Gallstone Disease & Cholecystitis

Meet the patient

A 45-year-old multiparous woman arrives two hours after a roast dinner with gripping right upper quadrant pain radiating to the right scapula, nauseated, restless, unable to find a comfortable position. She is afebrile, her white count is normal, and there is no Murphy sign — yet.[1]

Two questions decide her next twelve hours, and they decide every gallstone stem you will ever meet: is the stone stuck, and where? (the cystic duct, the common bile duct, or the ampulla) and is this septic? (Charcot, Reynolds, organ dysfunction). Hold those two questions and everything below slots into place.[3][4]

The 6-hour line — colic or cholecystitis?

Six hours is the hinge of the whole topic. Biliary "colic" is misleadingly named — the pain is constant, not colicky, building 30 to 60 minutes after a fatty meal as cholecystokinin drives the gallbladder against an obstructed cystic duct. It resolves within 2 to 6 hours as the stone falls back, leaving a well patient, a normal temperature, a normal white count, and no Murphy sign.[1]

Cross the six-hour line and the picture changes: the pain persists, fever appears, the white count rises, and Murphy turns positive. That is no longer colic — it is acute cholecystitis, the gallbladder is inflamed, and the patient now needs an admission, antibiotics, and an early operation.[3]

The named number rule: the 6-hour line. Under 6 hours, no fever, no Murphy equals colic; over 6 hours, fever, Murphy equals cholecystitis. Say it as one breath in a viva and you have earned the discriminator mark.[3]

One stone, four addresses — the disease is in the postcode

The same stone causes a different disease by where it lodges. This is the single idea that organises the whole topic, and it is the examiner's favourite framing.[1]

[1]

Three anatomical terms, used precisely in every exam: cholelithiasis (stones in the gallbladder), choledocholithiasis (stones in the CBD — primary brown-pigment stones formed in the duct, or secondary stones migrated from the gallbladder), and cholecystitis (inflammation of the gallbladder wall, almost always from cystic-duct obstruction; rarely acalculous in the critically ill).[1]

Cholesterol vs pigment — the face-off

Most stones are cholesterol; the rest are pigment, and the colour tells you the cause. Classify by dominant composition, because the composition points straight at a systemic disease in the patient.[1]

[1]

The one-line discriminator: brown equals bile ducts plus bacteria. If a stone is brown, soft and laminated, think infection in the ductal system, not the gallbladder — and look for the stricture or stasis that grew the bacteria.[1]

The 5 Fs — and the risk factors beyond them

Ten to fifteen percent of adults carry gallstones; in women the lifetime risk approaches 25 to 30 percent. Prevalence climbs with age — about 10 percent at forty, 20 to 30 percent over sixty — and the female-to-male ratio is roughly 2 to 1 in the reproductive years, narrowing after menopause.[1]

The ethnic gradient is the most striking in medicine: Pima Indian women of Arizona reach up to 70 percent prevalence; Native Americans, Chileans and Northern Europeans follow; sub-Saharan Africa is lowest. Brown pigment stones predominate across East and South-East Asia, where recurrent pyogenic cholangitis (Oriental cholangiohepatitis) is endemic.[1]

Risk factors beyond the 5 Fs — the list examiners probe when the patient is not "fat, forty, female":[1]

• Rapid weight loss — very-low-calorie diets and bariatric surgery; 30 to 70 percent form stones within six months.
• Total parenteral nutrition — gallbladder stasis from gut starvation.
• Ileal disease or resection, Crohn disease — loss of the bile-acid enterohepatic pool.
• Cirrhosis — pigment (hypersplenic haemolysis) and cholesterol (altered bile-acid pool).
• Diabetes — hypertriglyceridaemia and autonomic gallbladder dysmotility.
• Drugs — OCP and oestrogen raise biliary cholesterol; ceftriaxone forms calcium-ceftriaxone sludge (usually reversible); octreotide causes gallbladder hypomotility; clofibrate.
• Spinal cord injury, and prolonged fasting or critical illness — the substrate for acalculous cholecystitis.
• Haemolytic anaemias — sickle cell, hereditary spherocytosis, beta-thalassaemia, prosthetic valves, chronic malaria (black pigment stones).[1]

How the stone forms — and why cholesterol is a bile-chemistry disease

Cholesterol gallstone disease is a bile-chemistry and gallbladder-motility disorder, not a blood-cholesterol-level problem. Hepatic bile is a micellar solution in which bile acids and lecithin keep cholesterol soluble; when the cholesterol-to-bile-acid-plus-lecithin ratio rises, bile becomes supersaturated and the cholesterol saturation index exceeds 1.[1]

Five defects converge to make a cholesterol stone:[1]

1. Cholesterol hypersecretion into bile (genetic, OCP, obesity, rapid weight loss).
2. Gallbladder hypomotility and stasis — fasting, TPN, pregnancy (progesterone), octreotide, spinal injury.
3. Accelerated nucleation — pronucleating proteins (mucin glycoprotein, IgM, aminopeptidase-N, haptoglobin) overwhelm antinucleating apolipoprotein A-I; crystals form within hours.
4. Mucus hypersecretion by goblet cells — a gel matrix that traps crystals.
5. Altered bile-acid pool (ileal disease or resection) — fewer micelles, more precipitation.[1]

Crystals aggregate on the mucin matrix over months to years into few, large, yellow, faceted stones.[1]

Black pigment stones follow a different chain: any chronic haemolytic state overloads hepatocyte glucuronidation, the surplus unconjugated bilirubin is deconjugated by tissue (non-bacterial) beta-glucuronidase, and precipitates as insoluble calcium bilirubinate polymers — small, dark, fragile, spiculated, and about half radiopaque. Brown pigment stones are the product of bacterial infection: beta-glucuronidase-producing organisms (E. coli, Klebsiella, Enterobacter, Bacteroides, Clostridium perfringens) deconjugate bilirubin and hydrolyse lecithin inside the ducts, building a soft brown laminated stone of calcium bilirubinate, palmitate soaps and bacterial cytoplasm.[1]

From stone to inflammation — acute cholecystitis

A stone impacted in the cystic duct or Hartmann pouch converts a chemical irritant into ischaemia and then infection. The mucosa keeps absorbing water from the trapped bile, concentrating bile salts and phospholipase-A2-generated lysolecithin, which inflame the wall directly (chemical cholecystitis). Venous and lymphatic outflow is impeded, the wall becomes ischaemic, and the stagnant pressurised bile is seeded by bacteria ascending from the duodenum — E. coli, Klebsiella, Enterococcus, Enterobacter and anaerobes in descending frequency.[1]

The bedside and sonographic correlate is a thickened, oedematous wall with pericholecystic fluid, a positive sonographic Murphy sign, fever and leukocytosis — the TG18 diagnostic picture.[3]

From stone to sepsis — ascending cholangitis

Ascending cholangitis is a septic emergency, not a biliary nuisance. The biliary tree is normally a low-pressure sterile conduit. A CBD stone raises intraductal pressure, disrupts hepatocyte tight junctions and canalicular membranes, and allows bacteria and endotoxin to reflux into the circulation through the cholangiovenous and cholangiolymphatic pathways.[4]

Charcot triad — fever (often with rigors), RUQ pain, and jaundice — is present in only 50 to 70 percent and is frequently incomplete in the elderly. Reynolds pentad adds hypotension or shock and confusion, defining severe (Grade III) cholangitis whose mortality climbs to 25 to 50 percent without prompt decompression. Hypothermia, thrombocytopenia, lactic acidosis and oliguria are ominous.[4]

The management sentence is plain: resuscitate, broad-spectrum IV antibiotics within the hour, and urgent ERCP biliary decompression — drainage is the only intervention that lowers mortality.[5][7]

The other presentations — colic, duct stones, ileus, Mirizzi

Biliary colic is postprandial constant RUQ or epigastric pain (radiating to the right scapula or shoulder tip via the phrenic nerve C3 to C5) that builds over an hour and resolves within 2 to 6 hours, with nausea, vomiting and diaphoresis but no fever, no Murphy and a normal white count. The patient looks entirely well between attacks.[1]

Choledocholithiasis presents as obstructive (surgical) jaundice — yellow sclera and skin, pale stools, dark urine, pruritus — with a cholestatic LFT picture (raised ALP and GGT, conjugated bilirubin). ALT may transiently exceed 1000 U/L in acute obstruction, the "AST/ALT hepatitis" of biliary obstruction that is easily mistaken for viral hepatitis. A CBD stone may also precipitate cholangitis or pancreatitis.[1]

Gallstone ileus is mechanical small-bowel obstruction in an elderly woman: a large stone (over 2.5 cm) erodes through a cholecystoduodenal fistula and lodges at the terminal ileum. The classic Rigler triad on imaging — pneumobilia, small-bowel obstruction and an ectopic gallstone — clinches it. Bouveret syndrome is the proximal variant obstructing the duodenum or proximal jejunum, producing gastric outlet obstruction.[1]

Mirizzi syndrome — a stone in Hartmann pouch or the cystic duct compresses or erodes into the adjacent common hepatic duct, producing obstructive jaundice that mimics pancreatic head cancer. Pre-operative ERCP is essential to define anatomy and avoid catastrophic bile-duct injury at cholecystectomy.[1]

Atypical groups carry the hidden cholecystitis: the elderly (vague pain, confusion, silent gangrene or empyema), the diabetic (autonomic neuropathy blunts pain; higher rates of empyema, gangrene, emphysematous cholecystitis), pregnancy (biliary colic is the commonest non-obstetric surgical emergency), the immunocompromised (acalculous cholecystitis, CMV or Cryptosporidium cholangitis), and spinal cord injury (silent stones; autonomic dysreflexia may be the only clue).[1]

The killers that mimic gallstone pain — ECG before you label it colic

Any cause of RUQ or epigastric pain is in the differential; the skill is naming the mimic that, missed, kills the patient. Three dominate every viva: inferior MI, perforated peptic ulcer, and acute pancreatitis.[1]

[1]

Bedside signs — Murphy, Boas, Charcot, Reynolds, Courvoisier

These five named signs are the viva currency of gallstone disease — know each, with its numbers.[3]

Murphy sign. Palpate under the right costal margin in the mid-clavicular line during deep inspiration; the inflamed gallbladder descends onto the hand, producing sudden pain and an arrest of inspiration. It is positive only if the same manoeuvre in the left upper quadrant does not reproduce it. Sensitivity about 65 percent, specificity 87 to 97 percent for acute cholecystitis (lower in the elderly). The sonographic Murphy sign — focal tenderness over the ultrasound-localised gallbladder — is more specific.[3]

Boas sign is hyperaesthesia in the right subscapular area or referred pain to the right shoulder, from phrenic nerve (C3 to C5) irritation by an inflamed gallbladder against the diaphragm — non-specific but a viva favourite.[1]

Charcot triad (fever, RUQ pain, jaundice) and Reynolds pentad (Charcot plus hypotension and confusion) flag cholangitis severity; both are formalised in the TG18 cholangitis criteria below.[4]

Other bedside findings: jaundice (CBD obstruction), fever and rigors (cholangitis or empyema), hypotension with tachycardia and confusion (severe sepsis — senior review, ICU), peritonism (perforation — surgical emergency), a palpable RUQ mass (empyema or mucocele), scratch marks (chronic cholestatic pruritus).[1]

Investigations — ultrasound first, then risk-stratify the duct

The strategy is ultrasound first, then risk-stratify for CBD stones with LFTs and the ASGE criteria, reserving MRCP for intermediate risk and ERCP for high risk or therapy.[1]

Laboratory: full blood count (leukocytosis over 12 to 15 in cholecystitis or cholangitis; thrombocytopenia in severe sepsis), CRP (over 30 mg/L in inflammatory complications), LFTs (a cholestatic pattern with raised ALP, GGT and conjugated bilirubin suggests CBD obstruction; ALT over 150 U/L is highly predictive of choledocholithiasis — an ASGE criterion), serum lipase (over 3 times ULN confirms pancreatitis), PT/INR (deranged in chronic cholestasis; needed before ERCP or surgery), lactate (over 2 mmol/L in severe sepsis), two sets of blood cultures before antibiotics (positive in 30 to 60 percent of cholangitis), and U&E.[1]

[1]

Tokyo Guidelines 2018 — diagnostic criteria and three grades

TG18 is the international standard for diagnosis, severity grading, antimicrobial therapy and management of both acute cholecystitis and cholangitis. Reproduce the structure exactly.[3]

Acute cholecystitis — TG18 diagnostic criteria:[3]

1. Local signs — Murphy sign, or RUQ mass, pain or tenderness.
2. Systemic signs — fever over 38 degrees C, leukocytosis, or raised CRP.
3. Imaging — characteristic findings (stones, wall thickening, pericholecystic fluid, distension, sonographic Murphy).[3]

Suspected is one local plus one systemic, or one local plus imaging, or one systemic plus imaging; definite is one feature from each of the three groups.[3]

TG18 severity grading — acute cholecystitis:[3]

• Grade III (severe) — organ dysfunction: cardiovascular (needing dopamine or noradrenaline), neurological (decreased consciousness), respiratory (PaO2 under 60 mmHg or SpO2 under 90 percent), renal (oliguria, creatinine over 2 mg/dL, about 177 micromol/L), hepatic (PT-INR over 1.5), or haematological (platelets under 100).
• Grade II (moderate) — any one of: WCC over 18, palpable tender RUQ mass, fever over 39 degrees C, symptom duration over 72 hours, or marked local inflammation (gangrenous cholecystitis, pericholecystic or hepatic abscess, biliary peritonitis).
• Grade I (mild) — does not meet Grade II or III; otherwise healthy, no organ dysfunction.[3]

Acute cholangitis — TG18 diagnostic criteria:[4]

1. Systemic inflammation — fever or rigors, abnormal WCC, abnormal CRP, or abnormal procalcitonin.
2. Cholestasis — jaundice, or abnormal LFTs (ALP, GGT, AST, ALT, bilirubin over 2 mg/dL).
3. Imaging — biliary dilation plus evidence of a cause (stricture, stone, stent).[4]

Suspected is one item from each of the three; definite adds an identified cause to cholestasis and dilation.[4]

TG18 severity grading — acute cholangitis:[4]

• Grade III (severe) — organ dysfunction requiring ICU and urgent drainage: cardiovascular (hypotension needing noradrenaline or dopamine), neurological (disturbed consciousness), respiratory (PaO2 or SpO2 under 90 percent), renal (oliguria under 0.5 mL/kg/h, creatinine over 2 mg/dL), hepatic (PT-INR over 1.5), or haematological (platelets under 100).
• Grade II (moderate) — at least two of: abnormal WCC, fever over 39 degrees C, age 75 years or older, total bilirubin 5 mg/dL or more (about 85 micromol/L), or hypoalbuminaemia (below 0.7 times the lower limit of normal).
• Grade I (mild) — not Grade II or III; initially responsive to medical therapy.[4]

[3] [4]

ASGE 2019 — who needs ERCP before cholecystectomy

Risk-stratify the CBD before you scope it; ERCP carries its own pancreatitis and bleeding risk. The ASGE 2019 tiers direct that decision.[1]

• High risk (over 50 percent — proceed to ERCP): a CBD stone seen on ultrasound; or CBD dilation over 6 mm with gallbladder in situ; or total bilirubin over 4 mg/dL (about 70 micromol/L) plus a dilated duct or other strong predictor.
• Intermediate risk (10 to 50 percent — do EUS or MRCP): abnormal liver biochemistry tests, age over 55, or CBD dilation.
• Low risk (under 10 percent — proceed directly to cholecystectomy): none of the above.[1]

Management — resuscitation by syndrome

The principle is uniform across every syndrome: analgesia, fluid resuscitation, antibiotics when there is inflammation or sepsis, and a clear plan for definitive care. The doses below are the TG18 antimicrobial standard.[5][6]

Biliary colic

• Analgesia — an NSAID first-line: diclofenac 75 mg IM (or oral or PR if mild), which relieves pain and reduces sphincter of Oddi tone. Add an opioid if severe: morphine 5-10 mg IV titrated (or fentanyl 50-100 micrograms IV); pethidine offers no proven advantage over morphine.
• Antiemetic — ondansetron 4 mg IV or metoclopramide 10 mg IV.
• Investigations — FBC, CRP, LFTs, lipase, USS.
• Disposition — discharge once pain settles, with elective surgical referral for laparoscopic cholecystectomy and safety-netting for fever, persistent pain or jaundice.[1]

Acute cholecystitis

[6] [8]

Ascending cholangitis — the septic emergency

[5] [6] [7]

Gallstone pancreatitis

• Aggressive goal-directed IV fluids (lactated Ringer preferred; about 1.5 mL/kg/h for the first 12-24 hours, titrated to haematocrit and urine output); opioid analgesia; early enteral feeding unless severe.
• ERCP within 24 hours only if cholangitis or persistent biliary obstruction — routine ERCP does not reduce complications or mortality.[9]

Empyema, gangrene, perforation

IV antibiotics, fluid resuscitation, urgent CT if perforation is suspected, and urgent percutaneous cholecystostomy (the unfit) or surgical exploration.[1]

Management — definitive, stepwise

Definitive care follows the syndrome, and one operation — laparoscopic cholecystectomy — is the answer for almost every symptomatic patient.[1]

Asymptomatic gallstones — observe, with named exceptions

Observe. No cholecystectomy, no ursodeoxycholic acid, no further imaging beyond reassurance — silent stones become symptomatic at only 1 to 4 percent per year, with a cumulative 20-year risk of about 20 percent. Prophylactic cholecystectomy is reserved for:[11]

• Sickle cell disease and other major haemolytic anaemias in children.
• Transplant candidates (heart, kidney) before immunosuppression.
• Stones over 3 cm — gallbladder carcinoma risk.
• Porcelain gallbladder — up to 25 percent carcinoma risk.
• Gallbladder polyps over 1 cm or growing polyps.
• Selected Native American or other high-risk populations, and anticipated prolonged TPN or bariatric surgery.[11][12]

Biliary colic — the elective bed

Elective laparoscopic cholecystectomy. Once symptomatic, 30 percent recur within a year and 50 percent within five years; surgery prevents progression to cholecystitis, pancreatitis and cholangitis.[1]

Acute cholecystitis — the early operation

Early laparoscopic cholecystectomy within 72 hours of symptom onset. The Lyu 2018 meta-analysis of randomised trials confirms earlier surgery gives shorter total hospital stay, fewer complications, lower readmission, and equivalent conversion and bile-duct-injury rates compared with delayed (interval) cholecystectomy.[10]

Grade III cholecystitis with organ dysfunction is managed first with urgent percutaneous cholecystostomy plus IV antibiotics, with delayed interval cholecystectomy once the patient stabilises (TG18 flowchart).[8]

The critical view of safety — the technique that prevents the preventable catastrophe

The critical view of safety (CVS) is the named technique that prevents the preventable catastrophe. Bile-duct injury during laparoscopic cholecystectomy occurs in 0.2 to 0.5 percent of cases, and the injury is devastating — stricturing cholangitis, secondary biliary cirrhosis, and a lifetime of reconstructive surgery. CVS is the single most effective measure against it.[2]

Three requirements must be met before any structure is clipped or divided:[2]

1. Clear Calot triangle — bounded by the cystic duct inferiorly, the common hepatic duct medially, and the inferior edge of the liver superiorly.
2. Identify the cystic duct and cystic artery as the only two tubular structures crossing the triangle.
3. Clear the hepatocystic triangle of all fat and fibrous tissue so the gallbladder infundibulum (Hartmann pouch) is dissected off the liver bed — confirming that what is being clipped is only the cystic duct, not the common hepatic or common bile duct.[2]

Only then are the cystic duct and artery clipped and divided. Routine intra-operative cholangiography is advocated by some units; indocyanine green fluorescence cholangiography is gaining ground as an aid. Conversion to open (overall 2 to 10 percent, higher in acute or severe disease) is mandatory if the anatomy cannot be safely defined.[2]

Choledocholithiasis, cholangitis, ileus — the non-cholecystectomy pathways

Choledocholithiasis: ERCP with sphincterotomy plus balloon or basket trawl (with mechanical lithotripsy for large stones), then laparoscopic cholecystectomy during the same admission to prevent recurrence. Expert centres may do laparoscopic CBD exploration at cholecystectomy (transcystic or choledochotomy) in one operation; an unclearable stone is bridged with a plastic or self-expanding metal biliary stent.[1]

Acute cholangitis: antibiotics plus urgent ERCP biliary decompression — within 24 hours for Grade III, 24 to 48 hours for Grade II — achieving sphincterotomy, stone removal, and a stent or endoscopic nasobiliary drain. If ERCP fails or is unavailable, percutaneous transhepatic biliary drainage, rarely surgical drainage. Cholecystectomy follows once sepsis resolves.[4][5]

Gallstone pancreatitis: supportive care as for acute pancreatitis; ERCP within 24 hours only if cholangitis or persistent obstruction; cholecystectomy during the index admission — before discharge if mild, after recovery if severe.[9]

Mirizzi syndrome: pre-operative MRCP or ERCP to define anatomy and place a stent; open or subtotal cholecystectomy with intra-operative cholangiogram; a cholecystocholedochal fistula (Csendes type II to V) may need bile-duct repair or hepaticojejunostomy.[1]

Gallstone ileus: enterolithotomy — a small longitudinal enterotomy proximal to the obstruction to milk out the stone, closed transversely; run the entire small bowel (5 to 10 percent have more than one stone). Cholecystectomy and fistula repair are usually deferred to a second stage as most fistulae close spontaneously. Emergency surgery mortality is 10 to 20 percent.[1]

Ursodeoxycholic acid (UDCA) 10-15 mg/kg/day orally for 6 to 24 months dissolves only small (under 1 cm), radiolucent, cholesterol stones in a functioning gallbladder, with 50 percent recurrence within five years — rarely first-line, reserved for the unfit. MTBE contact dissolution and ESWL are historical niches.[1]

How gallstone patients come to harm — the preventable list

• An inferior MI mislabelled as biliary colic and sent home — the preventable death of the topic. ECG the older patient with epigastric pain first.
• The "mildly unwell" elderly jaundiced patient who actually has Grade III cholangitis and is sent home without ERCP.
• Routine ERCP in gallstone pancreatitis without cholangitis or obstruction — adds pancreatitis and bleeding risk, no benefit.
• A bile-duct injury from clipping before achieving the critical view of safety — 0.2 to 0.5 percent, devastating.
• Missing gangrene, perforation, empyema or emphysematous cholecystitis in a diabetic or elderly patient who presents atypically.
• Citing Murphy sign in biliary colic — by definition absent; the label hides progression to cholecystitis.
• Stones over 3 cm or porcelain gallbladder left unoperated, progressing to gallbladder carcinoma.
• Reading Courvoisier backwards — a palpable gallbladder with jaundice is NOT stones; missing the malignancy behind it.[1][2][3][4][9][12]

Complications — by category

[1]

Special populations — thresholds and presentations change

Pregnancy. Biliary colic is the commonest non-obstetric surgical emergency (progesterone slows gallbladder emptying). First-line is conservative — NPO, IV fluids, analgesia (NSAIDs avoided in the third trimester; use paracetamol and opioid). Laparoscopic cholecystectomy is safe in the second trimester (weeks 14 to 26) for recurrent colic or acute cholecystitis, with minimal rise in preterm labour or fetal loss; defer to postpartum for a single mild stable episode. ERCP for choledocholithiasis or cholangitis uses fetal lead shielding and minimal fluoroscopy.[1]

Diabetes. Higher rates of empyema, gangrene and emphysematous cholecystitis; atypical presentation (autonomic neuropathy blunts pain). A septic, mildly symptomatic diabetic with deranged LFTs warrants aggressive imaging; lower the threshold for surgery and optimise perioperative glucose. TG18 treats diabetes as a comorbidity warranting admission and IV antibiotics for any acute cholecystitis.[1]

Cirrhosis. Increased bleeding from portal hypertension and coagulopathy. Child-Pugh A tolerates laparoscopic cholecystectomy; Child-Pugh C (mortality up to 25 percent) is a relative contraindication — prefer percutaneous cholecystostomy; subtotal cholecystectomy often avoids hilum dissection.[1]

Children. Pigment stones predominate, from haemolytic disease (sickle cell, hereditary spherocytosis, beta-thalassaemia); prophylactic cholecystectomy is recommended in sickle cell once stones are detected, and laparoscopic cholecystectomy is well tolerated.[1]

Elderly. Atypical and late presentation with more comorbidity; higher incidence of gangrene, empyema, perforation and emphysematous cholecystitis — evaluate aggressively any septic elderly patient with deranged LFTs.[1]

Post-bariatric or rapid weight loss. 30 to 70 percent form gallstones within six months; ursodeoxycholic acid 600 mg/day orally for six months reduces the risk; cholecystectomy if symptomatic.[1]

Immunocompromised. Acalculous cholecystitis and opportunistic biliary infection (CMV, Cryptosporidium, Microsporidium, MAC) — broader work-up, lower threshold for imaging.[1]

Anticoagulated. Hold warfarin pre-operatively and bridge with LMWH if high thrombotic risk; INR under 1.5 before cholecystectomy. Omit DOACs on the morning of surgery and resume once haemostasis is secure. ERCP with sphincterotomy carries bleeding risk — consider balloon dilation of the sphincter or correct anticoagulation first.[1]

Regional deltas — the framework holds, the details bend

[1]

The landmark evidence an examiner expects you to cite, and what each changed:[1]

[10] [9] [1]

Prognosis and disposition

Asymptomatic stones are benign — 1 to 4 percent per year become symptomatic, 20 percent cumulative over 20 years; most patients are never operated. Biliary colic recurs in 30 percent at one year and 50 percent at five years if untreated, with excellent outcome after cholecystectomy. Acute cholecystitis with early cholecystectomy carries mortality under 1 percent in fit adults; Grade III mortality is 10 to 30 percent. Ascending cholangitis mortality is 2 to 7 percent in mild-to-moderate disease and 25 to 50 percent in Grade III, and early ERCP halves it. Gallstone pancreatitis survival is over 95 percent if mild, up to 30 percent mortality if severe and necrotising.[3][4]

Disposition maps onto the syndrome and the grade:[1]

• Biliary colic — discharge from ED with elective surgical referral.
• Acute cholecystitis Grade I or II — surgical ward, antibiotics, early lap chole.
• Acute cholecystitis Grade III — ICU and percutaneous drain first.
• Ascending cholangitis — admit (HDU or ICU if severe), antibiotics, urgent ERCP.
• Gallstone pancreatitis, mild — surgical or medical ward, cholecystectomy before discharge.
• Gallstone pancreatitis, severe — ICU, step-up approach for necrosis.
• Gallstone ileus, perforation, empyema, emphysematous — emergency surgery.[1]

The mantra, and the pearls

The mantra: Ultrasound first; colic gets an elective bed, cholecystitis gets an early operation, cholangitis gets the scope.[1][5]

Ward-round test — three stems

Stem 1 — the septic elderly patient (answer)

A 78-year-old man is referred from the medical ward as "mildly unwell" with a low-grade fever, slight confusion attributed to his baseline, and a bilirubin of 60 micromol/L. Ultrasound shows a dilated CBD. The surgical registrar suggests fluids and antibiotics overnight and "ERCP in the morning if no better". What is the right call? Model: This is Grade III ascending cholangitis until proven otherwise — the elderly present incompletely, and confusion with any organ dysfunction crosses the line. Run the Sepsis Six, take blood cultures, give piperacillin-tazobactam 4.5 g IV every 8 hours (with or without gentamicin 5-7 mg/kg once daily), and book urgent ERCP within 24 hours for sphincterotomy, stone extraction and a stent or nasobiliary drain. Biliary decompression is the only intervention that lowers mortality; waiting for the full Reynolds pentad is how these patients die.[4][6]

Stem 2 — the elderly woman with obstruction (answer)

An 82-year-old woman presents with three days of intermittent, colicky central abdominal pain, distension and vomiting. Her abdomen is tympanic and distended. A plain abdominal X-ray shows pneumobilia and dilated small-bowel loops, and CT confirms an ectopic gallstone at the terminal ileum. Name the syndrome, the imaging triad, and the operation. Model: This is gallstone ileus — mechanical small-bowel obstruction from a large gallstone that has eroded through a cholecystoduodenal fistula and lodged at the terminal ileum. The Rigler triad is pneumobilia plus small-bowel obstruction plus an ectopic gallstone. The operation is enterolithotomy — a longitudinal enterotomy proximal to the stone to milk it out, closed transversely, then run the entire small bowel for further stones (5 to 10 percent). Cholecystectomy and fistula repair are usually deferred to a second stage as most fistulae close spontaneously; emergency surgery carries 10 to 20 percent mortality.[1]

Stem 3 — the patient from Meet the patient, four years on (answer)

The 45-year-old multiparous woman returns four years later, still with her gallstones, now with a 3.5 cm stone and a calcified gallbladder wall on ultrasound. She remains asymptomatic. Does she need an operation now? Model: Yes — she now crosses into a prophylactic cholecystectomy indication even though she is asymptomatic. Stones over 3 cm and a porcelain (calcified) gallbladder (carcinoma risk up to 25 percent) are the classic indications, because long-standing large stones and mural calcification carry a markedly raised risk of gallbladder carcinoma. The benign natural history that justified observation no longer applies; offer elective laparoscopic cholecystectomy via the critical view of safety.[11][12]

References

1. [1]Portincasa P, Moschetta A, Palasciano G. Cholesterol gallstone disease Lancet, 2006.PMID 16844493
2. [2]Wakabayashi G, Iwashita Y, Hibi T, et al. Tokyo Guidelines 2018: surgical management of acute cholecystitis: safe steps in laparoscopic cholecystectomy for acute cholecystitis (with videos) J Hepatobiliary Pancreat Sci, 2018.PMID 29095575
3. [3]Yokoe M, Hata J, Takada T, et al. Tokyo Guidelines 2018: diagnostic criteria and severity grading of acute cholecystitis (with videos) J Hepatobiliary Pancreat Sci, 2018.PMID 29032636
4. [4]Kiriyama S, Kozaka K, Takada T, et al. Tokyo Guidelines 2018: diagnostic criteria and severity grading of acute cholangitis (with videos) J Hepatobiliary Pancreat Sci, 2018.PMID 29032610
5. [5]Miura F, Okamoto K, Takada T, et al. Tokyo Guidelines 2018: initial management of acute biliary infection and flowchart for acute cholangitis J Hepatobiliary Pancreat Sci, 2018.PMID 28941329
6. [6]Gomi H, Solomkin JS, Takada T, et al. Tokyo Guidelines 2018: antimicrobial therapy for acute cholangitis and cholecystitis J Hepatobiliary Pancreat Sci, 2018.PMID 29090866
7. [7]Mayumi T, Okamoto K, Takada T, et al. Tokyo Guidelines 2018: management bundles for acute cholangitis and cholecystitis J Hepatobiliary Pancreat Sci, 2018.PMID 29090868
8. [8]Okamoto K, Suzuki K, Takada T, et al. Tokyo Guidelines 2018: flowchart for the management of acute cholecystitis J Hepatobiliary Pancreat Sci, 2018.PMID 29045062
9. [9]Tse F, Yuan Y. Early routine endoscopic retrograde cholangiopancreatography strategy versus early conservative management strategy in acute gallstone pancreatitis Cochrane Database Syst Rev, 2012.PMID 22592743
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