Acute Cholecystitis

1. Definition

Acute cholecystitis is acute inflammation of the gallbladder, most commonly precipitated by obstruction of the cystic duct ^[1]. It is a complication of gallstone disease ^[1].

Let's break this down from first principles:

• "Chole-" = bile (Greek: cholē)
• "-cyst-" = bladder/sac (Greek: kystis)
• "-itis" = inflammation

So cholecystitis literally means "inflammation of the bile sac." The acute form implies a sudden, clinically significant inflammatory episode — as opposed to chronic cholecystitis, which is a smouldering, fibrotic process from repeated insults.

The key distinction to grasp early: this is not simply a stone blocking a duct and causing pain (that's biliary colic). Acute cholecystitis is what happens when the obstruction persists, the gallbladder becomes distended, and a cascade of chemical inflammation followed by secondary bacterial infection ensues ^[1][2][3].

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2. Epidemiology

2.1 Global & Hong Kong Context

• Gallstone disease affects approximately 10–15% of the adult population in Western countries; the prevalence in Hong Kong/Southern China is somewhat lower but rising with Westernisation of diet (higher fat, higher calorie intake) ^[2].
• Acute cholecystitis develops in ~1–3% of patients with symptomatic gallstones per year ^[2]. Once you become symptomatic with biliary colic, the risk of progression to cholecystitis or other complications is < 5% per year ^[2].
• Female predominance — follows the gallstone demographic ("5F" mnemonic: Fat, Female, Forty, Fertile, Family history) ^[2][4].
• In Hong Kong, there is additional relevance of pigment stones secondary to:
  • Recurrent pyogenic cholangitis (RPC / "Hong Kong disease") — associated with Clonorchis sinensis parasitic infestation from consumption of raw freshwater fish ^[5].
  • Haemolytic conditions endemic in Southern China (e.g. G6PD deficiency, thalassaemia) leading to black pigment stones ^[4].
• Acalculous cholecystitis accounts for approximately 5–10% of all acute cholecystitis cases and is predominantly seen in critically ill, hospitalised patients ^[2][3].

2.2 Age and Sex

• Peak incidence: 5th–6th decade
• Female:Male ratio approximately 3:1 (mirrors gallstone prevalence)
• Acalculous cholecystitis does not follow this sex distribution — it occurs in the critically ill regardless of sex

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3. Risk Factors

Risk factors for acute cholecystitis are essentially the risk factors for gallstones (since calculous cholecystitis is 90–95% of cases) plus factors that promote cystic duct obstruction and biliary stasis.

3.1 Risk Factors for Gallstone Formation

3.2 Additional Risk Factors Specific to Acalculous Cholecystitis

Acalculous cholecystitis classically occurs in hospitalised/critically ill patients ^[2][3]:

• Dehydration → bile inspissation
• Shock / systemic hypoperfusion → gallbladder ischaemia (microvascular occlusion)
• TPN → no enteral feeding → no CCK release → gallbladder stasis (↓CCK)
• Extensive burns, major operations, multiple trauma
• Sepsis / multi-organ dysfunction
• Prolonged ICU stay

The underlying mechanism is gallbladder ischaemia + bile stasis rather than mechanical obstruction by a stone ^[2][3].

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4. Anatomy and Function

Understanding the anatomy is essential because it directly explains the pathophysiology, clinical signs, surgical approach, and complications.

4.1 Gallbladder Anatomy

The gallbladder consists of: fundus, body, infundibulum (Hartmann's pouch), and neck ^[2][6].

• Fundus: The blind, rounded end that projects beyond the inferior border of the liver. It contacts the anterior abdominal wall at the tip of the 9th costal cartilage where the right lateral margin of the rectus abdominis crosses the costal margin — this is the Murphy's point, where you palpate for Murphy's sign.
• Body: The main portion, lies in a fossa on the visceral surface of the liver (segments IV and V).
• Infundibulum (Hartmann's pouch): A saccular outpouching at the junction of the body and neck. This is the most common site for stone impaction — stones collect here by gravity and get jammed into the narrow transition to the cystic duct. This is also where stones impact in Mirizzi syndrome, compressing the adjacent common hepatic duct ^[6].
• Neck: Tapered, S-shaped portion that leads into the cystic duct. Contains mucosal folds (spiral valves of Heister) which do not have a true sphincter function but can trap small stones.

4.2 Cystic Duct and Calot's Triangle

• The cystic duct (typically 2–4 cm long) connects the gallbladder neck to the common hepatic duct, forming the common bile duct (CBD).
• Calot's triangle (hepatocystic triangle): Bounded by the cystic duct inferiorly, the common hepatic duct medially, and the inferior surface of the liver superiorly. The cystic artery (usually a branch of the right hepatic artery) runs through this triangle.
  • Calot's triangle is the critical zone of dissection during cholecystectomy — inflammation in acute cholecystitis causes oedema and adhesions here, making surgery hazardous.

4.3 Blood Supply

• Cystic artery: Usually a branch of the right hepatic artery (in ~75% of individuals). It is an end-artery — there is no collateral supply to the gallbladder.
  • Why does this matter? In acute cholecystitis, the distended, inflamed gallbladder wall compresses its own blood supply. An end-artery with no collaterals → ischaemia → gangrenous cholecystitis (occurs in ~20% of cases) ^[3].

4.4 Venous and Lymphatic Drainage

• Venous drainage is via small cystic veins directly into the liver (segments IV and V) and partly via the cystic vein into the portal vein.
• Lymphatic drainage flows to the cystic duct lymph node (Lund's node / node of Calot) → hepatic nodes → coeliac nodes.

4.5 Nerve Supply

• Sympathetic: from the coeliac plexus (T7–T9).
• Parasympathetic: from the vagus nerve.
• Visceral afferents travel with sympathetic fibres to T7–T9 dermatomes — this explains why:
  • Biliary colic/cholecystitis pain is felt in the epigastrium/RUQ (T7–T9 dermatomes)
  • Pain can radiate to the right shoulder tip/interscapular area via the phrenic nerve (C3–C5), because the diaphragmatic peritoneum overlying the gallbladder fossa shares the same nerve supply (referred pain / Boas sign)

4.6 Gallbladder Function

• Storage and concentration of bile: Between meals, the sphincter of Oddi is tonically contracted, diverting bile into the gallbladder. The gallbladder concentrates bile 5–10× by absorbing water and electrolytes.
• Contraction and bile release: After a fatty meal, cholecystokinin (CCK) is released from I-cells of the duodenal mucosa → CCK causes gallbladder smooth muscle contraction + relaxation of sphincter of Oddi → bile ejected into the duodenum.
  • Why fatty meals trigger biliary colic: CCK-mediated contraction forces a stone against the cystic duct orifice or Hartmann's pouch → obstruction → increased intraluminal pressure → pain.

4.7 Biliary Tree Overview

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5. Aetiology

5.1 Calculous Cholecystitis (90–95%)

The most common cause — obstruction of the cystic duct by an impacted gallstone ^[1][2][3].

The stone typically impacts at Hartmann's pouch or the cystic duct itself. The type of stone matters for understanding the underlying disease but the pathophysiology of obstruction is the same regardless of stone type.

Types of gallstones (Hong Kong relevance):

Most gallstones are mixed stones ^[4].

5.2 Acalculous Cholecystitis (5–10%)

Not associated with gallstones. Caused by microvascular occlusion within the gallbladder wall leading to ischaemia and secondary infection ^[3].

Risk factors: hospitalised/critically ill patients — dehydration, shock, TPN, burns, sepsis, major surgery, prolonged illness with multi-organ dysfunction ^[2][3].

5.3 Rare Causes

• Tumour obstructing the cystic duct ( < 1%) ^[2]
• Biliary sludge (micro-lithiasis / biliary "mud"): precipitated calcium bilirubinate granules and cholesterol microcrystals in thick mucus; functionally behaves like small stones
• Parasitic (Ascaris blocking cystic duct — very rare)

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6. Pathophysiology

This is the most important section for understanding everything else. Let's walk through the cascade step by step.

6.1 The Pathophysiological Cascade (Calculous)

Step 1 — Obstruction: A gallstone impacts at Hartmann's pouch or the cystic duct → complete obstruction → no bile can enter or leave the gallbladder ^[2][3].

Step 2 — Distension: The gallbladder mucosa continues to secrete mucus but nothing can drain → progressive distension → raised intraluminal pressure ^[2].

Step 3 — Chemical inflammation (first 48 hours): Stagnant bile becomes concentrated. Lysolecithin, a normal bile constituent, reaches toxic concentrations and acts as a mucosal toxin, initiating chemical inflammation ^[2][3]. Phospholipase A converts lecithin (phosphatidylcholine) in bile to lysolecithin. Inflammatory mediators, particularly prostaglandins, are released, propagating the inflammatory response ^[2].

This is why NSAIDs (prostaglandin synthesis inhibitors) are first-line analgesics in biliary colic and cholecystitis — they directly target this pathophysiological mechanism.

Step 4 — Wall oedema and vascular compromise: The inflammatory oedema thickens the gallbladder wall. The distended gallbladder compresses its own blood supply (remember, the cystic artery is an end-artery). This creates a vicious cycle: ischaemia → more inflammation → more oedema → more ischaemia.

Step 5 — Secondary bacterial infection (15–30% of cases): Bacteria contaminate the biliary system secondarily — they do not initiate the process ^[2]. Common organisms include:

• Gram-negative rods: Escherichia coli (most common), Klebsiella pneumoniae, Enterobacter spp.
• Gram-positive: Enterococcus spp. ^[2]
• Anaerobes: Bacteroides fragilis (especially in severe/gangrenous cases)

These are enteric organisms — they reach the gallbladder via ascending infection from the duodenum through the cystic duct, or via haematogenous/lymphatic spread.

Step 6 — Complications if untreated:

• Empyema: Bacterial superinfection → pus fills the gallbladder
• Gangrenous cholecystitis (~20%): Ischaemic necrosis of the gallbladder wall ^[3]
• Perforation: Necrotic wall ruptures → localised (walled off by omentum) or free → biliary peritonitis
• Emphysematous cholecystitis: Infection by gas-forming organisms (e.g., Clostridium welchii/perfringens) → gas in the gallbladder wall

6.2 Mucocele / Hydrops

When the cystic duct is obstructed for a prolonged period without significant infection:

• All bilirubin within the gallbladder is absorbed by the mucosa
• The gallbladder fills with colourless mucoid fluid ("white bile")
• This is a mucocele (hydrops) — a distended gallbladder full of sterile mucus ^[2]

6.3 Pathophysiology of Acalculous Cholecystitis

Microvascular occlusion within the gallbladder → ischaemia → inflammation → secondary infection ^[3].

The mechanism is fundamentally different from calculous cholecystitis:

• No stone → no mechanical obstruction
• Instead, systemic hypoperfusion (shock, sepsis) + bile stasis (TPN, fasting, opioids reducing GB motility) → gallbladder wall ischaemia
• The ischaemic mucosa is more susceptible to bacterial invasion
• Progresses to gangrene and perforation faster than calculous cholecystitis

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7. Classification

7.1 By Aetiology

7.2 Tokyo Guidelines Severity Grading (TG18/TG13)

The Tokyo Guidelines classify acute cholecystitis by severity, which directly guides management ^[2]:

7.3 By Chronicity

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8. Clinical Features

8.1 Symptoms

8.2 Signs

8.3 Differentiating Features from Biliary Colic

This is a very high-yield comparison for exams ^[2][4]:

8.4 Signs of Complications

Certain clinical findings should alert you to complicated cholecystitis:

8.5 Complications of Gallstone Disease (Overview from Lecture Slides)

Complications of gallstone disease ^[1]:

• Mucocele of gallbladder
• Empyema of gallbladder
• Rupture of gallbladder
• Acute cholangitis
• Acute pancreatitis
• Cholecystoduodenal fistula
• Liver abscess

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9. Summary Comparison Table: Gallstone Disease Presentations

This is an essential "bird's-eye view" table ^[4]:

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Active Recall - Acute Cholecystitis

1. What is the pathophysiological sequence that leads from gallstone impaction to acute cholecystitis?

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Stone impaction at cystic duct/Hartmann's pouch → persistent obstruction → GB distension → bile stasis and concentration → chemical inflammation (lysolecithin as mucosal toxin; prostaglandins) in first 48h → secondary bacterial infection (15-30%: E. coli, Klebsiella, Enterococcus) → empyema/gangrene/perforation if untreated.

2. How do you clinically differentiate acute cholecystitis from biliary colic? Name at least 4 distinguishing features.

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(1) Duration: biliary colic < 6h vs cholecystitis > 6h. (2) Fever: absent in colic, present in cholecystitis. (3) Peritoneal signs: absent in colic (visceral pain only), present in cholecystitis (Murphy's sign, guarding, rebound). (4) Labs: normal WBC in colic vs leukocytosis/elevated CRP in cholecystitis. (5) Natural history: colic self-resolves; cholecystitis does not.

3. What is Murphy's sign, and why is it positive in cholecystitis but negative in cholangitis?

Your answer

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Murphy's sign = inspiratory arrest during deep palpation of RUQ. On inspiration, diaphragm descends, pushing inflamed gallbladder onto examiner's hand causing sharp pain. Positive in cholecystitis because the gallbladder itself is inflamed. Negative in cholangitis because the inflammation is in the CBD, not the gallbladder.

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

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(1) Presence of gallstones. (2) Distended GB (> 4 x 10 cm). (3) GB wall thickening > 3 mm. (4) Pericholecystic fluid/stranding. (5) Sonographic Murphy's sign.

5. Why does acute cholecystitis typically NOT cause jaundice? Name 3 exceptions where cholecystitis CAN present with jaundice.

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The obstruction is at the cystic duct, not the CBD — bile can still drain from liver through CHD/CBD into duodenum, so bilirubin metabolism is unaffected. Exceptions: (1) Mirizzi syndrome (stone in Hartmann's pouch compresses CHD). (2) Double impaction (stone in cystic duct AND distal CBD simultaneously, ~7%). (3) Concurrent choledocholithiasis. Also severe inflammation causing oedema compressing CBD (rare).

6. What is acalculous cholecystitis? Who gets it and why does it have higher mortality?

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Inflammation of GB without gallstones, caused by microvascular occlusion and ischaemia. Occurs in critically ill/hospitalised patients (dehydration, shock, TPN, burns, sepsis, major surgery). Higher mortality (up to 30-50%) because: (1) patients already critically ill, (2) ischaemic mechanism predisposes to earlier gangrene/perforation, (3) diagnosis often delayed as patients cannot communicate symptoms.

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References

^[1] Lecture slides: GC 200. RUQ pain, jaundice and fever Cholecytitis and cholangitis Imaging of GI system.pdf (p3–5) ^[2] Senior notes: felixlai.md (Cholecystitis sections, pp. 553–555; Gallstones overview, p. 508) ^[3] Senior notes: maxim.md (Acute calculous cholecystitis, Acute acalculous cholecystitis, pp. 130–136) ^[4] Senior notes: maxim.md (Gallstone diseases overview, stone composition table, symptomatic gallstones summary, pp. 130–131) ^[5] Senior notes: maxim.md (Recurrent pyogenic cholangitis, p. 136) ^[6] Senior notes: felixlai.md (Mirizzi syndrome — Gallbladder anatomy, pp. 572–573)

Differential Diagnosis of Acute Cholecystitis

When a patient presents with RUQ pain, fever, and signs of peritoneal irritation, acute cholecystitis is high on the list — but it is far from the only diagnosis. The differential is broad because the RUQ is a "busy neighbourhood": the gallbladder, liver, hepatic flexure of the colon, right kidney, right adrenal, duodenum, head of pancreas, right lower lung, and right hemidiaphragm all live here. Referred pain from distant structures (heart, right lung) can also localise to the RUQ.

The key to a logical differential is to think anatomically and then refine based on clinical features, lab findings, and imaging.

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Approach to the Differential Diagnosis

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Detailed Differential Diagnosis

1. Biliary Colic — The Most Important Differentiation

This is the single most critical distinction on exams and in clinical practice ^[2][3][4].

Biliary colic is caused by transient obstruction of Hartmann's pouch or the cystic duct by a gallstone — the gallbladder contracts (often in response to a fatty meal via CCK), presses a stone against the outlet, intraluminal pressure rises, and visceral pain occurs. Crucially, there is no true gallbladder wall inflammation ^[2][3].

Why is biliary colic "steady" and not truly colicky? The gallbladder is a muscular sac with tonic contraction — it does not have the rhythmic peristalsis of the intestine (which gives the classical crescendo-decrescendo "colicky" pattern). The name "biliary colic" is actually a misnomer ^[3].

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2. Acute Cholangitis

Charcot's triad (50–70%): Fever + RUQ pain + Jaundice ^[6][7] Reynold's pentad ( < 10%): Charcot's triad + Hypotension + Altered mental status ^[6][7]

This is a bacterial infection of the biliary tree secondary to CBD obstruction — fundamentally different from cholecystitis, where the problem is at the cystic duct/gallbladder ^[6][7].

How to differentiate from cholecystitis:

• Jaundice: Present in cholangitis (CBD obstruction prevents bilirubin from reaching the duodenum → conjugated hyperbilirubinaemia); usually absent in uncomplicated cholecystitis (the cystic duct obstruction does not block the CBD) ^[1][2]
• Tea-coloured urine: Present in cholangitis (conjugated bilirubin is water-soluble → filtered by kidneys); absent in cholecystitis ("No tea-colored urine" as per the lecture case vignette) ^[1]
• Murphy's sign: Positive in cholecystitis; typically negative in cholangitis (the gallbladder itself is not the inflamed organ)
• Cholestatic LFT pattern: Prominent in cholangitis (↑↑ ALP, ↑↑ GGT, ↑ conjugated bilirubin); may be mildly elevated or normal in cholecystitis ^[2][6]
• Blood culture is essential in cholangitis (bacteraemia is common) ^[7]

Why does cholangitis cause altered mental status? CBD obstruction + bacterial infection → cholangio-venous reflux (infected bile under pressure refluxes into the bloodstream through the hepatic sinusoids) → Gram-negative bacteraemia/sepsis → septic shock → encephalopathy. This is the pathophysiology behind Reynold's pentad.

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3. Choledocholithiasis (CBD Stones without Infection)

A gallstone that has migrated from the gallbladder through the cystic duct into the common bile duct ^[4]. This causes obstructive jaundice without necessarily causing infection (that distinction is what separates choledocholithiasis from cholangitis).

How to differentiate from cholecystitis:

• Jaundice is the hallmark — cholestatic LFT pattern (↑ ALP, ↑ GGT, ↑ conjugated bilirubin)
• Pain may be present but fever is typically absent (unless cholangitis develops)
• USG shows dilated CBD with gallstone rather than the 5 cardinal signs of cholecystitis ^[4]
• Can coexist with cholecystitis ("double impaction" — stone simultaneously in cystic duct AND distal CBD, ~7%) ^[4]

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4. Acute Pancreatitis

Epigastric pain that radiates to the back, often severe, constant, improved by sitting up or leaning forward, exacerbated by movement ^[8][9]. Gallstones are the most common cause of acute pancreatitis (a stone impacts at the ampulla of Vater, obstructing the pancreatic duct → duodeno-pancreatic reflux → premature trypsinogen activation → autodigestion) ^[8][9].

How to differentiate from cholecystitis:

• Location: Epigastric > RUQ (although overlap exists, especially with gallstone pancreatitis)
• Radiation: To the back (retropancreatic inflammation of the retroperitoneal structures) vs. right shoulder in cholecystitis
• Relief posture: Sitting up/leaning forward relieves pancreatitis pain (takes the pancreas away from the retroperitoneum); movement worsens cholecystitis pain
• Amylase/Lipase: Markedly elevated ( > 3× upper limit of normal) in pancreatitis; may be mildly elevated in cholecystitis but not to the same degree ^[8]
• Cullen's sign (periumbilical bruising) and Grey Turner's sign (flank bruising) — pathognomonic for severe necrotising pancreatitis (retroperitoneal haemorrhage tracking along tissue planes) — NOT seen in cholecystitis ^[9]
• Tetany from transient hypocalcaemia — fat saponification (liberated fatty acids bind calcium) — unique to pancreatitis ^[9]

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5. Peptic Ulcer Disease (PUD) / Perforated Peptic Ulcer

• Uncomplicated PUD: Epigastric pain related to meals (duodenal ulcer: pain relieved by eating; gastric ulcer: pain worsened by eating). No fever, no peritoneal signs. Can be distinguished by history and endoscopy.
• Perforated peptic ulcer: Sudden-onset, severe epigastric pain → becomes generalised → board-like rigidity → peritonitis. Air under the diaphragm on erect CXR (pneumoperitoneum). Usually no fever initially (chemical peritonitis from gastric acid, not infection).
  • Valentino's sign: Gastric/duodenal contents tracking down the right paracolic gutter → pain localises to the RLQ, mimicking acute appendicitis ^[10]
  • Distinguished from cholecystitis by the abrupt onset ("thunderclap"), absence of preceding biliary symptoms, and pneumoperitoneum on imaging

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6. Acute Appendicitis

Classically begins as periumbilical pain (visceral, poorly localised via T10 dermatome) then migrates to the RLQ (McBurney's point) as parietal peritoneal inflammation develops ^[10].

How to differentiate from cholecystitis:

• Location: RLQ (McBurney's point) vs. RUQ
• Migration pattern: Periumbilical → RLQ (appendicitis) vs. epigastric → RUQ (cholecystitis)
• Murphy's sign: Positive in cholecystitis, NOT in appendicitis
• Appendicitis-specific signs ^[10]: Pointing sign (McBurney's point), Rovsing's sign (RLQ pain on LLQ palpation), Psoas sign (retrocaecal appendix), Obturator sign (pelvic appendix)
• Age: Appendicitis peaks in 10–30 years; cholecystitis peaks in 40–60 years

However, beware:

• A high-riding/retrocaecal appendix can present with RUQ pain mimicking cholecystitis
• Right-sided diverticulitis (more common in Asian populations) can mimic either ^[10]

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7. Acute Hepatitis

Inflammation of the liver parenchyma from viral (HAV, HBV, HCV, HEV), alcoholic, drug-induced, or autoimmune causes ^[2].

How to differentiate from cholecystitis:

• Hepatocellular LFT pattern: Markedly ↑ AST and ALT (often > 10× ULN) with only mild ↑ ALP — this is the opposite of the cholestatic pattern seen in biliary obstruction
• Jaundice: Often present (hepatocyte dysfunction → impaired bilirubin conjugation/excretion)
• Tender hepatomegaly: Diffuse liver tenderness rather than focal RUQ/gallbladder point tenderness
• No Murphy's sign: The gallbladder is not inflamed
• Viral serology (HBsAg, anti-HAV IgM, etc.) clinches the diagnosis

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8. Liver Abscess

• Pyogenic liver abscess: Fever, RUQ pain, tender hepatomegaly, swinging fevers, rigors. Often secondary to biliary tract disease (ascending cholangitis) or portal pyaemia (from appendicitis, diverticulitis). Blood cultures often positive.
• Amoebic liver abscess: Travel history (endemic areas), diarrhoea, RUQ pain, tender hepatomegaly. Amoebic serology positive.

How to differentiate from cholecystitis:

• Hepatomegaly more prominent than gallbladder tenderness
• Murphy's sign negative (the gallbladder is not the source)
• USG/CT: Well-defined hepatic collection (abscess cavity) rather than the 5 cardinal signs of cholecystitis
• Liver abscess is listed as a complication of gallstone disease in the lecture slides — so the two can coexist ^[1]

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9. Right Lower Lobe Pneumonia / Pleuritis

This is a classic "trap" in exams. Basal pneumonia or pleurisy on the right side can cause referred RUQ pain via irritation of the diaphragmatic pleura (phrenic nerve, C3–C5 — same dermatomes as the shoulder/RUQ).

How to differentiate from cholecystitis:

• Respiratory symptoms: Cough (productive/dry), dyspnoea, pleuritic chest pain (sharp, worse on inspiration — different quality from the steady visceral pain of cholecystitis)
• Chest examination: Bronchial breathing, crepitations, dullness to percussion, decreased air entry over the right base
• CXR: Consolidation or pleural effusion in the right lower lobe
• Abdominal examination: May have RUQ tenderness but Murphy's sign is negative and there are no gallbladder-specific USG findings

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10. Myocardial Infarction (Inferior MI)

An inferior MI (right coronary artery territory) can present with epigastric pain that mimics biliary or pancreatic pathology ^[2][8]. The inferior surface of the heart sits on the diaphragm; ischaemic pain from the inferior myocardium can be referred to the epigastrium via vagal afferents.

How to differentiate from cholecystitis:

• Cardiovascular risk factors: Hypertension, diabetes, smoking, hyperlipidaemia, family history of IHD
• Associated features: Diaphoresis, breathlessness, radiation to jaw/left arm, haemodynamic instability
• ECG: ST elevation in leads II, III, aVF (inferior MI)
• Troponin: Elevated
• Murphy's sign negative, normal abdominal USG

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11. Sphincter of Oddi Dysfunction / Functional Gallbladder Disorder

• Pain typically lasts < 6 hours and occurs intermittently ^[5]
• Normal laboratory and radiological tests ^[5]
• Diagnosis of exclusion after structural causes are ruled out
• Sphincter of Oddi dysfunction: biliary-type pain caused by functional obstruction at the sphincter of Oddi (spasm or stenosis), without stones

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12. Other Differentials (by Region)

RUQ-specific ^[11]:

• Subphrenic abscess: Post-operative, fever, referred shoulder tip pain
• Fitz-Hugh-Curtis syndrome: Perihepatitis secondary to PID (Chlamydia trachomatis or Neisseria gonorrhoeae) — RUQ pain in a young sexually active female with vaginal discharge. Laparoscopy shows "violin-string" adhesions between liver capsule and anterior abdominal wall

Urological:

• Right renal/ureteric colic: Colicky flank pain radiating to the groin (loin-to-groin), haematuria, restless patient (in contrast to cholecystitis patients who lie still)
• Right pyelonephritis: Fever + loin pain + dysuria/frequency; costovertebral angle tenderness; pyuria on urinalysis

Gynaecological (in females of reproductive age):

• Ruptured ovarian cyst, ovarian torsion, ectopic pregnancy, PID — always ask about LMP, sexual history, vaginal discharge
• β-hCG is mandatory in any woman of reproductive age with acute abdominal pain

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Summary Differential Diagnosis Table

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Active Recall - Differential Diagnosis of Acute Cholecystitis

1. Name the key clinical features that differentiate biliary colic from acute cholecystitis.

Your answer

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Duration (< 6h vs > 6h), fever (absent vs present), peritoneal signs including Murphy's sign (absent vs present), lab findings (normal vs leukocytosis and raised CRP), natural history (self-resolving vs persistent/progressive). Pain character is steady in both (not truly colicky).

2. A patient presents with RUQ pain, fever, and jaundice. What is the most likely diagnosis and what clinical sign helps differentiate it from acute cholecystitis?

Your answer

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Most likely diagnosis is acute cholangitis (Charcot's triad: fever + RUQ pain + jaundice). Murphy's sign is typically NEGATIVE in cholangitis (inflammation is in the CBD, not the gallbladder) but POSITIVE in cholecystitis. Cholestatic LFT pattern and blood cultures further distinguish cholangitis.

3. Why can an inferior myocardial infarction mimic acute cholecystitis? What investigation must not be missed?

Your answer

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The inferior surface of the heart sits on the diaphragm; ischaemic pain from the inferior myocardium (RCA territory) is referred to the epigastrium via vagal afferents, mimicking biliary or upper GI pathology. An ECG must always be performed in acute upper abdominal pain. Troponin should be checked if suspicion remains.

4. How does acute pancreatitis differ from acute cholecystitis in terms of pain characteristics and relieving factors?

Your answer

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Pancreatitis: epigastric pain radiating to the BACK, relieved by sitting up or leaning forward (takes pancreas off retroperitoneum), exacerbated by movement. Cholecystitis: RUQ pain radiating to right shoulder/interscapular area, worsened by movement, patient lies still. Amylase/lipase > 3x ULN in pancreatitis.

5. List 3 conditions where acute cholecystitis can present with jaundice (exceptions to the usual rule of no jaundice in cholecystitis).

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(1) Mirizzi syndrome: stone impacted in Hartmann's pouch/cystic duct compresses the common hepatic duct. (2) Double impaction (~7%): stone simultaneously in cystic duct AND distal CBD. (3) Concurrent choledocholithiasis: separate stone migrated into the CBD. Also rarely: severe pericholecystic inflammation causing oedema compressing the CBD.

References

^[1] Lecture slides: GC 200. RUQ pain, jaundice and fever Cholecytitis and cholangitis Imaging of GI system.pdf (p3–5) ^[2] Senior notes: felixlai.md (Cholecystitis sections, pp. 553–556) ^[3] Senior notes: maxim.md (Acute calculous cholecystitis, Biliary colic, pp. 130–131) ^[4] Senior notes: maxim.md (Symptomatic gallstones summary table, Courvoisier's Law, p. 130) ^[5] Senior notes: felixlai.md (Differential diagnosis of biliary colic, pp. 510–511) ^[6] Senior notes: felixlai.md (Acute cholangitis, pp. 520–521) ^[7] Senior notes: maxim.md (Acute cholangitis, p. 135) ^[8] Senior notes: felixlai.md (Acute pancreatitis — clinical manifestation and DDx, pp. 579–580) ^[9] Senior notes: maxim.md (Acute pancreatitis, p. 138) ^[10] Senior notes: maxim.md (Acute appendicitis — differential diagnosis, p. 87) ^[11] Senior notes: maxim.md (Acute abdomen differential diagnosis by region, p. 43)

Diagnostic Criteria

Tokyo Guidelines (TG18/TG13) — The Standard Diagnostic Framework

The Tokyo Guidelines provide a structured, internationally accepted framework for diagnosing acute cholecystitis. The principle is straightforward: you need local inflammation + systemic inflammation + imaging confirmation ^[2][3][4].

Think of it as a three-legged stool — each leg strengthens the diagnosis:

Interpretation ^[2]:

• Suspected diagnosis = One item in A + One item in B (clinical diagnosis without imaging)
• Definite diagnosis = One item in A + One item in B + One item in C (clinically confirmed by imaging)

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Diagnostic Algorithm

The following algorithm represents the practical clinical approach when you suspect acute cholecystitis. It integrates history, examination, lab work, and imaging in a logical sequence.

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Investigation Modalities

Overview: What to Order and Why

When you suspect acute cholecystitis, you need investigations for three purposes:

1. Confirm the diagnosis (USG ± HIDA/MRCP)
2. Assess severity and rule out complications (bloods, CT)
3. Exclude differentials and identify coexisting biliary pathology (LFT, amylase, ECG, CXR)

Investigations to order ^[3][4]:

• Bloods: CBC D/C, LRFT, amylase, clotting, blood C/ST, X-match, lipid profile ^[3]
• USG abdomen (1st-line imaging) ^[3]
• CT abdomen + pelvis (to rule out complications) ^[3]
• HIDA scan or MRCP (if USG inconclusive) ^[3][4]

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A. Laboratory Investigations

1. CBC with Differentials

2. Liver Function Tests (LFT)

This is a subtle but critical point:

Liver chemistry is usually NORMAL in uncomplicated acute cholecystitis ^[2]. Why? Because the obstruction is at the cystic duct — bile can still flow freely from the liver through the common hepatic duct → CBD → duodenum. Bilirubin conjugation, excretion, and bile acid metabolism are all intact.

3. Amylase / Lipase

Always check amylase/lipase in suspected cholecystitis to exclude concurrent gallstone pancreatitis ^[3].

4. Clotting Profile (PT/INR)

• Needed pre-operatively (cholecystectomy is the definitive treatment)
• Prolonged PT may indicate vitamin K malabsorption from bile duct obstruction (fat-soluble vitamin absorption requires bile salts for micelle formation) or underlying liver disease

5. Blood Culture and Sensitivity

• Should be taken if there is high-grade fever, rigors, or suspicion of sepsis
• Helps guide targeted antibiotic therapy if secondary bacterial infection is present
• Particularly important if cholangitis is suspected (bacteraemia is common in cholangitis)

6. Group and Cross-Match

• Cholecystectomy carries a risk of haemorrhage (especially from the cystic artery or aberrant hepatic arterial anatomy)
• Blood should be available in case of intraoperative bleeding or conversion to open surgery

7. Other Bloods

• CRP: Marker of systemic inflammation; part of Tokyo criteria component B. Serial CRP is useful for monitoring treatment response.
• RFT (Renal function tests): Baseline assessment; dehydration from vomiting; pre-operative assessment; needed for severity grading (Tokyo Grade III includes renal dysfunction — Cr > 2.0 mg/dL)
• Lipid profile: Identifies risk factors for cholesterol gallstones (hyperlipidaemia) ^[3]

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B. Imaging Investigations

1. Abdominal Ultrasound (USG) — First-Line Imaging

USG is the first-line imaging modality for suspected acute cholecystitis ^[2][3][4]. It is readily available, non-invasive, no radiation, relatively quick, and can be performed at the bedside in an acutely unwell patient.

The 5 Cardinal USG Signs of Acute Cholecystitis ^[3]:

5 cardinal signs of acute cholecystitis — important! ^[3]

Sensitivity and Specificity:

• Sensitivity for gallstones: ~95%
• Sensitivity for acute cholecystitis (combined signs): ~85–90%
• Specificity: ~80% (wall thickening and pericholecystic fluid can occur in other conditions)

Limitations of USG ^[4]:

• Operator-dependent — accuracy varies with sonographer experience
• Limited by body habitus (excessive body fat) — sound waves attenuate in adipose tissue
• Limited by bowel gas — gas reflects ultrasound completely, obscuring structures behind it (especially distal CBD)
• Small stones ( < 3 mm) or stones in the cystic duct may be missed
• Cannot reliably visualise the distal CBD (bowel gas from the duodenum overlies it)

What else to look for on USG:

• CBD diameter: Normal CBD ≤ 6 mm (add 1 mm per decade of life over age 60; rule of thumb: 0.1 cm for every 10 years old ^[5]). Dilated CBD suggests coexisting choledocholithiasis or distal obstruction.
• Intrahepatic duct dilatation: Suggests proximal biliary obstruction
• Liver parenchyma: Look for abscess (liver abscess is a complication of gallstone disease ^[1])
• Causes of dilated CBD ^[5]: obstruction, aging, post-cholecystectomy

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2. Hepatobiliary Iminodiacetic Acid (HIDA) Scan — Second-Line (Gold Standard for Functional Assessment)

"HIDA" = Hepatobiliary IminoDiacetic Acid. The full name of the tracer is 99mTc-hepatic 2,6-dimethyliminodiacetic acid ^[2].

Principle:

• A radiotracer (99mTc-HIDA) is injected intravenously
• It is taken up by hepatocytes (like bilirubin) and excreted into the biliary system
• A gamma camera tracks the radiotracer as it flows through the bile ducts and into the gallbladder and duodenum
• Normal: the gallbladder should be visualised within 30 minutes (tracer fills the GB via the cystic duct) and the duodenum within 60 minutes ^[2]

Key Finding in Acute Cholecystitis:

• Non-visualisation of the gallbladder after 4 hours = cystic duct obstruction ^[2][3][5]
• The tracer fills the bile ducts and duodenum normally, but cannot enter the gallbladder because the cystic duct is blocked (by the impacted stone or surrounding oedema)
• A normal HIDA scan effectively excludes acute cholecystitis ^[2]

Sensitivity and Specificity:

• Sensitivity: ~95–97% (highest of all modalities for acute cholecystitis)
• Specificity: ~90%

When to use:

• Indicated when diagnosis remains unclear following abdominal USG or in atypical cases ^[2]
• Inconclusive USG ^[3]
• Acalculous cholecystitis (where stones are absent but cystic duct dysfunction is suspected)

Limitations ^[2]:

• Expensive and long study duration (up to 4 hours) → limits use as a first-line test
• Depends on hepatic excretion of bile → may not be useful in jaundiced patients (hepatocytes cannot excrete the tracer effectively when bilirubin is very high — bilirubin > 5 mg/dL significantly impairs accuracy) ^[2]
• False positives: prolonged fasting ( > 24 hours), TPN, chronic cholecystitis, severe hepatic disease — all cause non-filling of the GB without acute obstruction
• Morphine augmentation can improve specificity: morphine contracts the sphincter of Oddi (↑ SoD pressure), forcing any tracer in the CBD back up into the gallbladder — if the GB still doesn't fill, obstruction is confirmed ^[3]

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3. Magnetic Resonance Cholangiopancreatography (MRCP)

"MRCP" — magnetic resonance imaging specifically optimised for the biliary and pancreatic ductal systems.

Principle:

• Non-contrast, T2-weighted MRI sequence ^[5]
• Bile and pancreatic juice are bright (high signal) on T2 because they are fluid — this gives a beautiful "cholangiogram-like" image of the biliary tree without any contrast injection or invasive instrumentation

Role in Acute Cholecystitis:

• Superior to USG in detecting stones in the cystic duct ^[2] — the cystic duct is a notoriously difficult area for USG (small, tortuous, obscured by overlying bowel)
• Evaluate intrahepatic and extrahepatic bile ducts comprehensively ^[2]
• Useful when:
  • USG is inconclusive ^[3]
  • You suspect coexisting choledocholithiasis (CBD stones)
  • You need to assess biliary anatomy pre-operatively (e.g., Mirizzi syndrome, anatomical variants)
• Avoids complications associated with ERCP but is NOT therapeutic — it is purely diagnostic ^[5]

Limitations:

• Less readily available than USG
• Time-consuming (~30–45 minutes)
• Patient must lie still (difficult in acutely unwell or claustrophobic patients)
• Contraindicated in patients with certain metallic implants/pacemakers
• Cannot be performed at the bedside

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4. CT Abdomen and Pelvis

Role in Acute Cholecystitis:

• Usually unnecessary for diagnosis of uncomplicated acute cholecystitis ^[2] — USG is sufficient
• CT is primarily used to:
  • Detect complications: empyema, emphysematous cholecystitis (gas in GB wall — pathognomonic), perforation (pericholecystic abscess, free fluid), gangrenous cholecystitis ^[2][3]
  • Exclude alternative diagnoses when the clinical picture is unclear (acute pancreatitis, perforated PUD, appendicitis, liver abscess, malignancy)
  • Evaluate extent of inflammation in difficult cases

CT Findings in Acute Cholecystitis:

• Gallbladder wall oedema/thickening ^[2]
• Pericholecystic fat stranding
• Distended gallbladder
• Gallstones (CT only detects ~75% of gallstones because cholesterol stones are isodense to bile — USG is far superior for stones) ^[5]
• Gas in GB wall or lumen → emphysematous cholecystitis (air is black on CT → very conspicuous)
• Discontinuity of GB wall → perforation
• Rim enhancement of GB wall on contrast-enhanced CT → gangrenous cholecystitis

Limitations:

• Not useful for detecting gallstones compared to USG (only 75% sensitivity) ^[5]
• Radiation exposure
• IV contrast carries risk of allergic reaction and contrast nephropathy

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5. Abdominal X-Ray (AXR) and Erect Chest X-Ray (CXR)

These are not diagnostic for cholecystitis but are part of the acute abdomen workup:

AXR:

• Only ~15% of gallstones are radio-opaque on plain X-ray (only calcified stones) ^[4] — so AXR is insensitive for gallstones
• Mercedes Benz sign: A triradiate fissure pattern within a gallstone due to gas trapped in crevices of the stone — specific but rarely seen ^[4]
• May show porcelain gallbladder (calcified GB wall — associated with GB carcinoma)
• May show signs of complications: pneumobilia (gas in biliary tree → cholecystoenteric fistula), dilated bowel loops (gallstone ileus)

Erect CXR:

• Rule out right basal pneumonia/pleuritis (a common differential for RUQ pain)
• Rule out pneumoperitoneum (air under the diaphragm → perforated viscus, not cholecystitis)
• Check for pleural effusion (reactive effusion from subdiaphragmatic inflammation)

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6. Endoscopic Ultrasound (EUS)

Useful in choledocholithiasis ^[5] — very high sensitivity for detecting small CBD stones (even < 5 mm) that are missed by transabdominal USG (distal CBD is obscured by duodenal gas).

• Not routinely used for diagnosing cholecystitis itself
• May be useful when clinical suspicion of concurrent CBD stones is high but MRCP is inconclusive or unavailable

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7. ERCP (Endoscopic Retrograde Cholangiopancreatography)

• NOT a first-line diagnostic tool for cholecystitis — ERCP is invasive and carries risks (pancreatitis, perforation, bleeding)
• Both diagnostic and therapeutic ^[5]
• Reserved for when there is confirmed/suspected choledocholithiasis or cholangitis coexisting with cholecystitis
• Therapeutic role: sphincterotomy + stone extraction from the CBD; biliary stenting for decompression

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Investigation Summary Table

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Severity Assessment (Tokyo Guidelines Grading)

Once the diagnosis is confirmed, severity grading directly guides management ^[2][7]:

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Active Recall - Diagnosis of Acute Cholecystitis

1. State the three components of the Tokyo Guidelines diagnostic criteria for acute cholecystitis. What constitutes a suspected vs. definite diagnosis?

Your answer

Grade

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

2. List the 5 cardinal ultrasound signs of acute cholecystitis and explain the pathophysiological basis of pericholecystic fluid.

Your answer

Grade

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(1) Presence of gallstones (hyperechoic with posterior acoustic shadowing). (2) Distended GB > 4 x 10 cm. (3) GB wall thickening > 3 mm (with double wall sign from oedema). (4) Pericholecystic fluid/stranding. (5) Sonographic Murphy's sign. Pericholecystic fluid occurs because the inflamed, oedematous GB wall weeps inflammatory exudate into the surrounding peritoneal space.

3. What does a HIDA scan show in acute cholecystitis? Name two limitations of the HIDA scan.

Your answer

Grade

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HIDA shows non-visualisation of the gallbladder after 4 hours (tracer fills bile ducts and duodenum but cannot enter the GB due to cystic duct obstruction). Limitations: (1) expensive and long study duration (up to 4h), limiting first-line use; (2) depends on hepatic excretion, so unreliable in jaundiced patients (bilirubin > 5 mg/dL). Also false positives with prolonged fasting, TPN, chronic cholecystitis.

4. Why is the LFT usually normal in uncomplicated acute cholecystitis? What should you suspect if there is a cholestatic pattern?

Your answer

Grade

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The obstruction is at the cystic duct, not the CBD. Bile can still flow from the liver through the CHD and CBD into the duodenum, so bilirubin metabolism is unaffected. A cholestatic pattern (raised ALP, GGT, conjugated bilirubin) suggests concurrent choledocholithiasis, acute cholangitis, or Mirizzi syndrome (obstruction at the CBD/CHD level).

5. When is CT abdomen indicated in the workup of acute cholecystitis? Name three CT findings that suggest complicated cholecystitis.

Your answer

Grade

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CT is indicated to rule out complications or when diagnosis is unclear after USG. Three CT findings of complicated cholecystitis: (1) Gas in the GB wall or lumen = emphysematous cholecystitis. (2) Discontinuity of GB wall = perforation. (3) Rim enhancement/irregular wall thickening with surrounding stranding = gangrenous cholecystitis. Also: pericholecystic abscess collection.

6. Describe the Tokyo Guidelines severity grading for acute cholecystitis and its management implications.

Your answer

Grade

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Grade I (Mild): No organ dysfunction, mild inflammation → early laparoscopic cholecystectomy. Grade II (Moderate): WBC > 18000, palpable mass, duration > 72h, or marked local inflammation (gangrene/abscess/emphysematous) but no organ failure → early or delayed LC depending on expertise. Grade III (Severe): Any organ dysfunction (CVS, neuro, respiratory, renal, hepatic, haematological) → organ support + gallbladder drainage (percutaneous cholecystostomy) then delayed LC after stabilisation.

References

^[1] Lecture slides: GC 200. RUQ pain, jaundice and fever Cholecytitis and cholangitis Imaging of GI system.pdf (p3–5) ^[2] Senior notes: felixlai.md (Cholecystitis — Diagnosis sections, pp. 555–558; Severity grading, p. 558) ^[3] Senior notes: maxim.md (Acute calculous cholecystitis — Investigations, p. 131; Diagnostic criteria table, p. 131) ^[4] Senior notes: maxim.md (Biliary colic — Investigations, USG findings, p. 130; Symptomatic gallstones summary table, p. 130) ^[5] Senior notes: maxim.md (HBP investigations — USG, HIDA, MRCP, ERCP, CT, EUS, p. 119) ^[7] Senior notes: felixlai.md (Tokyo Guidelines severity grading table, p. 558)

Management of Acute Cholecystitis

Guiding Principles

The management of acute cholecystitis rests on three pillars, applied in sequence:

1. Resuscitation and supportive care — stabilise the patient
2. Medical treatment — control infection, inflammation, and symptoms
3. Definitive treatment — remove the gallbladder (the source of the problem) to prevent recurrence

The timing and approach to definitive treatment depend on the Tokyo Guidelines severity grading (Grade I–III), the duration of symptoms, and the patient's fitness for surgery.

Think of it this way: the gallbladder with its stone is a ticking bomb. Medical treatment defuses the immediate crisis. Surgery removes the bomb entirely.

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Management Algorithm

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1. Initial Resuscitation and Supportive Care

These measures apply to ALL patients regardless of severity grade. The aim is to stabilise the patient's physiology before any definitive intervention.

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2. Medical Treatment

A. Analgesia

Pain control with NSAIDs ^[2]

• First-line: NSAIDs (e.g., diclofenac, ketorolac, indomethacin)

  • Why NSAIDs first? The early inflammation in cholecystitis is mediated by prostaglandins released from the chemically irritated gallbladder mucosa (lysolecithin → phospholipase A → prostaglandins). NSAIDs inhibit cyclooxygenase (COX) → block prostaglandin synthesis → directly target the pathophysiological mechanism. They also reduce gallbladder pressure by relaxing smooth muscle. Evidence shows NSAIDs can reduce progression from biliary colic to cholecystitis.
  • Contraindications: renal impairment, peptic ulcer disease, coagulopathy, aspirin-sensitive asthma

• Second-line: Opioids (e.g., pethidine, morphine)

  • Used when NSAIDs are contraindicated or insufficient
  • Historical concern about morphine: It was traditionally taught that morphine causes sphincter of Oddi spasm and should be avoided. Current evidence suggests this is clinically insignificant at therapeutic doses, and morphine can be used safely. Pethidine was historically preferred but has no proven advantage and carries risk of seizures with repeated dosing.

• Adjuncts: Paracetamol (IV or oral), antispasmodics (hyoscine butylbromide)

B. IV Antibiotics

Acute cholecystitis is primarily an inflammatory process but secondary infection of gallbladder can occur as a result of cystic duct obstruction and bile stasis ^[2]

Antibiotics are given because:

1. 15–30% of cases develop secondary bacterial infection
2. You cannot reliably distinguish sterile chemical inflammation from infected cholecystitis clinically
3. Antibiotics prevent progression to empyema, gangrene, and sepsis
4. They are essential for treatment of pericholecystic abscess, emphysematous cholecystitis, and biliary sepsis ^[2]

Empirical antibiotic regimens — must cover Gram-negative aerobes and anaerobes ^[2]:

Why cover anaerobes? In complicated cholecystitis (gangrene, perforation, empyema), the ischaemic, necrotic gallbladder wall creates an anaerobic environment where organisms like Bacteroides fragilis and Clostridium species thrive. Metronidazole ("metro" = targeting anaerobic metabolism) is the classic anti-anaerobic agent.

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3. Definitive Surgical Treatment

The gallbladder is the source of the problem (it contains the stones, it is the organ that becomes inflamed). As long as it remains in situ, the patient is at risk of recurrent cholecystitis, empyema, gangrene, and gallstone migration into the CBD. Therefore:

The definitive treatment for acute cholecystitis is cholecystectomy — removal of the gallbladder.

A. Laparoscopic Cholecystectomy (LC) — The Gold Standard

Cholecystectomy (removal of gallbladder) — open or laparoscopic, delayed or early ^[1]

Laparoscopic cholecystectomy is the 1st-line definitive treatment for most patients ^[3][4].

Laparoscopic vs Open Cholecystectomy:

Indications for cholecystectomy ^[8][9]:

• Symptomatic gallstones with or without complications
• Acalculous cholecystitis
• Asymptomatic gallstones in high-risk patients:
  • Increased risk of gallbladder cancer: GB polyps > 1 cm, porcelain gallbladder, large gallstones > 3 cm ^[9]
  • Increased risk of gallstone complications: patients on long-term TPN, haemolytic disorders, gastric bypass (altered anatomy)
  • Concomitant liver surgery

Indications for conversion to open ^[9]:

• Cannot tolerate pneumoperitoneum (e.g., cardiopulmonary comorbidities — CO₂ insufflation increases intra-abdominal pressure → decreased venous return → cardiac compromise)
• Refractory coagulopathy
• Multiple prior abdominal surgeries (extensive adhesions)
• Gallbladder carcinoma (risk of tumour seeding from port sites)
• Failure to achieve the critical view of safety (anatomy unclear, bleeding, bile duct injury suspected)

B. Timing of Cholecystectomy: Early vs Delayed (Interval)

This is one of the most important management decisions and a high-yield exam topic ^[1].

Early or delayed surgery ^[1]:

"Early cholecystectomy is safe without increasing the risk of complications" ^[1]

The current evidence and guideline position:

• Early cholecystectomy should always be recommended unless contraindicated ^[7]
• 2013 Tokyo Guidelines: Surgery within 72 hours of symptom onset ^[7]
• 2018 Tokyo Guidelines: Even if > 72 hours has passed since symptom onset, there are still benefits to performing cholecystectomy early; recommended early LC in low-risk patients regardless of how much time has passed ^[7]
• 2016 WSES Guidelines: Early LC as long as completed within 10 days of symptom onset. Symptoms > 10 days → should not undergo early cholecystectomy (allow inflammation to subside) ^[7]

Why is early LC easier? ^[3]

• Initial inflammation: pericholecystic fluid in the dissection plane → easier dissection ^[3] — the oedema fluid actually creates a natural plane around the gallbladder that the surgeon can exploit
• After 72 hours: dense adhesions form at Calot's triangle ^[3] — fibrotic adhesions obliterate tissue planes, making identification of the cystic duct and artery hazardous

C. Severity-Guided Management (Tokyo Guidelines)

Emergency/Urgent LC is indicated for ^[3][4]:

• Complicated cholecystitis: gangrene, perforation, emphysematous cholecystitis ^[3][4]
• Disease progression despite best supportive care ^[3][4]

D. The Critical View of Safety (CVS) — Intraoperative Landmark

This is the single most important concept in cholecystectomy safety ^[8][9]:

Critical View of Safety (CVS) ^[9]:

1. Hepatocystic triangle clearance — Calot's triangle dissected free of all fat and fibrous tissue
2. Cystic plate clearance — the lower third of the gallbladder separated from the liver bed
3. Only two structures seen entering the gallbladder: the cystic duct and cystic artery ^[9]

Why is this so critical? Misidentification of the cystic duct is the commonest cause of biliary injury ^[8]. If the surgeon mistakes the CBD for the cystic duct and clips/divides it, the patient develops a devastating bile duct injury. The CVS ensures that the ONLY structures being divided are those that enter the gallbladder directly — nothing else.

If the critical view cannot be achieved ^[8]:

• Perform intraoperative cholangiography (IOC) to delineate anatomy
• Convert to open procedure
• Consider subtotal (partial) cholecystectomy — advocated when ductal and vascular structures in the triangle of Calot cannot be safely identified in the setting of severe acute inflammation ^[8]

E. Subtotal Cholecystectomy

• A bail-out procedure when the "critical view" is unachievable due to severe inflammation, dense adhesions, or Mirizzi syndrome
• The gallbladder fundus and body are removed, but the Hartmann's pouch/infundibulum is left behind (either closed or left open with a drain)
• Avoids dangerous dissection near the CBD and hepatic artery
• Leaves a small gallbladder remnant that may rarely develop recurrent stones or malignancy — but this is preferable to a bile duct injury

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4. Gallbladder Drainage (Non-Surgical Decompression)

When the patient cannot undergo cholecystectomy (too sick, organ failure, high surgical risk), you need an alternative way to decompress the infected, distended gallbladder.

Cholecystostomy — Drainage of the gallbladder. Open or percutaneous ^[1]

Indications for gallbladder drainage ^[1][7]:

• High surgical risk ^[1]
• Haemodynamically unstable ^[1]
• Difficult cholecystectomy ^[1]
• Severe acute cholecystitis (Grade III) ^[7]
• Late presentation > 72 hours after onset of symptoms (where early LC is not feasible) ^[7]
• Failure of medical (antibiotic) therapy ^[7]
• Contraindication to general anaesthesia ^[7]
• Not responding to antibiotics while waiting for interval LC ^[3]

A. Percutaneous Cholecystostomy (PTC) — First-Line Drainage

Percutaneous cholecystostomy ^[7]:

• Decompresses and drains the distended, inflamed, hydropic or purulent gallbladder ^[7]
• Indicated in management of acute cholecystitis in frail patients who are not fit for general anaesthesia ^[7]
• Can be placed under USG or CT guidance

Technique:

• Catheter is inserted over a guidewire that has been passed through the abdominal wall, through the liver, and into the gallbladder ^[7]
• By passing the catheter through the liver, the risk of bile leak around the catheter is minimised ^[7] — the liver parenchyma seals around the catheter tract (tamponade effect), preventing bile from tracking into the peritoneal cavity
• The catheter allows continuous drainage of infected bile/pus

It is both diagnostic AND therapeutic ^[2]: infected gallbladder is decompressed, bile can be sent for culture and sensitivity, and in calculous disease stones can potentially be extracted via the tube.

Specific complications of percutaneous cholecystostomy ^[3]:

• Catheter migration (dislodgement)
• Bile leakage around the tube
• Bowel injury (from needle insertion)

After stabilisation → definitive treatment is interval cholecystectomy ^[2][7]

B. Endoscopic Drainage — If Percutaneous Not Feasible

Endoscopic drainage: if percutaneous cholecystostomy is not feasible ^[3]:

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5. Management of Specific Situations

A. Acalculous Cholecystitis

Management: laparoscopic cholecystectomy or gallbladder drainage (if unfit) ^[3]

• These patients are typically critically ill (ICU patients) — surgical risk is high
• Percutaneous cholecystostomy is often the treatment of choice because they are usually unfit for surgery ^[2]
• Definitive treatment is interval cholecystectomy once the patient recovers ^[2]

B. Concurrent Choledocholithiasis

If investigations suggest coexisting CBD stones (cholestatic LFT, dilated CBD, visible CBD stone):

• Pre-operative ERCP → sphincterotomy + CBD stone extraction → followed by LC (two-stage approach)
• OR LC with intraoperative cholangiography (IOC) → laparoscopic CBD exploration if stones confirmed (single-stage approach)
• The approach depends on local expertise and resources

C. Complicated Cholecystitis

Emergency LC (or open cholecystectomy) is indicated for ^[3][4]:

• Gangrenous cholecystitis
• Gallbladder perforation
• Emphysematous cholecystitis
• Disease progression despite best supportive care

These are surgical emergencies — the necrotic/infected gallbladder must be removed urgently to prevent biliary peritonitis and overwhelming sepsis.

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6. Specific Complications of Cholecystectomy

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Management Summary Table

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Active Recall - Management of Acute Cholecystitis

1. Describe the initial medical management of acute cholecystitis. Why are NSAIDs the first-line analgesic?

Your answer

Grade

Show mark scheme

Initial: NPO (bowel rest, prevent CCK-mediated GB contraction), IV fluids (rehydration), IV antibiotics (cover Gram-negatives and anaerobes), analgesia, monitoring of vitals and I/O. NSAIDs are first-line because early inflammation is mediated by prostaglandins (from lysolecithin-induced chemical irritation). NSAIDs inhibit COX, blocking prostaglandin synthesis, directly targeting the pathophysiology. They also reduce gallbladder pressure.

2. Compare the advantages of early vs delayed cholecystectomy as stated in the lecture slides. Which is currently recommended?

Your answer

Grade

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Early (within 48-72h): avoids urgent operation, avoids recurrent symptoms, avoids readmission, shorter hospital stay. Delayed (interval at 8-12 weeks): avoids misdiagnosis, easier dissection, less septic complications, less serious complications. Current recommendation: Early cholecystectomy is safe without increasing risk of complications and should always be recommended unless contraindicated.

3. What is the Critical View of Safety in cholecystectomy? Why is it essential?

Your answer

Grade

Show mark scheme

Three criteria: (1) Hepatocystic triangle clearance (Calot's triangle dissected free of all tissue). (2) Cystic plate clearance (lower third of GB separated from liver bed). (3) Only two structures seen entering the gallbladder: cystic duct and cystic artery. Essential because misidentification of the cystic duct is the commonest cause of bile duct injury. If CVS cannot be achieved, perform IOC or convert to open.

4. List the indications for gallbladder drainage (cholecystostomy) in acute cholecystitis.

Your answer

Grade

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High surgical risk, haemodynamically unstable, difficult cholecystectomy, severe acute cholecystitis (Grade III), late presentation > 72h (where early LC not feasible), failure of medical/antibiotic therapy, contraindication to general anaesthesia, not responding to antibiotics while awaiting interval LC.

5. Explain why the percutaneous cholecystostomy catheter is passed through the liver rather than directly through the peritoneum into the gallbladder.

Your answer

Grade

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Passing the catheter through the liver parenchyma minimises the risk of bile leak. The liver tissue tamponades and seals around the catheter tract, preventing bile from tracking into the peritoneal cavity and causing biliary peritonitis. A direct transperitoneal approach would leave a tract through which bile could leak freely.

6. How does the Tokyo Guidelines severity grading guide the management approach for acute cholecystitis?

Your answer

Grade

Show mark scheme

Grade I (Mild, no organ dysfunction): Early laparoscopic cholecystectomy. Grade II (Moderate, marked local inflammation but no organ failure): Early LC if experienced centre, or IV antibiotics followed by interval LC at 6-8 weeks. Grade III (Severe, organ dysfunction present): Organ support + IV antibiotics + gallbladder drainage (percutaneous cholecystostomy first-line), then delayed LC after physiological recovery.

References

^[1] Lecture slides: GC 200. RUQ pain, jaundice and fever Cholecytitis and cholangitis Imaging of GI system.pdf (p8–12) ^[2] Senior notes: felixlai.md (Cholecystitis — Treatment sections, pp. 557–561) ^[3] Senior notes: maxim.md (Acute calculous cholecystitis — Initial management, Definitive treatment, Early vs Interval LC, GB drainage, pp. 131–132) ^[4] Senior notes: maxim.md (Symptomatic gallstones summary table — management approach, p. 130) ^[7] Senior notes: felixlai.md (Severity grading, timing of surgery guidelines, gallbladder drainage overview, pp. 558–561) ^[8] Senior notes: felixlai.md (Cholecystectomy — CVS, indications, partial cholecystectomy, pp. 513–515) ^[9] Senior notes: maxim.md (Cholecystectomy — indications, approach, CVS, operative procedure, pp. 133–134) ^[12] Senior notes: maxim.md (Acute cholangitis — Acute management RAD, IV Tazocin for severe, p. 135)

Complications of Acute Cholecystitis

Complications arise when acute cholecystitis is untreated or inadequately treated, allowing the pathophysiological cascade to progress beyond simple chemical inflammation into tissue destruction, infection, and structural damage. Understanding these complications follows logically from the pathophysiology we've already covered:

Stone impaction → distension → chemical inflammation → oedema → vascular compromise (end-artery cystic artery compressed) → ischaemia → necrosis → secondary infection → structural breakdown

Let's categorise these into: (A) Complications of the disease itself and (B) Complications of gallstone disease more broadly (since cholecystitis is a complication of gallstones, and gallstones cause additional problems beyond the gallbladder).

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A. Direct Complications of Acute Cholecystitis

These represent progression of the acute inflammatory and infective process within the gallbladder, arranged roughly in order of the pathophysiological cascade.

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1. Mucocele of the Gallbladder (Hydrops)

Mucocele of gallbladder ^[1]

Pathophysiology:

• Prolonged impaction of a stone in the cystic duct without significant cholecystitis (i.e., obstruction without marked infection) ^[13]
• Bile trapped within the gallbladder is gradually absorbed by the gallbladder mucosa — all the bilirubin is reabsorbed
• However, the gallbladder epithelium continues to secrete mucus — so the gallbladder progressively distends with colourless, mucoid fluid ("white bile") ^[13]
• The gallbladder becomes massively distended but typically non-tender (because there is no active inflammation) ^[13]

Clinical features:

• Palpable, non-tender RUQ mass (distended gallbladder)
• May remain asymptomatic for a prolonged period

Why does it matter?

• Mucocele can progress to oedema of the gallbladder wall, secondary infection, inflammation, and perforation ^[13]
• Early cholecystectomy is generally indicated to avoid complications ^[13]

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2. Gallbladder Empyema

Empyema of gallbladder ^[1]

Pathophysiology:

• When secondary bacterial infection of an obstructed gallbladder becomes overwhelming, the gallbladder fills with frank pus — this is an empyema (from Greek empyein = to suppurate)
• Essentially, the gallbladder becomes an intra-abdominal abscess
• The same enteric organisms (E. coli, Klebsiella, Enterococcus, anaerobes) that cause secondary infection in uncomplicated cholecystitis are responsible, but the bacterial load is much higher

Clinical features ^[3]:

• Tender RUQ mass + septic-looking ^[3]
• High-grade fever ( > 39°C), rigors, diaphoresis
• Markedly elevated WBC (often > 18,000)
• Patient appears toxic/systemically unwell

Management:

• Urgent IV antibiotics + emergency cholecystectomy or percutaneous cholecystostomy if unfit for surgery
• Empyema is a surgical emergency — untreated empyema progresses to gangrene and perforation

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3. Gangrenous Cholecystitis

Gangrenous cholecystitis — MOST common complication of cholecystitis ^[2]

Pathophysiology:

• The distended, inflamed gallbladder compresses its own blood supply (cystic artery — an end-artery with no collaterals)
• Progressive ischaemia → ischaemic necrosis of the gallbladder wall ^[2][3]
• Occurs in approximately 20% of cases of acute cholecystitis ^[3]
• More common in elderly, diabetics, and immunocompromised patients (impaired microcirculation)

Clinical features:

• Presence of a sepsis-like picture suggests the diagnosis ^[2]
• High fever, tachycardia, hypotension, leukocytosis
• Paradoxically, localised RUQ pain may decrease — because the sensory nerves in the gallbladder wall have been destroyed by necrosis (a dangerous sign that can be falsely reassuring)
• High WBC count is suggestive of a complicated form of cholecystitis such as gangrenous cholecystitis, perforation or associated cholangitis ^[2]

Diagnosis:

• CT abdomen: irregular/asymmetric wall thickening, lack of mural enhancement (ischaemic wall doesn't enhance with contrast), intraluminal membranes (sloughed mucosa), pericholecystic gas or fluid
• USG may show stranding, intraluminal membranes

Management:

• Emergency laparoscopic cholecystectomy or open cholecystectomy ^[3][4] — this is one of the indications for emergency surgery
• Delay increases the risk of perforation

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4. Gallbladder Perforation

Rupture of gallbladder ^[1]

Pathophysiology:

• Occurs after development of gangrene (perforation in ischaemic areas) ^[2]
• The necrotic, devitalised wall gives way → bile and pus leak out

Types of perforation ^[2]:

• Localised (contained) perforation — most common
  • Perforation is usually contained in the subhepatic space by the omentum and adjacent organs ^[2]
  • The greater omentum (the "policeman of the abdomen") wraps around the inflamed gallbladder and walls off the perforation
  • Results in pericholecystic or intrahepatic abscess ^[2]
• Free perforation
  • Uncontained leak of bile and pus into the general peritoneal cavity
  • Results in generalised peritonitis ^[2] — a surgical catastrophe
  • High mortality (~30%) — bile is extremely irritating to the peritoneum (chemical peritonitis) combined with bacterial contamination (septic peritonitis)
• Intrahepatic perforation
  • Abscess forms within the liver parenchyma adjacent to the gallbladder fossa (segments IV/V)
• Perforation into adjacent organs (duodenum, colon)
  • Leads to cholecystoenteric fistula formation (see below)

Clinical features:

• Contained: Persistent fever despite antibiotics, ongoing RUQ pain, possible palpable mass
• Free: Sudden worsening of pain → diffuse abdominal rigidity, rebound tenderness, hemodynamic instability, septic shock

Management:

• Emergency surgery (cholecystectomy + lavage)
• Abscess → percutaneous drainage ± delayed cholecystectomy

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5. Emphysematous Cholecystitis

Emphysematous cholecystitis ^[2][3]

This is a rare but life-threatening variant of acute cholecystitis.

Pathophysiology:

• Caused by secondary infection of the gallbladder wall with gas-forming organisms such as Clostridium perfringens ^[2]
• Other gas-formers include E. coli, Klebsiella, and anaerobic streptococci
• The ischaemic, necrotic gallbladder wall provides an ideal anaerobic environment for these organisms to proliferate and produce gas (by fermentation of glucose in tissue)
• Gas accumulates within the gallbladder wall and lumen

Clinical features ^[2][3]:

• Insidious onset ^[3] — may initially appear similar to uncomplicated cholecystitis
• Abdominal crepitus adjacent to gallbladder may be detected ^[2] — subcutaneous gas tracking from the inflamed gallbladder
• Unconjugated hyperbilirubinaemia may be present due to haemolysis induced by Clostridial infection ^[2] — Clostridium perfringens produces alpha-toxin (lecithinase/phospholipase C) that destroys red cell membranes → intravascular haemolysis → unconjugated bilirubin rises
• More common in diabetic patients (60–75% of cases) and elderly males — diabetes impairs microcirculation, predisposing to ischaemia

Diagnosis:

• AXR/CT: Gas in the gallbladder wall or lumen — pathognomonic finding
  • On AXR: curvilinear gas outlining the gallbladder wall
  • On CT: air densities (black) within the wall and lumen — very conspicuous
• CT A+P to rule out complications (e.g., empyema, emphysematous cholecystitis, perforation) ^[3]

Management:

• Emergency cholecystectomy ^[3][4] — this is a surgical emergency, as the risk of perforation is very high
• Broad-spectrum IV antibiotics including anti-anaerobic cover (metronidazole, plus piperacillin-tazobactam or carbapenems)
• High mortality (~15–25%) if untreated

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6. Cholecystoenteric Fistula and Gallstone Ileus

Cholecystoduodenofistula ^[1] Cholecystoenteric fistula → Gallstone ileus ^[2][6]

This is one of the most fascinating complications in surgery — a gallstone causing bowel obstruction.

Pathophysiology ^[2][6]:

• Fistula formation is more often due to long-standing pressure necrosis from stones than to acute cholecystitis ^[2]
• A large gallstone in the gallbladder chronically presses against the adjacent duodenal or colonic wall → pressure necrosis → erosion through both walls → formation of a direct communication (fistula) between the gallbladder and bowel lumen
• Cholecystoduodenal fistula is the most common type ^[6]
• Once the fistula is formed, the gallstone can pass from the gallbladder directly into the bowel lumen

Types of cholecystoenteric fistula ^[6]:

Gallstone ileus:

• Passage of gallstone through a cholecystoenteric fistula may lead to development of mechanical bowel obstruction usually in the terminal ileum ^[2]
• Why the terminal ileum? The terminal ileum, 2 feet proximal to the ileocaecal valve, is the narrowest portion of the small bowel ^[6]. A gallstone large enough to erode through the gallbladder wall (typically > 2.5 cm) will pass through the wider proximal small bowel but become impacted at this narrowest point.

Bouveret's syndrome ^[6]:

• Stone stuck at duodenum/stomach, causing gastric outlet obstruction (GOO) ^[6]
• A very large stone passes through a cholecystoduodenal fistula and impacts in the duodenal bulb or pylorus

Clinical features ^[6]:

• Features of distal small bowel obstruction: colicky abdominal pain, abdominal distension, vomiting (may be faeculent), absolute constipation
• Often elderly patients with a long history of gallstone disease

Investigations ^[6]:

• AXR: Rigler's triad ^[6]:
  1. Pneumobilia (gas in the biliary tree — air refluxes from the bowel through the fistula into the biliary system; present in ~40%)
  2. Small bowel obstruction (dilated small bowel loops with air-fluid levels)
  3. Ectopic gallstone (usually in the RIF, stuck near the ileocaecal valve; radio-opaque stone visible in ~10%)
• CT abdomen: GB wall thickening, Rigler's triad — CT is much more sensitive than AXR for detecting all three components ^[6]

Management ^[6]:

• Enterolithotomy to relieve SBO ^[6]
  • Exploratory laparotomy → proximal enterotomy (NOT over the stone because of ulceration at the impaction site) → milk the stone proximally for extraction ^[6]
  • Why not enterotomy at the stone? The bowel wall at the impaction site is ulcerated, oedematous, and friable from pressure necrosis — suturing over inflamed, unhealthy tissue risks anastomotic breakdown and leak. By milking the stone backwards (proximally) to healthier bowel, the enterotomy can be made in normal tissue, which heals reliably.
• Same-session or elective cholecystectomy + fistula repair ^[6]
  • There is debate about whether to address the fistula and gallbladder at the same operation (one-stage) or defer it. In the acutely obstructed, elderly patient, the priority is relieving the obstruction first; gallbladder surgery can wait.

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B. Complications of Gallstone Disease (Broader Context)

These are listed from the lecture slides as complications of gallstone disease ^[1]:

And from the comprehensive gallstone complications framework ^[13]:

In the gallbladder:

• Calculous cholecystitis
• CA gallbladder (chronic inflammation → dysplasia → carcinoma)
• Mucocele/hydrops

In the bile duct:

• Choledocholithiasis ± acute cholangitis
• Gallstone pancreatitis
• Obstructive jaundice

Perforation to other sites:

• Bowel: cholecystoenteric fistula → gallstone ileus
• Liver: liver abscess
• CBD: Mirizzi syndrome ^[13]

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C. Long-Term Complications (If Cholecystitis Becomes Chronic)

Recurrent episodes of acute cholecystitis or persistent smouldering inflammation lead to chronic cholecystitis, which has its own serious long-term complications:

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D. Complications of Cholecystectomy (Iatrogenic)

Since cholecystectomy is the definitive treatment, its complications are directly relevant to the management of acute cholecystitis.

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Complications Overview Diagram

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Active Recall - Complications of Acute Cholecystitis

1. What is the most common complication of acute cholecystitis? Explain the pathophysiology.

Your answer

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Gangrenous cholecystitis (occurs in ~20% of cases). Pathophysiology: distended, inflamed gallbladder compresses its own blood supply (cystic artery is an end-artery with no collaterals) → progressive ischaemia → ischaemic necrosis of the gallbladder wall. More common in elderly and diabetics. Suspect when septic picture develops with paradoxical decrease in localised pain (nerve destruction in necrotic wall).

2. List the complications of gallstone disease as shown in the lecture slides.

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Mucocele of gallbladder, empyema of gallbladder, rupture of gallbladder, acute cholangitis, acute pancreatitis, cholecystoduodenofistula, liver abscess.

3. What is Rigler's triad? In what condition is it seen and what is the definitive management?

Your answer

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Rigler's triad: (1) Pneumobilia, (2) Small bowel obstruction, (3) Ectopic gallstone (usually in RIF near ileocaecal valve). Seen in gallstone ileus (stone passes through cholecystoenteric fistula and impacts in terminal ileum). Management: enterolithotomy — proximal enterotomy (NOT over the stone due to ulceration), milk stone proximally for extraction, plus same-session or elective cholecystectomy and fistula repair.

4. What causes unconjugated hyperbilirubinaemia in emphysematous cholecystitis?

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Clostridium perfringens produces alpha-toxin (lecithinase/phospholipase C) that destroys red cell membranes → intravascular haemolysis → excess unconjugated bilirubin. This is distinct from the conjugated hyperbilirubinaemia of obstructive jaundice.

5. Why is gallbladder perforation usually contained rather than free? What is the natural barrier?

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Perforation is usually contained in the subhepatic space by the omentum and adjacent organs. The greater omentum ('policeman of the abdomen') wraps around the inflamed gallbladder and walls off the perforation, resulting in a pericholecystic or intrahepatic abscess rather than generalised peritonitis. Free perforation is less common but carries much higher mortality (~30%).

6. Name 3 late complications of cholecystectomy and the mechanism of post-operative diarrhoea.

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Late complications: (1) Bile duct stricture (thermal/ischaemic injury during dissection → fibrosis). (2) Post-cholecystectomy syndrome (persistent biliary colic or diarrhoea due to retained CBD stone, sphincter of Oddi dysfunction, or bile duct stricture). (3) Post-cholecystectomy choledocholithiasis (bile stasis from increased CBD calibre). Post-op diarrhoea mechanism: without the gallbladder to store and concentrate bile, bile drips continuously into the duodenum; excess bile salts reach the colon and cause secretory diarrhoea. Usually self-limiting.

References

^[1] Lecture slides: GC 200. RUQ pain, jaundice and fever Cholecytitis and cholangitis Imaging of GI system.pdf (p5) ^[2] Senior notes: felixlai.md (Complications of cholecystitis, pp. 561–562) ^[3] Senior notes: maxim.md (Acute calculous cholecystitis — Complications, p. 131) ^[4] Senior notes: maxim.md (Definitive treatment — emergency LC for complicated cholecystitis, p. 131) ^[6] Senior notes: maxim.md (Gallstone ileus, Rigler's triad, Bouveret's syndrome, pneumobilia DDx, p. 132) ^[13] Senior notes: felixlai.md (Complications of gallstones — in gallbladder, bile duct, and perforation sites, pp. 518–519) ^[14] Senior notes: maxim.md (Chronic cholecystitis — porcelain GB, CA gallbladder, p. 132) ^[15] Senior notes: maxim.md (Mirizzi syndrome — definition, Csendes classification, CA gallbladder association, p. 132) ^[16] Senior notes: maxim.md (Cholecystectomy — specific complications: immediate, early, late, pp. 133–134)