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Biliary colic

Biliary colic is a steady or intermittent aching pain in the upper abdomen, typically in the right upper quadrant, caused by the temporary obstruction of the cystic duct or common bile duct by a gallstone, resulting in gallbladder contraction against the blockage.^[1] This condition is a common manifestation of cholelithiasis, or gallstones, which are hardened deposits of digestive fluid that form in the gallbladder.^[2] Episodes of biliary colic usually last from 30 minutes to several hours and resolve spontaneously when the stone dislodges, distinguishing it from more severe complications like acute cholecystitis.^[3] The primary cause of biliary colic is gallstones, which develop due to imbalances in bile composition, such as excess cholesterol or bilirubin, or from incomplete emptying of the gallbladder.^[2] These stones, often asymptomatic until they migrate and obstruct a duct, are triggered by gallbladder contraction, frequently after consuming fatty meals that stimulate bile release.^[1] Less commonly, biliary colic can result from biliary strictures (narrowing of the ducts due to scar tissue) or biliary dyskinesia (impaired motility of the biliary tract).^[1] Risk factors include being female, age over 40, obesity, rapid weight loss, a family history of gallstones, and certain ethnic backgrounds such as Native American or Mexican American heritage.^[4] Symptoms of biliary colic characteristically include severe, cramp-like pain that may radiate to the back or right shoulder, accompanied by nausea and vomiting, but without fever or jaundice unless complications arise.^[3] The pain often intensifies steadily and then subsides gradually, occurring episodically rather than constantly.^[2] Diagnosis typically involves a medical history, physical examination, and imaging such as abdominal ultrasound to detect gallstones and rule out other conditions like pancreatitis or peptic ulcers.^[4] Management of biliary colic focuses on symptom relief and addressing the underlying gallstones, with initial treatment including pain medications like nonsteroidal anti-inflammatory drugs (NSAIDs) and a low-fat diet to minimize gallbladder stimulation.^[1] For recurrent episodes, laparoscopic cholecystectomy (surgical removal of the gallbladder) is the definitive treatment, as it prevents future attacks and is generally safe since the gallbladder is not essential for digestion.^[4] In cases where surgery is not immediately feasible, procedures like endoscopic retrograde cholangiopancreatography (ERCP) can remove obstructing stones.^[1] Prevention strategies emphasize maintaining a healthy weight, avoiding rapid dieting, and following a balanced, low-fat diet to reduce gallstone formation risk.^[2]

Clinical presentation

Symptoms

Biliary colic is characterized by intermittent episodes of severe abdominal pain resulting from transient obstruction of the biliary tract, typically by gallstones. The pain is often described as intense, steady, cramping, or squeezing in nature, building gradually to a peak before subsiding. It is commonly located in the right upper quadrant or epigastric region, just below the breastbone, and may radiate to the back between the shoulder blades or to the right shoulder.^[1]^[3]^[5] Episodes typically last from 30 minutes to several hours, distinguishing them from shorter or more prolonged pains associated with other conditions. The pain is frequently postprandial, occurring within hours after eating, particularly large or fatty meals that stimulate gallbladder contraction and bile release. Accompanying symptoms often include nausea, vomiting, and bloating, which may exacerbate discomfort during an attack.^[1]^[6]^[5] Unlike more severe biliary disorders such as acute cholecystitis or cholangitis, biliary colic episodes lack systemic inflammatory signs, including fever, chills, jaundice, or leukocytosis. This absence helps differentiate uncomplicated biliary colic, which resolves spontaneously once the obstruction passes, from complications requiring urgent intervention.^[1]^[5]^[3] The frequency and intensity of attacks can vary among individuals, influenced by factors such as gallstone size and mobility within the biliary tree. Smaller, more mobile stones may cause more frequent but shorter episodes due to partial or intermittent obstructions, while larger stones can lead to less frequent but potentially more severe pain. Gallstones represent the primary underlying cause of these symptoms.^[1]^[5]

Physical signs

Patients with biliary colic typically present with right upper quadrant or epigastric tenderness upon palpation during physical examination.^[7]^[8] This tenderness reflects visceral pain from gallbladder contraction against an obstructing gallstone but is generally milder than in inflammatory conditions like acute cholecystitis.^[9] In some cases, deep palpation may elicit inspiratory arrest due to pain, though this is less pronounced and less specific than the classic Murphy's sign seen in cholecystitis.^[10] Notably absent are signs of peritoneal irritation, such as rebound tenderness, voluntary or involuntary guarding, or rigidity, which help differentiate uncomplicated biliary colic from peritonitis or more severe abdominal pathologies.^[11]^[7] Vital signs are usually within normal limits, with patients remaining afebrile and without tachycardia in the absence of complications.^[7]^[8] Mild abdominal distension may occasionally be observed, potentially resulting from transient ileus secondary to severe pain.^[7]

Complications

Biliary colic, characterized by transient obstruction of the cystic duct by gallstones, can progress to more severe conditions if the obstruction persists or recurs frequently. Persistent impaction of a gallstone in the cystic duct may lead to acute cholecystitis, an inflammatory response in the gallbladder wall that manifests with prolonged pain, fever, and potential bacterial superinfection.^[8] Similarly, migration of stones into the common bile duct can cause cholangitis, an ascending bacterial infection presenting with the classic triad of abdominal pain, fever, and jaundice (Charcot's triad).^[8] Another critical progression is gallstone pancreatitis, where a stone obstructs the ampulla of Vater, leading to pancreatic inflammation with severe epigastric pain radiating to the back, nausea, and elevated pancreatic enzymes.^[8] These complications arise from the underlying gallstones that initially cause the colic episodes.^[8] Recurrent episodes of biliary colic can lead to chronic cholecystitis, contributing to structural changes in the biliary system over time. This repeated inflammation can result in gallbladder fibrosis, where the organ wall thickens and loses contractility, impairing its ability to store and release bile effectively.^[8] In rare cases, chronic calcification of the gallbladder wall leads to porcelain gallbladder, a condition marked by intramural calcium deposits that historically carried a high risk of malignancy but recent analyses indicate a much lower incidence of associated gallbladder cancer, ranging from 0% to 7%.^[12] Mirizzi syndrome represents another chronic complication, occurring when a large gallstone impacts in the cystic duct or gallbladder neck, causing extrinsic compression and obstruction of the adjacent common hepatic or bile duct, which can mimic malignancy on imaging.^[13] Long-standing biliary colic, particularly in the presence of large gallstones, elevates the risk of gallbladder cancer, a rare but aggressive malignancy linked to chronic inflammation and epithelial metaplasia.^[14] The relative risk of gallbladder cancer is approximately 4.9 times higher in individuals with a history of gallstones compared to those without, with most cases (69% to 100%) associated with cholelithiasis.^[15] Sphincter of Oddi dysfunction (SOD) can also emerge, involving abnormal contraction or stenosis of the sphincter, leading to recurrent biliary-type pain or even pancreatitis due to impaired bile and pancreatic flow; this is often classified into types based on pain, liver enzyme elevations, and ductal dilation.^[16]

Etiology

Causes

Biliary colic arises primarily from the transient obstruction of the cystic duct, most commonly by gallstones that form in the gallbladder.^[3] These stones develop when bile composition becomes imbalanced, leading to precipitation and solidification of its components.^[17] The predominant type, cholesterol gallstones, accounts for approximately 80% of cases in Western populations and forms due to bile supersaturation with cholesterol. This occurs when the liver secretes excess cholesterol relative to the solubilizing capacity of bile salts and lecithin, resulting in cholesterol crystal nucleation and aggregation within the gallbladder.^[3] Factors such as reduced bile salt secretion or impaired gallbladder motility exacerbate this imbalance, promoting stone growth over time.^[17] Pigment gallstones, comprising about 20% of cases, are less frequent but contribute to biliary colic through similar obstructive mechanisms. These dark brown or black stones arise from elevated bilirubin levels in bile, often secondary to chronic hemolysis in conditions like sickle cell anemia or from biliary tract infections that increase unconjugated bilirubin.^[18] Infections can also lead to bacterial deconjugation of bilirubin, facilitating calcium salt precipitation and stone formation.^[17] Biliary sludge serves as a key precursor to gallstone development in many instances. This viscous mixture of cholesterol crystals, calcium salts, and mucin glycoproteins accumulates in the gallbladder due to bile stasis, often from prolonged fasting or impaired gallbladder emptying.^[17] Sludge can evolve into frank stones or directly cause cystic duct obstruction, initiating colic episodes.^[18] Although gallstones represent the vast majority of causes, rare non-lithiasic etiologies include tumors, strictures, or parasitic infections that directly impede cystic duct patency. For example, cholangiocarcinomas or benign strictures from prior inflammation can narrow the duct, while parasites such as Ascaris lumbricoides or Fasciola hepatica may migrate into the biliary tree, mimicking stone-related obstruction.^[19]

Risk factors

Biliary colic, resulting from transient obstruction of the cystic duct by gallstones, shares risk factors with cholelithiasis, particularly those promoting cholesterol gallstone formation. The classic mnemonic "fair, fat, female, fertile" encapsulates key demographic susceptibilities: women face a twofold to threefold higher risk than men, largely due to estrogen's influence on hepatic cholesterol secretion and gallbladder motility.^[20] Obesity, defined by a body mass index greater than 30 kg/m², elevates risk by increasing biliary cholesterol saturation and impairing gallbladder emptying, with studies showing a dose-dependent association in both sexes.^[21] Multiparity further compounds this in women, as repeated pregnancies enhance estrogen exposure and promote bile stasis.^[20] Advancing age beyond 40 years independently heightens susceptibility, with prevalence rising sharply after this threshold due to cumulative metabolic changes.^[21] Lifestyle factors significantly modulate risk, including rapid weight loss, which mobilizes cholesterol stores and induces gallbladder hypomotility, potentially increasing gallstone formation by up to fourfold during very-low-calorie diets.^[22] High-calorie diets rich in saturated fats and refined sugars contribute by elevating hepatic cholesterol output and reducing bile acid synthesis, while sedentary behavior—such as prolonged sitting or low physical activity—impairs gallbladder contractility and correlates with a 20-30% higher incidence of symptomatic gallstones.^[23]^[24] Metabolic conditions amplify vulnerability through interrelated pathways. Type 2 diabetes doubles the risk via hyperinsulinemia and altered lipid metabolism, independent of obesity.^[25] Hyperlipidemia, particularly elevated low-density lipoprotein cholesterol, promotes cholesterol supersaturation in bile, with cohort studies linking dyslipidemia to a 1.5- to 2-fold increased odds of cholelithiasis.^[21] Insulin resistance, a core feature of metabolic syndrome, directly fosters gallbladder dysmotility and stone nucleation, even in non-obese individuals.^[26] Genetic predispositions play a notable role, with variants in the ABCG5/ABCG8 genes—encoding sterol transporters—associated with heightened cholesterol absorption and biliary excretion, conferring up to a 1.5-fold risk increase.^[27] These variants are more prevalent in certain ethnic groups, such as Native Americans and admixed Latinos with Mapuche ancestry, where gallstone prevalence can exceed 70% in susceptible populations, underscoring ethnic heritability.^[28]^[29]

Pathophysiology

Mechanism of pain

Biliary colic arises from the transient occlusion of the cystic duct by a gallstone, which impedes bile flow and leads to gallbladder distension as bile accumulates within the organ.^[8] This obstruction occurs intermittently, often triggered by meals containing fats that stimulate the release of cholecystokinin (CCK), prompting the gallbladder to contract forcefully against the blockage.^[20] The resulting increase in intraluminal pressure causes stretching of the gallbladder wall, generating the characteristic visceral pain of biliary colic.^[8] The pain is mediated by visceral afferent nerve fibers, primarily unmyelinated C-fibers, which detect the mechanical stretch and distension of the gallbladder wall.^[30] These C-fibers travel via the sympathetic splanchnic nerves, forming part of the greater, lesser, and least splanchnic pathways that convey nociceptive signals from the upper abdominal viscera to the spinal cord at thoracic levels T5-T9.^[31] This neural pathway contributes to the poorly localized, cramping quality of the pain, which may radiate to the right shoulder or back due to shared dermatomal projections.^[31] Pain typically resolves spontaneously as the gallstone dislodges and passes into the duodenum or back into the gallbladder, restoring bile flow and relieving the distension, thereby accounting for the episodic nature of biliary colic attacks that last from minutes to hours.^[8] In recurrent episodes, mediators such as prostaglandins are released from the gallbladder mucosa, amplifying the nociceptive response by sensitizing afferent nerve endings and enhancing gallbladder contractility against the obstruction.^[32] This prostaglandin-mediated sensitization can intensify pain during subsequent colic events, as evidenced by the efficacy of prostaglandin synthesis inhibitors like indomethacin in rapidly alleviating biliary pain.^[33]

Biliary physiology basics

The biliary system plays a crucial role in digestion by facilitating the storage, concentration, and release of bile, a fluid essential for lipid emulsification. Hepatocytes in the liver produce approximately 600 to 1000 mL of bile daily, an alkaline solution (pH 7.5–8.1) composed primarily of water, bile salts, cholesterol, phospholipids, and bilirubin.^[34] This bile is initially secreted into canaliculi and then modified by cholangiocytes before entering the gallbladder via the cystic duct during fasting states.^[35] The gallbladder, located in the right upper quadrant and attached to the liver, serves as a reservoir that concentrates bile up to 5 to 18 times by absorbing water and electrolytes through its mucosal layer, which features microvilli to enhance surface area.^[20] Stored bile in the gallbladder becomes more acidic (pH 5.2–6.0) and is released through the cystic duct into the common bile duct when needed for digestion.^[34] This release is hormonally regulated: postprandial fatty acids and amino acids in the duodenum stimulate I-cells to secrete cholecystokinin (CCK), which induces gallbladder contraction and ejects concentrated bile toward the duodenum.^[20] Coordinated with gallbladder contraction, CCK also relaxes the sphincter of Oddi, a muscular valve at the junction of the common bile duct, pancreatic duct, and duodenum, allowing controlled bile flow into the duodenal lumen via the ampulla of Vater.^[34] In the fasting state, the sphincter remains contracted, directing bile back to the gallbladder for storage.^[20] Secretin, another hormone from duodenal S-cells, complements this by increasing bile volume through enhanced bicarbonate secretion from cholangiocytes.^[34] Bile's composition is critical for maintaining cholesterol solubility and aiding fat digestion: it contains bile salts (derived from cholesterol and conjugated with glycine or taurine, such as taurocholic acid), phospholipids (primarily lecithin), and cholesterol in proportions that form mixed micelles.^[35] These amphipathic bile salts, with hydrophilic and hydrophobic regions, emulsify lipids by solubilizing cholesterol and phospholipids into 4–8 nm micelles, preventing precipitation and enabling efficient absorption of monoglycerides, fatty acids, and fat-soluble vitamins in the intestine.^[36] Approximately 95% of bile salts undergo enterohepatic recirculation via ileal absorption, conserving their synthesis from cholesterol.^[35]

Diagnosis

Clinical evaluation

The clinical evaluation of suspected biliary colic begins with a thorough history to characterize the pain and associated features. The pain typically has a sudden onset, is steady and moderate to severe, and is localized to the right upper quadrant or epigastrium, often radiating to the back or right shoulder blade.^[9]^[8] It commonly lasts 1 to 5 hours before resolving spontaneously as the obstructing gallstone dislodges from the cystic duct, and patients may report restlessness or pacing to seek comfort during episodes.^[37]^[38] Triggers such as ingestion of fatty or greasy meals are frequently noted, as these stimulate gallbladder contraction and exacerbate obstruction.^[39]^[8] Assessment of associated symptoms is essential, including nausea, vomiting, and dyspepsia (such as bloating or indigestion), which often accompany the pain.^[39]^[37] A history of recurrent episodes is common, with more than 90% of patients experiencing further attacks within 10 years if untreated.^[9] Inquiry should also cover the timing relative to meals, absence of fever or jaundice, and any alleviating factors, though the pain is generally self-limiting without specific positional relief.^[40]^[8] Physical examination focuses on the abdomen to identify tenderness and rule out signs of peritonitis. Mild to moderate right upper quadrant tenderness may be elicited on palpation, but the patient is typically afebrile with normal vital signs and no palpable masses.^[39]^[8] Absence of rebound tenderness, involuntary guarding, or rigidity helps exclude peritoneal irritation or complications like acute cholecystitis.^[38] The patient may appear uncomfortable or diaphoretic during active pain but often normalizes after resolution.^[37] Initial laboratory tests are performed to support the diagnosis and exclude complications. In uncomplicated biliary colic, results are usually normal, including liver enzymes (such as AST and ALT), bilirubin, alkaline phosphatase, amylase, and lipase.^[39]^[38] A complete blood count may show a normal white blood cell count, though mild leukocytosis can occasionally occur without indicating infection.^[8] Elevated liver function tests or bilirubin suggest possible choledocholithiasis and warrant further investigation.^[40]

Imaging studies

Abdominal ultrasound serves as the first-line imaging modality for diagnosing biliary colic, offering high sensitivity and specificity for detecting gallstones greater than 2 mm in diameter, as well as assessing gallbladder wall thickness and common bile duct dilation.^[41] It achieves a sensitivity exceeding 95% and specificity approaching 100% for cholelithiasis in symptomatic patients, making it the preferred initial test due to its non-invasive nature, lack of radiation, and widespread availability.^[42] Findings such as mobile echogenic foci with posterior acoustic shadowing confirm gallstones, while wall thickening greater than 3 mm or duct dilation beyond 6 mm may suggest associated complications.^[43] In cases of suspected acalculous biliary colic, hepatobiliary iminodiacetic acid (HIDA) scintigraphy evaluates gallbladder function by measuring the ejection fraction after cholecystokinin stimulation.^[44] A gallbladder ejection fraction below 35-40% indicates biliary dyskinesia, supporting the diagnosis when ultrasound shows no stones but clinical suspicion persists.^[44] This functional assessment has a sensitivity of 86-96% and specificity of 90% for detecting cystic duct obstruction or motility disorders in acalculous scenarios.^[45] Computed tomography (CT) and magnetic resonance imaging (MRI), particularly MR cholangiopancreatography (MRCP), are secondary options reserved for evaluating complications such as choledocholithiasis in patients with biliary colic.^[46] CT demonstrates choledocholithiasis with 88-96% sensitivity and 88-98% specificity but is less effective for simple colic due to poorer visualization of non-calcified gallstones.^[47] MRCP provides non-invasive ductal imaging with 93% sensitivity and 96% specificity for bile duct stones greater than 5 mm, aiding in cases where ultrasound is inconclusive.^[42] Endoscopic ultrasound (EUS) is particularly valuable for identifying small gallstones or microlithiasis missed by transabdominal ultrasound, offering superior resolution in the distal common bile duct and gallbladder. It achieves 94-98% sensitivity for cholecystolithiasis and choledocholithiasis, especially for stones under 5 mm, with specificity up to 97%.^[42] EUS is recommended when standard imaging is negative but symptoms suggest persistent biliary pathology.^[41]

Differential diagnosis

Biliary colic, characterized by episodic right upper quadrant abdominal pain often postprandial, must be differentiated from other conditions presenting with similar upper abdominal discomfort to avoid misdiagnosis.^[8] Gastrointestinal disorders frequently mimic biliary colic. Peptic ulcer disease may cause epigastric pain that worsens with fasting or at night, distinguished by response to antacids and upper endoscopy findings, unlike the meal-triggered, self-resolving nature of biliary colic.^[8] Gastroesophageal reflux disease (GERD) presents with burning epigastric or chest pain exacerbated by lying down, relieved by antacids, and lacking the colicky radiation to the back seen in biliary colic.^[8] Acute pancreatitis often involves steady epigastric pain radiating to the back, accompanied by nausea and vomiting, and is differentiated by elevated serum amylase and lipase levels.^[5] Cardiac conditions such as myocardial infarction or angina can refer pain to the upper abdomen, particularly in atypical presentations. These are ruled out through electrocardiography (ECG) showing ischemic changes and elevated cardiac troponins, which are absent in biliary colic.^[1] Other mimics include renal colic from ureteric stones, which typically causes flank pain radiating to the groin with hematuria, contrasting the right upper quadrant focus and lack of urinary symptoms in biliary colic.^[8] Lower lobe pneumonia may produce right upper abdominal pain due to diaphragmatic irritation, but features respiratory symptoms like cough and fever, absent in uncomplicated biliary colic.^[1] Musculoskeletal pain, such as costochondritis, is localized and worsens with movement or palpation, differing from the visceral, steady pain of biliary colic that radiates to the shoulder.^[1] Functional disorders like irritable bowel syndrome (IBS) can cause recurrent abdominal pain but lack organic findings on imaging or labs, such as gallstones confirmed by ultrasound in biliary colic, and are associated with altered bowel habits rather than postprandial triggers.^[5]

Management

Conservative approaches

Conservative approaches to managing biliary colic emphasize non-invasive strategies to alleviate acute symptoms and promote gallbladder rest, particularly for mild episodes that are self-limiting. Initial management often involves bed rest to minimize physical activity that could exacerbate pain, allowing the body to recover without further stimulation of the biliary system.^[48] This is typically combined with fasting or a clear liquid diet during the acute phase to prevent gallbladder contraction triggered by cholecystokinin release from food intake, thereby reducing the risk of recurrent colic while the obstructing gallstone passes.^[9] Once symptoms subside, a gradual reintroduction of a low-fat diet is recommended to support ongoing gallbladder rest and prevent irritation. This dietary shift limits fat intake to approximately 25-40 grams per day, focusing on lean proteins, fruits, vegetables, and whole grains while avoiding fried foods, fatty meats, and high-cholesterol items that could provoke attacks.^[49] Applying heat to the upper right abdomen, such as with a warm compress or heating pad for 15-20 minutes, can provide symptomatic relief by relaxing smooth muscles and improving local blood flow during pain episodes.^[50] Supportive measures like antispasmodics (e.g., hyoscyamine) may be used if needed to ease spasms, alongside these non-pharmacological steps.^[9] For mild, uncomplicated cases, outpatient observation is appropriate, with patients monitored in a primary care setting to ensure resolution without progression to complications. This approach allows for self-resolution in many instances, with follow-up to assess recurrence.^[51] Adequate hydration through clear fluids like water or broth is encouraged to maintain fluid balance, especially if nausea limits intake, and short-term avoidance of dietary triggers such as high-fat meals helps prevent immediate recurrence.^[52]^[53]

Pharmacological treatments

The primary pharmacological approach to managing acute biliary colic focuses on symptom relief, particularly for pain and associated nausea. Nonsteroidal anti-inflammatory drugs (NSAIDs), such as intravenous ketorolac at a dose of 30 mg, are recommended as first-line analgesics due to their efficacy in reducing biliary pain comparable to opioids, while avoiding sphincter of Oddi contraction and minimizing adverse effects like respiratory depression.^[54]^[55] For severe pain unresponsive to NSAIDs, opioids such as meperidine may be used, though they carry risks of sedation and dependency.^[9] Antiemetics, including ondansetron at 4-8 mg intravenously, are commonly administered to alleviate nausea and vomiting, which frequently accompany biliary colic episodes.^[56]^[57] For patients unsuitable for surgery, ursodeoxycholic acid (UDCA) serves as a nonsurgical option to dissolve small cholesterol gallstones, typically administered orally at 8-10 mg/kg daily for 6-24 months to achieve partial or complete dissolution in suitable candidates.^[58] This therapy is particularly indicated for radiolucent stones less than 1 cm in diameter in functioning gallbladders.^[59] Following successful dissolution with UDCA, prophylactic administration of the drug at a reduced dose (e.g., 300 mg daily) is employed in high-risk patients to mitigate gallstone recurrence, which can occur at rates of up to 50% within five years without maintenance therapy.^[60] However, UDCA is ineffective against pigment stones or calcified calculi greater than 1 cm, and its overall success rate remains limited by high recurrence and prolonged treatment duration.^[59]^[61]

Surgical interventions

Surgical interventions are indicated for patients with recurrent episodes of biliary colic, complications such as acute cholecystitis or pancreatitis, or high-risk features including diabetes mellitus that elevate the likelihood of severe outcomes from gallstone disease.^[62]^[9]^[63] Laparoscopic cholecystectomy serves as the gold standard treatment for symptomatic cholelithiasis causing biliary colic, offering a definitive resolution by removing the gallbladder and preventing further stone formation.^[62]^[9] This minimally invasive procedure achieves symptom relief in over 90% of cases, with a low major complication rate of 1-2%, including risks such as bile duct injury (0.1-0.6%) and conversion to open surgery (2-15% in uncomplicated cases).^[64]^[65]^[62] Open cholecystectomy is reserved for situations where laparoscopic access is challenging, such as severe inflammation, extensive adhesions from prior surgery, or suspected gallbladder malignancy.^[62]^[66] This approach involves a larger incision and is associated with longer hospital stays (typically 3 additional days) and recovery periods compared to the laparoscopic method.^[9] For patients with common bile duct stones contributing to biliary colic, endoscopic retrograde cholangiopancreatography (ERCP) is employed to extract the stones endoscopically, often in conjunction with cholecystectomy to address the underlying gallbladder pathology.^[67]^[68] ERCP is particularly indicated when imaging confirms choledocholithiasis, with success rates exceeding 90% for stone clearance but carrying risks of pancreatitis or bleeding in 5-10% of procedures.^[69]^[67]

Epidemiology

Prevalence and incidence

Biliary colic represents the primary symptomatic presentation of cholelithiasis, occurring when gallstones intermittently obstruct the cystic duct. Globally, the prevalence of gallstones is estimated at approximately 6% among adults, though rates are higher in developed countries, ranging from 10% to 20% due to dietary and lifestyle factors such as high-fat intake and obesity.^[70]^[71] Recent US surveys show gallstone prevalence increasing from 7.4% in the late 1980s to 13.9% as of 2020, reflecting rising obesity rates.^[72] Autopsy studies in Western populations have reported even higher figures, with gallstone prevalence reaching 20-30% in individuals over 60 years, particularly among women.^[73]^[8] Among those with gallstones, only a subset develop symptoms annually; the incidence of biliary colic is 1-4% per year in asymptomatic stone carriers.^[74] This risk escalates with advancing age, with annual incidence rates in Western populations increasing from about 0.2% in those under 40 years to 1.4% in those over 60.^[75] In the United States, gallstone disease affects roughly 20 million individuals, with symptomatic presentations such as biliary colic occurring in a subset (approximately 20-30%), and approximately 335,000 emergency department visits annually for uncomplicated cases.^[8]^[76] The majority of gallstone cases (up to 80%) remain asymptomatic, contributing to underreporting in population-based studies, as biliary colic often emerges as the first clinical manifestation in 20-30% of affected patients.^[77]^[78]

Demographic patterns

Biliary colic, a manifestation of symptomatic gallstone disease, exhibits a marked predominance in women, with a female-to-male ratio of approximately 2:1 in affected populations.^[79] This disparity is attributed to hormonal influences, particularly estrogen, which promotes cholesterol saturation in bile. The condition peaks in incidence post-menopause, as prolonged exposure to female hormones during reproductive years contributes to gallstone formation, though risk remains elevated thereafter due to cumulative factors like obesity.^[15] Multiparous women face even higher susceptibility, with each additional pregnancy increasing the likelihood through repeated exposure to progesterone and estrogen, which impair gallbladder motility.^[80] Ethnic variations in biliary colic are pronounced, reflecting genetic and environmental influences on gallstone prevalence. Among Native American populations, particularly the Pima Indians, gallstone disease affects 60-70% of adult women, representing one of the highest rates globally and leading to frequent episodes of biliary colic.^[81] In contrast, prevalence is substantially lower among individuals of African descent, ranging from 5-10% in sub-Saharan African cohorts, where dietary and genetic factors contribute to reduced cholesterol gallstone formation.^[82] These disparities underscore the role of ancestry in disease susceptibility, with admixed Hispanic populations showing intermediate rates. Age is a key determinant, with biliary colic being rare in individuals under 20 years, comprising less than 1% of cases, and incidence rising sharply after age 40 as gallbladder function declines and metabolic changes accumulate.^[83] In developing nations, urban residents experience higher rates than rural counterparts, driven by lifestyle shifts toward sedentary behavior and Westernized diets that promote obesity.^[84] Socioeconomic patterns link biliary colic to affluent Western societies, where obesity epidemics—prevalent in higher-income groups—exacerbate gallstone risk through altered lipid metabolism and insulin resistance.^[71] In these settings, the condition correlates with elevated body mass index, a modifiable factor amplified by access to calorie-dense foods and reduced physical activity.^[85]

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keeping a diary of food and symptoms to help you identify trigger foods; avoiding fatty foods and excess oils when cooking as these make the gallbladder squeeze ...Symptoms · Treatment · Home Care<|control11|><|separator|>
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Obesity has broadly been described as the main risk factor of GD; mainly women with a BMI higher than 30 have twice the risk of developing gallstones.Missing: colic socioeconomic Western