Jaundice

Last updated 31 May 2026 · Gastroenterology / Hepatology

📋 Key Information Summary

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Jaundice is the yellow discolouration of skin and sclerae due to elevated serum bilirubin (>25 µmol/L); it is a clinical sign, not a diagnosis — the underlying aetiology must be determined urgently.
Classify jaundice into pre-hepatic (haemolysis/ineffective erythropoiesis), hepatic (hepatocellular dysfunction), and post-hepatic (biliary obstruction) to direct investigations and management.
Pre-hepatic jaundice: unconjugated hyperbilirubinaemia with elevated LDH, low haptoglobin, reticulocytosis; consider autoimmune haemolytic anaemia, G6PD deficiency, hereditary spherocytosis, and haemolytic disease of the newborn.
Hepatic jaundice: mixed conjugated/unconjugated rise with elevated ALT/AST; causes include viral hepatitis (A–E), alcohol-related liver disease, drug-induced liver injury (DILI), autoimmune hepatitis, and Wilson disease.
Post-hepatic jaundice: predominantly conjugated hyperbilirubinaemia with elevated ALP, GGT, and dilated bile ducts on imaging; common causes are gallstones, pancreatic head tumours, and cholangiocarcinoma.
Hepatitis A and E are faecal-oral; Hepatitis B, C, and D are blood-borne. Australia has funded vaccines for Hepatitis A (at-risk groups) and Hepatitis B (universal infant programme since 2000).
Chronic Hepatitis B affects ~220,000 Australians, disproportionately impacting Aboriginal and Torres Strait Islander peoples and culturally diverse communities; Hepatitis C has been largely curable since direct-acting antivirals (DAAs) became PBS-listed in 2016.
Drug-induced liver injury (DILI) accounts for ~10% of hepatotoxicity presentations; paracetamol overdose remains the leading cause of acute liver failure in Australia.
Red flags requiring urgent specialist referral or ED presentation: bilirubin >100 µmol/L, coagulopathy (INR ≥1.5), encephalopathy, ascending cholangitis (Charcot's triad/Raynaud's pentad), suspected biliary obstruction, or progressive jaundice in pregnancy.
Always take a thorough medication history (including complementary and herbal preparations) in any patient presenting with jaundice — many commonly prescribed Australian drugs are hepatotoxic.
Aboriginal and Torres Strait Islander Australians have significantly higher rates of hepatitis B carriage and hepatocellular carcinoma; culturally safe testing, linkage to care, and community-based screening programmes are essential.
Immediate management priorities: stabilise the patient, identify and treat the cause (e.g., N-acetylcysteine for paracetamol toxicity, antivirals for hepatitis B/C, ERCP for obstructive jaundice), and escalate to hepatology or gastroenterology when indicated.

Introduction & Australian Epidemiology

Jaundice (icterus) is the clinical manifestation of hyperbilirubinaemia — a serum total bilirubin exceeding approximately 25 µmol/L. At this threshold, bilirubin deposits in the sclerae (scleral icterus), mucous membranes, and skin, producing the characteristic yellow discolouration. Jaundice is not a disease itself but a cardinal sign of an underlying disorder affecting bilirubin metabolism, hepatic function, or biliary drainage. A systematic diagnostic approach is essential to identify the cause promptly, as some aetiologies demand emergent intervention.

In Australia, jaundice accounts for a substantial proportion of presentations to general practice, emergency departments, and inpatient medical units. The Australian Institute of Health and Welfare (AIHW) reports that liver disease is among the top 20 causes of death nationally, with chronic hepatitis B and C contributing significantly to the burden of cirrhosis and hepatocellular carcinoma (HCC). Alcohol-related liver disease remains the most common cause of hepatic jaundice in many metropolitan centres, while viral hepatitis — particularly hepatitis B — predominates in remote and Indigenous communities.

Key epidemiological data for Australia include:

Hepatitis B: An estimated 220,000 Australians are living with chronic hepatitis B (CHB), with a diagnosis rate of ~60% and treatment rate of only ~12–15%. Prevalence is disproportionately high among Aboriginal and Torres Strait Islander peoples (particularly in the Northern Territory), people born in endemic regions (China, South-East Asia, sub-Saharan Africa, Pacific Islands), and people who inject drugs (PWID).
Hepatitis C: Approximately 115,000 Australians are living with chronic hepatitis C. Since the introduction of PBS-funded direct-acting antivirals (DAAs) in March 2016, over 90,000 people have been treated, with cure rates exceeding 95%. However, reinfection and undiagnosed populations remain concerns.
Hepatitis A: Australia has low endemicity, but outbreaks occur — particularly among men who have sex with men (MSM), travellers returning from endemic regions, and in some Indigenous communities. Vaccination is funded for at-risk groups under the National Immunisation Program (NIP).
Hepatitis D: Rare in Australia; estimated 5,000–10,000 co-infected individuals, predominantly among those with CHB from endemic regions.
Hepatitis E: Historically considered a travel-associated infection, locally acquired hepatitis E (genotype 3) is increasingly recognised, often linked to consumption of undercooked pork or wild game.
Drug-induced liver injury (DILI): Accounts for approximately 10% of all acute hepatitis presentations in Australian tertiary centres. Paracetamol overdose is the single most common cause of acute liver failure nationally, responsible for ~50% of cases referred to liver transplant units.
Gallstone disease: Affects 10–15% of the Australian adult population and is the most common cause of post-hepatic (obstructive) jaundice.

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Clinical Pearl: In any patient presenting with jaundice, always consider the urgency of the presentation. Painless obstructive jaundice may indicate malignancy (pancreatic head, cholangiocarcinoma) and requires urgent imaging and specialist referral. Painful jaundice with fever suggests cholangitis — a medical emergency.

Jaundice Diagnostic Model (Pre-Hepatic / Hepatic / Post-Hepatic)

A structured anatomical classification of jaundice guides the diagnostic workup. The bilirubin pathway — from haem breakdown to intestinal excretion — can be disrupted at three sites: before the liver (pre-hepatic), within the liver (hepatic), or after the liver (post-hepatic/obstructive).

Bilirubin Metabolism Overview

Bilirubin is the end-product of haem degradation. Senescent red blood cells are phagocytosed by splenic macrophages, releasing haem → biliverdin → unconjugated (indirect) bilirubin. This is albumin-bound and transported to hepatocytes, where it is conjugated by UDP-glucuronosyltransferase (UGT1A1) to form conjugated (direct) bilirubin, which is water-soluble and excreted into bile. Conjugated bilirubin is converted by gut bacteria to urobilinogen (excreted in stool as stercobilin) and urobilin (excreted by kidneys).

Classification and Key Features

Feature	Pre-Hepatic	Hepatic (Hepatocellular)	Post-Hepatic (Obstructive)
Mechanism	Excess bilirubin production (haemolysis) or ineffective erythropoiesis	Impaired hepatocyte uptake, conjugation, or excretion	Mechanical obstruction to bile flow in intra- or extrahepatic ducts
Bilirubin type	Predominantly unconjugated (indirect)	Mixed conjugated and unconjugated	Predominantly conjugated (direct)
ALT / AST	Normal or mildly elevated	Markedly elevated (>10× ULN in acute hepatitis)	Mildly to moderately elevated
ALP / GGT	Normal	Normal to mildly elevated	Markedly elevated (>3× ULN)
Haemolysis markers	↑ LDH, ↓ haptoglobin, ↑ reticulocytes	Normal	Normal
Urine bilirubin	Absent	Present (if conjugated component)	Strongly positive
Urine urobilinogen	Increased	Variable	Absent or decreased
Stool colour	Dark (increased stercobilin)	Variable — may be pale	Pale / clay-coloured (acholic)
Key imaging	Ultrasound: normal liver, enlarged spleen	Ultrasound: may show diffuse liver disease, fatty changes, or cirrhosis	Ultrasound: dilated bile ducts; CT/MRCP/EUS for level and cause
Common causes (Australia)	Autoimmune haemolytic anaemia, G6PD deficiency, hereditary spherocytosis, haemolytic transfusion reaction, malaria (returned traveller)	Viral hepatitis (A–E), alcohol-related liver disease, DILI, autoimmune hepatitis, Wilson disease, NAFLD/NASH	Choledocholithiasis, pancreatic head tumour, cholangiocarcinoma, ampullary carcinoma, primary sclerosing cholangitis

Stepwise Diagnostic Approach

Confirm Jaundice

Clinical examination (scleral icterus in natural light), serum total and direct bilirubin, LFTs (ALT, AST, ALP, GGT), FBC, LDH, haptoglobin, reticulocyte count.

Classify by Bilirubin Fraction

Unconjugated predominance → pre-hepatic or Gilbert syndrome. Conjugated predominance → hepatic or post-hepatic.

Pattern Recognition

Hepatitic pattern (↑↑ ALT/AST) vs cholestatic pattern (↑↑ ALP/GGT) vs haemolytic pattern (↑↑ LDH, ↓ haptoglobin, ↑ retics).

Targeted Investigations

Viral serology, autoimmune markers, iron studies, caeruloplasmin, α1-antitrypsin; ultrasound abdomen as first-line imaging for cholestasis.

Escalate / Refer

Urgent gastroenterology or hepatology referral if obstructive jaundice, suspected malignancy, acute liver failure, or unclear aetiology.

Gilbert Syndrome

Gilbert syndrome (constitutional hepatic dysfunction) affects 5–10% of the Australian population and is the most common cause of isolated unconjugated hyperbilirubinaemia. It is a benign condition caused by reduced UGT1A1 activity (UGT1A1*28 promoter polymorphism). Bilirubin typically fluctuates between 20–80 µmol/L, rises with fasting, illness, or stress, and all other liver tests are normal. No treatment is required — reassure the patient and document the diagnosis to prevent unnecessary future investigations.

Viral Hepatitis (A, B, C, D, E)

Viral hepatitis is a major cause of jaundice in Australia and worldwide. Five hepatitis viruses (A through E) are well characterised, each with distinct epidemiology, transmission routes, clinical courses, and management strategies. Understanding these differences is essential for appropriate testing, treatment, notification, and public health intervention.

Hepatitis A (HAV)

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Transmission: Faecal-oral — contaminated food/water, person-to-person (including sexual transmission in MSM), and rarely via blood. Self-limiting; no chronic form. Notifiable disease in all Australian states and territories.

Australian epidemiology: Low endemicity with ~300–1,000 notifications per year. Outbreaks have occurred among MSM (2017–2018 multi-state outbreak), travellers to endemic regions (South-East Asia, Indian subcontinent, Pacific Islands), and in some Aboriginal and Torres Strait Islander communities in remote areas. The NIP funds hepatitis A vaccination for Aboriginal and Torres Strait Islander children in high-incidence areas (NT, QLD, WA) and for other at-risk groups.

Clinical course: Incubation 15–50 days (mean 28 days). Prodrome of fever, malaise, nausea, anorexia, followed by jaundice (in ~70% of adults). Children <6 years are often anicteric. IgM anti-HAV confirms acute infection. Recovery is complete in >99% of cases. Fulminant hepatic failure is rare (~0.1–0.3% of cases) but carries significant mortality.

Hepatitis B (HBV)

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Critical: Chronic hepatitis B affects ~220,000 Australians and is the leading cause of hepatocellular carcinoma (HCC) in Australia. Many carriers are undiagnosed. All adults from high-risk groups should be screened (HBsAg, anti-HBs, anti-HBc).

Transmission: Blood-borne and sexually transmitted — perinatal (vertical), unprotected sexual contact, sharing injecting equipment, needlestick injuries, and household contact in endemic regions. Australia introduced universal infant hepatitis B vaccination in 2000 (now a hexavalent vaccine at birth, 2, 4, and 6 months).

Natural history:

Acute infection: Incubation 30–180 days (mean 75 days). Most adults (>95%) clear the virus; <5% develop chronic infection. Neonates/infants have a 90% risk of chronicity if infected.
Chronic HBV phases: Immune-tolerant → immune-active (HBeAg-positive hepatitis) → inactive carrier (HBeAg-negative) → reactivation. Phases guide treatment decisions.
Complications: Cirrhosis (20–30% of chronic carriers over 20–30 years), HCC (annual risk 0.5–1% with cirrhosis), liver failure.

Serological interpretation:

Marker	Interpretation
HBsAg +	Active infection (acute or chronic)
Anti-HBs +	Immunity (vaccination or past infection)
Anti-HBc + (IgM)	Acute infection
Anti-HBc + (total, IgG)	Past or chronic infection (exposure marker)
HBeAg +	High viral replication, infectivity
Anti-HBe +	Seroconversion; lower replication
HBV DNA (quantitative)	Viral load — guides treatment decisions

Treatment of chronic HBV: Indications for antiviral therapy include active hepatitis (elevated ALT, high HBV DNA), cirrhosis (regardless of ALT/HBV DNA), immunosuppression, pregnancy (to prevent vertical transmission), and co-infection with HCV/HDV/HIV.

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Entecavir

Baraclude® · Nucleoside analogue

Adult dose 0.5 mg PO once daily (1 mg if lamivudine-resistant)

Duration Long-term; often indefinite. Endpoint: HBsAg loss (functional cure) rare

Renal adjustment Yes — reduce dose if CrCl <50 mL/min

PBS status ✔ PBS Authority Required

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Tenofovir alafenamide (TAF)

Vemlidy® · Nucleotide analogue (2nd generation)

Adult dose 25 mg PO once daily

Duration Long-term; preferred in patients with renal or bone concerns

Renal adjustment Generally well tolerated; no adjustment required until CrCl <15 mL/min

PBS status ✔ PBS Authority Required

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Tenofovir disoproxil fumarate (TDF)

Viread® · Nucleotide analogue (1st generation)

Adult dose 245 mg PO once daily

Duration Long-term

Renal adjustment Yes — adjust interval if CrCl <50 mL/min; monitor renal function and bone density

PBS status ✔ PBS Authority Required

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Tenofovir and renal monitoring: TDF can cause proximal renal tubular dysfunction and reduced bone mineral density. TAF (Vemlidy®) is now preferred for most patients, particularly those aged >60, with renal impairment, osteoporosis, or concomitant nephrotoxic agents. Monitor eGFR, phosphate, and urine albumin-creatinine ratio (ACR) every 6–12 months on TDF.

Hepatitis C (HCV)

Transmission: Primarily blood-borne — sharing needles/syringes (PWID), nosocomial (historically, before screening of blood products), needlestick injuries, and rarely sexual transmission. Vertical transmission occurs in ~5% of HCV-positive mothers.

Australian epidemiology: Approximately 115,000 Australians living with chronic HCV; ~80% have genotype 1, ~15% genotype 3. The Australian Government's National Hepatitis C Strategy 2023–2030 aims to eliminate HCV as a public health threat by 2030 (WHO target).

Diagnosis: Anti-HCV antibody (screening) → HCV RNA by PCR (confirmation of active infection and viral load quantification). All patients with positive HCV RNA should be assessed for treatment.

Treatment — Direct-Acting Antivirals (DAAs):

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Sofosbuvir/Velpatasvir

Epclusa® · NS5B + NS5A inhibitor (pangenotypic)

Adult dose 400/100 mg PO once daily for 12 weeks

Notes Pangenotypic; first-line for most genotypes. Add ribavirin for decompensated cirrhosis (Child-Pugh B/C)

Renal adjustment Not required (sofosbuvir cleared hepatically); safe in CKD including dialysis (TGA-approved)

PBS status ✔ PBS Authority Required

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Glecaprevir/Pibrentasvir

Mavyret® · NS3/4A + NS5A inhibitor (pangenotypic)

Adult dose 300/120 mg (3 tablets) PO once daily with food for 8 weeks (treatment-naïve, non-cirrhotic)

Notes 8-week course for treatment-naïve non-cirrhotic patients. 12 weeks for treatment-experienced or compensated cirrhosis. Preferred in CKD/dialysis.

Renal adjustment No dose adjustment; safe in severe CKD and haemodialysis

PBS status ✔ PBS Authority Required

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PBS access for HCV treatment: Since March 2016, all Australians with confirmed chronic HCV infection (HCV RNA positive) can access DAA therapy through the PBS without liver staging or fibrosis restrictions. GPs with s100 prescriber status (or via hepatologist/gastroenterologist referral) can initiate treatment. SVR12 (sustained virological response at 12 weeks post-treatment) = cure. Test for HCV RNA 12 weeks after completing therapy.

Hepatitis D (HDV)

Transmission: Blood-borne; requires co-infection with HBV (HDV uses HBsAg as its envelope). Three patterns: co-infection (acute HBV + HDV simultaneously), superinfection (HDV acquired on chronic HBV), and chronic HDV.

Australian epidemiology: Estimated 5,000–10,000 people, predominantly from endemic regions (Mediterranean, Eastern Europe, Central Asia, sub-Saharan Africa, Amazon basin). Screen all HBsAg-positive patients for anti-HDV antibodies.

Clinical significance: HDV co-infection accelerates liver fibrosis and increases the risk of cirrhosis, HCC, and liver-related mortality 2–3-fold compared to HBV mono-infection.

Treatment: Pegylated interferon-alpha (Peg-IFN-α) was the standard of care for many years, with low response rates (~25–30%). Bulevirtide (Hepcludex®), an entry inhibitor targeting the NTCP receptor, was TGA-approved in 2023 and is now the preferred first-line agent for chronic HDV. Refer to hepatology for management.

Hepatitis E (HEV)

Transmission: Faecal-oral (contaminated water in developing countries); zoonotic (undercooked pork, wild game — genotype 3, locally acquired in Australia). Rarely via blood transfusion.

Australian epidemiology: Primarily travel-associated (genotypes 1 and 2 in South Asia, Africa). Locally acquired genotype 3 infections are increasingly recognised, particularly in NSW, QLD, and VIC.

Clinical course: Usually self-limiting. Incubation 2–10 weeks. Similar clinical presentation to hepatitis A. IgM anti-HEV confirms acute infection. Chronic hepatitis E (genotype 3) can occur in immunocompromised patients (organ transplant recipients, HIV with low CD4) and requires antiviral treatment (ribavirin 600–1000 mg PO daily for 12–24 weeks; refer to hepatology/infectious disease).

Special concern: High mortality in pregnant women in endemic regions (genotype 1; up to 20–30% in third trimester). Locally acquired genotype 3 does not carry the same pregnancy-related risk.

Summary Comparison of Hepatitis Viruses

Feature	HAV	HBV	HCV	HDV	HEV
Genome	RNA	DNA	RNA	RNA	RNA
Transmission	Faecal-oral	Blood, sexual, perinatal	Blood-borne	Blood-borne (needs HBV)	Faecal-oral, zoonotic
Chronicity	None	~5% adults; ~90% neonates	~75% (pre-DAA era)	~70% (superinfection)	Rare (immunosuppressed)
Vaccine	Yes (NIP — at-risk)	Yes (NIP — universal)	No	HBV vaccine (cross-protects)	Yes (not in Australia)
Treatment	Supportive	Entecavir, TAF, TDF	DAAs (Epclusa, Mavyret)	Bulevirtide, Peg-IFN-α	Supportive; ribavirin if chronic
Notifiable (AU)	Yes	Yes	Yes	Yes	Yes

Drug-Related Jaundice (DILI)

Drug-induced liver injury (DILI) is a leading cause of acute hepatitis and jaundice in Australia, accounting for approximately 10% of all acute hepatitis presentations to tertiary centres. DILI is defined as liver injury attributed to a medication, herbal product, or dietary supplement, after exclusion of other causes. It can mimic virtually any liver disease pattern — hepatocellular, cholestatic, or mixed — and ranges from mild, asymptomatic liver enzyme elevations to fulminant hepatic failure requiring transplantation.

Classification of DILI

Hepatocellular

ALT ≥3× ULN, R ratio ≥5

Paracetamol, isoniazid, rifampicin, NSAIDs (diclofenac), anticonvulsants (sodium valproate, phenytoin), statins (rare), anti-TNF agents, herbal preparations.

Higher risk of acute liver failure (Hy's Law: ALT >3× ULN + bilirubin >2× ULN)

Cholestatic

ALP ≥2× ULN, R ratio ≤2

Flucloxacillin, amoxicillin-clavulanate, anabolic steroids, oral contraceptive pill, chlorpromazine, erythromycin estolate.

Usually self-limiting on drug withdrawal; flucloxacillin cholestasis may persist for months

Mixed

ALT and ALP both elevated, R ratio 2–5

Sulfonamides, nitrofurantoin, phenytoin, ampicillin, tricyclic antidepressants, herbal products.

Variable prognosis; manage by withdrawal and supportive care

R ratio = (ALT/ULN) ÷ (ALP/ULN). This ratio helps classify the injury pattern and guides prognosis.

Common Hepatotoxic Drugs in Australia

Drug / Class	Pattern	Key Features
Paracetamol	Hepatocellular	Dose-dependent toxicity. Single dose >150 mg/kg or >10 g (whichever is less) is potentially hepatotoxic. Therapeutic doses can cause toxicity in chronic alcohol use, malnutrition, enzyme inducers. NAC is the antidote (see below).
Flucloxacillin	Cholestatic	Most common cause of DILI-related hospitalisation in Australia. Risk increases with age >55, duration >2 weeks, and cumulative dose. Can cause prolonged cholestasis (vanishing bile duct syndrome). HLA-B*57:01 association.
Amoxicillin-clavulanate	Cholestatic / Mixed	Second most common antibiotic-related DILI. Typically presents 1–6 weeks after starting treatment. More common in men, age >40.
Isoniazid	Hepatocellular	Risk increases with age >35, alcohol use, concurrent rifampicin. Monitor LFTs at baseline, 2 weeks, 4 weeks, then monthly. Educate patients to stop if symptomatic.
Statins	Hepatocellular (rare)	Clinically significant DILI is rare (<1:100,000). Mild ALT elevations (1–3× ULN) occur in ~1% and usually resolve. Do not routinely monitor LFTs beyond baseline.
Herbal & complementary medicines	Variable	Kava, green tea extract (EGCG), comfrey (pyrrolizidine alkaloids), black cohosh, turmeric supplements (high-dose). Always ask about non-prescription products.
Sodium valproate	Hepatocellular	Dose-dependent; higher risk in children <2 years and polypharmacy. Hyperammonaemia can occur even with normal LFTs.
Methotrexate	Hepatocellular / Fibrosis	Cumulative dose-related. Monitor LFTs and FBC every 2–4 weeks initially, then every 1–3 months. Consider FibroScan® or liver biopsy if persistent ALT elevations.

Paracetamol Toxicity — Australian Management

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Paracetamol overdose is the most common cause of acute liver failure in Australia. Present to the nearest ED immediately. Activated charcoal (50 g) if within 1–2 hours of ingestion. Measure serum paracetamol level at ≥4 hours post-ingestion and plot on the Rumack-Matthew nomogram. Start N-acetylcysteine (NAC) if above the treatment line, or if in doubt. The Australasian College for Emergency Medicine (ACEM) recommends early consultation with a clinical toxicologist or Poisons Information Centre (13 11 26).

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N-Acetylcysteine (NAC)

Parvolex® · Antidote for paracetamol toxicity

Indication Paracetamol overdose above Rumack-Matthew treatment line; acute liver failure of any cause

Adult dose (IV) Modified 2-bag protocol (Australasian standard): Bag 1: 200 mg/kg in 500 mL 5% dextrose over 4 hours. Bag 2: 100 mg/kg in 1000 mL 5% dextrose over 16 hours. Total: 300 mg/kg over 20 hours.

Paediatric dose Same mg/kg dosing as adults; adjust fluid volumes for weight

Monitoring Paracetamol level at 4h post-ingestion, LFTs, INR, VBG (pH), renal function. Recheck paracetamol at end of Bag 1 if late or staggered ingestion.

Adverse effects Anaphylactoid reactions (non-allergic — histamine-mediated; more common with rapid infusion). Nausea, vomiting, rash. Do NOT stop NAC for mild reactions — slow infusion rate and give antihistamine.

PBS status ✔ PBS (hospital use)

Management Principles for DILI

Suspect: Always consider DILI in the differential of jaundice or unexplained liver enzyme elevation. Take a comprehensive medication history including OTC, herbal, and supplement use.
Stop the culprit: Immediate withdrawal of the suspected agent is the single most important intervention. Most DILI resolves within weeks to months of drug cessation.
Exclude other causes: Viral hepatitis serology, autoimmune markers (ANA, ASMA, anti-LKM), iron studies, caeruloplasmin, abdominal ultrasound.
Apply Hy's Law: ALT >3× ULN + total bilirubin >2× ULN (without biliary obstruction) = ~10% risk of fatal or transplant-requiring outcome. Refer urgently to hepatology.
NAC for non-paracetamol acute liver failure: Emerging evidence supports NAC use in non-paracetamol acute liver failure with early (coma grade I–II) encephalopathy, improving transplant-free survival.
Corticosteroids: Consider in DILI with autoimmune features (drug-induced autoimmune hepatitis pattern — e.g., nitrofurantoin, methyldopa, infliximab). Refer to hepatology. Not routinely recommended for DILI.
Report: Notify the Therapeutic Goods Administration (TGA) via the Adverse Event Reporting System (AERS). Document the reaction in the patient's medical record and My Health Record.

Red Flag Pointers for Jaundice

Not all jaundice requires emergency evaluation, but several clinical and laboratory features should trigger urgent assessment, referral, or ED presentation. The following red flags help identify patients at risk of serious or life-threatening liver disease.

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Immediate ED referral is required for any patient with jaundice AND signs of acute liver failure (encephalopathy, coagulopathy), ascending cholangitis, or haemodynamic instability.

Clinical Red Flags

Red Flag	Significance	Action
Jaundice + confusion / drowsiness / asterixis	Hepatic encephalopathy — suggests acute or chronic liver failure	ED presentation. Urgent VBG (ammonia), LFTs, INR, glucose. Consider transfer to liver transplant centre.
Jaundice + fever + RUQ pain (Charcot's triad)	Ascending cholangitis	ED presentation. IV antibiotics (piperacillin-tazobactam 4.5 g IV TDS or ceftriaxone 2 g IV OD + metronidazole 500 mg IV TDS). Urgent ERCP.
Charcot's triad + hypotension + altered mental status (Reynolds' pentad)	Suppurative cholangitis — surgical/ERCP emergency	Resuscitation, IV antibiotics, emergency ERCP. High mortality without intervention.
Painless progressive jaundice + weight loss	Pancreatic head tumour, cholangiocarcinoma, or other malignancy	Urgent CT abdomen (pancreas protocol) and referral to gastroenterology/oncology. Two-week wait pathway if available.
Jaundice in pregnancy	May indicate pre-eclampsia/HELLP syndrome, acute fatty liver of pregnancy (AFLP), intrahepatic cholestasis of pregnancy (ICP), or viral hepatitis	Urgent obstetric and medical review. Check BP, urinalysis, LFTs, platelets, LDH, coagulation. HELLP and AFLP are obstetric emergencies requiring delivery.
INR ≥1.5 + jaundice	Significant hepatocellular dysfunction; possible acute liver failure	Urgent hepatology referral. Assess for transplant criteria (King's College criteria). Consider NAC if non-paracetamol ALF.
Jaundice + pruritus + pale stools + dark urine	Obstructive jaundice pattern	Urgent abdominal ultrasound to assess bile duct diameter. If dilated, refer for MRCP/ERCP/EUS.
Jaundice + signs of chronic liver disease (spider naevi, palmar erythema, ascites, gynaecomastia, caput medusae)	Decompensated cirrhosis	Urgent hepatology referral. Manage complications: ascites (diuretics, paracentesis), variceal bleeding (terlipressin, banding), encephalopathy (lactulose, rifaximin).
Jaundice + new rash + eosinophilia	DILI with hypersensitivity features (DRESS syndrome)	Stop suspected drug immediately. Refer to dermatology and hepatology. Systemic corticosteroids may be required.
Bilirubin >100 µmol/L	Severe hyperbilirubinaemia — always pathological	Urgent investigation and specialist review. Do not attribute to Gilbert syndrome at this level.

Laboratory Red Flags

ALT >1,000 U/L: Acute hepatocellular injury — consider viral hepatitis, DILI (paracetamol, isoniazid), ischaemic hepatitis (shock liver), autoimmune hepatitis, Wilson disease (especially age <40).
ALP >3× ULN with GGT elevation: Cholestatic picture — ultrasound to exclude obstruction. If obstructed, urgent ERCP referral.
Albumin <30 g/L + INR >1.5: Synthetic dysfunction — chronic liver disease or acute liver failure. Urgent hepatology input.
AFP >200 ng/mL: Strongly suggestive of hepatocellular carcinoma in the setting of chronic liver disease. Urgent triple-phase CT or MRI and hepatology/oncology referral.
Sodium <130 mmol/L in cirrhosis: Dilutional hyponatraemia — predictor of poor prognosis. Fluid restriction; avoid over-diuresis.

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King's College Criteria for Acute Liver Failure — refer for emergency liver transplant assessment if met:
Paracetamol-induced ALF: Arterial pH <7.3 (after resuscitation) OR all three: INR >6.5, creatinine >300 µmol/L, Grade III–IV encephalopathy.
Non-paracetamol ALF: INR >6.5 (regardless of grade of encephalopathy) OR any three of: age <10 or >40, aetiology (non-A/non-B hepatitis, idiosyncratic DILI, Wilson disease), jaundice to encephalopathy interval >7 days, INR >3.5, bilirubin >300 µmol/L.

Investigations

The investigation of jaundice should be systematic and guided by the clinical pattern (pre-hepatic, hepatic, post-hepatic). Below is a structured approach to first-line and second-line investigations available in the Australian healthcare setting.

First-Line Investigations

Essential Serum total and direct (conjugated) bilirubin MBS item 66556. Differentiates conjugated vs unconjugated hyperbilirubinaemia. Unconjugated predominance → pre-hepatic/Gilbert. Conjugated predominance → hepatic or post-hepatic.

Essential Liver function tests (LFTs) MBS item 66556. ALT, AST, ALP, GGT, total protein, albumin. Pattern recognition: hepatitic (↑ ALT/AST) vs cholestatic (↑ ALP/GGT) vs mixed.

Essential Full blood count (FBC) MBS item 66512. Anaemia with reticulocytosis suggests haemolysis. Macrocytosis may indicate alcohol use or folate deficiency. Thrombocytopenia may indicate cirrhosis or DIC.

Essential Haemolysis screen LDH, haptoglobin, reticulocyte count, direct Coombs test (DAT). ↑ LDH + ↓ haptoglobin + ↑ reticulocytes = haemolysis. DAT positive → autoimmune haemolytic anaemia.

Essential Coagulation studies (INR, APTT) MBS item 66556. INR ≥1.5 with jaundice suggests significant liver synthetic dysfunction or acute liver failure. Does not respond to vitamin K if due to hepatocellular failure.

Essential Abdominal ultrasound (US) MBS item 55038. First-line imaging for suspected cholestasis/obstruction. Assess bile duct diameter (intrahepatic ducts >4 mm, CBD >7 mm suggest obstruction), gallbladder stones, liver parenchyma, spleen size. Sensitivity ~90% for detecting CBD dilation.

Second-Line Investigations (Targeted by Pattern)

Available Viral hepatitis serology HBsAg, anti-HBs, anti-HBc (± HBV DNA); anti-HCV (± HCV RNA); IgM anti-HAV; IgM anti-HEV. MBS item 69316/69325. Order if hepatitic pattern or risk factors.

Available Autoimmune hepatitis markers ANA, anti-smooth muscle antibody (ASMA), anti-LKM-1, serum IgG levels. Consider if young woman with hepatitic pattern, or DILI not resolving after drug withdrawal.

Available Iron studies + ferritin Elevated transferrin saturation and ferritin with raised ALT → consider hereditary haemochromatosis (HFE gene testing C282Y/H63D). Common in Australian Caucasians (~1:200 carrier rate).

Available Caeruloplasmin + serum copper + 24-hour urine copper Consider Wilson disease in any patient aged <40 with unexplained hepatitis or cirrhosis. Low caeruloplasmin + high urine copper is diagnostic. Refer for slit-lamp examination (Kayser-Fleischer rings).

Available α1-Antitrypsin level and phenotype Consider if young patient with liver disease and/or emphysema. PiZZ phenotype is the most severe deficiency.

Specialist MRCP (Magnetic Resonance Cholangiopancreatography) MBS item 63000+. Non-invasive assessment of biliary tree. Preferred over ERCP for diagnostic purposes (visualising strictures, stones, PSC). Refer if US suggests obstruction but cause unclear.

Specialist ERCP (Endoscopic Retrograde Cholangiopancreatography) Therapeutic (stone extraction, stent placement, sphincterotomy) + diagnostic. Indicated for choledocholithiasis, obstructive jaundice requiring decompression, cholangitis. Risk of pancreatitis (~3–5%).

Specialist EUS (Endoscopic Ultrasound) Superior for small CBD stones, ampullary lesions, pancreatic head masses. Allows FNA/biopsy of pancreatic masses. Refer to gastroenterologist.

Specialist Liver biopsy Indicated when non-invasive investigations are inconclusive — staging of chronic hepatitis, suspected autoimmune hepatitis, infiltrative disease, unexplained cholestasis. Percutaneous (US-guided), transjugular, or laparoscopic approach.

Available FibroScan® (transient elastography) Non-invasive liver stiffness measurement for fibrosis staging. Available in most Australian hepatology centres and some GP practices. MBS item 12515 (since November 2022, via specialist referral).

Special Populations

🤰

Pregnancy

HELLP syndrome: Haemolysis, Elevated Liver enzymes, Low Platelets — variant of severe pre-eclampsia. Presents in 2nd–3rd trimester. Obstetric emergency requiring delivery regardless of gestational age.

Acute fatty liver of pregnancy (AFLP): Rare but life-threatening. Nausea, vomiting, jaundice, coagulopathy, hypoglycaemia. Emergency delivery is the definitive treatment.

Intrahepatic cholestasis of pregnancy (ICP): Pruritus (especially palms and soles) without rash; elevated bile acids (>40 µmol/L) and mild ALT elevation. Ursodeoxycholic acid 10–15 mg/kg/day PO. Increased risk of stillbirth; recommend delivery at 36–37 weeks. ✔ PBS General Benefit

Hepatitis B in pregnancy: All pregnant women should be screened (HBsAg) at first antenatal visit. If HBV DNA >200,000 IU/mL, commence tenofovir (TDF or TAF) from 28–32 weeks to reduce vertical transmission risk. Neonate receives HBV immunoglobulin (HBIG) + vaccine within 12 hours of birth.

Hepatitis C in pregnancy: DAAs are not currently recommended in pregnancy (insufficient safety data). Treat post-partum. Screen for vertical transmission at 18 months (anti-HCV) or 2 months (HCV RNA).

Contraindicated drugs: Pegylated interferon, ribavirin (teratogenic — Category X), statins (generally avoided).

👶

Paediatrics

Neonatal jaundice: Physiological jaundice peaks at day 3–5 (term), day 5–7 (preterm). Pathological if onset <24 hours, rising >8.5 µmol/L/hr, total bilirubin >340 µmol/L (term), or duration >14 days. Check direct Coombs, FBC, blood group, G6PD. Use Australian NICE-aligned phototherapy guidelines.

Biliary atresia: Presents with persistent jaundice (>14 days) + acholic stools + dark urine. Must be diagnosed by 6–8 weeks for optimal Kasai portoenterostomy outcome. Use the Australian Biliary Atresia Stool Colour Chart (distributed at birth).

Paediatric hepatitis B: Universal infant vaccination on NIP (birth dose within 24 hours, then at 2, 4, 6 months as hexavalent). Chronic HBV in children: monitor ALT, HBV DNA, HBeAg every 6–12 months. Refer to paediatric hepatology for treatment consideration.

G6PD deficiency: X-linked; significant prevalence in Mediterranean, African, and South-East Asian populations. Avoid oxidant drugs (primaquine, sulfonamides, dapsone, nitrofurantoin). Neonatal jaundice may be severe.

Wilson disease: Usually presents age 5–35 with hepatitis, haemolytic anaemia, or neuropsychiatric symptoms. Paediatric hepatology referral for penicillamine or trientine chelation.

👴

Elderly

Higher risk of DILI: Polypharmacy, altered drug metabolism, renal impairment. Flucloxacillin cholestatic hepatitis is particularly common in patients >55 years. Always consider medication review.

Malignancy: Painless obstructive jaundice in an elderly patient is pancreatic head carcinoma until proven otherwise. Urgent CT and gastroenterology referral.

Alcohol-related liver disease: May present late with decompensation (ascites, variceal bleeding, encephalopathy). Elderly patients have reduced hepatic reserve and poorer tolerance to physiological stress.

Drug dose adjustments: Reduced hepatic blood flow and enzyme activity with ageing. Start low, go slow. Review all medications — deprescribe where possible.

🫘

Renal Impairment

Drug dose adjustments: Entecavir requires renal dose adjustment. TAF is preferred over TDF in CKD. NAC dosing in hepato-renal syndrome should follow standard protocols (no adjustment), but fluid balance requires careful monitoring.

Hepatorenal syndrome: Functional renal failure in advanced cirrhosis. Type 1 (rapid, doubling creatinine to >226 µmol/L in <2 weeks) has very poor prognosis. Treat with terlipressin (Renalase®) + albumin. Refer for transplant assessment.

HCV in dialysis patients: DAAs can be safely used. Glecaprevir/pibrentasvir (Mavyret®) is the preferred regimen in haemodialysis. PBS-listed.

🟤

Hepatic Impairment

Child-Pugh score: Classifies cirrhosis severity (A, B, C) using bilirubin, albumin, INR, ascites, and encephalopathy. Guides drug dosing and prognosis.

Contraindicated medications: Avoid hepatotoxic drugs entirely. Most DAAs are safe in compensated cirrhosis (Child-Pugh A) but some require dose adjustment or are contraindicated in decompensated disease (glecaprevir/pibrentasvir contraindicated in Child-Pugh B/C).

Variceal screening: All patients with cirrhosis should have upper GI endoscopy at diagnosis to screen for oesophageal/gastric varices. If large varices, commence non-selective beta-blocker (carvedilol 6.25–12.5 mg OD) or endoscopic band ligation.

🛡️

Immunocompromised

HIV co-infection: HIV/HBV co-infected patients: tenofovir (TAF or TDF) + emtricitabine or lamivudine as backbone (treats both viruses). HIV/HCV co-infected: same DAA regimens as HIV-negative; check drug interactions with antiretrovirals (consult Liverpool HIV Interactions database).

Transplant recipients: HBV prophylaxis is mandatory for HBsAg-positive transplant patients (entecavir or tenofovir indefinitely). Chronic HEV infection must be considered in transplant recipients with unexplained hepatitis — reduce immunosuppression if possible, and treat with ribavirin.

Chemotherapy-induced HBV reactivation: All patients commencing immunosuppressive therapy (rituximab, systemic corticosteroids >4 weeks, stem cell transplant) should be screened for HBV (HBsAg, anti-HBc, anti-HBs). Prophylactic entecavir or tenofovir if HBsAg+ or anti-HBc+ with high-risk regimen.

CMV hepatitis: Consider in transplant recipients and severely immunocompromised patients. Check CMV PCR. Treat with valganciclovir 900 mg PO BD or ganciclovir 5 mg/kg IV BD.

Aboriginal and Torres Strait Islander Health Considerations

Aboriginal and Torres Strait Islander Health

Aboriginal and Torres Strait Islander Australians experience a significantly higher burden of liver disease, viral hepatitis, and hepatocellular carcinoma compared to the non-Indigenous population. Culturally safe, trauma-informed, and community-based approaches are essential to improve outcomes.

Hepatitis B — The Priority

Chronic hepatitis B prevalence in Aboriginal and Torres Strait Islander peoples is estimated at 2–6% in some remote NT communities — up to 10× the national average (~0.9%).
Vertical (perinatal) and early childhood transmission remain significant routes in remote communities. The NIP provides hepatitis B vaccination at birth for all Aboriginal and Torres Strait Islander neonates, with catch-up programmes for older children and adults.
Hepatocellular carcinoma (HCC) incidence is 3–4× higher in Aboriginal and Torres Strait Islander peoples than in non-Indigenous Australians, largely driven by chronic HBV and higher rates of alcohol-related liver disease.
Only ~40% of Aboriginal and Torres Strait Islander people with chronic HBV are diagnosed, and fewer than 15% are on antiviral treatment. Closing this gap is a national priority under the National Hepatitis B Strategy 2023–2030.

Hepatitis C and the Elimination Goal

Aboriginal and Torres Strait Islander peoples are disproportionately affected by hepatitis C, with prevalence estimates 2–3× higher than non-Indigenous Australians, particularly among those with a history of injecting drug use.
PBS access to DAAs without liver staging restrictions has improved treatment uptake, but barriers remain: geographic remoteness, stigma, low health literacy, and limited culturally safe services.
Community-controlled health organisations (ACCHOs) play a vital role in hepatitis C testing, treatment, and harm reduction (needle and syringe programmes, opioid substitution therapy).

Key Barriers and Facilitators

Access to specialist care

Many remote communities have no hepatologist or gastroenterologist. Telehealth consultations (MBS items 99200–99215) and visiting specialist outreach programmes are essential. The Royal Flying Doctor Service (RFDS) provides emergency retrieval and remote consultations.

Cultural safety

Liver disease and hepatitis carry significant stigma. Ensure culturally safe communication (use local language interpreters where needed), gender-concordant care where preferred, and involve Aboriginal Health Workers/Practitioners (AHW/Ps) in all stages of care.

Screening and testing

Opportunistic screening for HBV and HCV should occur during routine health assessments (MBS Item 715 for Aboriginal and Torres Strait Islander peoples). Point-of-care testing (e.g., dried blood spots for HBV/HCV) is being piloted in remote settings.

Liver cancer surveillance

All Aboriginal and Torres Strait Islander people with chronic HBV or cirrhosis should be enrolled in a 6-monthly HCC surveillance programme (liver ultrasound ± AFP). Many eligible patients are not currently receiving surveillance — systems-based solutions within ACCHOs are needed.

Social determinants of health

Overcrowded housing, food insecurity, limited clean water access in some remote communities, and higher rates of alcohol and substance use contribute to hepatitis transmission and liver disease progression. Addressing these determinants is fundamental to improving liver health outcomes.

Community-controlled health services

ACCHOs such as the Kimberley Aboriginal Medical Services (KAMS), Central Australian Aboriginal Congress, and Apunipima Cape York Health Council deliver integrated hepatitis care, including chronic disease management, antiviral prescribing, and liver cancer surveillance. Support and fund these models.

📋

Recommended resource: The RACGP National Guide to Preventive Healthcare for Aboriginal and Torres Strait Islander People (4th edition, 2024) includes comprehensive guidance on hepatitis B screening, vaccination, and management in primary care. Available free at www.racgp.org.au.

📚 References

1. Australasian Society for HIV, Viral Hepatitis and Sexual Health Medicine (ASHM). ASHM Hepatitis B Prescribing Guide. Sydney: ASHM; 2023. Available at: www.ashm.org.au.
2. Australian Government Department of Health and Aged Care. National Hepatitis B Strategy 2023–2030. Canberra: Commonwealth of Australia; 2023.
3. Australian Government Department of Health and Aged Care. National Hepatitis C Strategy 2023–2030. Canberra: Commonwealth of Australia; 2023.
4. Australian Institute of Health and Welfare (AIHW). Aboriginal and Torres Strait Islander Health Performance Framework: Hepatitis B and C. Canberra: AIHW; 2023.
5. The Royal Australian College of General Practitioners (RACGP). National Guide to a Preventive Health Assessment for Aboriginal and Torres Strait Islander People. 4th edn. Melbourne: RACGP; 2024.
6. Hepatitis B Virus (HBV) Guidelines Panel. Recommendations for Testing, Managing, and Treating Hepatitis B. American Association for the Study of Liver Diseases (AASLD); 2024. Available at: www.hcvguidelines.org.
7. Pawlotsky J-M, Negro F, Aghemo A, et al. EASL recommendations on treatment of hepatitis C: final update of the series. J Hepatol. 2020;73(5):1170–1218.
8. Chalasani N, Bonkovsky HL, Fontana R, et al. Features and outcomes of 899 patients with drug-induced liver injury: the DILIN prospective study. Gastroenterology. 2015;148(7):1340–1352.
9. Acute Liver Failure Study Group (ALSG). Rumack BH, Matthew H. Acetaminophen poisoning and toxicity. Pediatrics. 1975;55(6):871–876. (Rumack-Matthew nomogram, widely used in Australian EDs.)
10. Wong RJ, Gish R, Frederick T, et al. The impact of race/ethnicity on the clinical epidemiology of hepatocellular carcinoma. J Clin Gastroenterol. 2022;56(2):e150–e158.
11. Thompson AJ, Nguyen T, Pezolt D, et al. The public health impact of direct-acting antivirals for hepatitis C in Australia: an update. Aust N Z J Public Health. 2023;47(3):100050.
12. Heydtmann M, Georgiou P, Demediuk C, et al. Bulevirtide for chronic hepatitis delta: real-world experience. J Hepatol. 2023;78(Suppl 1):S2–S3. (TGA approval 2023, Australian context.)
13. Endigeri M, Kowdley KV. Primary sclerosing cholangitis and cholangiocarcinoma. In: Schiff's Diseases of the Liver. 12th edn. Wiley-Blackwell; 2018:617–644.
14. Royal Australian and New Zealand College of Obstetricians and Gynaecologists (RANZCOG). Intrahepatic Cholestasis of Pregnancy. Clinical Guideline C-Obs 43. Melbourne: RANZCOG; 2022.
15. O'Grady JG, Alexander GJ, Hayllar KM, Williams R. Early indicators of prognosis in fulminant hepatic failure. Gastroenterology. 1989;97(2):439–445. (King's College Criteria.)

for PBS scripts. Utilise ACCHS pharmacies and Remote Area Aboriginal Health Worker programs for medication supply in remote areas. Avoid initiating benzodiazepines; support holistic pain management including community-based exercise programs.

Preventive health

Promote bone health: encourage vitamin D supplementation (1000 IU daily in deficient individuals), smoking cessation support, reduction of alcohol intake, and weight-bearing exercise. MBS Item 715 health checks provide a structured opportunity to assess bone health, screen for osteoporosis risk factors, and discuss musculoskeletal health in a culturally safe context.

Quick Reference: Differential Diagnosis at a Glance

Costovertebral dysfunction

Paracetamol ± NSAID; manual therapy

2–6 weeks

Provocable on palpation; no red flags

Thoracic compression fracture

Paracetamol; ± calcitonin; DXA + osteoporosis Rx

6–12 weeks healing

Elderly; osteoporosis; acute onset

ACS (posterior MI)

Aspirin 300 mg, GTN, heparin; urgent PCI

Time-critical

ECG, troponin; CV risk factors

Aortic dissection

IV labetalol; urgent CT aortogram; surgery (Type A)

Time-critical

Tearing pain; BP differential >20 mmHg

Vertebral osteomyelitis

IV antibiotics (vancomycin + ceftriaxone initially); ID consult

6 weeks IV antibiotics

Fever, elevated CRP, IV drug use

Biliary colic / cholecystitis

Paracetamol ± morphine; lap cholecystectomy

Surgical within 72 h (cholecystitis)

RUQ/infrascapular; post-prandial; RUQ US

📚 References

1. Briggs AM, Smith AJ, Straker LM, Bragge P. Thoracic spine pain in the general population: prevalence, incidence and associated factors in children, adolescents and adults. A systematic review. BMC Musculoskelet Disord. 2009;10:77.
2. National Health and Medical Research Council (NHMRC). Evidence-based management of acute musculoskeletal pain. Canberra: NHMRC; 2003 (updated 2020).
3. Australian Institute of Health and Welfare (AIHW). Aboriginal and Torres Strait Islander Health Performance Framework: Summary report 2023. Canberra: AIHW; 2023.
4. Deyo RA, Rainville J, Kent DL. What can the history and physical examination tell us about low back pain? JAMA. 1992;268(6):760–765.
5. Stochkendahl MJ, Kjaer P, Hartvigsen J, et al. National Clinical Guidelines for non-surgical treatment of patients with recent onset low back pain or lumbar radiculopathy. Europ Spine J. 2018;27(1):60–75.
6. Erwin WM, Jackson PC, Homonko DA. Innervation of the human costovertebral joint: implications for clinical back pain syndromes. J Manipulative Physiol Ther. 2000;23(6):395–403.
7. Royal Australian College of General Practitioners (RACGP). Guidelines for preventive activities in general practice. 9th edn. Melbourne: RACGP; 2018 (updated 2023).
8. Hirsch JA, Singh V, Falco FJE, et al. Thoracic facet joint interventions. Pain Physician. 2016;19(4):E581–E593.
9. Erwin WM, Jackson PC. The costovertebral joint: anatomy, biomechanics, and clinical significance in thoracic back pain syndromes. J Can Chiropr Assoc. 2003;47(2):112–120.
10. Strayer RJ, Gunnerson JM, Brown LH, et al. Aortic dissection: clinical features, diagnosis, and management. Aust Crit Care. 2019;32(2):144–153.
11. Ombregt L. A system of orthopaedic medicine. 3rd edn. Edinburgh: Churchill Livingstone Elsevier; 2013. Chapter 18: Thoracic spine.
12. Lin CC, Chen KH, Li DM, et al. Characteristics and outcomes of patients presenting with thoracic back pain to the emergency department. Emerg Med Australas. 2020;32(5):805–811.

for PBS-listed medicines at participating pharmacies.

Cultural safety

Engagement with Aboriginal Community Controlled Health Organisations (ACCHOs) is essential. Cultural safety training for non-Indigenous clinicians, use of Aboriginal Health Workers and Liaison Officers, and incorporation of traditional healing practices alongside Western medicine improve treatment adherence and outcomes. Avoidance of eye contact, respect for gender-sensitive examination practices, and understanding of sorry business protocols are critical elements of culturally safe care.

Medication adherence

Complex DMARD regimens with frequent monitoring requirements present adherence challenges. Long-acting depot injections (e.g., methotrexate SC) may improve adherence compared to oral regimens. Community pharmacy partnerships through the Indigenous Pharmacy Programmes improve medication management.

Specific conditions

Rheumatic heart disease (RHD) requires secondary prophylaxis with benzathine penicillin G (BPG) 1.2 MU IM every 3–4 weeks for a minimum of 10 years or until age 21 (whichever is longer). RHD registers (e.g., NT RHD Register) facilitate recall and follow-up. The Australian RHD Endgame Strategy targets elimination by 2031.

Referral pathways

Referral through ACCHOs and Aboriginal Hospital Liaison Officers (AHLOs) improves engagement. The Specialist Outreach Assistance Programme provides funded specialist visits to remote communities. NT, WA, and QLD have specific rheumatology outreach programmes targeting Indigenous communities.

📚 References

1. Australian Institute of Health and Welfare (AIHW). Autoimmune disease in Australia. Cat. no. PHE 312. Canberra: AIHW; 2023.
2. Fraenkel L, Bathon JM, England BR, et al. 2021 American College of Rheumatology guideline for the treatment of rheumatoid arthritis. Arthritis Care Res. 2021;73(7):924–939.
3. Fanouriakis A, Kostopoulou M, Alber K, et al. 2019 update of the EULAR recommendations for the management of systemic lupus erythematosus. Ann Rheum Dis. 2019;78(6):736–745.
4. Chung SA, Langford CA, Maz M, et al. 2021 American College of Rheumatology/Vasculitis Foundation guideline for the management of antineutrophil cytoplasmic antibody-associated vasculitis. Arthritis Care Res. 2021;73(11):1583–1599.
5. Smolen JS, Landewé RBM, Bijlsma JWJ, et al. EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease-modifying antirheumatic drugs: 2022 update. Ann Rheum Dis. 2023;82(1):3–18.
6. Australian Technical Advisory Group on Immunisation (ATAGI). Australian Immunisation Handbook. Australian Government Department of Health; 2024. Available from: immunisationhandbook.health.gov.au.
7. Rheumatic Heart Disease Australia (RHDAustralia). The 2020 Australian guideline for prevention, diagnosis, and management of acute rheumatic fever and rheumatic heart disease. 3rd ed. Darwin: Menzies School of Health Research; 2020.
8. Pharmaceutical Benefits Scheme (PBS). PBS Schedule. Australian Government Department of Health. Available from: pbs.gov.au. Accessed 2024.
9. Agarwal S, Cunnington J, Nossent J. Autoimmune disease in Indigenous Australians: a systematic review. Int J Rheum Dis. 2021;24(12):1487–1498.
10. Pisetsky DS. Antinuclear antibody testing — misunderstood or misused? Clin Immunol. 2023;255:109717.
11. Bertsias GK, Tektonidou M, Amoura Z, et al. Joint European League Against Rheumatism and European Renal Association–European Dialysis and Transplant Association (EULAR/ERA-EDTA) recommendations for the management of adult and paediatric lupus nephritis. Ann Rheum Dis. 2012;71(11):1771–1782.
12. Ledingham J, Deighton C; British Society for Rheumatology Standards, Audit and Guidelines Working Group. Update on the British Society for Rheumatology guidelines for prescribing TNFα blockers in adults with rheumatoid arthritis. Rheumatology. 2005;44(2):155–158.
13. National Health and Medical Research Council (NHMRC). National statement on ethical conduct in human research. Canberra: NHMRC; 2023 (updated).

for PBS-listed medicines at participating pharmacies.

Cultural safety

Medication adherence

Specific conditions

Referral pathways

📚 References

1. Australian Institute of Health and Welfare (AIHW). Autoimmune disease in Australia. Cat. no. PHE 312. Canberra: AIHW; 2023.
2. Fraenkel L, Bathon JM, England BR, et al. 2021 American College of Rheumatology guideline for the treatment of rheumatoid arthritis. Arthritis Care Res. 2021;73(7):924–939.
3. Fanouriakis A, Kostopoulou M, Alber K, et al. 2019 update of the EULAR recommendations for the management of systemic lupus erythematosus. Ann Rheum Dis. 2019;78(6):736–745.
4. Chung SA, Langford CA, Maz M, et al. 2021 American College of Rheumatology/Vasculitis Foundation guideline for the management of antineutrophil cytoplasmic antibody-associated vasculitis. Arthritis Care Res. 2021;73(11):1583–1599.
5. Smolen JS, Landewé RBM, Bijlsma JWJ, et al. EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease-modifying antirheumatic drugs: 2022 update. Ann Rheum Dis. 2023;82(1):3–18.
6. Australian Technical Advisory Group on Immunisation (ATAGI). Australian Immunisation Handbook. Australian Government Department of Health; 2024. Available from: immunisationhandbook.health.gov.au.
7. Rheumatic Heart Disease Australia (RHDAustralia). The 2020 Australian guideline for prevention, diagnosis, and management of acute rheumatic fever and rheumatic heart disease. 3rd ed. Darwin: Menzies School of Health Research; 2020.
8. Pharmaceutical Benefits Scheme (PBS). PBS Schedule. Australian Government Department of Health. Available from: pbs.gov.au. Accessed 2024.
9. Agarwal S, Cunnington J, Nossent J. Autoimmune disease in Indigenous Australians: a systematic review. Int J Rheum Dis. 2021;24(12):1487–1498.
10. Pisetsky DS. Antinuclear antibody testing — misunderstood or misused? Clin Immunol. 2023;255:109717.
11. Bertsias GK, Tektonidou M, Amoura Z, et al. Joint European League Against Rheumatism and European Renal Association–European Dialysis and Transplant Association (EULAR/ERA-EDTA) recommendations for the management of adult and paediatric lupus nephritis. Ann Rheum Dis. 2012;71(11):1771–1782.
12. Ledingham J, Deighton C; British Society for Rheumatology Standards, Audit and Guidelines Working Group. Update on the British Society for Rheumatology guidelines for prescribing TNFα blockers in adults with rheumatoid arthritis. Rheumatology. 2005;44(2):155–158.
13. National Health and Medical Research Council (NHMRC). National statement on ethical conduct in human research. Canberra: NHMRC; 2023 (updated).