Gallstones are the root cause of most of the conditions in this lecture. Understanding where a stone lodges determines the clinical syndrome: ^{[5] [6]}

"Complications of gallstone disease: Mucocele of gallbladder, Empyema of gallbladder, Rupture of gallbladder, Acute cholangitis, Acute pancreatitis, Cholecystoduodenofistula, Liver abscess" ^[1]

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"F/55, known history of gallstone disease, acute right upper quadrant abdominal pain, fever with nausea and vomiting, no tea-coloured urine. Physical examination: 37.5°C, no jaundice. Tender +ve, guarding +ve, rebound +ve, Murphy's sign +ve." ^[1]

Why these features matter — explained from first principles:

• RUQ pain > 6 hours: A gallstone impacts at Hartmann's pouch or cystic duct. Initially the pain is visceral (vague, epigastric — from gallbladder distension stretching visceral peritoneum). As inflammation spreads transmurally to the parietal peritoneum overlying the gallbladder fossa, pain localises to the RUQ (somatic component). This is why the patient has guarding and rebound tenderness — signs of parietal peritoneal irritation. ^[7]

• Fever with nausea/vomiting: Gallbladder wall inflammation → bacterial translocation → systemic inflammatory response. The fever is typically low-grade initially (37.5°C in this case). High fever (> 39°C) should make you think of complications (empyema, gangrenous cholecystitis, cholangitis). ^[7]

• No tea-coloured urine, no jaundice: This is the key distinguishing feature from cholangitis or choledocholithiasis. In isolated acute cholecystitis, the cystic duct is blocked but the CBD remains patent — bile still flows normally from liver to duodenum. Therefore there is no conjugated hyperbilirubinaemia, no dark urine, and no pale stools. ^{[1] [8]}

"Murphy's sign +ve" ^[1]

How to elicit it: Place your hand at the gallbladder fossa (junction of right costal margin and lateral border of rectus abdominis, roughly at the tip of the 9th costal cartilage). Ask the patient to take a deep breath. On inspiration, the diaphragm pushes the liver and gallbladder inferiorly — the inflamed gallbladder descends onto your palpating fingers. The patient catches their breath (inspiratory arrest) due to sudden sharp pain. ^{[8] [9]}

Why it works: The inflamed gallbladder is tender; deep inspiration brings it into contact with the examining hand. The sign is highly sensitive (97%) but only moderately specific (48%) — other RUQ pathology (e.g. hepatitis, liver abscess) can occasionally produce a positive result. ^[7]

Sonographic Murphy's sign: The same manoeuvre performed with the ultrasound probe over the gallbladder. More specific because you can confirm the probe is directly over the gallbladder. ^[9]

"Acute inflammation of gallbladder. Obstruction of cystic duct. Complication of gallstone disease. Chemical inflammation → bacterial infection." ^[1]

What the pathology specimens show: an opened, inflamed gallbladder with multiple dark irregular stones beside a centimetre scale — obstruction + chemical/bacterial inflammation made tangible. ^[1]

The sequence (from first principles):

1. Stone impacts cystic duct → gallbladder outlet obstruction
2. Bile stasis → concentrated bile salts cause chemical injury to the gallbladder mucosa (this is the initial "chemical cholecystitis")
3. Mucosal injury → release of prostaglandins and lysolecithin → further inflammation
4. Bacterial translocation (secondary infection): bacteria colonise the stagnant bile — this is a secondary event, not the primary cause. Common organisms: E. coli, Klebsiella, Enterococcus, Bacteroides ^{[7] [10]}

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Bloods in acute cholecystitis:

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The initial management of acute cholecystitis is resuscitation and supportive care to stabilise the patient before definitive surgical treatment:

1. Nil by mouth (NBM) — rest the GI tract, reduce CCK stimulation
2. IV fluids — the patient is often dehydrated from vomiting and poor oral intake
3. IV antibiotics — target gut organisms (Gram-negatives + anaerobes)
   • Cefuroxime + Metronidazole (commonly used in HK)
   • Alternatives: Augmentin ± aminoglycoside, Piperacillin-tazobactam (Tazocin) for severe cases ^{[1] [10]}
4. Analgesia — NSAIDs (first-line for biliary colic), opioids if needed
5. Monitor for deterioration — worsening sepsis, generalised peritonitis → urgent intervention

Not explicitly on the GC200 slides but important for completeness and exam purposes:

• Definition: Acute cholecystitis without gallstones — caused by gallbladder ischaemia from microvascular occlusion
• Risk factors: Critically ill / ICU patients, dehydration, shock (systemic hypoperfusion), TPN (↓CCK → GB stasis)
• Key point: Higher mortality than calculous cholecystitis
• Management: Laparoscopic cholecystectomy or gallbladder drainage (if unfit) ^[6]

"M/75, history of cholecystectomy and biliary operations. Progressive upper abdominal pain. Fever, chills, rigors. Tea-coloured urine. Physical examination: 39°C, confusion and shock, jaundice. Tender +ve, guarding +ve, rebound -ve." ^[1]

Key differences from cholecystitis (from first principles):

1. Tea-coloured urine and jaundice → CBD obstruction → conjugated bilirubin spills into blood → excreted by kidneys (water-soluble) → dark urine. Also pale stools (no bilirubin reaching gut).
2. Fever with chills and rigors → this is bacteraemia/sepsis. Obstructed bile becomes infected, and high intraductal pressure forces bacteria into the systemic circulation via hepatic sinusoids and peribiliary venous plexus.
3. Confusion and shock → this patient has Reynolds pentad — the most severe form of cholangitis (suppurative/toxic cholangitis). This is a surgical emergency.
4. Rebound tenderness -ve → unlike cholecystitis, cholangitis primarily involves the biliary ducts (retroperitoneal/deep), not the gallbladder wall against the parietal peritoneum. Peritoneal signs are less prominent.

"Charcot's triad: fever + RUQ pain + jaundice. Reynolds pentad: Charcot's triad + confusion + shock." ^[1]

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"Bacteria in bile: Gram-negative rods, Enterococci, (Anaerobes). Bile duct obstruction: stones, tumour, benign stricture." ^[1]

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Why Gram-negatives dominate: The biliary tree communicates with the duodenum via the ampulla of Vater. Gut flora (predominantly Gram-negative rods and anaerobes) ascend into the biliary tree, especially when the sphincter of Oddi is disrupted (e.g. post-sphincterotomy, post-cholecystectomy, post-biliary operations — as in this lecture case). ^[10]

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• USG abdomen (first-line): Dilated CBD ( > 8mm), ± visible CBD stone (only seen in ~1/3 cases due to obscuring duodenal gas), dilated intrahepatic ducts ^{[5] [6]}
• MRCP: If USG inconclusive; excellent for visualising CBD stones and biliary anatomy non-invasively ^[6]
• CT abdomen: High sensitivity for bile duct dilatation; can detect complications (abscess, perforation) and exclude other diagnoses ^[7]

Ultrasound is the first-line investigation for hepatobiliary pathology. ^[11]

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The lecture integrates with the broader topic of obstructive jaundice. The approach: ^{[6] [13]}

1. Confirm obstruction: USG → look for dilated intrahepatic ducts (= extrahepatic cholestasis)
2. Identify level of obstruction: Proximal (intrahepatic) vs distal (CBD/ampullary)
3. Identify cause: Stone vs tumour vs stricture
4. Further workup: MRCP (non-invasive) or ERCP (if therapeutic intent)

Courvoisier's Law: "In painless jaundice, if the gallbladder is palpable, the cause is unlikely to be gallstone." ^[6]

• Why: Chronic gallstones → repeated cholecystitis → fibrosed, contracted GB → cannot distend
• Malignant obstruction → GB has no prior fibrosis → distends with back-pressure
• Exceptions: Double impaction (stone in cystic duct + stone in CBD), Mirizzi syndrome, RPC ^[6]

^[6]

GC 092 establishes the four key presentations of gallstones (biliary colic, cholecystitis, cholangitis, pancreatitis) ^[16] — GC 200 then deep-dives into cholecystitis and cholangitis specifically. The management principle from GC 092: "90% of acute cholecystitis settled with bed rest, antibiotics, elective cholecystectomy" ^[16] — while GC 200 updates this to emphasise that early cholecystectomy is now preferred. ^[1]

When acute cholangitis is caused by tumour rather than stones, the management shifts from stone extraction to stenting (plastic or metallic) via ERCP or PTBD for palliation, ± curative surgery (Whipple procedure for CA head of pancreas, hepatectomy for cholangiocarcinoma). The principle of biliary decompression remains the same. ^{[6] [12]}

Biliary pancreatitis is the most common cause of acute pancreatitis worldwide. A stone impacting the ampulla blocks both the pancreatic and bile ducts. Management: initial conservative care → ERCP for stone removal (especially if concurrent cholangitis) → interval cholecystectomy to prevent recurrence. The 2024 SAQ Q5 directly tests this connection. ^[14]