Gallstones — Symptoms, Causes & Treatment | MyMedicPlus

Gallstones (cholelithiasis) are solid crystalline deposits that form within the gallbladder or biliary tract when bile becomes supersaturated with cholesterol, bilirubin, or calcium salts. They affect approximately 10–15% of adults in Western populations — rising to 25% of women over 60 years old — making gallstone disease one of the most prevalent gastrointestinal conditions worldwide, with an estimated 20 million affected in the USA alone. Gallstones are classified by composition: cholesterol stones (80% of cases in Western populations — pale, faceted, often multiple) form from bile supersaturated with cholesterol relative to bile salts and lecithin; pigment stones (20%) are composed of calcium bilirubinate from excess unconjugated bilirubin and are associated with haemolytic anaemia and liver disease. Approximately 80% of gallstones remain asymptomatic ('silent gallstones') and are found incidentally on imaging. Symptomatic gallstones cause recurrent biliary colic — severe right upper quadrant pain from gallbladder contraction against a stone obstructing the cystic duct — and can progress to serious life-threatening complications including acute cholecystitis, choledocholithiasis (common bile duct stones causing jaundice), gallstone pancreatitis (the most common cause of acute pancreatitis in non-alcohol users), and ascending cholangitis, a potentially fatal biliary infection.

Cholesterol gallstones (80% in Western populations) form from bile that is supersaturated with cholesterol relative to the bile acid and lecithin content required to keep cholesterol solubilised in micellar solution. Three pathophysiological mechanisms contribute: lithogenic bile (excess biliary cholesterol secretion from hepatic upregulation of HMG-CoA reductase activity, or reduced bile acid synthesis from down-regulation of CYP7A1); gallbladder hypomotility (impaired gallbladder emptying reduces the time for cholesterol crystal nucleation to be diluted by fresh bile — a key mechanism in pregnancy, prolonged fasting, parenteral nutrition, and spinal cord injury); and accelerated cholesterol crystal nucleation (mucin glycoproteins and calcium salts act as pro-nucleating factors). Risk factors follow the '4 F's mnemonic' — Female (oestrogen increases cholesterol secretion and reduces gallbladder motility; combined oral contraceptives increase gallstone risk 2-fold), Fat (obesity — hepatic over-production of cholesterol; BMI above 30 carries 2–3-fold increased gallstone risk; paradoxically, rapid weight loss from bariatric surgery or crash dieting creates a lithogenic state from mobilisation of cholesterol into bile), Forty (gallstone prevalence rises progressively with age — 20% of women and 8% of men by age 40; 30% of women by age 60), Fertile (pregnancy — elevated progesterone reduces gallbladder contractility; gallstone incidence doubles during pregnancy; new gallstones detected in 2–4% of pregnancies). Additional risk factors: Crohn's disease and ileal resection (reduced bile acid reabsorption depletes the bile acid pool, leaving bile supersaturated with cholesterol); prolonged TPN; spinal cord injury; certain medications (ceftriaxone, octreotide, clofibrate). Pigment stones (20% — black pigment from excess unconjugated bilirubin in haemolytic anaemias; brown pigment from bile stasis and infection) are associated with cirrhosis, sickle cell disease, hereditary spherocytosis, and biliary infections.

Biliary colic is the characteristic symptom of symptomatic gallstones — a severe, constant (despite the name, not colicky — it is a sustained cramp), cramping upper right quadrant or epigastric pain caused by gallbladder smooth muscle contraction against a stone transiently occluding the cystic duct; it typically begins 30–60 minutes after a fatty meal (cholecystokinin released by fat in the duodenum triggers gallbladder contraction), builds to maximum intensity within 30–60 minutes, remains severe for 1–5 hours, and then gradually resolves — its constant (not cramping) nature distinguishes it from bowel colic. Pain radiates to the right shoulder or interscapular back in 50% of cases (referred pain via phrenic nerve/diaphragmatic irritation). Nausea and vomiting accompany most biliary colic episodes. Fever, rigors, or persistent pain beyond 6 hours suggest transition to acute cholecystitis (secondary infection and wall inflammation). Obstructive jaundice (yellowing of the skin and sclerae), dark urine (bilirubinuria), and pale stools (acholic — absent bile pigment in stool from common bile duct obstruction) indicate choledocholithiasis (stone in the common bile duct). Charcot's triad (fever, jaundice, and right upper quadrant pain) is pathognomonic of ascending cholangitis — a life-threatening biliary infection requiring emergency decompression. Reynold's pentad adds hypotension and altered consciousness — indicating septic shock from suppurative cholangitis.

Abdominal ultrasound (transabdominal) is the first-line and most cost-effective investigation for suspected gallstone disease — sensitivity above 95% for gallbladder stones (echogenic foci with posterior acoustic shadowing), 80–85% for gallbladder polyps, and 50–70% for common bile duct (CBD) stones (CBD dilation above 6 mm in the absence of cholecystectomy — above 8 mm post-cholecystectomy — is a reliable surrogate marker for CBD stones even when stones are not directly visualised). Ultrasound also assesses gallbladder wall thickness (above 3 mm indicates cholecystitis), pericholecystic fluid (acute cholecystitis), and CBD diameter. Liver function tests: elevated alkaline phosphatase (ALP) and gamma-glutamyltransferase (GGT) with or without elevated bilirubin indicate biliary obstruction from CBD stones; elevated alanine aminotransferase (ALT) and aspartate aminotransferase (AST) suggest hepatocyte injury from biliary obstruction or acute cholangitis; elevated lipase (above 3 times upper limit of normal) and amylase confirm acute pancreatitis. MRCP (magnetic resonance cholangiopancreatography): the gold standard non-invasive imaging modality for the biliary tree — provides exquisite delineation of bile duct anatomy, identifies CBD stones with sensitivity 85–92% and specificity 93–97%, detects biliary strictures, and maps ductal anatomy before surgery; replaces diagnostic ERCP (reducing procedural risk from ERCP-related pancreatitis) and guides the decision for therapeutic ERCP. EUS (endoscopic ultrasound): superior to MRCP for distal CBD stones and ampullary pathology — used when MRCP is inconclusive or unavailable. CT abdomen: not sensitive for uncomplicated gallstones (calcium content only in pigment stones) but essential for complications — perforation, abscess, acute pancreatitis severity assessment (CT severity index — modified Balthazar scoring: necrosis plus extrapancreatic complications).

Laparoscopic cholecystectomy is the definitive, gold standard treatment for symptomatic gallstones — performed in the majority of cases as a day procedure or 23-hour admission under general anaesthesia; it carries a 0.1–0.5% major complication rate (bile duct injury — the most serious: occurs in 0.3–0.5% and may require hepaticojejunostomy biliary reconstruction), 5% minor complication rate, and returns patients to normal activity within 1–2 weeks. Critical view of safety (CVS) — a standardised visual documentation of the cystic artery and cystic duct before division — is the recommended technique to minimise bile duct injury. Open cholecystectomy (Kocher right subcostal incision) is reserved for cases where laparoscopic completion is unsafe (dense adhesions, unclear anatomy, haemorrhage). ERCP (endoscopic retrograde cholangiopancreatography) with sphincterotomy and stone extraction: performed for confirmed or suspected CBD stones; the endoscope is advanced transorally into the duodenum, the ampulla of Vater is cannulated, sphincterotomy cuts the sphincter of Oddi, and stones are extracted with a Dormia basket or balloon catheter — subsequent laparoscopic cholecystectomy is performed within the same admission or within 2 weeks. Gallstone pancreatitis: ERCP with CBD stone clearance within 24–72 hours if concurrent cholangitis or persistent biliary obstruction is present; cholecystectomy during the same hospitalisation after mild gallstone pancreatitis resolves (within 3–5 days) — prevents 25–30% 4-week recurrence risk if deferred. For acute cholecystitis: IV fluids, nil by mouth, IV antibiotics (piperacillin-tazobactam or cefuroxime + metronidazole), and early laparoscopic cholecystectomy within 72 hours of symptom onset (Tokyo Guidelines 2018 — reduces conversion rate and complication rate versus interval cholecystectomy); percutaneous cholecystostomy for those unfit for surgery.

Acute cholecystitis (gallbladder inflammation from persistent cystic duct obstruction with secondary bacterial infection — Escherichia coli, Klebsiella, Enterococcus) affects 20% of symptomatic gallstone patients within 10 years — causing localised peritonitis, Murphy's sign (positive in 97% — inspiratory arrest during right subcostal palpation due to movement of the inflamed gallbladder against the examiner's hand), fever, and leukocytosis; empyema (pus-filled gallbladder) and gangrene (ischaemic wall necrosis with risk of perforation) are severe variants requiring emergency surgery. Gallstone pancreatitis — caused by a migratory stone temporarily or persistently impacting the ampulla of Vater and obstructing the pancreatic duct — is the most common cause of acute pancreatitis in the UK (40%) and the most common non-alcohol cause globally; severity ranges from mild oedematous pancreatitis (Ranson score below 3) requiring 3–5 days supportive care to severe necrotising pancreatitis with systemic inflammatory response, multiorgan failure, and 30% mortality requiring ICU care, antibiotics (prophylaxis for infected necrosis), and interventional drainage (endoscopic, percutaneous, or surgical). Ascending cholangitis: bacterial infection of the bile duct from CBD stone causing biliary stasis — presents with Charcot's triad (fever, jaundice, right upper quadrant pain) or Reynold's pentad in severe cases; requires emergency IV antibiotics and urgent biliary drainage (ERCP or percutaneous transhepatic cholangiography); mortality without drainage is 50%. Gallbladder cancer: rare but strongly associated with gallstones — long-standing gallstones (present in over 90% of gallbladder cancers), gallbladder polyps above 10 mm, and porcelain gallbladder; 5-year survival below 15% for advanced disease — prophylactic cholecystectomy for polyps above 10 mm or rapidly growing polyps is recommended.

Maintain a healthy body weight through Mediterranean dietary pattern and regular physical activity (150 minutes moderate aerobic exercise weekly) — obesity is the most important modifiable risk factor for cholesterol gallstone formation. Avoid rapid or crash dieting — weight loss above 1.5 kg/week massively increases biliary cholesterol saturation and gallstone risk; a gradual weight loss of 0.5–1 kg/week is safe. If bariatric surgery or very low calorie diet (VLCD below 800 kcal/day) is planned, ursodeoxycholic acid (UDCA) 500 mg twice daily for 6 months reduces gallstone formation by 40% in this high-risk period. Dietary measures: increase dietary fibre (soluble fibre from oat bran, legumes, and psyllium reduces biliary cholesterol saturation); reduce saturated fat and refined carbohydrates (stimulate hepatic cholesterol secretion); adequate protein intake prevents biliary stasis. Coffee consumption (4 or more cups per day): associated with 25% reduced gallstone risk — caffeine stimulates gallbladder motility and reduces biliary cholesterol saturation. Moderate physical activity is consistently associated with 20–40% reduced gallstone risk, independent of weight, through enhanced gallbladder motility and improved insulin sensitivity. Women taking oral contraceptives (particularly high-oestrogen preparations) or hormone replacement therapy (HRT) have increased gallstone risk — transdermal rather than oral oestrogen (for HRT) avoids the hepatic first-pass effect and carries lower gallstone risk.

Go to A&E or call emergency services immediately for: severe constant upper right abdominal pain lasting more than 6 hours (possible acute cholecystitis); fever above 38.5°C combined with abdominal pain and jaundice — Charcot's triad — (ascending cholangitis — a life-threatening biliary infection requiring emergency IV antibiotics and urgent ERCP drainage); sudden worsening abdominal pain spreading across the abdomen with rigidity (peritonitis from gallbladder perforation); and vomiting blood or signs of shock. See your GP or gastroenterology clinic urgently for: jaundice, pale stools, and dark urine (suggesting common bile duct stone causing obstruction); new or worsening biliary colic episodes; and any episode of suspected gallstone pancreatitis (severe upper abdominal and back pain with nausea). Known gallstone carriers who develop new or changing symptoms should not delay — gallbladder complications can deteriorate rapidly and become life-threatening.