MD, FACP, FACG, Clinical Professor, School of Pharmacy, Professor of Medicine, Director of Digestive Diseases, Medical Director of Nutrition Support, Medical Director of Gastrointestinal Endoscopy, Internal Medicine Department, University of Mississippi Medical Center

Nothing to disclose.

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine

eMedicine Salary Employment

James L Achord, MD, Professor Emeritus, Department of Medicine, Division of Digestive Diseases, University of Mississippi School of Medicine

Nothing to disclose.

Chief Editor

Julian Katz, MD, Clinical Professor of Medicine, Drexel University College of Medicine; Consulting Staff, Department of Medicine, Section of Gastroenterology and Hepatology, Hospital of the Medical College of Pennsylvania

Nothing to disclose.


Biliary colic is a symptom of discomfort and is often not accompanied by any clinical signs. It represents one of the causes of epigastric pain. It is the most common presentation of symptomic gallstone disease (cholelithiasis/choledocholithiasis). Because this is a symptom, numerous other disease processes may result in pain that is similar to biliary colic, and, certainly, biliary colic is not the most common cause of epigastric pain. For this reason, other disease processes should be considered during the evaluation of patients being considered to have biliary colic. (See image belows and Images 1, 3.)

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Mechanism of biliary colic.

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Gallbladder stones.

Careful history and examination are cornerstones to making an accurate clinical diagnosis, essentially because of the high incidence of gallstones in the population and because most gallstones are asymptomatic. The potential disastrous implications of a misdiagnosis as biliary colic instead of alternative diagnoses that may present with epigastric pain (eg, atypical myocardial ischemia) cannot be overemphasized. Patients also can be particularly unhappy and frustrated when their pain is not resolved following cholecystectomy. The differential diagnosis section lists other important medical conditions one should consider in patients who present with possible biliary colic (see Differentials).

History should elicit the nature, intensity, location, duration, onset, cessation, associated factors, aggravating factors, relieving factors, radiation, and frequency (NILDOCARRF) of the pain (see History). The pain of biliary colic is listed inaccurately as a colic. This term implies a paroxysmal pain that waxes and wanes, when, in actuality, the pain of biliary colic is generally a constant and slowly progressive pain. The pain generally follows a meal and may wake up a person several hours later. In fact, pain immediately with a meal is not characteristic of biliary colic.

It is important while taking the history that one evaluates the risk factors for stone formation, addresses and excludes other potential causes for the pain, and concurrently evaluates medical comorbidities that may influence management (eg, cardiovascular disease).

This visceral pain is believed to result from impaction of a gallstone in the cystic duct and/or ampulla of Vater. The resulting impaction causes distension of the gallbladder and/or biliary tract, and this distension activates visceral afferent sensory neurons. The resultant pain is commonly localized poorly and generally refers midline to the representative dermatomes T8/9 (mid epigastrium, right upper quadrant), although it may radiate to the right upper quadrant. Localized pain or persistent pain generally represents a complication of cholelithiasis or choledocholithiasis (eg, cholecystitis, cholangitis, pancreatitis).

Biliary colic is the presenting symptom in 80% of patients with gallstone disease who seek medical care; however, only 10-20% of all individuals with gallstones experience severe gallstone pain. The risk of developing biliary pain or stone-related complications in asymptomatic patients is low, at 1-2% per year. For this reason, clinical practice favors treatment of only symptomatic disease, with the exception of a few unique circumstances. Two thirds of patients presenting with their first attack of biliary colic have recurrent pain within 2 years.

Nonpain symptoms that may be associated with biliary colic are inconsistently relieved with cholecystectomy (approximately 44%) and are more likely relieved in the presence of gallstones than in acalculous disease.

Fatty food intolerance (fatty dyspepsia) is not a symptom of biliary colic.


A gallstone produces visceral pain by obstructing the cystic duct or ampulla of Vater, resulting in distention of the gallbladder or biliary tree. Pain is relieved when the gallstone migrates back into the gallbladder, passes through the ampulla, or falls back into the common bile duct (CBD). The pain of biliary colic may accompany sphincter of Oddi spasm. (See image below and Image 2.)

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Potential sites of gallbladder stones.



United States

Asymptomatic individuals with gallstones develop pain at an annual rate of 1-4%, with approximately 10% of individuals developing symptoms in 10 years and 20% developing symptoms in 20 years.


Limited international data appear to support a similar incidence of biliary colic in all populations with gallstones. The incidence of gallstones is greater in some races and cultures than in others.


By definition, uncomplicated gallstone disease is not associated with signs or symptoms of systemic disease, such as fever, jaundice, or leukocytosis. Patients with uncomplicated gallstone disease experience self-limited pain. Presentation is associated with only limited morbidity and never mortality, despite some patients' perception of the severity of pain and its significance. The frequency of progression to acute cholecystitis is 10-30%. Ibuprofen use may decrease the likelihood of progression.


In the United States, the prevalence of gallstone disease is highest among Hispanic Americans and Native Americans, especially the Pima Indians of Arizona, with 75% of women developing cholesterol gallstones by early adulthood.


Biliary colic is more common in women than in men, primarily related to the 2- to 3-fold increased incidence of cholelithiasis in women.


The incidence of biliary colic depends on the incidence of gallstones. For this reason, the condition is rare in patients younger than 20 years and increases with age, occurring in approximately 2-4% of men older than 60 years and approximately 3-8% of age-matched women.


Note that, in general, there is no clear association between the presence of gallstones and upper abdominal pain.[1]



The risk factors for cholelithiasis have been outlined in the eMedicine article Cholelithiasis.

A postulate explaining the greater nocturnal occurrence of biliary colic pain concerns the biliary anatomy. The horizontal lie of the gallbladder upon recumbency (sleeping) is believed to predispose patients to stone migration and subsequent impaction.

Laboratory Studies

Imaging Studies


Histologic Findings

Cholecystectomy specimens often show changes consistent with chronic cholecystitis (see Cholecystitis). Gallstones are found in most surgical specimens.

Medical Care

Supportive measures are indicated for patients with uncomplicated biliary colic, with symptoms usually resolving within 2-3 hours. Continuous or recurrent symptoms despite analgesia likely herald a complication of gallstone disease, most commonly acute cholecystitis.

Surgical Care

No acute surgical intervention is warranted because uncomplicated biliary colic resolves with conservative treatment.


Early surgical consultation is appropriate if symptoms do not resolve in the expected time frame. Persistent symptoms suggest the possibility of acute cholecystitis. In those in whom a diagnosis is established and symptoms resolve, elective consultation is appropriate.


During the acute attack, patients typically are anorectic. After resolution of the attack, some authors favor avoidance of high-fat meals. Controlled data are lacking to support this approach, and a liberal healthy diet is not unreasonable. A diet to prepare an individual for surgery is advised (eg, weight reduction in patients who are obese).


Bed rest usually is recommended until the pain resolves; patients may resume full activity thereafter.

Medication Summary

NSAIDs and/or opiate agonists are used to provide pain relief. Nausea is treated with antiemetics and intravenous fluids for consequent dehydration.

Class Summary

Pain control is essential to quality patient care. NSAIDs have analgesic, anti-inflammatory, and antipyretic activities. They are used for mild to moderate pain. Their mechanism of action is unknown, but they may inhibit cyclooxygenase activity and prostaglandin synthesis. Other mechanisms may exist (eg, inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, various cell membrane functions). Opioid analgesics act at the CNS mu receptors. They are inexpensive and have proven effective.

Meperidine (Demerol)

Clinical Context:  Analgesic with multiple actions similar to those of morphine; may produce less constipation, smooth-muscle spasm, and depression of cough reflex than equal analgesic doses of morphine.

Hydromorphone (Dilaudid)

Clinical Context:  Potent semisynthetic opiate agonist similar in structure to morphine. Approximately 7- to 8-times as potent as morphine on mg-to-mg basis, with shorter or similar duration of action (ie, 4-5 h).

Ibuprofen (Motrin, Advil, Ibuprin)

Clinical Context:  Indicated for patients with mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.

Ketorolac (Toradol)

Clinical Context:  Inhibits prostaglandin synthesis by decreasing activity of cyclooxygenase, which results in decreased formation of prostaglandin precursors.

Class Summary

The CNS vomiting center (VC) may be stimulated directly by GI irritation. Increased activity of central neurotransmitters, dopamine in the chemoreceptor trigger zone, or acetylcholine in the VC appears to be a major mediator for inducing vomiting. Antidopaminergic agents (eg, metoclopramide, phenothiazines) are effective for nausea due to GI irritation.

Metoclopramide (Reglan)

Clinical Context:  Dopamine antagonist that stimulates acetylcholine release in the myenteric plexus. Acts centrally on chemoreceptor triggers in the floor of the fourth ventricle, which provides important antiemetic activity.

Prochlorperazine (Compazine)

Clinical Context:  May relieve nausea and vomiting by blocking postsynaptic mesolimbic dopamine receptors through anticholinergic effects and depressing reticular activating system.

Ondansetron (Zofran)

Clinical Context:  5-HT-3 receptor antagonist used when other classes fail or are contraindicated.

Further Inpatient Care

Further Outpatient Care

Inpatient & Outpatient Medications





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Mechanism of biliary colic.

Gallbladder stones.

Potential sites of gallbladder stones.


HIDA (or gallbladder) scan.

HIDA (or gallbladder) scan.

HIDA (or gallbladder) scan.