Jaundice

Introduction: definition

Yellowing of the skin and the sclerae (white of eyes) caused by bilirubin, a bile pigment.

Jaundice usually requires a serum bilirubin > 35-40 microM.

It is clasically divided into 3 types: pre-hepatic, hepatic (hepatocellular) and post-hepatic (obstructive).

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Pre-hepatic

Haemolysis
- congenital: neonatal (physiological) or hereditary spherocytosis
- acquired: at heart valves, blood transfusion

Glucuronyl transferase deficiency
- common: Gilbert's syndrome
- rare: Crigler-Najjar syndrome

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Hepatic (hepatocellular)

Acute
Acute hepatitis
- viral (A, B, C, EBV)
- leptospirosis
- EtOH

Drugs
- paracetamol
- anti-TB
- statins

Toxins
- chloroform
- phosphorus
- amanita phalloides (deathcap mushroom)

Chronic
Chronic liver disease
- EtOH
- chronic hepatitis
- cirrhosis

Cancer
- secondaries (metastasis)
- hepatoma

Congenital
- Dubin-Johnson syndrome (failure to excrete conjugated bilirubin)

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Post-hepatic (cholestatic or obstructive)

Intrahepatic
Drugs
-Antibiotics
- anabolic steroids
- OCP

Other
- PBC
- acute hepatitis

Extrahepatic
Intraluminal
- choledocholithiasis
- CF
- parasites

Intramural
- biliary atresia
- traumatic stricture (ERCP)
- cholangiocarcinoma
- PSC
- ampullary Ca

Extramural
- pancreatitis
- cancer head of pancreas
- portal lymphadenopathy
- Mirizzi's syndrome

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History

Characterise presenting symptoms
Age
- old: cancer

Jaundice
- sudden-onset: viral
- intermittent: stones
- slowly progressive: cancer
- worse when do not eat (or ill): Gilbert's

Pain
- intermittent: stones
- constant epigastric ('boring through'): cancer
- none: cancer

Cholestasis
- dark urine
- pale stools
- itch

Cholestatic (post-hepatic): questions to ask
- stones: indigestion, fat intolerance
- cholangitis: fever / rigors
- cancer: weight loss / diabetes mellitus

Hepatocellular: questions to ask
- hepatocellular: easy bruising
- EtOH: 'CAGE' questions
- leptospirosis: occupation (farm / sewage workers)
- drugs: OCP, phenothiazines
- toxins: mushrooms
- autoimmune: thyroid disease, diabetes mellitus (CAH, PBC)

- viral (general): malaise, anorexia
- viral (EBV): sore throat, rash
- viral (Hep B): gone off cigarettes, sexual history, IVDU, injections / transfusions in last 6 months
- viral (Hep A): contacts, foreign travel

Pre-hepatic: questions to ask
- Gilbert's: family history of jaundice
- Haemolysis: heart valve

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Examination

General
- colour: lemon-yellow tinge (haemolytic, low Hb), deep jaundice (hepatocellular / cholestatic)
- cholecystitis: inspection (lying still), observations (raised temp and pulse)

Sigmata of chronic liver disease
- palmar erythema
- clubbing
- spider naevi
- gynaecomastia
- loss of axillary hair
- testicular atrophy

Stigmata of chronic EtOH-related liver disease
- Dupuytren's contracture
- parotitis

Other peripheral signs
- pallor (low Hb)
- nodes (EBV / cancer)

Abdominal signs (on palpation)
- hepatomegaly: cirrhosis / cancer
- splenomegaly: cirrhosis / EBV

- Murphy's sign: place palm flat on RUQ and ask patient to breathe in - pain is felt here in acute cholecystitis (with no pain in the LUQ when test is repeated there)
- palpable gallbladder: Courvoisier's law

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Courvoisier's law

- if in the presence of jaundice the gallbladder is palpable, then the jaundice is unlikely to be due to a stone
- rare exception stone in CBD causing jaundice and 2nd stone in Hartmann's pouch causing mucocoele
- the converse is NOT true: in Ca pancreas the gallbladder may be enlarged but not clinically palpable

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Investigation

	PRE-HEPATIC	HEPATIC*	CHOLESTATIC
BILIRUBIN	< / = 100 microM unconjugated	unconjugated + conjugated	? > 1000 microM >conjugated
URINE	N colour ** no bilirubin inc. urobilinogen	? dark +/- bilirubin +/- urobilinogen	dark bilirubin no urobilinogen
STOOL	N colour inc. urobilinogen	N colour	pale dec. stercobilinogen
AST / ALT / GGT	N	+	~ / +
ALK PHOSP	N	~ /inc. +	increased ++
PT	N	+ *** partially corrects ćvit K	+ *** corrects ć vit K
ALBUMIN	N	-	N
GLUCOSE	N	-	+ if pancreatic Ca
SEROLOGY	-	hep A IgM HBsAg EBV Abs   AMA (PBC) ANA, SmM (CAH)	-
RETICULOCTYE COUNT	+	N	N
HAPTOGLOBINS	-	N	N
COOMBES’ TEST	+/-	-	-

* most hepatic causes cause a mix of both hepatocellular dysfunction and intrahepatic cholestasis

** although urobilinogen is colourless, the urine will turn brown when left to stand (as urobilinogen is converted to urobilin by oxidaion on contact with air)

*** hepatocellular damage = increased PT due to decreased hepatic synthesis of prothrombin (so NOT correctable with vit K)
cholestasis = increased PT due to decreased vit K absorption (so correctable with vit K)

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Further Investigation

Non-invasive
- AXR
- USS
- CT
- MRCP (magnetic resonance cholangiopancreatography)

Invasive
- ERCP (endoscopic retrograde cholangiopancreatography)
- PTC (percutaneous transhepatic cholangiography)
- needle biopsy
- laparotomy

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Management of Obstructive Jaundice

- correct PT with vit K (PO)
- ERCP with sphincterotomy / Dormia basket / stent insertion
- decide about subsequent surgical management (cholecystectomy / Whipple's...)

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