Hepatitis

Acutely unwell + jaundice – consider

• Viral hepatitis A-E
• Infectious – EBV, CMV, adenovirus, Q fever, HIV, syphillis
• Alcoholic hepatitis
• Drug-induced hepatitis
• Wilson’s disease
• Autoimmune hepatitis
• Acute cholangitis
• Acute cholecystitis

Causes:

Infectious causes:

• Hepatotropic viruses:
  • Hepatitis A Virus(HAV)
  • Hepatitis B Virus (HBV)
  • Hepatitis C Virus (HCV)
  • Hepatitis D Virus (HDV)
  • Hepatitis E Virus (HEV)
• Nonhepatotropic virus:
  • Epstein-Barr virus (EBV)
  • Cytomegalovirus (CMV)
  • Herpes simplex virus (HSV)
  • Coxsackievirus
  • Adenovirus
  • Dengue virus
  • Coronavirus-19(COVID-19)
• Bacteria, fungi, and parasites 

Toxin or substance-related causes include: 

• Alcohol-related: fatty liver disease, acute alcoholic hepatitis, or alcoholic cirrhosis
• Drugs and toxins
  • Dose-dependent, e.g. acetaminophen (paracetamol)
  • Non-dose-dependent, e.g., idiosyncratic drug reaction most commonly related to antibiotics and anticonvulsants but also statins, NSAIDs, herbal/nutritional supplements
  • Other toxins, e.g., mushroom (Amanita phalloides), herbal and dietary supplements, carbon tetrachloride, sea anemone sting  

Immunologic or inflammatory conditions 

• Autoimmune hepatitis
• Biliary disease such as primary biliary cholangitis or primary sclerosing cholangitis.

Metabolic or hereditary 

• Nonalcoholic fatty liver disease
• Hemochromatosis
• Wilson’s disease

Pregnancy-related 

• Preeclampsia
• Acute fatty liver of pregnancy
• HELLP syndrome

Ischemic and Vascular 

• Cardiogenic/Distributive shock
• Hypotension
• Heatstroke
• Cocaine, methamphetamine, ephedrine
• Acute Budd-Chiari syndrome
• Sinusoidal obstruction syndrome

Miscellaneous 

• Acute fatty liver of pregnancy
• Malignancy
• Eclampsia
• HELLP syndrome
• Reye’ syndrome
• Primary graft non-function after liver transplantation

Viral Hepatitis

	A	B	C	D	E
Agent	Enterovirus Capsid ssRNA	Hepadna Enveloped dsDNA	Unclassified enveloped ssRNA	Unclassified Enveloped ssRNA	Unclassified unenveloped ssRNA
Transmission	Fecal-oral→ ingestion of contaminated food/water Raw shell fish	Blood borne→ parenteral sex IVDU Blood transfusions	Blood borne→ parenteral sex IVDU Blood transfusions	Blood borne→ parenteral Contaminated water	Waterborne→ Faecal-oral→ Sexual
Incubation	Short 2 – 6 weeks  by time symptoms appear, most of virus shed in faeces	Long 4wk-3mth	Intermediate 2wk-6mths	Intermediate 4-7 wks – ALWAYS with HBV	Short 6 weeks
Clinical features	Asymptomatic or Mild – self limiting disease	acute hepatitis with resolution chronic hepatitis fulminant hepatitis → necrosis→ Hep D infection	progression to cirrhosis is common	acute severe hepatitis mild HBV hep converted to fulminant disease chronic → cirrhosis	self-limiting disease N.B. high mortality rate in pregnancy Fs
Carrier state?	No	Yes	Yes	Yes – but rare	Unknown
Chronic hepatitis?	No	Yes(5-10%)	Yes(>85%)	Yes	No
Hepatocellular carcinoma?	No	Yes	Yes	Yes, but no ↑ above HBV	Unknown, unlikely
Distribution	Worldwide Endemic in countries with poor hygeince	Worldwide	Worldwide	Areas worldwide	SE Asia, India, Middle East, Africa, Mexico
Public Health Measures	Hygiene Vaccination	VaccinationEducation	EducationNO vaccine	Vaccine for Hep B	NO vaccine
Notes	Benign & self-limiting (mild and asymptomatic)		Episodic ↑ in serum liver transaminases is common	Requires B

Bloods

Acute hepatitis

• LFT
• FBC
• EUC
• INR
• paracetamol
• HAV IgM
• HBsAg + anti-HBc IgM
• anti-HCV & HCV RNA
• HEV IgM (if travel)
• EBV VCA IgM
• CMV IgM
• HIV Ag/Ab.

Chronic hepatitis

• LFT
• FBC
• INR
• viral: HBsAg/anti-HBs/anti-HBc, anti-HCV ± RNA
• metabolic: ferritin/TSAT
• fasting glucose & lipids
• ceruloplasmin
• α1-antitrypsin
• autoimmune:
  • ANA
  • Smooth Muscle Antibodies (SMA)
  • Liver-Kidney Microsome (LKM)
  • Anti-Mitochondrial Antibodies (AMA) 
  • IgG
• AFP
• iron studies
• exposure-driven serologies (Q-fever, Brucella) if risk factors.

Acute hepatitis (symptom onset or ALT rise < 6 weeks)

Step	What you really need	Why it matters
Baseline chemistry & severity markers	• Full LFT panel, FBC, EUC, albumin ± glucose • INR/PT (ACUTE liver failure risk) • ± Paracetamol level • ± ethanol • ± pregnancy test	Establish pattern (hepatocellular vs cholestatic) and detect fulminant failure early. INR > 1.5 and any encephalopathy → urgent referral.
Universal viral screen	• HAV IgM • HBsAg + anti-HBc IgM (more sensitive than HBsAg alone) • HCV Ab ± RNA (RNA if Ab+, or if very early exposure) • Consider HEV IgM if traveler / pork exposure	These four are responsible for >90 % of proven acute viral hepatitis in Australia. HAV IgM is mandatory because it is the commonest travel-related cause and is not chronic
‘Mild ALT’ (<10 × ULN) additional viruses	• EBV VCA IgM • CMV IgM • HIV Ag/Ab combo	EBV/CMV classically give ALT < 500 U/L and a mono-like prodrome. HIV may present with a mononucleosis-type hepatitis. These are adjuncts, not first-line.
If ALT > 1000 U/L or INR rising	• Autoimmune markers: – ANA – ASMA – anti-LKM – IgG • Wilson screen in <40 y (serum caeruloplasmin, 24-h urinary copper)	Severe aminotransferase elevation can herald autoimmune hepatitis or Wilson crisis;
Imaging	RUQ USS (± doppler)	Exclude biliary obstruction, Budd–Chiari.

Chronic hepatitis / unexplained abnormal LFTs (≥ 6 months)

Domain	Key tests	First-pass rationale
Viral	HBsAg anti-HBs anti-HBc (total ± IgM) – HBeAg if HBsAg+ HBV DNA anti-HCV – HCV RNA if Ab+ HIV	Characterize HBV phase rule out occult HBV confirm viraemic HCV (RNA) before referral for DAA therapy.
Metabolic / iron	Fasting ferritin + transferrin saturation	Hereditary haemochromatosis common in Aus (1:150).
Steatosis / NASH	Fasting lipids glucose/HbA1c, BMI, waist	Part of cardiometabolic work-up.
AIH Autoimmune Hepatis PBC (Primary biliary cholangitis) PSC (Primary sclerosing cholangitis)	ANA ASMA anti-LKM-1 AMA IgG IgM	all three conditions may first appear as unexplained abnormal LFTs. Overlap syndromes – up to 15 % of patients fulfil criteria for both AIH and PBC or AIH and PSC, and treatment hinges on recognising both components.
Copper / A1AT	Ceruloplasmin ± 24-h urinary copper (age < 40) quantitative α1-antitrypsin	Screen rare but treatable metabolic CLDs.
Others when epidemiologically indicated	Q-fever serology Brucella ACE sarcoid imaging	Only if occupational/exposure history (e.g. abattoir, livestock) or granulomatous liver disease They are not part of a routine CLD panel
Tumour surveillance	Baseline AFP liver USS if cirrhosis risk	HCC surveillance per ASHM/HCC consensus