Gallstones

Solid deposits, primarily of cholesterol or bilirubin, that form within the gallbladder and can obstruct biliary flow, causing biliary colic, cholecystitis, or other complications.

1. Definition

Cholelithiasis literally means "chole" (bile) + "lith" (stone) + "iasis" (condition) — the formation of stones within the gallbladder.

Choledocholithiasis adds "choledocho-" (common bile duct) — stones within the common bile duct (CBD). The vast majority of CBD stones are secondary, meaning they form in the gallbladder and then migrate through the cystic duct into the CBD. Primary CBD stones (forming de novo within the duct) are uncommon in Western populations but notably more common in Asia, particularly in the context of Recurrent Pyogenic Cholangitis (RPC) ^[1]^[2].

The clinical importance of gallstones lies in their spectrum of presentation:

~80% are asymptomatic — discovered incidentally on imaging ^[2].
~3% of asymptomatic patients become symptomatic per year ^[1].
~2/3 of asymptomatic patients remain symptom-free over 20 years ^[1].
Once symptomatic, patients tend to have recurrent bouts of biliary colic.
< 5% of symptomatic patients develop complications per year ^[1].

The complications of gallstones — acute cholecystitis, choledocholithiasis, acute cholangitis, gallstone pancreatitis, Mirizzi syndrome, gallstone ileus, and gallbladder carcinoma — form a huge chunk of hepatobiliary surgery and are extremely high-yield for exams.

Courvoisier's Law

In painless obstructive jaundice with a palpable (enlarged) gallbladder, the cause is unlikely to be gallstones. Why? A gallbladder that has harboured stones undergoes repeated episodes of cholecystitis → fibrosis → contracted, non-distensible wall. So when a CBD obstruction occurs (e.g., from a stone), the gallbladder cannot distend. A palpable gallbladder in this setting therefore suggests a non-stone cause (e.g., periampullary tumour — pancreatic head cancer, cholangiocarcinoma, ampullary carcinoma) ^[2].

Exceptions to Courvoisier's Law: (i) Double impaction — stone simultaneously in cystic duct and distal CBD; (ii) Mirizzi syndrome; (iii) RPC ^[2].

Saint's Triad = Gallstones + Hiatal hernia + Colonic diverticulosis (three common conditions co-existing in obese, Western-diet patients — not causally linked but frequently seen together) ^[2].

2. Epidemiology

Factor	Detail
Prevalence	10–15% of adults in developed countries; lower in Africa/Asia but rising with westernization of diet
Sex	Female:Male ≈ 3:1 (oestrogen effect)
Age	Increases with age; peak incidence in 40s–60s
Geography (HK-relevant)	Cholesterol stones predominate overall, but brown pigment stones are relatively more common in Hong Kong/SE Asia due to higher prevalence of biliary parasites and RPC ^[1]^[2]
Asymptomatic	~80% remain asymptomatic ^[2]
Complications	< 5% of symptomatic patients/year develop complications ^[1]

3. Risk Factors

The classic mnemonic is the "5 Fs": Fat, Female, Forty, Fertile, Family ^[1]^[2].

3.1 Cholesterol Stones (85% of all gallstones)

Category	Risk Factor	Mechanism
Demographics	Female sex	Oestrogen ↑ hepatic HMG-CoA reductase → ↑ cholesterol secretion into bile; also ↓ bile salt secretion
	Age > 40 ("Forty")	Cumulative cholesterol supersaturation over time
	Pregnancy ("Fertile")	Progesterone ↓ gallbladder motility → stasis; oestrogen ↑ cholesterol secretion
	Obesity ("Fat")	↑ Cholesterol synthesis and biliary secretion
	Family history	1st degree relative → 2× risk; genetic polymorphisms in cholesterol transporters (ABCG5/G8)
Medical	Rapid weight loss / bariatric surgery	Mobilisation of body cholesterol + gallbladder stasis from low caloric intake
	Diabetes mellitus	Autonomic neuropathy → impaired GB emptying; ↑ cholesterol saturation of bile
	Liver cirrhosis	Impaired bile salt synthesis → ↑ cholesterol-to-bile-salt ratio
	Crohn's disease / ileal resection	Loss of terminal ileum → ↓ bile salt reabsorption → ↓ bile salt pool → supersaturation
	TPN / prolonged fasting	No CCK stimulus → gallbladder stasis ("JCCK" — no food, no CCK) ^[2]
Drugs	OCP / HRT (oestrogen)	Same mechanism as pregnancy
	Fibrates	↑ Biliary cholesterol secretion
	Octreotide	↓ GB motility

3.2 Pigment Stones (15% of all gallstones)

Type	Risk Factor	Mechanism
Black pigment	Chronic haemolysis (thalassaemia, hereditary spherocytosis, sickle cell disease, G6PD deficiency)	↑ Unconjugated bilirubin production → supersaturation of calcium bilirubinate in bile
	Chronic liver disease / cirrhosis	Impaired conjugation of bilirubin
Brown pigment	Biliary infection / parasites (E. coli, Klebsiella, Clonorchis sinensis, Ascaris lumbricoides)	Bacterial β-glucuronidase deconjugates bilirubin glucuronide → unconjugated bilirubin precipitates with calcium → calcium bilirubinate stones ^[1]^[2]
	Biliary stasis / strictures / RPC	Stasis predisposes to bacterial colonisation and stone formation
	Low-protein diet (historically in SE Asia)	Relative enzyme deficiency → ↑ deconjugation of bilirubin ^[2]

Hong Kong Context

Brown pigment stones and RPC ("Hong Kong disease") are disproportionately important in the local exam setting. These stones form de novo within the intrahepatic ducts (not the gallbladder), driven by parasitic/bacterial infection → β-glucuronidase → unconjugated bilirubin → calcium bilirubinate precipitation. The left intrahepatic ducts are preferentially affected ^[2].

4. Anatomy & Function of the Biliary System

Understanding biliary anatomy is essential to understanding where stones get stuck and what symptoms they cause.

4.1 Gallbladder Anatomy

The gallbladder is a pear-shaped, muscular sac sitting on the undersurface of the liver (segments IVB and V).

Part	Description	Clinical Significance
Fundus	Blind-ended tip, projects beyond the liver edge at the tip of the 9th costal cartilage (intersection with lateral border of rectus abdominis)	Palpable when distended; site of Murphy's sign localisation
Body	Main storage area	Concentrates bile 5–10× by active absorption of water and electrolytes
Infundibulum (Hartmann's pouch)	Outpouching at the junction of body and neck	Most common site of gallstone impaction → biliary colic, Mirizzi syndrome ^[1]^[2]
Neck	Narrow, S-shaped, continuous with cystic duct	Transition zone to cystic duct

4.2 Cystic Duct

Contains the spiral valves of Heister — mucosal folds that resist distension and regulate bile flow (not true valves).
Joins the common hepatic duct (CHD) to form the common bile duct (CBD).
Normal CBD diameter: ≤ 6 mm (add 1 mm per decade over 60; post-cholecystectomy up to 10 mm is acceptable) ^[3].

4.3 Calot's Triangle (Hepatobiliary Triangle)

Border	Structure
Medial	Common hepatic duct
Inferior	Cystic duct
Superior	Inferior surface of the liver (segment V)

Contents: Cystic artery (branch of right hepatic artery), cystic lymph node (node of Lund/Calot), connective tissue, sometimes an accessory hepatic duct.

Critical View of Safety (CVS)

During laparoscopic cholecystectomy, the surgeon must achieve the Critical View of Safety before clipping any structure: (1) Calot's triangle is cleared of fat and fibrous tissue; (2) The lower third of the gallbladder is separated from the liver bed; (3) Only two structures should be seen entering the gallbladder (cystic duct and cystic artery). This prevents misidentification and inadvertent CBD injury — the most feared complication of cholecystectomy.

4.4 Sphincter of Oddi

Muscular sphincter at the ampulla of Vater controlling flow of bile and pancreatic juice into the duodenum.
Acts as a mechanical barrier to ascending duodenal infection — disruption (e.g., post-sphincterotomy, stent placement) predisposes to cholangitis ^[1].

4.5 Biliary Physiology

Hepatocytes secrete ~600 mL of bile/day.
Between meals, the sphincter of Oddi is closed → bile diverted into the gallbladder via the cystic duct.
Gallbladder concentrates bile by absorbing water and electrolytes (up to 10-fold).
After a meal (especially fatty), duodenal I-cells release cholecystokinin (CCK) → gallbladder contracts + sphincter of Oddi relaxes → bile flows into the duodenum.
Bile salts emulsify fats for absorption; they are reabsorbed in the terminal ileum and recycled to the liver via the portal vein (enterohepatic circulation).

Why does a fatty meal trigger biliary colic? Fat in the duodenum → CCK release → gallbladder contraction against an obstructed cystic duct (stone in Hartmann's pouch/cystic duct) → ↑ intraluminal pressure → visceral pain.

5. Pathophysiology of Gallstone Formation

5.1 Cholesterol Stone Formation

The formation of cholesterol stones requires three key defects (the "lithogenic triad"):

Supersaturation: Cholesterol is insoluble in water. It is kept in solution by bile salts and phospholipids forming mixed micelles. When cholesterol secretion exceeds the solubilising capacity → supersaturated ("lithogenic") bile → cholesterol crystals precipitate.
Nucleation: Pronucleating factors (mucin glycoproteins secreted by gallbladder epithelium, calcium salts, prostaglandins) accelerate crystal aggregation. Antinucleating factors (apolipoprotein A-I, A-II) inhibit it. The balance determines whether crystals form.
Gallbladder stasis: Impaired gallbladder emptying allows crystals to remain and grow rather than being flushed into the duodenum.

5.2 Pigment Stone Formation

Black Pigment Stones

Formed within the gallbladder.
Composed of calcium bilirubinate + calcium carbonate + calcium phosphate polymerized into a hard, jet-black stone.
Pathophysiology: ↑ unconjugated bilirubin in bile (from chronic haemolysis or impaired hepatic conjugation) → supersaturation → precipitation with calcium.
Radiopaque (due to calcium content) — unlike cholesterol stones.

Brown Pigment Stones

Formed within the bile ducts (intrahepatic or CBD) — this is the key distinction.
Composed of calcium bilirubinate + bacterial cell bodies + fatty acid soaps.
Pathophysiology: bacterial infection (E. coli, Klebsiella) → bacterial β-glucuronidase hydrolyses conjugated bilirubin glucuronide → unconjugated bilirubin + glucuronic acid → unconjugated bilirubin precipitates with calcium ^[1]^[2].
Parasitic infection (Clonorchis sinensis, Ascaris lumbricoides) causes epithelial damage → bacterial translocation → same cascade ^[2].
Radiopaque but softer and more friable than black stones.

6. Classification of Gallstones

6.1 By Composition

Feature	Cholesterol Stones	Black Pigment Stones	Brown Pigment Stones
Frequency	~85% (Western)	~10%	~5% (but higher in Asia)
Composition	> 70% cholesterol by weight	Calcium bilirubinate polymers	Calcium bilirubinate + bacterial debris
Location of formation	Gallbladder	Gallbladder	Bile ducts (intra/extrahepatic)
Radiolucency	Radiolucent (< 10% radiopaque)	Radiopaque	Radiopaque (soft)
Colour	Yellow-green, greasy	Jet black, hard	Earthy brown, soft, friable
Associated conditions	Obesity, oestrogen, Western diet	Chronic haemolysis, cirrhosis	Biliary infection/parasites, RPC
Sterile vs infected	Sterile	Sterile	Infected
Multiplicity	Often multiple, faceted	Multiple, small	Few, large, soft

6.2 By Location (Clinical Classification)

Location	Term	Key Clinical Consequence
Gallbladder	Cholelithiasis	Biliary colic, acute/chronic cholecystitis
Cystic duct	Cholelithiasis	Biliary colic, acute cholecystitis, Mirizzi syndrome
CBD	Choledocholithiasis	Obstructive jaundice, cholangitis, gallstone pancreatitis
Intrahepatic ducts	Hepatolithiasis	RPC, cholangiocarcinoma
Ampulla of Vater	Choledocholithiasis	Gallstone pancreatitis, cholangitis

7. Possible Clinical Presentations of Gallstones — Overview

This is the roadmap. Gallstones can present in many ways depending on where the stone lodges and what it obstructs ^[2]:

8. Clinical Features

8.1 Asymptomatic Gallstones

The majority (80%) — found incidentally on USG, CT, or at laparotomy ^[2].
Risk of future complications: 1–4% per year ^[2].
Generally managed conservatively (watchful waiting) unless specific indications for prophylactic cholecystectomy exist (see Management section later).

8.2 Biliary Colic (Uncomplicated Symptomatic Gallstones)

Mechanism: Gallbladder contracts (usually post-prandially, triggered by CCK) against a stone transiently impacted in Hartmann's pouch or the cystic duct → ↑ intraluminal pressure → visceral pain via splanchnic afferents ^[1]^[2].

Feature	Detail	Pathophysiological Basis
Site	RUQ / epigastric / substernal	Visceral afferents from the gallbladder travel with splanchnic nerves to T7–T9 → referred to the epigastrium/RUQ
Onset	Abrupt	Sudden impaction of stone
Character	Steady, intense, dull, constant — NOT truly colicky (the name is misleading!)	The gallbladder and cystic duct lack peristalsis, so there are no rhythmic waves of pain — it is a sustained contraction against a fixed obstruction ^[2]
Radiation	Right shoulder / right scapula / interscapular	Referred pain via the phrenic nerve (C3–C5) from diaphragmatic peritoneal irritation, or via splanchnic afferents to T7–T9 dermatomes
Duration	≥ 30 min, plateaus within 1 hour, subsides < 6 hours	If > 6 hours → suspect acute cholecystitis ^[1]^[2]
Timing	After a fatty meal; can wake patient from sleep	Fatty meal → CCK → gallbladder contraction
Associated	Sweating, nausea, vomiting	Vagal stimulation from visceral pain
NOT exacerbated by	Movement	It is visceral pain, not parietal peritoneal — no somatic component
NOT relieved by	Squatting, bowel movements, passage of flatus	Distinguishes from colonic/rectal pathology
Between attacks	Patient feels completely well	Transient obstruction self-resolves → stone falls back into GB

Key distinction: Biliary colic is episodic — discrete attacks with completely well intervals. If pain becomes continuous > 6 hours with fever and localised tenderness → think acute cholecystitis ^[1]^[2].

Exam Trap: 'Biliary Colic' is NOT Colicky

Despite its name, biliary colic is a steady, constant pain — not the waxing-and-waning "colicky" pain seen in ureteric or intestinal colic. This is because the gallbladder and cystic duct have no peristalsis — so the pain is from sustained distension against a fixed obstruction, not from rhythmic muscular contractions ^[2].

Investigations for Biliary Colic:

USG gallbladder: Gold standard — hyperechoic stone with posterior acoustic shadowing, gravity-dependent (rolling stone sign when patient turns lateral) ^[2]^[3].
AXR: Only ~15% of gallstones are radiopaque (pigment stones). May see Mercedes-Benz sign (gas in fissures of stone) — low sensitivity.
Bloods: CBC, LFT (should be normal in uncomplicated biliary colic — if cholestatic pattern, think choledocholithiasis), amylase/lipase (rule out pancreatitis) ^[2].

8.3 Acute Cholecystitis

Definition: Acute inflammation of the gallbladder ^[3].

Pathology: Obstruction of cystic duct → complication of gallstone disease → chemical inflammation → bacterial infection ^[3].

8.3.1 Acute Calculous Cholecystitis (90–95%)

Mechanism: Prolonged gallstone impaction at Hartmann's pouch / cystic duct → stagnant bile → gallbladder distension (mucocele/hydrops) → concentrated bile salts cause chemical inflammation (first 48 hours) → secondary bacterial infection (E. coli, Klebsiella, Strep faecalis) ^[2]^[3].

Symptoms:

Symptom	Detail	Pathophysiological Basis
Pain	Starts as biliary colic but more constant, longer > 6 hours	Persistent obstruction → ongoing distension + inflammation → transition from visceral to parietal peritoneal pain
Fever + chills	Low-grade initially, may spike with secondary infection	Chemical then bacterial inflammation → systemic inflammatory response
Nausea / vomiting	Common	Vagal stimulation, ileus from peritoneal inflammation

Signs:

Sign	Detail	Pathophysiological Basis
Murphy's sign	Inspiratory arrest during deep palpation of RUQ — the inflamed gallbladder descends with inspiration and contacts the examiner's hand, causing pain and reflex inspiratory arrest	Parietal peritoneal inflammation overlying the inflamed gallbladder fundus
RUQ tenderness with guarding	Localised peritonism	Inflammation extending to parietal peritoneum
Low-grade fever	37.5–38.5°C typically	Inflammatory cytokines
Tachycardia	In proportion to fever / pain	Sympathetic response

USG findings — 5 cardinal signs of acute cholecystitis ^[2]:

Presence of gallstones
Distended GB ( > 4 × 10 cm)
GB wall thickening > 3 mm
Pericholecystic fluid / stranding (from wall oedema)
Sonographic Murphy sign (maximal tenderness when USG probe pressed directly over the GB)

If USG is inconclusive:

HIDA scan (hepatobiliary iminodiacetic acid): Non-visualisation of the gallbladder (because radiotracer cannot enter through the obstructed cystic duct) = positive for acute cholecystitis. Sensitivity ~95%.
MRCP with morphine augmentation: Morphine ↑ sphincter of Oddi pressure → forces bile into the gallbladder; non-filling confirms cystic duct obstruction ^[2].

8.3.2 Acute Acalculous Cholecystitis (5–10%)

Mechanism: Microvascular occlusion within the gallbladder wall → ischaemia → inflammation and infection, NOT associated with gallstones ^[1]^[2].

Classically occurs in critically ill / hospitalised patients: ICU patients, those on TPN, extensive burns, sepsis, major operations, multiple trauma, prolonged illness with multi-organ dysfunction ^[1]^[2].
Risk factors: Dehydration, shock (systemic hypoperfusion), TPN (no CCK stimulation → stasis) ^[2].
Clinical presentation is similar to calculous cholecystitis (fever, RUQ pain, leucocytosis) but with higher mortality ^[2].
Management: Laparoscopic cholecystectomy or gallbladder drainage (percutaneous cholecystostomy) if unfit for surgery ^[1]^[2].

8.3.3 Complications of Acute Cholecystitis

Complication	Mechanism	Clinical Features
Gallbladder empyema	Persistent cystic duct obstruction + purulent bacterial infection → pus fills the gallbladder	Tender RUQ mass + septic-looking patient, high swinging fever ^[2]
Gangrenous cholecystitis (20%)	Continued distension → ↓ mural blood flow → ischaemic necrosis of gallbladder wall	Worsening sepsis, may paradoxically have decreased pain (nerve necrosis)
Perforation → biliary peritonitis	Necrotic GB wall ruptures (less common as usually wrapped by omentum)	Generalized peritonitis, haemodynamic instability
Emphysematous cholecystitis	Secondary infection with gas-forming organisms (e.g., Clostridium welchii/perfringens)	Insidious onset, abdominal crepitus; gas in GB wall on imaging ^[2]
Cholecystoenteric fistula + gallstone ileus	Chronic inflammation → GB wall erodes into adjacent bowel (usually duodenum) → stone passes into bowel → mechanical SBO	See gallstone ileus section below

8.4 Chronic Cholecystitis

Mechanism: Recurrent acute cholecystitis or persistent mechanical irritation by gallstones → chronic inflammatory infiltrate → fibrosis and thickening of GB wall ^[1]^[2].

Symptoms:

Repeated attacks of biliary colic with well intervals.
Vague dyspepsia, fat intolerance, bloating (less specific).

Signs:

Often minimal between attacks.
Contracted, thick-walled gallbladder on USG.

Complications:

CA gallbladder — chronic inflammation → dysplasia → carcinoma sequence ^[2].
Porcelain gallbladder: Calcification of GB wall due to extensive scarring. Carries 2–3% risk of malignancy → absolute indication for cholecystectomy even if asymptomatic ^[1]^[2].
Typhoid carrier state: Gallbladder infected by Salmonella typhi → chronic carriage in bile ^[2].

USG findings: Contracted gallbladder with wall thickening and gallstones ^[2].

8.5 Choledocholithiasis (CBD Stones)

Mechanism: Gallstones migrate from the gallbladder through the cystic duct into the CBD → obstruction of bile flow → upstream biliary dilatation.

Symptoms ^[1]:

Symptom	Detail	Pathophysiological Basis
Jaundice	Most common manifestation — yellowish discolouration of skin/sclera	Obstructed bile flow → conjugated bilirubin refluxes into blood → deposited in tissues
	Transient jaundice if stone temporarily impacts ampulla then moves	"Ball-valve" effect at the ampulla
	Progressive jaundice if stone completely impacts	Complete CBD obstruction
RUQ / epigastric pain	More prolonged > 6 hours than typical biliary colic	Stone in CBD causes sustained obstruction; resolves when stone passes or is removed
Dark urine ("coca-cola urine")		Conjugated bilirubin (water-soluble) filtered by kidneys
Pale/clay-coloured stools		No bilirubin reaching the gut → no stercobilinogen
Pruritus		Bile salt deposition in skin
Nausea / vomiting		Vagal stimulation

Signs:

Jaundice (scleral icterus first — albumin in sclera has high affinity for bilirubin).
RUQ tenderness (variable).
Cholestatic LFT pattern: ↑ ALP, ↑ GGT, ↑ conjugated bilirubin; AST/ALT may be mildly elevated.
Dilated CBD on USG ( > 6 mm, or > 10 mm post-cholecystectomy).

8.6 Acute Cholangitis

Mechanism: Biliary obstruction + stasis → bacterial infection of the biliary tract ^[1]^[2]. Obstruction alone causes obstructive jaundice; bacteria alone without obstruction are usually cleared. It is the combination that produces cholangitis ^[1].

Normal biliary defences (all of which must be overwhelmed) ^[1]:

Continuous flushing action of bile flow
Bacteriostatic activity of bile salts
Biliary mucous + secretory IgA (anti-adherence factors)
Sphincter of Oddi — mechanical barrier to ascending duodenal bacteria

Bacteriology ^[1]^[2]:

Gram-negative rods: E. coli (most common), Klebsiella pneumoniae, Enterobacter sp., Pseudomonas (especially if stent in situ)
Gram-positive: Enterococcus sp.
Anaerobes: Bacteroides fragilis

Clinical Features:

Feature	Pathophysiological Basis
Charcot's triad (present in 50–70%) ^[2]: Fever + RUQ pain + Jaundice	Infection → fever; obstruction → jaundice and upstream pressure → pain
Reynolds' pentad ( < 10%) ^[2]: Charcot's triad + Hypotension + Altered mental status	Biliary sepsis → septic shock → end-organ hypoperfusion including cerebral

Charcot's Triad vs Reynolds' Pentad

Charcot's triad = the classic triad of acute cholangitis (Fever + Jaundice + RUQ pain). Present in only ~50–70% of cases.

Reynolds' pentad = Charcot's triad + hypotension + altered mental status → indicates suppurative cholangitis with septic shock — a life-threatening emergency requiring urgent biliary decompression. Present in < 10% of cases ^[1]^[2].

8.7 Gallstone Pancreatitis

Mechanism: Gallstone migrates to the ampulla of Vater → transient or persistent obstruction → reflux of bile into the pancreatic duct → premature activation of pancreatic enzymes (trypsinogen → trypsin) → autodigestion of pancreatic parenchyma ^[1]^[4].

Gallstones are the most common cause of acute pancreatitis (55%) ^[4].

Clinical Features ^[1]^[2]:

Feature	Detail	Pathophysiological Basis
Epigastric pain	Severe, constant, radiating to the back, improves with leaning forward	Pancreas is retroperitoneal → pain referred to the back; leaning forward reduces stretch on retroperitoneal structures
Nausea / vomiting	Prominent	Inflammation + ileus
Fever	Due to chemical inflammation (not necessarily infection)	SIRS response from cytokine release
Cullen's sign	Periumbilical bruising	Retroperitoneal haemorrhage tracking along the falciform ligament to the umbilicus ^[2]
Grey Turner's sign	Flank bruising	Retroperitoneal haemorrhage tracking to the flanks ^[2]
Fox's sign	Inguinal ligament bruising	Retroperitoneal haemorrhage tracking inferiorly
Tetany	Transient hypocalcaemia	Fat saponification: lipase → fat necrosis → release of fatty acids → precipitate with calcium → ↓ serum calcium ^[2]

8.8 Mirizzi Syndrome

Mechanism: Common hepatic duct (CHD) obstruction caused by extrinsic compression from a stone impacted in Hartmann's pouch or the cystic duct ^[1]^[2].

Feature	Detail
Presentation	Fever, jaundice, RUQ pain — may mimic cholangitis or cholecystitis
Key sign	Jaundice with palpable gallbladder — an exception to Courvoisier's Law ^[2]
Chronic inflammation	May erode into the bile duct wall → cholecystobiliary fistula (cholecystohepatic or cholecystocholedochal) ^[1]^[2]
Association	CA gallbladder — recurrent inflammation + biliary stasis ^[1]^[2]

Csendes Classification ^[1]^[2]:

Type	Description
I	External compression of CHD, no fistula
II	Fistula involving < 1/3 of CBD circumference
III	Fistula involving 1/3–2/3 of CBD circumference
IV	Fistula involving > 2/3 of CBD circumference (complete destruction)
V	Any type + cholecystoenteric fistula (5A: no gallstone ileus; 5B: with gallstone ileus) ^[2]

8.9 Gallstone Ileus

Mechanism: Chronic cholecystitis → gallstone erodes through the GB wall into adjacent bowel through a cholecystoenteric fistula (most commonly cholecystoduodenal) → large stone ( > 2.5 cm) passes through the bowel → impacts at the narrowest point of the small bowel (terminal ileum, ~2 feet proximal to the ileocaecal valve) → mechanical small bowel obstruction ^[2].

Bouveret's Syndrome: A variant where the stone impacts in the duodenum or stomach, causing gastric outlet obstruction (GOO) ^[2].

Clinical Features: Features of distal small bowel obstruction — colicky abdominal pain, vomiting (may be faeculent), abdominal distension, absolute constipation.

Investigations:

AXR: Rigler's triad ^[2]:
1. Pneumobilia (air in biliary tree — through the cholecystoenteric fistula)
2. Small bowel obstruction
3. Ectopic gallstone (usually in RIF, at ileocaecal valve)
CT abdomen: Gallbladder wall thickening + Rigler's triad — much more sensitive than AXR.

Other causes of pneumobilia (DDx on AXR): Emphysematous cholecystitis, post-ERCP, post-cholecystectomy, blunt abdominal trauma, sphincter of Oddi incompetence ^[2].

8.10 Gallbladder Cancer

Covered briefly here as a complication of chronic gallstone disease:

95% of patients with gallbladder carcinoma have gallstones — one of the strongest risk factors ^[1].
Risk factors ("4P") ^[2]: Polyps ( > 1 cm), Porcelain gallbladder, Primary sclerosing cholangitis, Pancreatobiliary duct anomalous junction (a/w choledochal cyst).
Female predominance (M:F = 1:2–3) ^[1].
Very poor prognosis: most discovered late and unresectable at diagnosis — 5-year OS < 5% ^[2].
Spreads via direct invasion (liver segments IV and V), lymphatics (cystic duct node → pericholedochal → hilar → coeliac/SMA nodes), and haematogenous (lung, peritoneum) ^[1].

8.11 Recurrent Pyogenic Cholangitis (RPC)

Also called "Hong Kong disease" / Oriental cholangiohepatitis ^[1]^[2].

Mechanism: Parasitic infestation (e.g., Clonorchis sinensis from raw freshwater fish) → biliary epithelial damage → bacterial translocation → stricture formation → biliary stasis → bacterial β-glucuronidase → deconjugation of bilirubin → brown pigment stone formation de novo within intrahepatic ducts → cycle of obstruction, infection, and further stone formation ^[1]^[2].

Feature	Detail
Age/Sex	Middle-aged, equal M:F
Location	Usually starts in left intrahepatic ducts ^[2]
Stone type	Brown pigment (calcium bilirubinate) — NOT cholesterol
Clinical	Recurrent episodes of acute cholangitis (Charcot's triad) — 1–2 episodes/year ^[2]
Complications	Biliary sepsis, liver abscess, pancreatitis, cirrhosis (chronic biliary obstruction), cholangiocarcinoma ^[2]

9. Summary Table: Symptomatic Gallstones at a Glance

	Biliary Colic	Acute Cholecystitis	Choledocholithiasis	Acute Cholangitis
Mechanism	Stone transiently stuck at Hartmann's pouch / cystic duct	Inflammation of GB due to gallstone / biliary sludge	Migration of gallstones into CBD	Bacterial infection secondary to CBD obstruction
Pain	RUQ, < 6h	RUQ, > 6h	RUQ, > 6h	RUQ
Fever	No	Yes	±	Yes (with rigors)
Jaundice	No	Usually No	Yes	Yes
Murphy's sign	No	Yes	No	No
Labs	Normal	↑ WBC, CRP	Cholestatic LFT (↑ALP, ↑GGT, ↑bilirubin)	↑ WBC, CRP + cholestatic LFT
Imaging	USG: stone + shadow	USG: 5 cardinal signs	USG: dilated CBD + stone	USG: dilated CBD + stone
Management	Elective LC	Resuscitation, IV antibiotics, LC	Supportive, biliary decompression, LC	Resuscitation, IV antibiotics, biliary decompression, LC

High Yield Summary

Gallstones are classified by composition: Cholesterol (85%, radiolucent), Black pigment (haemolysis, radiopaque), Brown pigment (infection/parasites, radiopaque, form in ducts).
5Fs: Fat, Female, Forty, Fertile, Family — risk factors for cholesterol stones.
80% of gallstones are asymptomatic; 3%/year become symptomatic.
Biliary colic = steady (NOT colicky) RUQ pain < 6h after fatty meal, no fever, no jaundice, self-resolving.
Acute cholecystitis = pain > 6h + fever + Murphy's sign; 5 USG cardinal signs (gallstones, distended GB, wall thickening > 3mm, pericholecystic fluid, sonographic Murphy's sign).
Choledocholithiasis = obstructive jaundice + cholestatic LFT + dilated CBD on USG.
Charcot's triad (Fever + Jaundice + RUQ pain) = acute cholangitis; Reynolds' pentad adds hypotension + AMS = suppurative cholangitis / septic shock.
Gallstone pancreatitis = most common cause of acute pancreatitis (55%); epigastric pain radiating to back.
Courvoisier's Law: Painless jaundice + palpable GB = unlikely gallstones (think periampullary tumour).
Mirizzi syndrome: CHD obstruction by stone in Hartmann's pouch; Csendes classification (Types I–V).
Gallstone ileus: Rigler's triad = pneumobilia + SBO + ectopic gallstone.
RPC ("Hong Kong disease"): Brown pigment stones forming de novo in intrahepatic ducts (usually left); parasites → β-glucuronidase → unconjugated bilirubin → calcium bilirubinate stones.
Porcelain gallbladder = absolute indication for cholecystectomy (risk of GB carcinoma).

Active Recall - Gallstones

1. Name the three types of gallstones, their composition, radiolucency, and where they form.

Your answer

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Cholesterol (>70% cholesterol, radiolucent, form in GB); Black pigment (calcium bilirubinate polymers, radiopaque, form in GB, assoc. with haemolysis); Brown pigment (calcium bilirubinate + bacterial cell bodies, radiopaque, form in bile ducts, assoc. with infection/parasites/RPC).

2. A patient presents with RUQ pain lasting 2 hours after a fatty meal, no fever, and normal bloods. What is the diagnosis, and why is the name misleading?

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Biliary colic. Name is misleading because pain is STEADY/CONSTANT, not colicky — the gallbladder and cystic duct lack peristalsis so there are no rhythmic contractions.

3. List the 5 cardinal USG signs of acute cholecystitis.

Your answer

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1. Gallstones present; 2. Distended GB (>4x10cm); 3. GB wall thickening >3mm; 4. Pericholecystic fluid/stranding; 5. Sonographic Murphy sign.

4. What is Courvoisier's Law? Name three exceptions.

Your answer

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In painless obstructive jaundice with a palpable gallbladder, the cause is unlikely gallstones (fibrosed GB cannot distend). Exceptions: double impaction, Mirizzi syndrome, RPC.

5. Explain the pathophysiology of brown pigment stone formation in RPC.

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Parasitic/bacterial infection of bile ducts causes epithelial damage and bacterial translocation. Bacteria (E. coli, Klebsiella) produce beta-glucuronidase which deconjugates bilirubin glucuronide to unconjugated bilirubin. Unconjugated bilirubin precipitates with calcium to form calcium bilirubinate (brown pigment) stones. Stasis and strictures perpetuate the cycle.

6. What is Rigler's triad and in what condition is it seen?

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Rigler's triad: pneumobilia + small bowel obstruction + ectopic gallstone — seen in gallstone ileus (stone erodes through cholecystoenteric fistula, impacts at terminal ileum).

References

^[1] Senior notes: felixlai.md (Gastrointestinal Diseases — Cholelithiasis, Choledocholithiasis, Acute Cholangitis, Mirizzi Syndrome, Gallbladder Cancer, Acute Pancreatitis, RPC sections) ^[2] Senior notes: maxim.md (Gallstone Diseases, Biliary Colic, Acute Cholecystitis, Mirizzi Syndrome, Gallstone Ileus, RPC, Acute Cholangitis, Acute Pancreatitis, GB Carcinoma sections) ^[3] Lecture slides: GC 200. RUQ pain, jaundice and fever Cholecytitis and cholangitis Imaging of GI system.pdf ^[4] Lecture slides: Acute pancreatitis.pdf

Differential Diagnosis of Gallstones

The differential diagnosis of gallstones must be approached systematically because gallstones themselves present in many different ways — and at each presentation (RUQ pain, jaundice, cholangitis, pancreatitis), there is a different differential list. The key clinical skill is to determine (1) is this gallstone-related or not? and (2) if gallstone-related, which specific gallstone complication is it?

Think of the differential as concentric circles: first, distinguish among the various gallstone presentations themselves (biliary colic vs. cholecystitis vs. choledocholithiasis vs. cholangitis vs. pancreatitis), and second, distinguish gallstone disease from non-gallstone conditions that mimic it.

1. The Clinical Problem: Where Does the Stone Sit?

Before considering non-gallstone diagnoses, you must first differentiate within the gallstone spectrum, because the management is radically different:

The key differentiating features among gallstone presentations themselves were covered in detail in the Clinical Features section. The summary table below is useful for rapid ward-round differentiation ^[1]^[2]:

Feature	Biliary Colic	Acute Cholecystitis	Choledocholithiasis	Acute Cholangitis	Gallstone Pancreatitis
Pain duration	< 6h	> 6h	> 6h	Variable	Hours–days
Fever	No	Yes	±	Yes (with rigors)	Yes (chemical)
Jaundice	No	Usually No	Yes	Yes	±
Murphy's sign	No	Yes	No	No	No
Labs	Normal	↑WBC, CRP	Cholestatic LFT	↑WBC + cholestatic LFT	↑ Amylase/lipase ≥ 3× ULN
Key imaging	USG: stone + shadow	USG: 5 cardinal signs	USG: dilated CBD	USG: dilated CBD	CT (if severe)

2. Differential Diagnosis by Presenting Complaint

The DDx changes depending on how the patient walks in. Let's go through each major presentation.

2.1 DDx of RUQ Pain (Biliary Colic / Acute Cholecystitis Presentation)

This is the most common exam scenario: a patient with RUQ pain after a fatty meal. The differential is broad because many structures occupy or refer pain to the RUQ.

Category	Condition	How to Differentiate from Gallstones
Biliary	Gallbladder polyps (adenoma, cholesterolosis, adenomyomatosis)	USG: polyps are not gravity-dependent and have no posterior acoustic shadow (unlike stones which are gravity-dependent with shadowing) ^[1]^[2]^[5]
	Sphincter of Oddi dysfunction	Pain < 6h, intermittent; normal laboratory and radiological tests; diagnosed by manometry ^[1]
	Functional gallbladder disorder	Pain < 6h, intermittent; normal laboratory and radiological tests; diagnosed by HIDA with CCK-stimulated ejection fraction < 35% ^[1]
Hepatic	Acute hepatitis (viral, alcoholic, drug-induced)	Markedly ↑ AST/ALT (hepatocellular pattern, NOT cholestatic); history of viral exposure, alcohol, drugs; USG: no stones, may show hepatomegaly
	Liver abscess (pyogenic or amoebic)	Swinging fever, tender hepatomegaly; USG/CT: hypoechoic/hypodense lesion in liver parenchyma; travel history (amoebic) ^[1]
	Hepatocellular carcinoma	Chronic liver disease background; AFP elevated; CT: arterial enhancement with portal venous washout
Gastroduodenal	Peptic ulcer disease (gastric/duodenal ulcer)	Epigastric burning, meal-related (DU relieved by food, GU worsened); OGD diagnostic; perforation → pneumoperitoneum on erect CXR ^[1]
Pancreatic	Acute pancreatitis	Epigastric pain radiating to the back, improves leaning forward; ↑ amylase/lipase ≥ 3× ULN; gallstones may be the cause (gallstone pancreatitis is both a complication of gallstones AND a differential for RUQ pain) ^[1]
Intestinal	Acute appendicitis (retrocaecal/high appendix)	Pain typically starts periumbilical then migrates to RIF; McBurney's point tenderness; CT: inflamed appendix with periappendiceal fat stranding ^[1]
Pulmonary/Cardiac	Right lower lobe pneumonia	Cough, sputum, pleuritic chest pain referred to RUQ; CXR: consolidation in RLL ^[1]
	Pleurisy	Pleuritic pain, friction rub; CXR may show effusion
	Myocardial infarction (inferior MI)	Epigastric pain, diaphoresis, nausea; ECG: ST changes in II, III, aVF; troponin elevated ^[1]
Renal	Right renal colic	Loin-to-groin pain, haematuria; CT KUB: ureteric stone; differentiated from gallstone on lateral AXR view (renal stone is posterior, gallstone is anterior) ^[2]
Musculoskeletal	Costochondritis / intercostal pathology	Reproducible with palpation of chest wall; no peritoneal signs

The Dangerous Mimics

Two conditions that mimic biliary colic but carry life-threatening consequences if missed:

Inferior myocardial infarction — can present as pure epigastric/RUQ pain with nausea and vomiting, especially in elderly/diabetic patients. Always do an ECG in anyone with upper abdominal pain.
Right lower lobe pneumonia — diaphragmatic irritation refers pain to the RUQ. Always get an erect CXR in any patient with RUQ pain and fever ^[1].

2.2 DDx of Obstructive Jaundice (Choledocholithiasis Presentation)

When a patient presents with jaundice + cholestatic LFT, you must differentiate stone from tumour because the management diverges completely. The lecture slides emphasise: "Painless progressive obstructive jaundice in the elderly is malignant biliary obstruction until proven otherwise" ^[3]^[5].

The differential of obstructive jaundice is classically organised by the anatomical relationship to the bile duct wall ^[3]:

Location	Cause	Key Distinguishing Features
Intraluminal	Choledocholithiasis	Intermittent/fluctuating jaundice, colicky pain, history of gallstones; USG: stone in CBD
	RPC (Recurrent Pyogenic Cholangitis)	SE Asian patient, recurrent cholangitis episodes, intrahepatic ductal dilatation with stones, left lobe predominance ^[1]^[2]
Mural (wall of duct)	Cholangiocarcinoma	Painless progressive jaundice; perihilar (Klatskin) → early jaundice; CA19-9 ↑; MRCP: stricture without stone ^[3]^[5]
	Primary sclerosing cholangitis (PSC)	Young male with IBD (especially UC); multifocal strictures + dilatation ("beading" on MRCP); ↑ ALP; p-ANCA +ve ^[1]
Extramural (extrinsic compression)	CA head of pancreas	Painless progressive obstructive jaundice; palpable gallbladder (Courvoisier's sign); double duct sign on CT (dilated CBD + pancreatic duct); weight loss; new-onset DM ^[5]^[6]
	Periampullary carcinoma	Jaundice + melaena (ulceration into duodenum); ampullary tumour visible on duodenoscopy at ERCP
	Lymphadenopathy (porta hepatis nodes)	History of lymphoma, metastatic disease; CT: enlarged nodes compressing CBD
	Mirizzi syndrome	Gallstone at Hartmann's pouch compressing CHD extrinsically; jaundice with palpable GB (exception to Courvoisier's Law); biliary dilatation above level of GB neck with normal CBD below ^[1]^[2]

Differentiating stone vs tumour at the bedside — the critical clinical question ^[3]:

Feature	Gallstone (Benign)	Malignant Biliary Obstruction
Pain	Present (colicky/RUQ)	Painless (or dull, progressive)
Jaundice pattern	Fluctuating / intermittent	Progressive, unrelenting
Fever	Common (cholangitis)	Uncommon (unless stent-related)
Weight loss	Uncommon	Marked
Palpable GB	Not palpable (fibrosed from chronic cholecystitis)	Palpable (Courvoisier's Law)
Age	Any age	Elderly
History	Previous biliary colic / stones	May have new-onset DM, back pain

Imaging approach ^[5]: Ultrasound / CT is first-line for obstructive jaundice to determine: (i) size of bile duct (dilated = obstructive), (ii) level of obstruction (intrahepatic vs hilar vs distal), (iii) cause of obstruction (stone vs mass), and (iv) other associated features (staging for malignant disease; complications for benign disease e.g., gallstones) ^[5].

2.3 DDx of Fever + Jaundice + RUQ Pain (Cholangitis Presentation)

When the patient presents with Charcot's triad or Reynolds' pentad, the differential includes ^[1]:

Condition	How to Differentiate
Acute cholangitis (from choledocholithiasis)	Most common cause; dilated CBD with stone on USG; cholestatic LFT + leucocytosis
RPC	SE Asian patient; intrahepatic pigment stones; strictures on MRCP; recurrent episodes ^[1]^[2]
Acute cholecystitis with choledocholithiasis	Murphy's sign positive; GB wall thickening on USG; CBD may also be dilated
Liver abscess (pyogenic / amoebic)	Swinging fever; USG/CT: focal intrahepatic collection; blood cultures may grow gut organisms; no biliary dilatation unless secondary ^[1]
Infected choledochal cyst	Young patient (usually < 10y); RUQ mass + pain + jaundice + fever; USG: cystic dilatation of bile duct; MRCP for anatomy ^[5]
Biliary leaks (post-surgical)	History of recent biliary surgery; biloma on imaging
Acute pancreatitis	May coexist; epigastric pain radiating to back; ↑ amylase/lipase ^[1]
Acute hepatitis	Hepatocellular LFT pattern (AST/ALT > > ALP); viral serology positive
Malignant biliary obstruction with secondary infection	Progressive jaundice → superimposed infection (especially post-stent); mass on CT; CA19-9 elevated ^[3]^[5]

2.4 DDx of Acute Pancreatitis

When gallstone pancreatitis is suspected, you must exclude other causes of acute pancreatitis. The mnemonic GAME ID is useful ^[2]:

Letter	Cause	Clue
G	Gallstones (MC — 55%) ^[4]	History of biliary colic; ↑ ALP; stones on USG
A	Alcohol (35%) ^[4]	History of binge drinking; ↑ AST; MCV elevated
M	Metabolic (hypertriglyceridaemia, hypercalcaemia)	Lipid panel; calcium level
E	ERCP (post-procedural)	Within 24h of ERCP
I	Idiopathic (10%)	Diagnosis of exclusion
D	Drugs (NSAIDs, steroids, azathioprine, valproate)	Drug history
	Others: trauma, infections (mumps), autoimmune (SLE), tumours, pancreatic divisum	Context-dependent

3. DDx of Gallbladder Polyps vs Gallstones on USG

This is a specific but commonly tested differentiation ^[2]^[5]:

Feature	Gallstone	Gallbladder Polyp
Gravity dependence	Yes — moves with position change (rolling stone sign)	No — fixed to wall
Posterior acoustic shadow	Yes	No
Shape	Variable	Sessile or pedunculated
Vascularity on Doppler	None	May show flow

Why does this matter?

Polyps ≥ 1 cm carry significant malignant potential (up to 46% if 1.5 cm) and are an indication for cholecystectomy even if asymptomatic. Gallstones alone without symptoms can be observed. The USG characteristics above are how you tell them apart ^[2]^[5].

4. Important Principles to Distinguish Pre-hepatic, Hepatic, and Obstructive Jaundice

This is foundational to the differential diagnosis of any jaundice and highly relevant when a patient with "gallstones" presents with yellow skin ^[3]:

Feature	Pre-hepatic (Haemolysis)	Hepatic (Hepatocellular)	Post-hepatic (Obstructive)
Bilirubin type	Unconjugated	Mixed	Conjugated
Urine colour	Normal	Dark	Tea-coloured (conjugated bilirubin is water-soluble → filtered by kidneys)
Stool colour	Normal/dark	Variable	Pale / clay-coloured (no bilirubin reaching gut)
Pruritus	No	±	Yes (bile salt deposition in skin)
LFT pattern	↑ unconj. bilirubin	↑ AST/ALT > > ALP	↑ ALP, ↑ GGT > > AST/ALT
Examples	Thalassaemia, G6PD, sickle cell	Hepatitis, cirrhosis, drugs	Gallstones, tumours, PSC

History-taking tip from the senior notes ^[3]: Ask about urine colour (tea-coloured = obstructive) and stool colour (pale, floating, foul-smelling steatorrhoea = obstructive). Also exclude non-biliary causes of dark urine: rifampicin, Pyridium, beetroot ^[3].

5. Diagnostic Approach Algorithm

Once you suspect gallstone disease, the following algorithmic thinking helps you navigate the DDx:

6. Less Common but Important Differentials (Hong Kong Context)

Condition	Relevance	Key Features
Recurrent pyogenic cholangitis (RPC)	"Hong Kong disease" — must consider in any local patient with recurrent cholangitis + intrahepatic stones	Brown pigment stones in intrahepatic ducts (especially left lobe); stasis + stricturing + recurrent infection cycle; parasites (Clonorchis sinensis); complications include cholangiocarcinoma ^[1]^[2]
Choledochal cyst	Congenital dilatation of biliary system; most diagnosed before age 10	RUQ mass + pain + jaundice + fever; pancreatitis; risk of cholangiocarcinoma; Todani classification (Type I most common); excision + Roux-en-Y hepaticojejunostomy ^[2]^[5]
Cholangiocarcinoma	Can mimic choledocholithiasis with obstructive jaundice	Painless progressive jaundice; Klatskin tumour (perihilar) most common; CA 19-9 elevated; differentiate from stone on MRCP (stricture without stone vs. filling defect) ^[1]
Pancreatic carcinoma	CA head of pancreas is the classic cause of painless obstructive jaundice	Double duct sign on CT; Courvoisier's sign positive (palpable non-tender GB); new-onset DM; weight loss ^[5]^[6]
IgG4-related cholangitis	Immune-mediated; can mimic cholangiocarcinoma	Mostly elderly males; ↑ serum IgG4; steroid-responsive; associated with autoimmune pancreatitis ^[3]

High Yield DDx Summary for Exams

When asked "DDx of gallstones", think systematically:

Differentiate within gallstone complications first: biliary colic vs cholecystitis vs choledocholithiasis vs cholangitis vs pancreatitis vs Mirizzi vs gallstone ileus — use pain duration, fever, jaundice, Murphy's sign, and labs.
Then differentiate from non-gallstone mimics based on the presenting complaint:
- RUQ pain: PUD, hepatitis, liver abscess, appendicitis, RLL pneumonia, inferior MI, renal colic
- Obstructive jaundice: CA head of pancreas (Courvoisier +), cholangiocarcinoma, PSC, Mirizzi, choledochal cyst
- Cholangitis: RPC, liver abscess, infected choledochal cyst, biliary leak
- Pancreatitis: GAME ID (Gallstones, Alcohol, Metabolic, ERCP, Idiopathic, Drugs)
Imaging first-line: USG/CT to determine duct size, level of obstruction, cause, and associated features ^[5].
Courvoisier's Law helps distinguish stone from tumour: palpable GB + painless jaundice = tumour until proven otherwise.
Polyp vs stone on USG: polyp = fixed, no shadow; stone = gravity-dependent, posterior acoustic shadow.

Active Recall - DDx of Gallstones

1. A 65-year-old woman presents with painless progressive jaundice and a palpable non-tender gallbladder. What is the most likely diagnosis and why?

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Malignant biliary obstruction (most likely CA head of pancreas or distal cholangiocarcinoma). Courvoisier's Law: palpable GB in painless jaundice means the GB wall is NOT fibrosed from chronic cholecystitis, so the cause is unlikely gallstones. The progressive nature and painlessness point to malignancy.

2. How do you differentiate a gallbladder polyp from a gallstone on ultrasound?

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Gallstone: gravity-dependent (moves with position change / rolling stone sign) + posterior acoustic shadow. Polyp: fixed to wall (not gravity-dependent) + no posterior acoustic shadow. Polyps may show vascularity on Doppler.

3. Name the two dangerous mimics of biliary colic that must not be missed, and what initial investigation should be done for each.

Your answer

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1. Inferior myocardial infarction - do an ECG. 2. Right lower lobe pneumonia - do an erect CXR. Both can present with RUQ/epigastric pain and nausea.

4. A patient in Hong Kong presents with recurrent episodes of Charcot's triad. USG shows intrahepatic ductal dilatation with stones, predominantly in the left lobe. What is the diagnosis and what type of stones would you expect?

Your answer

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Recurrent pyogenic cholangitis (RPC / Hong Kong disease). Expect brown pigment stones (calcium bilirubinate + bacterial cell bodies) formed de novo in intrahepatic ducts, driven by parasitic/bacterial infection and beta-glucuronidase activity.

5. What is the GAME ID mnemonic for causes of acute pancreatitis? Which is the most common cause?

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G = Gallstones (most common, 55%), A = Alcohol (35%), M = Metabolic (hyperTG, hyperCa), E = ERCP, I = Idiopathic (10%), D = Drugs (NSAIDs, steroids, azathioprine, valproate). Others include trauma, infections, autoimmune, tumours.

References

^[1] Senior notes: felixlai.md (Cholelithiasis, Cholecystitis, Acute Cholangitis, Mirizzi Syndrome, Acute Pancreatitis, Cholangiocarcinoma, Gallbladder Cancer, RPC sections) ^[2] Senior notes: maxim.md (Gallstone Diseases, Biliary Colic, Acute Cholecystitis, Choledocholithiasis, Mirizzi Syndrome, Gallstone Ileus, RPC, Acute Cholangitis, Acute Pancreatitis, GB Polyps, GB Carcinoma, Pancreatic Carcinoma, Choledochal Cyst sections) ^[3] Lecture slides: GC 200. RUQ pain, jaundice and fever Cholecytitis and cholangitis Imaging of GI system.pdf ^[4] Lecture slides: Acute pancreatitis.pdf ^[5] Lecture slides: Malignant biliary obstruction.pdf ^[6] Senior notes: maxim.md (Pancreatic carcinoma section)

Diagnostic Criteria, Diagnostic Algorithm & Investigation Modalities

1. Diagnostic Criteria by Clinical Presentation

Gallstones don't have a single set of diagnostic criteria — the criteria change depending on which clinical syndrome the patient is presenting with. Think of it as asking: "What is the stone doing right now?" Each scenario has its own formal criteria or clinical definition.

1.1 Biliary Colic — Clinical Diagnosis

There are no formal "criteria" for biliary colic per se. It is a clinical diagnosis confirmed by imaging. You diagnose it by putting together the story and the ultrasound:

Component	Required
Characteristic pain	Steady (not colicky) RUQ/epigastric pain, < 6 hours, post-prandial (fatty meal), radiating to right shoulder/scapula
No systemic inflammation	Afebrile, normal WCC, normal CRP
Normal or near-normal LFT	If cholestatic LFT → think choledocholithiasis; if ↑ amylase → think pancreatitis
USG: gallstones present	Hyperechoic stone with posterior acoustic shadowing, gravity-dependent ^[2]^[3]
No GB wall abnormality	No wall thickening, no pericholecystic fluid, no sonographic Murphy's sign

The key principle: biliary colic = stone + characteristic pain + no inflammation + no obstruction. The moment you add fever, leucocytosis, positive Murphy's sign, or cholestatic LFT, you've moved beyond simple biliary colic into a complication.

1.2 Acute Cholecystitis — Tokyo Guidelines (TG18/TG13) Diagnostic Criteria

The Tokyo Guidelines provide the standard diagnostic criteria for acute cholecystitis ^[1]^[2]^[3]. The diagnosis is made by combining local signs, systemic signs, and imaging findings.

Category	Criteria
A: Local signs of inflammation	Murphy's sign; RUQ mass / pain / tenderness
B: Systemic signs of inflammation	Fever; Leukocytosis; Elevated CRP
C: Imaging findings	Imaging findings characteristic of acute cholecystitis (see USG 5 cardinal signs below)

Interpretation ^[1]:

Diagnosis Level	Requirement
Suspected diagnosis	One item in A + One item in B
Definite diagnosis	One item in A + One item in B + C (confirmatory imaging)

Tokyo Guidelines — Must Know!

The Tokyo criteria are straightforward: local signs + systemic signs = suspected; add imaging confirmation = definite. In the exam, if you are asked "how do you diagnose acute cholecystitis?", state the Tokyo criteria explicitly. The 5 cardinal USG signs are the imaging component ^[2]:

Presence of gallstones
Distended GB ( > 4 × 10 cm)
GB wall thickening > 3 mm
Pericholecystic fluid / stranding
Sonographic Murphy sign

The Tokyo Guidelines also grade severity (important for management decisions):

Grade	Severity	Definition
Grade I (Mild)	No organ dysfunction; mild inflammatory disease in an otherwise healthy patient	Does not meet Grade II or III criteria
Grade II (Moderate)	Associated with any of: WCC > 18,000; palpable RUQ mass; duration > 72h; marked local inflammation (gangrenous, emphysematous, pericholecystic abscess, hepatic abscess, biliary peritonitis)	Significant local inflammation but no organ dysfunction
Grade III (Severe)	Associated with organ dysfunction in any one system	Cardiovascular (hypotension requiring pressors), neurological (↓ consciousness), respiratory (PaO2/FiO2 < 300), renal (oliguria, Cr > 2.0), hepatic (INR > 1.5), haematological (platelets < 100,000)

Why does severity grading matter? Because Grade I → elective/early LC; Grade II → early LC with more careful perioperative support; Grade III → initial organ support + percutaneous cholecystostomy (PTC) if unfit for surgery, with delayed LC once stabilised ^[2].

1.3 Acute Cholangitis — Tokyo Guidelines (TG18) Diagnostic Criteria

The TG18 criteria for acute cholangitis follow a similar logic — systemic inflammation + biliary obstruction ^[1]:

Component	Criteria
A: Systemic inflammation	Fever ( > 38°C) / shaking chills OR Laboratory evidence of inflammatory response (abnormal WCC / ↑ CRP / other changes)
B: Cholestasis	Jaundice OR Abnormal liver chemistries (↑ AST/ALT/ALP/GGT)
C: Imaging	Biliary dilatation on imaging AND Evidence of aetiology (stone, stricture, or stent on imaging)

Interpretation ^[1]:

Diagnosis Level	Requirement
Suspected diagnosis	One item in A + One item in B
Definite diagnosis	Suspected diagnosis + BOTH items in C (biliary dilatation + identified aetiology on imaging)

Severity grading of acute cholangitis (TG18):

Grade	Severity	Definition
Grade I (Mild)	Responds to initial medical treatment (antibiotics + supportive care)	No organ dysfunction, responds within 24–48h
Grade II (Moderate)	Does not respond to initial treatment; requires biliary drainage	Two or more of: WCC > 12,000 or < 4,000; fever ≥ 39°C; age ≥ 75; bilirubin ≥ 5 mg/dL; albumin < 0.7× lower normal limit
Grade III (Severe)	Organ dysfunction in any one system	Same organ dysfunction criteria as cholecystitis Grade III — this is essentially Reynolds' pentad territory: septic shock + altered mental status ^[1]^[2]

Cholangitis Grading Drives Urgency of Drainage

Grade III (severe) cholangitis = urgent biliary drainage within 24 hours (ERCP first-line). Do NOT wait. Grade II = early biliary drainage within 24–48 hours. Grade I = may respond to antibiotics alone, but if no improvement → biliary drainage. The key teaching point: the sicker the patient, the more urgent the drainage ^[2]^[3].

1.4 Choledocholithiasis — Risk Stratification (Not Formal "Criteria")

Choledocholithiasis does not have formal diagnostic criteria like cholecystitis/cholangitis. Instead, you risk-stratify to decide which investigation to use — this is the critical decision-making step ^[1]^[2]:

Risk Level	Predictors	Next Investigation
High risk	CBD stone visible on USG; or clinical acute cholangitis; or bilirubin > 4 mg/dL + dilated CBD	Proceed directly to ERCP (diagnostic + therapeutic) ^[1]^[2]
Intermediate risk	Abnormal LFT (cholestatic pattern) but no stone seen on USG; dilated CBD ( > 8 mm) without visible stone; age > 55; clinical gallstone pancreatitis	MRCP or EUS first (non-invasive confirmation before committing to ERCP) ^[1]^[2]
Low risk	Normal LFT, normal CBD calibre, no clinical features of obstruction	No further biliary imaging needed — proceed to elective cholecystectomy ± intraoperative cholangiogram (IOC) ^[1]

Why not just do ERCP on everyone? Because ERCP is invasive with significant complications (post-ERCP pancreatitis in 3–10%, perforation, haemorrhage, cholangitis). It should be reserved for cases where you are confident there IS a CBD stone to treat, or when the patient needs urgent therapeutic drainage ^[1]^[2].

1.5 Gallstone Pancreatitis — Diagnostic Criteria

Acute pancreatitis (of any cause) requires 2 out of 3 of the following ^[1]:

Criterion	Detail
1. Characteristic abdominal pain	Epigastric pain radiating to the back, severe, persistent
2. Serum amylase or lipase ≥ 3× upper limit of normal	Lipase preferred (more sensitive, stays elevated longer)
3. Imaging findings	CT/MRI showing pancreatic inflammation (oedema, necrosis, peripancreatic fluid)

You attribute it to gallstones (rather than alcohol/other causes) when:

Gallstones are present on USG
↑ ALP (suggests biliary origin rather than alcoholic — suspect gallstones if ALP elevated) ^[2]
↑ ALT > 3× ULN within 48h has high positive predictive value for gallstone aetiology
No history of significant alcohol intake
↑ AST more suggestive of alcohol ^[2]

2. Master Diagnostic Algorithm

The following algorithm synthesises the approach from first presentation to definitive investigation. This is how you should think on a ward round:

3. Investigation Modalities — Detailed Breakdown

3.1 Bedside & Laboratory Investigations

Investigation	What to Order	Key Findings & Interpretation	Pathophysiological Basis
CBC with differential count	FBC, WCC, neutrophils, band forms	Normal in biliary colic; ↑ WCC with left shift in cholecystitis/cholangitis; very high WCC ( > 18,000) → gangrenous cholecystitis/perforation ^[1]	Bacterial infection → bone marrow releases immature neutrophils (bands)
CRP	Inflammatory marker	Elevated in cholecystitis, cholangitis; serial monitoring useful for treatment response	Acute-phase reactant synthesised by liver in response to IL-6
LFT	Bilirubin, ALP, GGT, AST, ALT, albumin	Normal in biliary colic; Liver chemistry usually NORMAL in acute cholecystitis but mild elevation may occur ^[1]; cholestatic pattern (↑ ALP, ↑ GGT > > ↑ AST/ALT) in choledocholithiasis/cholangitis; ↑ AST/ALT early, then ↑ ALP/GGT later in the course of biliary obstruction ^[1]	ALP/GGT are located on the canalicular membrane of hepatocytes → biliary obstruction → bile backs up → ↑ synthesis and release of these enzymes; AST/ALT leak from damaged hepatocytes due to bile toxicity
	Conjugated bilirubin predominates	In obstructive jaundice, bilirubin is conjugated but cannot be excreted → refluxes into blood	Conjugated bilirubin is water-soluble → filtered by kidneys → dark/tea-coloured urine; no bilirubin reaches gut → pale stools
Serum amylase / lipase	Lipase preferred	≥ 3× ULN → diagnose acute pancreatitis; lipase rises within 4–8 hours, peaks at 24 hours, persists up to 2 weeks ^[1]; amylase rises earlier but returns to normal faster (3–5 days)	Pancreatic acinar cell injury → enzyme leak into blood. Lipase is more specific (amylase also elevated in salivary gland disease, macroamylasaemia, bowel obstruction)
Clotting profile	PT/INR	May be prolonged in obstructive jaundice	No bile salts in gut → no fat absorption → no vitamin K absorption (fat-soluble vitamin) → ↓ synthesis of factors II, VII, IX, X → prolonged PT ^[1]
Blood cultures	Aerobic + anaerobic bottles	Must send in suspected cholangitis BEFORE starting antibiotics ^[2]	Bacteraemia in cholangitis from translocation of gut organisms (E. coli, Klebsiella) through inflamed biliary mucosa into portal/systemic circulation
RFT	Urea, creatinine, electrolytes	Assess for dehydration, sepsis-related AKI, baseline before contrast imaging	Sepsis → pre-renal AKI; obstructive jaundice → hepatorenal syndrome (rare)
Urinalysis	Bilirubin, urobilinogen	Conjugated bilirubin positive in obstructive jaundice; urobilinogen absent (because no bilirubin reaches the gut to be converted) ^[1]	Confirms obstructive mechanism
Tumour markers	CA 19-9, CEA	NOT diagnostically useful (lack sensitivity and specificity); useful for monitoring after resection for recurrence ^[1]	CA 19-9 elevated in cholangiocarcinoma, pancreatic cancer, but also in benign cholangitis, pancreatitis — low specificity
Cardiac markers + ECG	Troponin, 12-lead ECG	Exclude myocardial infarction as a mimic of epigastric/RUQ pain ^[1]	Inferior MI (RCA territory) → diaphragmatic irritation → referred epigastric/RUQ pain
Erect CXR	PA chest film	Rule out right lower lobe pneumonia (RUQ pain mimic); air under diaphragm (perforated viscus); pleural effusion (pancreatitis complication)	Diaphragmatic irritation from RLL consolidation → referred RUQ pain
AXR	Supine abdomen	Only ~15% gallstones visible (pigment stones are radiopaque); Mercedes-Benz sign (gas in stone fissures); pneumobilia (gallstone ileus, post-ERCP); Rigler's triad (pneumobilia + SBO + ectopic stone = gallstone ileus) ^[2]; sentinel loop / colon cut-off sign (pancreatitis)	Limited sensitivity — USG is far superior for gallstones

LFT Interpretation in Biliary Disease — A Key Concept

The temporal evolution of LFT in biliary obstruction is important ^[1]:

Early (first 24–48h): ↑ AST and ALT — because back-pressure of bile causes hepatocyte damage → transaminase leak. ALT may transiently spike to > 1000 IU/L, mimicking hepatitis.
Later (days to weeks): ↑ ALP and GGT predominate — the classic "cholestatic pattern" — as the biliary epithelium upregulates ALP synthesis in response to obstruction.
If you catch the patient early, the LFT may look "hepatocellular" and fool you into thinking it's hepatitis. Always repeat LFT in 24–48h — the pattern will shift to cholestatic if it's truly obstructive.

3.2 Imaging Modalities

3.2.1 Transabdominal Ultrasound (USG)

USG is the initial standard imaging study of choice for suspected gallstone disease ^[1]^[2]^[3].

Why USG first? It is readily available, quick, non-invasive, no radiation, no contrast, inexpensive, and has excellent sensitivity for gallbladder stones (~95%). It simultaneously assesses the liver, bile ducts, and pancreas.

Finding	Significance	Pathophysiological Basis
Hyperechoic focus with posterior acoustic shadowing	Gallstone in GB	Stone reflects all ultrasound waves (hyperechoic) and blocks transmission behind it (shadow) ^[2]
Gravity-dependent / rolling stone sign	Confirms stone (not polyp)	Stone is mobile, moves when patient changes position; polyp is fixed to wall ^[1]^[2]
Distended GB ( > 4 × 10 cm)	Cystic duct obstruction (cholecystitis, mucocele)	Bile cannot exit → accumulation → distension
GB wall thickening > 3 mm	Inflammation (cholecystitis)	Oedema and inflammatory infiltrate in GB wall
Double-wall sign	Wall oedema in cholecystitis	Intramural oedema separates mucosal and serosal layers
Pericholecystic fluid	Cholecystitis with serosal inflammation	Exudate from inflamed GB serosa
Sonographic Murphy sign	Acute cholecystitis	Pressing USG probe over GB reproduces maximum tenderness (localises inflammation to GB specifically)
Contracted, thick-walled GB	Chronic cholecystitis	Fibrosis from repeated inflammation ^[2]
Dilated CBD ( > 8 mm)	Biliary obstruction (choledocholithiasis, tumour)	Back-pressure from distal obstruction dilates the duct proximally ^[1]^[2]
Stone in CBD	Choledocholithiasis	Only visible in ~1/3 of cases — distal CBD often obscured by duodenal gas ^[1]^[2]
Dilated intrahepatic ducts	Proximal/hilar obstruction	Obstruction at or above the hilum (Klatskin tumour, RPC)
Wall calcification	Porcelain gallbladder	Chronic inflammation → dystrophic calcification of GB wall

Limitations of USG ^[1]^[2]:

Operator-dependent — quality varies with sonographer experience
Limited by body habitus (obesity) and bowel gas (obscures distal CBD and pancreas)
Poor sensitivity for distal CBD stones (~50%) — the duodenum overlies the distal CBD
Cannot assess pancreatic necrosis or stage malignancy

CBD diameter rule of thumb ^[2]: Normal ≤ 6 mm. Add ~1 mm per decade over 60. Post-cholecystectomy, up to 10 mm may be acceptable (the CBD dilates to compensate for loss of the gallbladder reservoir). If ≥ 8 mm with gallstones and biliary pain → suspicious for choledocholithiasis ^[1].

3.2.2 HIDA Scan (Cholescintigraphy)

"HIDA" = Hepatic IminoDiacetic Acid — a technetium-99m labelled radiotracer (99mTc-HIDA) that is taken up by hepatocytes and excreted into bile, mimicking bilirubin metabolism ^[1]^[2].

Aspect	Detail
Principle	Radiotracer injected IV → taken up by liver → excreted into bile → normally fills GB within 30 min and enters duodenum within 60 min
Positive for acute cholecystitis	Non-visualisation of the gallbladder after 4 hours (because the cystic duct is obstructed → tracer cannot enter GB) ^[1]
Chronic cholecystitis	Delayed or reduced GB filling ^[2]
Normal HIDA	Excludes acute cholecystitis — high negative predictive value ^[1]
Sensitivity/Specificity	~95% / ~90% — highly accurate but expensive and time-consuming
Limitation	Not useful in jaundiced patients — the liver cannot excrete the tracer if bilirubin is very high (competitive inhibition at the hepatocyte canalicular membrane) ^[1]
Morphine augmentation	Morphine IV → ↑ sphincter of Oddi pressure → forces bile into the GB if the cystic duct is patent → if GB still not seen, confirms obstruction. Used when HIDA is equivocal ^[2]
When to use	When USG is inconclusive and clinical suspicion for acute cholecystitis remains high ^[1]^[2]

3.2.3 MRCP (Magnetic Resonance Cholangiopancreatography)

"MRCP" is a non-contrast, T2-weighted MRI sequence that exploits the fact that stationary fluid (bile, pancreatic juice) appears bright white on T2, giving a "cholangiogram-like" image without any contrast or endoscopy ^[2].

Aspect	Detail
Principle	T2 weighting → static fluid (bile) = bright signal; surrounding soft tissue = dark. Creates a "roadmap" of the biliary tree and pancreatic duct
Sensitivity for CBD stones	~90–95% (far superior to USG for CBD/cystic duct stones)
Advantages	Non-invasive, no contrast, no radiation, no sedation; superior to USG for cystic duct and distal CBD stones; can differentiate inflammatory from neoplastic masses on T2 images ^[1]
Limitations	NOT therapeutic — can only diagnose, cannot treat (unlike ERCP); lower spatial resolution for very small stones ( < 3 mm); claustrophobia; not widely available in emergency settings; contraindicated with some metallic implants
When to use	Intermediate risk of choledocholithiasis — when you want to confirm/exclude CBD stones before committing to ERCP ^[1]^[2]; to delineate biliary anatomy before surgery; Mirizzi syndrome workup ^[1]

MRCP has largely replaced diagnostic ERCP for choledocholithiasis. The principle is: use MRCP to diagnose, then proceed to ERCP only if a stone is confirmed and needs extraction ^[1].

3.2.4 EUS (Endoscopic Ultrasound)

Aspect	Detail
Principle	High-frequency ultrasound transducer mounted on an endoscope → positioned in the duodenum or stomach → gives close-range, high-resolution images of the CBD, pancreas, and ampulla without bowel gas interference
Sensitivity for CBD stones	~95% — equivalent to or better than MRCP, especially for small stones ( < 5 mm)
Advantages	Overcomes the bowel gas limitation of transabdominal USG; excellent for distal CBD; can assess pancreatic masses and perform FNA/biopsy simultaneously
Limitations	Invasive (requires sedation, endoscopy); operator-dependent; not universally available
When to use	Intermediate risk of choledocholithiasis when MRCP is contraindicated (e.g., metallic implants); when MRCP is negative but clinical suspicion remains high ^[1]; staging of periampullary/pancreatic tumours ^[2]

3.2.5 ERCP (Endoscopic Retrograde Cholangiopancreatography)

ERCP is both diagnostic and therapeutic — but should be reserved for patients with HIGH risk of CBD stones or who need urgent biliary drainage ^[1]^[2]^[3].

Aspect	Detail
Principle	Side-viewing duodenoscope → cannulation of the ampulla of Vater → contrast injection into CBD/pancreatic duct → fluoroscopic imaging; allows simultaneous intervention
Diagnostic findings	Filling defects (stones), strictures, dilatation, cholecystobiliary fistula (Mirizzi), tumour
Therapeutic capabilities	Sphincterotomy (cutting the sphincter of Oddi to widen the ampullary opening); stone extraction (balloon or basket); mechanical lithotripsy (crushing large stones); biliary stent placement (for obstruction from stricture/tumour); biliary drainage (for cholangitis) ^[1]^[2]
Complications	Post-ERCP pancreatitis (3–10%) — most common; perforation; haemorrhage (post-sphincterotomy); cholangitis; basket impaction. Reduced by prophylactic rectal NSAIDs or temporary pancreatic stent ^[2]
When to use	High risk of CBD stone (stone seen on imaging, acute cholangitis, bilirubin > 4 + dilated CBD) ^[1]; urgent biliary drainage in acute cholangitis (first-line, Grade II–III) ^[2]^[3]; confirmed CBD stone on MRCP/EUS needing extraction
When NOT to use	Low/intermediate probability of CBD stone without prior non-invasive confirmation; sole diagnostic purpose when MRCP/EUS can answer the question

3.2.6 CT Abdomen (with Contrast)

Aspect	Detail
Principle	Cross-sectional imaging with IV contrast; arterial, portal venous, and delayed phases
Sensitivity for gallstones	Only ~75% — many cholesterol stones are isodense with bile on CT ^[2]. USG is superior for gallbladder stones
When CT excels	Complications of cholecystitis (empyema, emphysematous cholecystitis — gas in GB wall, perforation, abscess) ^[2]; staging malignancy (cholangiocarcinoma, pancreatic cancer, GB cancer — assessing vascular invasion, LN involvement, distant metastases) ^[1]^[5]; acute pancreatitis — gold standard (Sn 90%, Sp 100%) for detecting necrosis, peripancreatic collections; CT changes may NOT appear within first 24 hours ^[1]; gallstone ileus (Rigler's triad much more sensitive on CT than AXR) ^[2]
Specific CT findings	Emphysematous cholecystitis: gas within GB wall/lumen; Porcelain GB: curvilinear calcification of GB wall; Double duct sign: dilated CBD + dilated pancreatic duct → pancreatic head mass ^[2]; Pancreatic necrosis: lack of enhancement with IV contrast ^[1]

3.2.7 PTC (Percutaneous Transhepatic Cholangiography)

Aspect	Detail
Principle	Percutaneous needle inserted through the liver into an intrahepatic bile duct under fluoroscopic guidance → contrast injection → imaging of biliary tree
Diagnostic	Visualisation of biliary tree anatomy above an obstruction
Therapeutic	PTBD (percutaneous transhepatic biliary drainage) — external drain or internal stent to decompress obstructed bile ducts
Preferred over ERCP when	Obstruction at or above the confluence of hepatic ducts (e.g., Klatskin tumour, PSC, RPC) — ERCP cannot access above a complete hilar obstruction ^[2]; failed ERCP; surgically altered anatomy (e.g., Roux-en-Y) making endoscopic access impossible
Complications	Bacteraemia (antibiotic prophylaxis required), haemobilia, bile leak, pneumothorax ^[2]

3.2.8 Intraoperative Cholangiogram (IOC)

Aspect	Detail
Principle	During laparoscopic cholecystectomy, contrast is injected via the cystic duct under fluoroscopy → images the CBD in real-time
Purpose	Detects residual/unsuspected CBD stones (present in ~5–10% of patients undergoing LC for gallstones); confirms biliary anatomy to avoid CBD injury
When to use	Low risk of CBD stones → LC with IOC (instead of pre-op MRCP); any case where anatomy is uncertain during surgery ^[1]

4. Investigation Strategy by Clinical Scenario — Summary Table

Clinical Scenario	First-Line Imaging	Second-Line / Confirmatory	Therapeutic
Biliary colic	USG (stones, no GB inflammation)	—	— (→ Elective LC)
Acute cholecystitis	USG (5 cardinal signs)	HIDA scan (if USG inconclusive); CT (if complications suspected) ^[1]^[2]	— (→ LC or PTC)
Choledocholithiasis (low risk)	USG	IOC during LC	LC + IOC
Choledocholithiasis (intermediate risk)	USG	MRCP or EUS ^[1]^[2]	ERCP if stone confirmed
Choledocholithiasis (high risk)	USG	—	ERCP directly (diagnostic + therapeutic) ^[1]^[2]
Acute cholangitis	USG (dilated CBD, stone, r/o liver abscess)	MRCP if ERCP delayed/unavailable	ERCP (1st line) ^[2]^[3]
Gallstone pancreatitis	USG (gallstones, CBD)	CT abdomen (if severe / after 72h); MRCP for CBD stone if intermediate risk	ERCP (if concurrent cholangitis or confirmed CBD stone) ^[1]
Mirizzi syndrome	USG (dilated ducts above GB neck, stone at neck, contracted GB) ^[1]	MRCP (high sensitivity); CT (r/o malignancy) ^[1]	ERCP (diagnostic + stenting) ^[1]
Gallstone ileus	AXR (Rigler's triad)	CT abdomen (much more sensitive) ^[2]	Surgical (enterolithotomy)
Malignant biliary obstruction	USG + CT ^[5]	MRCP; EUS (staging + FNA)	ERCP (stenting for palliation) or PTC (if hilar obstruction)

Imaging for obstructive jaundice ^[5]: The lecture slides emphasise that USG / CT should assess: (i) Size of bile duct, (ii) Level of obstruction, (iii) Cause of obstruction, (iv) Other associated features — staging for malignant disease; complications for benign disease (gallstones) ^[5].

5. Specific USG Findings Summary — Visual Checklist

Condition	USG Findings
Gallstone	Hyperechoic + posterior acoustic shadow + gravity-dependent ^[2]
GB polyp	Hyperechoic + NO posterior shadow + NOT gravity-dependent + may have vascularity on Doppler ^[2]
Acute cholecystitis	5 cardinal signs (stones, distended GB, wall > 3mm, pericholecystic fluid, sono-Murphy) ^[2]
Chronic cholecystitis	Contracted GB + wall thickening + stones ^[2]
Choledocholithiasis	Dilated CBD > 8 mm ± visible stone (only 1/3 seen due to bowel gas) ^[1]^[2]
Porcelain GB	Curvilinear echogenic focus with posterior shadowing in GB wall (calcification)
Mirizzi syndrome	Dilated ducts ABOVE GB neck + stone at GB neck + normal CBD BELOW stone + contracted GB ^[1]
Cholangitis	Dilated CBD ± stone; may show liver abscess ^[2]
GB cancer	Thickened irregular wall > 3 mm; mass protruding into lumen; loss of GB-liver interface; LN ^[1]

High Yield Summary — Diagnosis of Gallstones

Biliary colic = clinical diagnosis; USG confirms stones + normal GB wall + no systemic inflammation.
Acute cholecystitis = Tokyo criteria: 1 local sign + 1 systemic sign = suspected; + imaging = definite. 5 cardinal USG signs are the imaging gold standard.
HIDA scan = second-line when USG is inconclusive; non-visualisation of GB = cystic duct obstruction = cholecystitis.
Acute cholangitis = TG18 criteria: systemic inflammation + cholestasis = suspected; + biliary dilatation with identified cause on imaging = definite. Severity grading dictates urgency of biliary drainage.
Choledocholithiasis = risk-stratify: High → ERCP directly; Intermediate → MRCP/EUS first; Low → LC + IOC.
USG is first-line for all gallstone presentations. It is limited for distal CBD stones (bowel gas).
MRCP has replaced diagnostic ERCP — use MRCP to confirm, ERCP to treat.
ERCP is reserved for high-risk CBD stones and urgent biliary drainage — it is invasive with significant complication risk (pancreatitis 3–10%).
CT is best for complications (emphysematous cholecystitis, perforation, pancreatitis necrosis, staging malignancy) and is NOT the first choice for detecting gallstones (only 75% sensitivity).
LFT evolution: Early obstruction → ↑ AST/ALT; Later → ↑ ALP/GGT (cholestatic pattern). Always repeat LFT in 24–48h.
Always send blood cultures in suspected cholangitis BEFORE antibiotics.
Always do ECG + erect CXR to exclude MI and RLL pneumonia as RUQ pain mimics.

Active Recall - Diagnosis of Gallstones

1. State the Tokyo Guidelines diagnostic criteria for acute cholecystitis, including what constitutes 'suspected' vs 'definite' diagnosis.

Your answer

Show mark scheme

A = Local signs (Murphy's sign, RUQ mass/pain/tenderness). B = Systemic signs (fever, leucocytosis, elevated CRP). C = Imaging findings (characteristic of acute cholecystitis). Suspected = 1 item in A + 1 item in B. Definite = 1A + 1B + C.

2. A patient has RUQ pain, mildly elevated ALP and bilirubin, but USG shows no CBD stone although the CBD is dilated to 9mm. What risk category is this for choledocholithiasis and what investigation do you order next?

Your answer

Show mark scheme

Intermediate risk (cholestatic LFT + dilated CBD but no stone seen on USG). Order MRCP or EUS to confirm/exclude CBD stone before committing to ERCP.

3. Why is HIDA scan not useful in a jaundiced patient with suspected acute cholecystitis?

Your answer

Show mark scheme

HIDA depends on hepatic excretion of the radiotracer into bile. In jaundiced patients, high serum bilirubin competitively inhibits hepatocyte uptake/excretion of the tracer, so the biliary system (including GB) cannot be visualised regardless of cystic duct patency.

4. List the 5 cardinal USG signs of acute cholecystitis.

Your answer

Show mark scheme

1. Presence of gallstones. 2. Distended GB (>4x10cm). 3. GB wall thickening >3mm. 4. Pericholecystic fluid/stranding. 5. Sonographic Murphy sign.

5. Explain why the LFT pattern in early biliary obstruction may mimic hepatitis, and what happens to the pattern over time.

Your answer

Show mark scheme

Early (first 24-48h): back-pressure of bile causes hepatocyte damage, so AST/ALT spike markedly (hepatocellular pattern), mimicking hepatitis. Over days: biliary epithelium upregulates ALP synthesis in response to obstruction, so ALP and GGT rise and predominate (cholestatic pattern). Always repeat LFT in 24-48h to see the shift.

6. When should you proceed directly to ERCP rather than MRCP/EUS for suspected choledocholithiasis?

Your answer

Show mark scheme

High risk of CBD stones: CBD stone visible on USG, clinical acute cholangitis, or bilirubin >4 with dilated CBD. ERCP is both diagnostic and therapeutic in these scenarios. Also indicated for urgent biliary drainage in Grade II-III cholangitis.

References

^[1] Senior notes: felixlai.md (Cholelithiasis, Cholecystitis — Tokyo criteria, Acute Cholangitis — TG18 criteria, Mirizzi Syndrome, Acute Pancreatitis, Gallbladder Cancer diagnostic sections) ^[2] Senior notes: maxim.md (Gallstone Diseases, Biliary Colic investigations, Acute Cholecystitis — 5 cardinal signs and Tokyo table, Choledocholithiasis — risk stratification, Acute Cholangitis — urgent investigations, HBP investigations — USG/EUS/CT/HIDA/MRCP/PTC/ERCP, Gallstone Ileus, GB Polyps) ^[3] Lecture slides: GC 200. RUQ pain, jaundice and fever Cholecytitis and cholangitis Imaging of GI system.pdf ^[5] Lecture slides: Malignant biliary obstruction.pdf

Management of Gallstones — Treatment Algorithm & Modalities

The management of gallstones is dictated by a single question: "What is the stone doing right now?" The treatment is entirely different for an asymptomatic stone sitting quietly in the gallbladder versus one causing septic shock from cholangitis. Let's work through each scenario systematically.

1. Overarching Principles

Before diving into specifics, three management principles apply across all gallstone presentations:

Resuscitate first, investigate second, intervene third — especially in cholangitis and pancreatitis. You cannot ERCP a dead patient.
Remove the gallbladder to prevent recurrence — almost every gallstone complication eventually leads back to laparoscopic cholecystectomy (LC) as the definitive treatment to eliminate the stone factory ^[1]^[2].
Biliary decompression is life-saving in obstruction with sepsis — when bacteria are trapped behind an obstruction, antibiotics alone cannot penetrate adequately because bile is not flowing. You must physically drain the system ^[1]^[2]^[3].

2. Master Management Algorithm

3. Management by Clinical Scenario

3.1 Asymptomatic Gallstones

Most gallstones (80%) are asymptomatic. The question is: when do you leave them alone versus operate prophylactically?

Default approach: Watchful waiting ^[2]

Risk of future complications: only 1–4% per year ^[2]
Risk factor modification: weight management, dietary changes, control of diabetes
Ursodeoxycholic acid (UDCA): An oral bile acid that works by reducing cholesterol secretion into bile and promoting cholesterol desaturation → gradual dissolution of cholesterol stones over months to years. Only effective for cholesterol stones (not pigment), small stones ( < 1 cm), and functioning gallbladder (patent cystic duct). Rarely used in practice because of low efficacy and high recurrence (50% within 5 years after stopping) ^[2].

Indications for prophylactic cholecystectomy in asymptomatic patients ^[1]^[2]:

Indication	Rationale
Porcelain gallbladder	Calcification of GB wall → 2–3% risk of malignancy → absolute indication for cholecystectomy ^[1]^[2]
GB polyps ≥ 1 cm	Risk of malignancy 46% at 1.5 cm; adenomatous polyps ≥ 1 cm (or ≥ 8 mm if underlying PSC) ^[2]
Large gallstones > 3 cm	Increased risk of GB carcinoma ^[2]
Concomitant haemolytic disorders	Ongoing production of pigment stones; stones will inevitably become symptomatic
Patients on long-term TPN	No CCK stimulus → perpetual GB stasis → high risk of cholecystitis ^[1]
Gastric bypass / bariatric surgery	Altered anatomy makes future ERCP extremely difficult; rapid weight loss → stone formation
Concomitant liver surgery	Opportunistic removal during another hepatobiliary procedure

3.2 Biliary Colic

Acute management ^[2]:

NPO (nil by mouth) — rest the gut, reduce CCK stimulation
Analgesia — NSAIDs are preferred first-line (e.g., diclofenac, ketorolac) ^[2]
- Why NSAIDs? They inhibit prostaglandin synthesis → reduce gallbladder mucosal inflammation and smooth muscle spasm. They also avoid opioid-related sphincter of Oddi spasm (morphine → ↑ sphincter of Oddi pressure → worsens biliary obstruction).
- If NSAIDs contraindicated (renal impairment, PUD, allergy) → pethidine (meperidine) or paracetamol + codeine. Morphine should be AVOIDED due to sphincter of Oddi spasm ^[1].
IV fluids if dehydrated/vomiting
Anti-emetics (ondansetron, metoclopramide)

Definitive management: Elective laparoscopic cholecystectomy ^[2]

Rationale: once symptomatic, patients tend to have recurrent bouts; elective LC reduces risk of future complications from 25% to 8% ^[2].
Timing: can be arranged as an outpatient/elective procedure during the same admission or within weeks.

3.3 Acute Cholecystitis

The management follows a structured approach: initial stabilisation → definitive surgery.

Initial Medical Stabilisation

Intervention	Detail	Rationale
NPO	Nil by mouth	Bowel rest; reduce CCK-driven GB contraction against obstruction
IV fluids	Crystalloid resuscitation	Replace losses from vomiting, fever, third-spacing
IV antibiotics ^[3]	Cefuroxime + Metronidazole (mild-moderate); Piperacillin-tazobactam (Tazocin) (severe) ^[2]^[3]; Alternatives: Ampicillin-sulbactam; Metronidazole + 3rd-gen cephalosporin; Metronidazole + fluoroquinolone ^[1]	Acute cholecystitis is initially chemical inflammation but secondary bacterial infection occurs (E. coli, Klebsiella, Strep. faecalis) → must cover gram-negatives + anaerobes
Analgesia	NSAIDs first-line; avoid morphine	Pain control; morphine → sphincter of Oddi spasm
Monitor	Vitals, I/O, serial bloods	Detect deterioration: ↑ temperature/pulse, ↓ BP/consciousness/urine output, ↑ abdominal tenderness ^[1]

Definitive Treatment: Cholecystectomy [3]

"Surgical treatment = Cholecystectomy (removal of gallbladder) — open or laparoscopic, delayed or early" ^[3].

The critical decision is timing — early vs. delayed (interval):

Early LC: within 48–72 hours of symptom onset ^[3]	Delayed (Interval) LC: after 6–12 weeks ^[3]
Advantages: avoid urgent operation, avoid recurrent symptoms, avoid readmission, shorter hospital stay ^[3]	Advantages: avoid misdiagnosis, easier dissection, less septic complications, less serious complications ^[3]
Initial inflammation creates pericholecystic fluid → easier tissue-plane dissection ^[2]	After 72h: dense adhesions form at Calot's triangle → difficult dissection ^[2]
Higher risk of bleeding and post-op infections; higher conversion-to-open rate ^[2]	Separate admission; fibrosis makes GB mobilisation difficult; chance of recurrence while waiting ^[2]

"Early cholecystectomy is safe without increasing the risk of complications" ^[3] — current evidence and guidelines favour early LC (within 72h) as the standard of care for most patients with acute cholecystitis, as it avoids the morbidity of a second admission and the risk of recurrent complications during the waiting period.

Management by Tokyo Severity Grade ^[1]^[2]:

Grade	Management
Grade I (Mild)	Early LC (within 72h) — 1st line for most patients ^[2]^[3]
Grade II (Moderate)	Early LC with experienced surgeon + careful perioperative support. If local resources/expertise insufficient → antibiotics + delayed LC ^[1]
Grade III (Severe)	Initial organ support + GB drainage → delayed LC when stabilised ^[1]^[2]
Complicated (gangrene, perforation, emphysematous)	Emergency LC regardless of grade — disease progression despite best supportive care ^[2]

Emergency vs Early vs Interval LC

Emergency LC = performed urgently (same day) for life-threatening complications — gangrene, perforation, emphysematous cholecystitis, or clinical deterioration despite antibiotics ^[2].
Early LC = within 48–72 hours of symptom onset — the current standard of care for Grade I–II ^[3].
Interval LC = delayed 6–12 weeks after initial conservative management — reserved for late presentations ( > 72h where dense adhesions have already formed), or when early surgery is not feasible ^[2].

Cholecystostomy (GB Drainage) [3]

"Drainage of the gallbladder — open or percutaneous. Indications: high surgical risk, haemodynamically unstable, difficult cholecystectomy" ^[3].

Modality	Detail
Percutaneous transhepatic cholecystostomy (PTC) ^[2]^[3]	Catheter inserted percutaneously through the liver into the GB under USG/CT guidance. Trans-hepatic route minimises risk of bile leak (liver tissue tamponades the tract). Decompresses and drains the inflamed/purulent GB. Specific complications: catheter migration, bile leakage, bowel injury ^[2]
Endoscopic drainage	If PTC not feasible: transpapillary drainage via ERCP (catheter placed through cystic duct → either nasobiliary drain externally or internal pigtail stent into duodenum); or transmural EUS-guided drainage (EUS-guided needle puncture of GB → dilation → stent/LAMS placement) ^[1]^[2]

GB drainage is a bridge — it stabilises the patient until they are fit for definitive cholecystectomy.

Laparoscopic Cholecystectomy — Operative Details

Aspect	Detail
Approach	Laparoscopic (95% of cases) vs. open (Kocher's subcostal incision) ^[1]^[2]
Advantages of lap	Less pain, shorter hospital stay, faster recovery, better cosmesis, early return of GI function ^[1]
Disadvantages of lap	Higher risk of major bile duct injury; conversion to open may be needed ^[1]
Positioning	Reversed Trendelenburg (head up) — allows gravity to retract bowel inferiorly, exposing the GB; slightly rotated to left ^[2]
Port placement	4 ports: 10 mm umbilical (camera), 10 mm epigastric (operating), 5 mm right subcostal (dynamic retraction), 5 mm right flank (static retraction of fundus) ^[2]
Pneumoperitoneum	CO₂ insufflation to ~15 mmHg via Hasson open technique at umbilicus ^[2]
Key landmarks	Retract GB fundus cephalad + Hartmann's pouch laterally → identify Rouviere's sulcus (right posterior portal pedicle) as safety landmark ^[2]

Critical View of Safety (CVS) — the most important concept in cholecystectomy ^[1]^[2]:

CVS Criteria	Why
1. Hepatocystic triangle (Calot's triangle) cleared of all fat and fibrous tissue	Ensures no hidden structures (accessory ducts, aberrant arteries)
2. Lower third of GB separated from the cystic plate (liver bed)	Confirms the plane between GB and liver
3. Only two structures seen entering the gallbladder: cystic duct and cystic artery	Misidentification of the cystic duct is the commonest cause of biliary injury ^[1] — CVS prevents this by ensuring ONLY 2 structures are connected to the GB before clipping/dividing

Critical View of Safety

Never clip or divide ANY structure during cholecystectomy until the CVS is achieved. If the CVS cannot be obtained due to severe inflammation or unclear anatomy → perform intraoperative cholangiogram (IOC) to delineate the anatomy, or convert to open surgery. Conversion to open is NOT a failure — it is a safety decision ^[1]^[2].

Partial (subtotal) cholecystectomy is advocated when ductal and vascular structures in Calot's triangle cannot be safely identified in severe acute inflammation — you leave the posterior wall of the GB attached to the liver bed (Fenestrating technique) or amputate at Hartmann's pouch (Reconstituting technique) ^[1].

Indications for open cholecystectomy ^[2]:

Indication	Rationale
Cannot tolerate pneumoperitoneum	Cardiopulmonary comorbidities → CO₂ absorption + increased intra-abdominal pressure → ↓ venous return, ↑ PaCO₂
Refractory coagulopathy	High bleeding risk with laparoscopic approach
Multiple previous abdominal surgeries	Dense adhesions make port placement and dissection hazardous
Suspected GB carcinoma	Risk of port-site seeding; need for wider resection with LN dissection ^[2]

Indications for cholecystectomy (comprehensive) ^[1]^[2]:

Category	Specific Indication
Symptomatic gallstones	With or without complications (biliary colic, cholecystitis, choledocholithiasis, pancreatitis) ^[1]^[2]
Asymptomatic — high risk of GB cancer	Porcelain gallbladder (absolute); GB polyps ≥ 1 cm; large stones > 3 cm ^[1]^[2]
Asymptomatic — high risk of complications	Long-term TPN; haemolytic disorders; post-bariatric surgery ^[1]
Acalculous cholecystitis	GB inflammation without stones — definitive treatment is cholecystectomy ^[1]
Concomitant surgery	During other hepatobiliary procedures

3.4 Choledocholithiasis (CBD Stones)

The management has two components: (1) Remove the CBD stone and (2) Remove the gallbladder to prevent recurrence.

CBD Stone Removal — Risk-Stratified Approach [1][2]

Risk Level	Approach
High suspicion (CBD stone on USG, clinical cholangitis, bilirubin > 4 + dilated CBD)	ERCP first → sphincterotomy + stone extraction → interval LC with IOC ^[1]
Intermediate suspicion (cholestatic LFT, dilated CBD without visible stone)	MRCP or EUS first → if stone confirmed → ERCP → LC ^[1]^[2]
Low suspicion (normal LFT, normal CBD)	LC with IOC → if stone found intraoperatively → laparoscopic ECBD or post-op ERCP ^[1]

ERCP — Stone Extraction Techniques [1][2]

"First-line approach: Endoscopic retrograde cholangiopancreatography ± biliary stenting" ^[3].

Step	Detail	Why
Endoscopic sphincterotomy	Electrocautery incision through the biliary sphincter of Oddi	Eliminates the principal anatomic barrier to stone passage; widens the ampullary opening for instrument access ^[1]
Stone extraction	Wire baskets (Dormia basket — snares the stone); Stone extraction balloon (Fogarty-type — inflated above stone, pulled down to sweep stone out); Mechanical lithotripsy (crushes large stones that cannot be extracted whole) ^[1]^[2]	Different tools for different stone sizes/shapes
Papillary balloon dilation (balloon sphincteroplasty)	Alternative to sphincterotomy — dilates ampulla with a balloon to preserve the sphincter	Concerns about long-term sphincter incompetence and ascending cholangitis with sphincterotomy; however, balloon dilation carries higher risk of post-ERCP pancreatitis ^[1]

Complications of ERCP ^[1]^[3]:

Timing	Complication	Detail
Short-term	Pancreatitis (most common, 3–10%)	Reduced by prophylactic rectal NSAIDs or temporary pancreatic stent
	Perforation	Two types: Intraperitoneal (duodenal perforation → free gas under diaphragm on CXR → requires operative treatment) vs. Retroperitoneal (bile duct perforation at ampulla → retroperitoneal gas, NO free gas under diaphragm → usually conservative management as it seals spontaneously) ^[1]
	Bleeding	Post-sphincterotomy haemorrhage
	Infection / cholangitis	Incomplete drainage → residual obstruction + instrumentation
Long-term	Stone recurrence	Especially if gallbladder not removed
	Papillary stenosis	Scarring of sphincterotomy site

Relative contraindications for ERCP ^[3]:

Altered GI anatomy e.g., Billroth II gastrectomy, Roux-en-Y ^[3] — the afferent limb anatomy makes duodenoscope access to the ampulla technically very difficult or impossible
Gastric/bowel obstruction
Severe coagulopathy (INR > 1.5, platelets < 50,000) — risk of post-sphincterotomy bleeding

Surgical Exploration of CBD (ECBD) [1][2]

When ERCP fails or is contraindicated, CBD stones must be managed surgically.

Approach	Detail
Transcystic exploration (1st line)	Catheter inserted via the cystic duct → cholangiogram → stone extraction with balloon/basket → advantage: avoids opening the CBD itself ^[2]
Choledochotomy (2nd line)	Direct incision into the CBD → stone removed through the defect → choledochoscopy to confirm complete clearance → T-tube or primary closure ^[2]
Percutaneous choledochoscopy	Via mature T-tube tract (6–8 weeks post-insertion) — stones retrieved with baskets/balloons under direct vision ^[1]
Advantage	Can be performed as one-stage surgery together with LC ^[2]

T-tube placement after choledochotomy ^[1]:

Function	Detail
Post-operative biliary decompression	Keeps CBD pressure low while the choledochotomy suture line heals
Prevents bile leakage from suture line	Safety valve — bile drains externally if pressure rises
Access for post-operative cholangiogram	Check tube cholangiogram at 7–10 days to exclude residual stones
Access for choledochoscopy	After 6–8 weeks (fibrous tract formation), scope can be passed through the tract to extract residual stones ^[1]
Complications	Bile leak, infection, tube dislodgement, bile duct obstruction ^[1]^[2]

Modern practice often favours primary closure of the choledochotomy (without T-tube) if a biliary stent is in situ, as T-tubes have been shown to increase complications ^[2].

3.5 Acute Cholangitis

The management is encapsulated by the mnemonic "RAD" — Resuscitation, Antibiotics, Drainage ^[2].

"Keep the patient fast. Intravenous fluid. Intravenous antibiotics: Cefuroxime, Metronidazole, Piperacillin + tazobactam" ^[3].

Step	Detail	Rationale
R — Resuscitation	NPO, IV fluids, monitor vitals and I/O Q1h ^[2]	Correct dehydration, prevent shock; close monitoring to detect clinical deterioration early
A — Antibiotics (broad-spectrum, IV) ^[2]^[3]	Mild: IV Augmentin (amoxicillin-clavulanate) or cefuroxime + metronidazole; Severe: IV Tazocin (piperacillin-tazobactam) × 7 days ^[2]^[3]	Must cover enteric gram-negatives (E. coli, Klebsiella) + anaerobes (Bacteroides); antibiotics alone fail in 15% because bile flow is obstructed → drug cannot reach the infected bile ^[1]
D — Drainage	Urgent if Reynolds' pentad, or not responding to antibiotics within 24h ^[2]	Obstruction impairs antibiotic secretion into bile → you MUST physically decompress the biliary tree

Biliary Drainage Modalities — Hierarchy [1][2][3]

QMH practice: ERCP → PTBD → ECBD ^[1].

Modality	Detail	When to Use
ERCP (1st line) ^[2]^[3]	Biliary drainage and decompression — aspirate bile and pus → inject contrast → place plastic stent (temporary, requires scheduled change) with or without sphincterotomy; stone removal now or interval ERCP after sepsis resolves ^[2]	First-line for acute cholangitis ^[3]; mortality < 5% with endoscopic drainage
PTBD (Percutaneous transhepatic biliary drainage)	Transhepatic catheter inserted into intrahepatic bile duct (not CBD) under fluoroscopic guidance; external drainage (easy output monitoring) but risk of fluid/electrolyte losses; can be internalised later ^[2]	When ERCP unsuccessful or contraindicated (e.g., altered anatomy — Billroth II, Roux-en-Y; poor respiratory function) ^[2]^[3]; preferred for proximal/hilar obstruction (Klatskin tumour, RPC) where ERCP cannot access intrahepatic ducts
Surgical ECBD ^[3]	Decompression by exploration of common bile duct — open approach for emergency cases; laparoscopic approach in selected elective cases ^[3]	Indications: failure of endoscopic drainage; deterioration despite endoscopic drainage ^[3]; mortality ~30% (much higher than endoscopic/percutaneous drainage) — last resort ^[2]

RAD for Cholangitis — Must Know!

Resuscitation → Antibiotics → Drainage. The key teaching point: antibiotics ALONE will fail if the obstruction is not relieved — biliary obstruction impairs antibiotic secretion into bile. If the patient has Reynolds' pentad (septic shock) or fails to improve within 24h of antibiotics → urgent biliary drainage ^[2]^[3].

In unstable patients during ERCP: aspirate bile and pus to decompress the biliary tree FIRST before injecting contrast — contrast injection into an obstructed, infected system can worsen bacteraemia ^[2].

Long-Term Management After Cholangitis [2]

Cause	Long-Term Plan
Gallstone	ERCP stone removal (if not done acutely) + LC (early preferred over interval) ^[2]
Benign/malignant stricture	Endoscopic stent placement or definitive surgical resection ^[2]
RPC	Regular ductal clearance (USG surveillance, ERCP to remove stones/dilate strictures); resection of affected hepatobiliary segment + biliary-enteric anastomosis (e.g., hepaticojejunostomy) if atrophic liver segment, failed non-operative treatment, or suspected cholangiocarcinoma ^[2]

Note: ascending cholangitis can recur even after LC because of ERCP-induced CBD dilatation or age-related CBD dilatation allowing stasis and ascending infection ^[2].

3.6 Gallstone Pancreatitis

Management has two phases: (1) Treat the acute pancreatitis and (2) Prevent recurrence by removing the gallbladder + addressing any CBD stone.

Acute Phase — Supportive Care [1]

Intervention	Detail	Rationale
NPO → early enteral nutrition	Start oral/NG feeding within 24–72h if tolerated; nasojejunal (NJ) feeding if oral not possible; TPN only if enteral route fails	Early enteral nutrition maintains gut mucosal barrier → reduces bacterial translocation → ↓ infected necrosis; TPN associated with gut atrophy and infection
IV fluids	Aggressive crystalloid resuscitation (goal-directed: urine output > 0.5 mL/kg/h)	Pancreatitis causes massive third-space fluid losses → hypovolaemia → pancreatic ischaemia → necrosis
Analgesia	NSAIDs for mild pain; opioids for severe pain; morphine should be AVOIDED (sphincter of Oddi spasm) ^[1]	Pethidine/fentanyl preferred if opioids needed
Antibiotics	Prophylactic antibiotics generally NOT recommended; may be considered if pancreatic necrosis > 30% on CT → imipenem/meropenem ^[1]	Target enteric organisms; antibiotics that penetrate necrosis: carbapenems, fluoroquinolones, metronidazole ^[1]
Monitoring	Vitals, I/O, serial bloods (WCC, CRP, calcium, LFT, amylase), severity scoring (Ranson, APACHE II, BISAP, CTSI)	Detect organ failure early; guide escalation to ICU

Addressing the Biliary Component [1]

Scenario	Action
Concurrent cholangitis or confirmed persistent CBD stone	ERCP within 24 hours of admission — sphincterotomy + stone extraction ^[1]
CBD obstruction suspected but no cholangitis	ERCP within 24–72h if visible stone on imaging, dilated CBD, or worsening LFT ^[1]
No evidence of CBD obstruction	ERCP is NOT indicated ^[1]; perform LFT, MRCP, or EUS to confirm before proceeding

Cholecystectomy After Recovery [1]

Severity	Timing
Mild pancreatitis	Cholecystectomy within the same index hospitalisation (can be performed safely within a week of recovery) ^[1]
Severe necrotizing pancreatitis	Delay cholecystectomy (interval LC) until active inflammation subsides and fluid collections resolve or stabilise ^[1]

The rationale for same-admission cholecystectomy in mild disease: if you discharge the patient and bring them back later, ~30% will have a recurrent biliary event (colic, cholecystitis, recurrent pancreatitis, cholangitis) in the interval — this is an avoidable risk ^[1].

3.7 Mirizzi Syndrome [1][2]

Csendes Type	Management
Type I (no fistula)	Laparoscopic or open cholecystectomy ^[2]
Type II–V (with fistula)	Open surgery — subtotal cholecystectomy (severe inflammation impedes safe dissection of Calot's triangle) + CBD repair: closure of fistula / choledochoplasty / bilioenteric anastomosis (choledochojejunostomy) depending on size of defect ^[2]
Pre-operative	ERCP for biliary stenting (temporary decompression) ^[1]

Why subtotal cholecystectomy? The dense inflammatory adhesions around Hartmann's pouch make full dissection of Calot's triangle extremely hazardous — attempting a complete cholecystectomy risks catastrophic CBD injury. Leaving the posterior GB wall attached to the liver bed (and removing the rest) is safer ^[2].

3.8 Gallstone Ileus [2]

Step	Detail	Rationale
Enterolithotomy	Exploratory laparotomy → identify impacted stone → make proximal enterotomy (NOT over the stone — the bowel wall overlying the stone is ulcerated and friable → high leak risk if incised there) → milk the stone proximally for extraction ^[2]	Relieve the mechanical SBO — this is the life-saving step
Cholecystectomy + fistula repair	Same-session or elective depending on patient fitness ^[2]	Remove the source and close the fistula to prevent recurrence

3.9 RPC (Recurrent Pyogenic Cholangitis) [2]

Phase	Management
Acute	Resuscitation + IV antibiotics + biliary drainage (ERCP is difficult for intrahepatic stones → PTBD preferred; or T-tube drainage; or hepaticocutaneojejunostomy (HCJ) = a surgical access conduit for repeated biliary interventions) ^[2]
Long-term prevention	Regular ductal clearance: USG surveillance + ERCP to remove stones and dilate strictures
Surgical	Resection of affected hepatobiliary segment + biliary-enteric anastomosis (e.g., hepaticojejunostomy) — indications: atrophic liver segment, failed non-operative treatment, suspected cholangiocarcinoma ^[2]

4. Summary Table — Management at a Glance

Presentation	Initial Mx	Definitive Mx
Asymptomatic	Watchful waiting; UDCA if cholesterol stone	Prophylactic LC only if high risk (porcelain GB, polyp ≥ 1 cm, large stones, TPN)
Biliary colic	NSAIDs, NPO, antiemetics	Elective LC
Acute cholecystitis	NPO, IVF, IV antibiotics	Early LC (within 72h); PTC if unfit; Emergency LC if complicated
Choledocholithiasis	Risk-stratify	ERCP + sphincterotomy + stone extraction → LC
Acute cholangitis	RAD: Resuscitate + Antibiotics + Drainage	ERCP (1st line drainage) → LC
Gallstone pancreatitis	Supportive (IVF, analgesia, NPO → early enteral feeding)	ERCP if cholangitis/CBD stone → LC same admission (mild) or interval (severe)
Mirizzi	ERCP stenting	LC (Type I) or open subtotal cholecystectomy + CBD repair (Type II–V)
Gallstone ileus	Resuscitation	Enterolithotomy → LC + fistula repair

High Yield Summary — Management of Gallstones

Elective LC is the definitive treatment for almost all symptomatic gallstone disease — it removes the stone factory.
Early LC (within 72h) is the standard of care for acute cholecystitis — safe, single-admission, avoids recurrence while waiting.
Critical View of Safety: clear Calot's triangle, expose cystic plate, see ONLY 2 structures (cystic duct + artery) → prevents bile duct injury. If CVS not achieved → IOC or convert to open.
Tokyo severity grading guides cholecystitis management: Grade I–II → early LC; Grade III → organ support + GB drainage (PTC) → delayed LC.
Cholecystostomy indications: high surgical risk, haemodynamically unstable, difficult cholecystectomy.
Choledocholithiasis: risk-stratify → High = ERCP directly; Intermediate = MRCP/EUS first; Low = LC + IOC.
RAD for cholangitis: Resuscitation → Antibiotics (cefuroxime + metronidazole or Tazocin) → Drainage (ERCP 1st line).
QMH drainage hierarchy: ERCP → PTBD → surgical ECBD.
ERCP complications: pancreatitis (most common), perforation (intra- vs retroperitoneal), bleeding, cholangitis.
ERCP contraindications: altered GI anatomy (Billroth II, Roux-en-Y), bowel obstruction, severe coagulopathy.
Gallstone pancreatitis: ERCP within 24h if concurrent cholangitis; ERCP NOT indicated if no CBD obstruction; LC same admission if mild, interval if severe.
Morphine should be AVOIDED in biliary/pancreatic pain → sphincter of Oddi spasm. NSAIDs preferred.
Prophylactic antibiotics NOT recommended in pancreatitis unless necrosis > 30% → carbapenems.

Active Recall - Management of Gallstones

1. What is the RAD approach for acute cholangitis and when is urgent biliary drainage indicated?

Your answer

Show mark scheme

R = Resuscitation (NPO, IVF, monitor vitals/IO). A = Antibiotics (IV Augmentin or cefuroxime + metronidazole for mild; Tazocin for severe). D = Drainage (ERCP 1st line). Urgent drainage indicated if: Reynolds' pentad (shock + AMS), or failure to improve within 24h of antibiotics. Rationale: biliary obstruction impairs antibiotic secretion into bile.

2. State the three criteria for the Critical View of Safety during laparoscopic cholecystectomy and explain why it is essential.

Your answer

Show mark scheme

1. Hepatocystic triangle cleared of all fat/fibrous tissue. 2. Lower third of GB separated from cystic plate (liver bed). 3. Only two structures seen entering GB (cystic duct and cystic artery). Essential because misidentification of the cystic duct is the commonest cause of bile duct injury. If CVS not achieved, perform IOC or convert to open.

3. A patient has mild gallstone pancreatitis with no evidence of cholangitis or CBD obstruction. Outline the management plan including timing of cholecystectomy.

Your answer

Show mark scheme

Acute: Supportive care (NPO then early enteral nutrition, IV fluids, analgesia with NSAIDs - avoid morphine, monitoring). ERCP is NOT indicated in absence of CBD obstruction. Cholecystectomy: perform within the same index hospitalisation (within 1 week of recovery) for mild pancreatitis to prevent recurrent biliary events (30% risk if discharged without LC).

4. Compare early vs interval cholecystectomy for acute cholecystitis: timing, advantages, and disadvantages of each.

Your answer

Show mark scheme

Early LC: within 48-72h of symptom onset. Advantages: avoid recurrent symptoms, readmission, shorter hospital stay, single admission, easier dissection (pericholecystic fluid creates tissue planes). Disadvantages: higher bleeding risk, higher conversion-to-open rate. Interval LC: after 6-12 weeks. Advantages: avoid misdiagnosis, easier dissection (resolved inflammation), less septic complications. Disadvantages: separate admission, fibrosis makes mobilisation difficult, chance of recurrence while waiting. Current evidence favours early LC.

5. List the indications for cholecystostomy in acute cholecystitis and name three drainage modalities.

Your answer

Show mark scheme

Indications: high surgical risk, haemodynamically unstable, difficult cholecystectomy, Grade III severity, late presentation >72h, failure of antibiotic therapy. Modalities: 1. Percutaneous transhepatic cholecystostomy (PTC) - 1st line. 2. Endoscopic transpapillary drainage via ERCP. 3. EUS-guided transmural drainage (needle + LAMS).

6. What is the QMH biliary drainage hierarchy for acute cholangitis, and what are the indications for surgical ECBD?

Your answer

Show mark scheme

Hierarchy: ERCP (1st line) then PTBD (if ERCP fails/contraindicated) then surgical ECBD (last resort). Indications for surgical ECBD: failure of endoscopic drainage, clinical deterioration despite endoscopic drainage. Open approach for emergency; laparoscopic in selected elective cases. Mortality of surgical ECBD is ~30%.

References

^[1] Senior notes: felixlai.md (Treatment of Cholelithiasis, Treatment of Choledocholithiasis, Cholecystitis treatment — Tokyo grading, GB drainage overview, ERCP complications, Acute Cholangitis treatment, Acute Pancreatitis — prevention/cholecystectomy timing, Mirizzi syndrome treatment sections) ^[2] Senior notes: maxim.md (Asymptomatic gallstones, Biliary colic management, Acute cholecystitis — early vs interval LC and PTC, Cholecystectomy — indications/CVS/operative details, Choledocholithiasis management, Acute cholangitis — RAD, Gallstone ileus management, Mirizzi syndrome management, RPC management sections) ^[3] Lecture slides: GC 200. RUQ pain, jaundice and fever Cholecytitis and cholangitis Imaging of GI system.pdf (slides on cholecystectomy — open/lap/early/delayed, cholecystostomy indications, cholangitis management — antibiotics and ERCP/ECBD)

Complications of Gallstones

Gallstones are one of those conditions where the complications are arguably more important than the disease itself. An asymptomatic stone sitting in the gallbladder is harmless — it is what happens when it moves, obstructs, inflames, or erodes that causes the full spectrum of surgical pathology. The complications are best understood by thinking about where the stone is and what it is doing to the surrounding structures.

1. Framework: Complications Organised by Anatomical Site

The lecture slides provide a clean list of gallstone complications ^[3]:

Complications of gallstone disease ^[3]:

Mucocele of gallbladder

Empyema of gallbladder

Rupture of gallbladder

Acute cholangitis

Acute pancreatitis

Cholecystoduodenal fistula

Liver abscess

Building on this, we can organise all complications into three anatomical categories ^[1]^[2]:

Additionally, there are complications of cholecystectomy itself — which are just as examinable ^[2].

2. Complications in the Gallbladder

2.1 Acute Cholecystitis

Pathology: Acute inflammation of gallbladder → Obstruction of cystic duct → Complication of gallstone disease → Chemical inflammation → bacterial infection ^[3].

This is the most common complication of symptomatic gallstones. The pathophysiology was covered in detail in the Clinical Features section: prolonged cystic duct obstruction → bile concentration → chemical inflammation (first 48h) → secondary bacterial infection (E. coli, Klebsiella, Strep. faecalis) ^[2]. The key concept is that acute cholecystitis is the gateway to a cascade of progressively more dangerous complications if left untreated.

2.2 Mucocele of Gallbladder (Hydrops) [1][3]

Mechanism: Prolonged impaction of a stone in the cystic duct without active cholecystitis → bile within the gallbladder gets absorbed (since no fresh bile can enter) → but the gallbladder epithelium continues to secrete mucus → the gallbladder becomes distended with colourless, mucoid fluid (not bile) = "white bile" ^[1].

Feature	Detail	Pathophysiological Basis
Palpable gallbladder	May be palpable on examination	GB distended with mucus
Usually non-tender	No active inflammation (unlike cholecystitis)	Cystic duct obstruction without bacterial infection or chemical irritation
Complications	Can progress to oedema of GB wall, secondary infection, inflammation, and perforation ^[1]	Chronic distension compromises mural blood flow → ischaemia → predisposes to bacterial superinfection
Management	Early cholecystectomy is generally indicated to avoid complications ^[1]	Even though it may persist with few consequences, the risk of progression justifies removal

The distinction from acute cholecystitis is important: mucocele = distended but non-inflamed, non-tender GB; cholecystitis = distended, inflamed, tender GB with systemic signs.

2.3 Empyema of Gallbladder [2][3]

Mechanism: Acute cholecystitis with persistent cystic duct obstruction → secondary bacterial infection becomes fulminant → pus fills the gallbladder (empyema = "pus within a cavity"). This is essentially an intracystic abscess.

Feature	Detail	Pathophysiological Basis
Clinical presentation	Tender RUQ mass + septic-looking patient ^[2]; high swinging fever, rigors, marked leucocytosis	Walled-off collection of pus under pressure → systemic sepsis
Distinction from simple cholecystitis	Much more toxic-appearing; GB is palpable as a tense, exquisitely tender mass	Pus under pressure within a closed space; GB wall is stretched and inflamed beyond simple cholecystitis
Risk	Can progress to gangrene, perforation, or biliary sepsis	Ongoing bacterial proliferation with compromised mural blood supply
Management	Urgent intervention: emergency LC or percutaneous cholecystostomy if unfit for surgery ^[1]	Must decompress the infected collection

2.4 Gangrenous Cholecystitis [1]

Mechanism: Continued distension of the gallbladder → increased intraluminal pressure exceeds mural perfusion pressure → ischaemic necrosis of the gallbladder wall (gangrene). This is the MOST common complication of cholecystitis ^[1], occurring in approximately 20% of cases ^[2].

Feature	Detail	Pathophysiological Basis
Clinical clue	Presence of a sepsis-like picture suggests the diagnosis ^[1]; paradoxically, patient may report decreased RUQ pain	Nerve endings in the GB wall are destroyed by necrosis → pain may transiently decrease even as the patient becomes more systemically unwell
Lab findings	Markedly elevated WCC ( > 18,000), CRP; blood cultures may be positive	Full-thickness necrosis → bacterial invasion of wall → bacteraemia
Imaging	CT: irregular/absent GB wall enhancement; intraluminal membranes; pericholecystic abscess	Non-enhancing areas of wall = necrotic tissue (no blood supply to take up contrast)
Management	Emergency cholecystectomy — gangrenous GB will not resolve with antibiotics alone ^[2]	Necrotic tissue cannot be sterilised; only removal prevents perforation

Beware the 'Improving' Patient

A patient with acute cholecystitis whose pain suddenly decreases but whose systemic status worsens (↑ tachycardia, ↑ fever, ↑ WCC) may have developed gangrenous cholecystitis — the pain improves because the nerves in the GB wall are dead. This is a surgical emergency, not an improvement.

2.5 Emphysematous Cholecystitis [1][2]

Mechanism: Secondary infection of the gallbladder wall with gas-forming organisms — most commonly Clostridium perfringens (welchii) — producing gas within the GB wall and lumen ^[1]^[2].

Feature	Detail	Pathophysiological Basis
Clinical presentation	Insidious onset; abdominal crepitus adjacent to the gallbladder ^[1]^[2]	Gas produced by Clostridia dissects through tissue planes
Labs	Unconjugated hyperbilirubinaemia may be present ^[1]	Clostridial infection produces toxins that cause haemolysis → ↑ unconjugated bilirubin from RBC destruction ^[1]
Imaging	CT/AXR: gas within GB wall and/or lumen — pathognomonic	Gas produced by bacterial fermentation
Risk factors	Elderly males, diabetics (impaired immunity + microvascular disease → GB ischaemia)	DM → microangiopathy → ischaemic GB wall → anaerobic bacteria thrive in necrotic tissue
Management	Emergency cholecystectomy — high mortality if untreated ^[2]	Gas gangrene progresses rapidly; antibiotics alone cannot penetrate gas-filled necrotic tissue

2.6 Gallbladder Perforation (Rupture of Gallbladder) [1][2][3]

Mechanism: Occurs after development of gangrene → perforation in ischaemic areas of the GB wall ^[1]. The outcome depends on whether the perforation is contained or free.

Type	Detail	Pathophysiological Basis
Contained (most common)	Perforation is walled off by the omentum and adjacent organs → localised pericholecystic abscess or intrahepatic abscess ^[1]	The greater omentum ("policeman of the abdomen") migrates to seal off the perforation site
Free perforation	Rare (omentum usually prevents this) → generalised biliary peritonitis	Bile is a chemical irritant and contains bacteria → diffuse peritoneal inflammation → septic shock
Perforation into adjacent organ	GB wall erodes into duodenum, colon, or stomach → cholecystoenteric fistula ^[1]	Long-standing pressure necrosis from an impacted stone rather than acute inflammation ^[1]
Management	Emergency surgery: contained → drainage + cholecystectomy; free → laparotomy, washout, cholecystectomy; fistula → see gallstone ileus section	Uncontained bile peritonitis is rapidly fatal without surgery

2.7 Chronic Cholecystitis and Its Complications

Chronic cholecystitis itself is a complication of recurrent gallstone disease (repeated episodes of acute cholecystitis or persistent mechanical irritation → fibrosis and thickening of GB wall) ^[2]. It then predisposes to further complications:

Complication	Mechanism
Porcelain gallbladder	Chronic inflammation → extensive scarring → dystrophic calcification of GB wall ^[2]; 2–3% risk of malignancy → absolute indication for cholecystectomy even if asymptomatic ^[1]^[2]
CA Gallbladder	Chronic inflammation → dysplasia → carcinoma sequence; 95% of patients with GB carcinoma have gallstones ^[1]; chronic cholecystitis is the single strongest risk factor
Typhoid carrier state	Salmonella typhi colonises the chronically inflamed gallbladder → chronic biliary carriage ^[2]; cholecystectomy may be needed to eradicate carriage

3. Complications in the Bile Duct

3.1 Choledocholithiasis

Stone migrates from GB through cystic duct into CBD → obstructive jaundice, cholestatic LFT. This is a complication in itself but also the gateway to the three major duct complications below ^[1].

3.2 Acute Cholangitis [3]

The most common complication of CBD stones (along with gallstone pancreatitis) ^[1]. Biliary obstruction + stasis → bacterial infection of the biliary tract. Covered in detail in previous sections.

Severity	Clinical Correlate
Mild-moderate	Charcot's triad (fever, jaundice, RUQ pain) — responds to antibiotics
Severe / Suppurative	Reynolds' pentad (Charcot's triad + hypotension + altered mental status) → biliary sepsis → septic shock → multi-organ failure if not drained urgently ^[1]^[2]

Key concept: 15% of patients will NOT respond to antibiotics alone and require emergency biliary decompression ^[1] — because the obstruction prevents antibiotics from being secreted into bile.

3.3 Acute Pancreatitis [3]

Gallstones are the most common cause of acute pancreatitis (55%) ^[4]. Mechanism: stone impacts at the ampulla of Vater → reflux of bile into the pancreatic duct → premature activation of trypsinogen → autodigestion of pancreas → release of inflammatory mediators (SIRS) ^[2].

The complications of pancreatitis itself are extensive and deserve detailed coverage:

Local Complications (Revised Atlanta Classification)

Complication	Time	Mechanism	Management
Acute peripancreatic fluid collection	< 4 weeks	Inflammatory exudate around the pancreas, no defined wall	Usually self-resolves; no intervention unless infected
Pancreatic pseudocyst	≥ 4 weeks	Encapsulated collection of pancreatic juice/debris with a well-defined fibrous wall but NO epithelial lining (hence "pseudo-")	Observe if small and asymptomatic; drain if symptomatic ( > 6 cm), infected, or compressing adjacent structures — endoscopic (EUS-guided cystogastrostomy), percutaneous, or surgical drainage
Acute necrotic collection	< 4 weeks	Areas of non-viable pancreatic or peripancreatic tissue ± fluid, no mature wall	Usually managed conservatively; intervene if infected
Walled-off necrosis	≥ 4 weeks	Maturation of necrotic collection into an encapsulated mixed solid-liquid mass	If infected → step-up approach: percutaneous/endoscopic drainage → if fails, minimally invasive necrosectomy → open necrosectomy as last resort
Infected necrosis	Usually > 2 weeks	Bacterial translocation from the gut into necrotic tissue	Suspect if clinical deterioration after initial improvement, gas bubbles within necrosis on CT → antibiotics (carbapenems) + drainage/necrosectomy

Systemic Complications

Complication	Mechanism
SIRS / Sepsis	Massive cytokine release (TNF-α, IL-1, IL-6) from pancreatic and peripancreatic necrosis → systemic inflammatory response
Organ failure	Respiratory (ARDS — inflammatory mediators → ↑ alveolar-capillary permeability + pleural effusions from diaphragmatic inflammation); Renal (pre-renal AKI from hypovolaemia + direct cytokine-mediated tubular injury); Cardiovascular (distributive shock from SIRS)
Hypocalcaemia / Tetany	Fat saponification: lipase → fat necrosis → release of fatty acids → precipitate with calcium → ↓ serum calcium → Chvostek's/Trousseau's sign ^[2]
Hyperglycaemia	Destruction of islets of Langerhans (β-cells) → insulin deficiency
Cullen's sign / Grey Turner's sign	Retroperitoneal haemorrhage tracking along tissue planes: periumbilical (Cullen's) and flanks (Grey Turner's) ^[2]
Splenic vein thrombosis	Inflammation of pancreatic tail adjacent to splenic vein → thrombosis → left-sided portal hypertension → gastric varices
Pseudoaneurysm	Pancreatic enzymes erode into adjacent arteries (splenic, gastroduodenal, pancreaticoduodenal) → severe and fatal haemorrhage ^[1]

Pseudoaneurysm — A Hidden Killer

Suspect pseudoaneurysm if a patient with pancreatitis develops sudden haemorrhagic shock or haematemesis. Severe and fatal haemorrhage can occur following endoscopic drainage in patients with an unsuspected pseudoaneurysm ^[1]. Always perform CT angiography before draining pancreatic collections to rule this out. Treatment is angiographic embolisation or surgery.

3.4 Mirizzi Syndrome [1][2]

Stone impacted in Hartmann's pouch/cystic duct → extrinsic compression of the common hepatic duct → obstructive jaundice. Chronic inflammation → erosion of bile duct wall → cholecystobiliary fistula (Csendes Types II–V) ^[1]^[2]. Long-term: association with CA gallbladder due to recurrent inflammation and biliary stasis ^[2].

4. Complications from Perforation / Erosion to Other Sites

4.1 Cholecystoenteric Fistula and Gallstone Ileus [1][2][3]

Mechanism: Chronic cholecystitis → GB wall erodes through into adjacent bowel (usually duodenum) via a cholecystoenteric fistula → large stone ( > 2.5 cm) passes into the bowel → impacts at the narrowest point of the small bowel (terminal ileum, ~2 feet proximal to the ileocaecal valve) → mechanical small bowel obstruction ^[2].

"Cholecystoduodenal fistula" ^[3] is the term used on the lecture slides.

Fistula Type	Consequence
Cholecystoduodenal (most common)	Symptomatic gallstone ileus — distal SBO ^[2]
Cholecystocolic	Usually asymptomatic (large bowel has a wider lumen) ^[2]
Cholecystogastric	Rare; gastric outlet obstruction

Bouveret's syndrome: Stone impacts in the duodenum or stomach, causing gastric outlet obstruction (GOO) rather than SBO ^[2].

Diagnostic triad on AXR/CT — Rigler's triad ^[2]:

Pneumobilia (air in biliary tree — through the fistula)
Small bowel obstruction
Ectopic gallstone (usually in RIF at ileocaecal valve)

4.2 Liver Abscess [1][3]

Mechanism: Two routes:

Direct extension: GB perforation (contained) → pericholecystic abscess extends into liver parenchyma → intrahepatic abscess ^[1].

Ascending cholangitis: CBD obstruction → biliary sepsis → ascending infection into intrahepatic ducts → pyogenic liver abscess.

Feature	Detail
Presentation	Swinging fever, RUQ pain, tender hepatomegaly; may mimic cholangitis
Imaging	USG/CT: hypoechoic/hypodense intrahepatic collection
Management	Percutaneous drainage + IV antibiotics; treat underlying cause (cholecystectomy, CBD clearance)

5. Complications of Cholecystectomy

These are complications of the treatment of gallstones and are highly examinable ^[2]:

5.1 Immediate Complications

Complication	Detail	Pathophysiological Basis
Conversion to open surgery	5% in elective cases, 25% in emergency cases — NOT a failure ^[2]	Dense adhesions, unclear anatomy, uncontrolled bleeding, or inability to achieve CVS
GA risks	Aspiration, cardiovascular events, anaphylaxis	General anaesthesia-related
Bleeding	From liver bed (middle hepatic vein close to GB fossa), cystic artery, trocar sites ^[2]	Venous bleeding from liver bed is the most common
Damage to neighbouring structures	Bile leakage (biliary tree), bleeding (cystic artery), pneumoperitoneum-related injury (duodenum, transverse colon, hepatic flexure) ^[2]	Thermal/mechanical injury during dissection, trocar insertion injuries

5.2 Early Complications (Days to Weeks)

Complication	Detail	Pathophysiological Basis
Biliary leakage	From cystic duct stump or duct of Luschka; incidence ~0.5% ^[2]	Cystic duct clip slippage or necrosis of duct stump; duct of Luschka = small accessory bile ductule in the GB fossa draining directly into the liver bed, often injured during GB dissection
	If noted intra-op: repair + T-tube placement ^[2]
	Delayed presentation (post-op D2–10): fever, RUQ pain, deranged LFT; Ix: USG/CT → HIDA scan/MRCP; Mx: ERCP stent (minor leak) or laparotomy + lavage + Roux-en-Y hepaticojejunostomy (major leak) ^[2]	Bile is a chemical and bacterial irritant → bile peritonitis if not contained
Post-op jaundice	Dropped or missed CBD stones ^[2]	Stones dislodged during manipulation → fall into CBD → obstruction
Post-op cholangitis	Infected residual stone	Obstruction + bacteria
Post-op diarrhoea	Initial uncoordinated excessive bile salt excretion + fat malabsorption ^[2]	Loss of GB reservoir → continuous bile flow into duodenum → excess bile salts reach colon → stimulate colonic secretion (bile salt diarrhoea); resolves in weeks as the body adapts
Bleeding	Liver bed, cystic artery, trocar sites ^[2]	May present as haemodynamic instability or drain output

5.3 Late Complications

Complication	Detail	Pathophysiological Basis
Bile duct stricture	Most feared long-term complication; Mx: reconstruction ± hepaticojejunostomy ^[2]	Thermal injury, clip placement on CBD (misidentified as cystic duct), ischaemic injury → fibrosis → stricture — this is why CVS is so critical
Subphrenic abscess	Collection in the subphrenic/subhepatic space; Mx: drainage + antibiotics ^[2]	Residual bile/blood in the operative field becomes infected
Post-cholecystectomy syndrome	Persistent symptoms (e.g., biliary colic, diarrhoea) after operation ^[2]	Causes: residual CBD stone, bile duct stricture, sphincter of Oddi dysfunction, bile salt diarrhoea, or non-biliary cause (PUD, IBS) that was the true cause of symptoms all along
Post-cholecystectomy choledocholithiasis	CBD stones forming after cholecystectomy ^[2]	Bile stasis due to increased CBD calibre — loss of GB storage function → CBD dilates to compensate → stasis predisposes to stone formation ^[2]

Post-Cholecystectomy Syndrome

If a patient returns with RUQ pain after cholecystectomy, don't just dismiss it. Investigate systematically:

Retained/new CBD stone — check LFT, USG for dilated CBD, MRCP
Bile duct stricture — MRCP/ERCP
Bile leak — HIDA scan, USG for collection
Sphincter of Oddi dysfunction — manometry
Non-biliary cause — was the original diagnosis correct? Consider PUD (OGD), IBS, chronic pancreatitis

The most common cause of post-cholecystectomy syndrome is actually a non-biliary condition that was present before surgery and not addressed ^[2].

6. Complications Specific to RPC

Because RPC (Recurrent Pyogenic Cholangitis) is particularly relevant to Hong Kong, its complications deserve separate mention ^[2]:

Complication	Mechanism
Recurrent biliary sepsis	Ongoing cycle of stasis → infection → stones → more stasis ^[2]
Liver abscess	Direct extension of intrahepatic infection
Pancreatitis	Stones migrating to ampulla
Cirrhosis	Chronic biliary obstruction → secondary biliary cirrhosis ^[2]
Cholangiocarcinoma	Chronic inflammation → malignant transformation of biliary epithelium — mandates long-term surveillance ^[2]

7. Master Complications Summary Table

Site	Complication	Key Feature / Mechanism
Gallbladder	Mucocele	Mucus-filled distended GB, "white bile", non-tender
	Empyema	Pus-filled GB, septic patient, tender mass
	Gangrenous cholecystitis (most common Cx of cholecystitis)	Ischaemic necrosis of wall, paradoxical ↓ pain
	Emphysematous cholecystitis	Gas-forming organisms (C. perfringens), gas in wall, crepitus, haemolysis
	Perforation	Contained (abscess) or free (biliary peritonitis)
	Porcelain GB	Calcified wall, 2–3% cancer risk, absolute indication for LC
	CA Gallbladder	95% have gallstones, chronic inflammation → dysplasia → carcinoma
Bile Duct	Choledocholithiasis	Obstructive jaundice, cholestatic LFT
	Acute cholangitis	Obstruction + infection; Charcot's triad / Reynolds' pentad
	Gallstone pancreatitis	Stone at ampulla → reflux → autodigestion; most common cause of pancreatitis
	Mirizzi syndrome	CHD compression by Hartmann's pouch stone; cholecystobiliary fistula
Other Sites	Cholecystoduodenal fistula → gallstone ileus	SBO; Rigler's triad (pneumobilia, SBO, ectopic stone)
	Liver abscess	Direct extension or ascending cholangitis
Post-LC	Bile duct injury / stricture	Most feared; prevented by CVS
	Biliary leakage	Cystic duct stump or duct of Luschka
	Post-cholecystectomy syndrome	Persistent symptoms; investigate for retained stone, stricture, SOD, non-biliary cause

High Yield Summary — Complications of Gallstones

Gangrenous cholecystitis is the MOST common complication of acute cholecystitis (~20%); suspect when sepsis picture worsens but pain paradoxically decreases (nerve necrosis).
Emphysematous cholecystitis: gas-forming organisms (C. perfringens); gas in GB wall on CT; may cause unconjugated hyperbilirubinaemia from haemolysis; emergency LC.
Mucocele: prolonged cystic duct obstruction without inflammation → "white bile"; GB is palpable but non-tender.
Empyema: pus-filled GB; tender RUQ mass + septic patient.
Perforation: usually contained by omentum → pericholecystic abscess; free perforation → biliary peritonitis (surgical emergency).
Cholecystoenteric fistula → gallstone ileus: Rigler's triad = pneumobilia + SBO + ectopic stone; stone impacts at terminal ileum; Bouveret's = GOO.
Porcelain GB: calcified GB wall → 2–3% malignancy risk → absolute indication for cholecystectomy.
CA gallbladder: 95% have gallstones; chronic inflammation → dysplasia → carcinoma; very poor prognosis (5-year OS < 5%).
Cholangitis complications: biliary sepsis → Reynolds' pentad → multi-organ failure if not drained.
Pancreatitis complications: pseudocyst, infected necrosis, pseudoaneurysm, hypocalcaemia (fat saponification), ARDS, splenic vein thrombosis.
Complications of LC: biliary leakage (cystic duct stump / duct of Luschka), bile duct injury/stricture (most feared — prevented by CVS), post-cholecystectomy syndrome.
RPC complications: biliary sepsis, liver abscess, cirrhosis (chronic obstruction), cholangiocarcinoma (chronic inflammation).

Active Recall - Complications of Gallstones

1. What is the most common complication of acute cholecystitis, and what is the paradoxical clinical clue that suggests it?

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Gangrenous cholecystitis (occurs in ~20% of cases). Paradoxical clue: pain may DECREASE because nerve endings in the GB wall are destroyed by ischaemic necrosis, but systemic signs WORSEN (rising tachycardia, fever, WCC). A sepsis-like picture suggests the diagnosis.

2. Explain the pathophysiology of mucocele of the gallbladder, including why it contains 'white bile'.

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Prolonged stone impaction in cystic duct WITHOUT cholecystitis. No fresh bile can enter the GB, so existing bile is absorbed by the GB mucosa. However, the GB epithelium continues to secrete mucus. The GB becomes distended with colourless mucoid fluid (white bile). It is palpable but non-tender because there is no active inflammation.

3. Why does emphysematous cholecystitis cause unconjugated hyperbilirubinaemia? Name the causative organism.

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Emphysematous cholecystitis is caused by Clostridium perfringens (welchii). Clostridial toxins cause haemolysis (destruction of red blood cells), releasing haemoglobin which is broken down to unconjugated bilirubin. This exceeds the liver's conjugation capacity, causing unconjugated hyperbilirubinaemia.

4. Name three late complications of laparoscopic cholecystectomy and explain the mechanism of each.

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1. Bile duct stricture: thermal/clip injury to CBD during surgery causes ischaemia and fibrosis leading to stricture formation. 2. Post-cholecystectomy syndrome: persistent symptoms due to retained CBD stone, stricture, SOD dysfunction, or non-biliary cause misdiagnosed as gallstone disease. 3. Post-cholecystectomy choledocholithiasis: loss of GB storage function causes CBD dilatation and bile stasis, predisposing to new stone formation in the CBD.

5. A patient with chronic pancreatitis from gallstones develops sudden massive GI haemorrhage. What is the likely complication and how would you investigate and manage it?

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Pseudoaneurysm: pancreatic enzymes erode into adjacent arteries (splenic, gastroduodenal, pancreaticoduodenal). Investigate with CT angiography. Manage with angiographic embolisation (1st line) or surgery. Important: always rule out pseudoaneurysm with CT angiography BEFORE attempting endoscopic drainage of pancreatic collections.

6. List the complications of RPC that are relevant to the Hong Kong context.

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1. Recurrent biliary sepsis (stasis-infection-stone cycle). 2. Liver abscess (intrahepatic extension). 3. Pancreatitis (stone migration to ampulla). 4. Secondary biliary cirrhosis (chronic biliary obstruction). 5. Cholangiocarcinoma (chronic inflammation of biliary epithelium leading to malignant transformation). Mandates long-term surveillance.

References

^[1] Senior notes: felixlai.md (Complications of gallstones, Complications of cholecystitis — gangrenous/emphysematous/perforation/cholecystoenteric fistula, Mucocele, Mirizzi syndrome, RPC, Acute pancreatitis complications — pseudoaneurysm, Gallbladder cancer) ^[2] Senior notes: maxim.md (Acute cholecystitis complications — empyema/gangrene/perforation/emphysematous/gallstone ileus, Chronic cholecystitis — porcelain GB/CA GB, Mirizzi syndrome, Gallstone ileus — Rigler's triad, RPC complications, Cholecystectomy specific complications — immediate/early/late, Acute pancreatitis — Cullen's/Grey Turner's/hypocalcaemia, Post-cholecystectomy syndrome) ^[3] Lecture slides: GC 200. RUQ pain, jaundice and fever Cholecytitis and cholangitis Imaging of GI system.pdf (Complications of gallstone disease slide; Acute cholecystitis pathology slide) ^[4] Lecture slides: Acute pancreatitis.pdf

Gallstones

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