Haematemesis and Melaena

Last updated 31 May 2026 · Gastroenterology

📋 Key Information Summary

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Upper gastrointestinal (GI) bleeding presents as haematemesis (fresh blood or "coffee-ground" vomitus) and/or melaena (black, tarry stools) and constitutes a medical emergency requiring rapid assessment and resuscitation.
The most common causes of upper GI bleeding are peptic ulcer disease (~40%), oesophagitis/gastritis (~30%), Mallory-Weiss tears (~10–15%), and oesophageal varices (~10%).
The Glasgow-Blatchford Score (GBS) is the recommended pre-endoscopy risk stratification tool; a GBS of 0–1 identifies very-low-risk patients safe for outpatient management.
All haemodynamically unstable patients require immediate resuscitation with IV access, crystalloid fluids, group-and-save or crossmatch, and transfusion targeting Hb ≥70 g/L.
Proton pump inhibitors (PPIs) — IV pantoprazole 80 mg bolus then 8 mg/hr infusion — should be commenced empirically for suspected peptic ulcer bleeding before endoscopy.
Upper GI endoscopy (OGD) within 24 hours of presentation is standard; for variceal bleeding or haemodynamic instability, emergency endoscopy within 12 hours is required.
Mallory-Weiss tears are mucosal lacerations at the gastro-oesophageal junction, typically following forceful vomiting; 80–90% stop bleeding spontaneously and rarely require intervention beyond supportive care.
Oesophageal varices carry a mortality of 15–20% per episode; initial pharmacotherapy with IV terlipressin (or octreotide/somatostatin) plus IV ceftriaxone is mandatory before endoscopy.
NSAIDs and aspirin are the most common drug-associated causes of upper GI bleeding; co-prescription of a PPI significantly reduces risk.
Warfarin and direct oral anticoagulants (DOACs) increase bleeding severity; reversal agents (vitamin K, prothrombin complex concentrate, idarucizumab, andexanet alfa) should be considered in life-threatening haemorrhage.
Dual antiplatelet therapy (DAPT) post-PCI carries significant GI bleeding risk; PPI co-prescription is strongly recommended.
Aboriginal and Torres Strait Islander Australians have significantly higher rates of Helicobacter pylori infection and peptic ulcer disease, contributing to greater upper GI bleeding burden.
All patients with peptic ulcer bleeding should be tested for H. pylori and treated if positive to prevent rebleeding.

Introduction & Australian Epidemiology

Upper gastrointestinal (GI) bleeding is defined as haemorrhage originating proximal to the ligament of Treitz, presenting as haematemesis (vomiting of fresh or altered blood), melaena (black, tarry, foul-smelling stools), or both. It is one of the most common gastrointestinal emergencies encountered in Australian emergency departments and primary care, with an estimated annual incidence of 80–150 per 100,000 adults in Australia and New Zealand.

The condition carries an overall in-hospital mortality of approximately 5–10%, though mortality rises to 15–20% in variceal bleeding and in patients with significant comorbidities. Prompt recognition, risk stratification, resuscitation, and timely endoscopy are the cornerstones of management.

Australian Burden of Disease

Approximately 25,000–30,000 hospital admissions per year in Australia are attributable to upper GI bleeding.
Peptic ulcer disease remains the single most common aetiology, accounting for 35–45% of cases. The prevalence of Helicobacter pylori in Australia is approximately 15–20% in non-Indigenous adults but significantly higher (30–70%) in Aboriginal and Torres Strait Islander communities.
Aspirin and NSAID use accounts for an increasing proportion of upper GI bleeds, particularly in the ageing population on cardiovascular prophylaxis.
Alcohol-related liver disease and hepatitis B/C-associated cirrhosis drive the burden of variceal bleeding, disproportionately affecting Indigenous Australians and populations in regional and remote areas.
Men are affected approximately twice as often as women, and incidence increases sharply after age 60.
The AIHW reports that gastrointestinal diseases are among the top 10 causes of disease burden in Australia, with upper GI bleeding contributing significantly to hospital bed days and healthcare costs.

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Clinical urgency: Any patient presenting with haematemesis or melaena should be triaged as Category 2 (emergency) or Category 1 (if haemodynamically unstable) under the Australasian Triage Scale. Do not delay resuscitation for diagnostic investigations.

Causes of Upper GI Bleeding

The causes of upper GI bleeding are broadly classified by anatomical site and underlying mechanism. A systematic approach ensures that life-threatening causes are not overlooked.

Classification by Site

Site	Causes	Approximate Frequency
Oesophagus	Oesophagitis (reflux, eosinophilic), oesophageal varices, Mallory-Weiss tear, oesophageal carcinoma, oesophageal ulcer	~25%
Stomach	Gastric ulcer, erosive gastritis, gastric varices, gastric carcinoma, Dieulafoy lesion, gastric antral vascular ectasia (GAVE / "watermelon stomach")	~40%
Duodenum	Duodenal ulcer (anterior and posterior), erosive duodenitis, duodenal varices	~25%
Aorto-enteric fistula	Post aortic graft surgery; can present with catastrophic "herald bleed"	<1%
Hepatobiliary / Pancreatic	Hæmobilia (post-trauma, post-biopsy), pancreatic pseudoaneurysm rupture	<1%

Classification by Mechanism

Ulceration / erosion: Peptic ulcer disease (most common), NSAID/aspirin-related gastropathy, H. pylori-associated gastritis, stress ulceration in critically ill patients.
Portal hypertensive: Oesophageal and gastric varices secondary to cirrhosis or non-cirrhotic portal hypertension.
Mechanical / traumatic: Mallory-Weiss tear, foreign body ingestion, iERCP-related, post-operative.
Vascular: Dieulafoy lesion, angiodysplasia, GAVE, hereditary haemorrhagic telangiectasia.
Neoplastic: Oesophageal, gastric, or duodenal malignancy.
Coagulopathy-related: Anticoagulant or antiplatelet use, thrombocytopenia, chronic liver disease with coagulopathy.

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Key clinical point: In approximately 5–10% of upper GI bleeds, no cause is identified at initial endoscopy. Repeat endoscopy, capsule endoscopy, or CT angiography may be required for obscure GI bleeding.

Mallory-Weiss Syndrome

Mallory-Weiss syndrome refers to longitudinal mucosal lacerations at or near the gastro-oesophageal junction (GEJ), typically precipitated by forceful or prolonged vomiting, retching, or straining. The tear involves the mucosa and submucosa but not the muscularis propria, distinguishing it from Boerhaave syndrome (oesophageal perforation).

Aetiology and Risk Factors

Alcohol binge and vomiting: The most common precipitant; accounts for 50–70% of cases.
Severe retching: From any cause including chemotherapy-induced vomiting, hyperemesis gravidarum, gastroenteritis.
Heavy meals followed by vomiting.
Hiatal hernia: Present in up to 75% of Mallory-Weiss cases — increases mucosal vulnerability at the GEJ.
Coagulopathy or anticoagulant use increases the risk and severity of bleeding.
Coughing, straining at stool, seizures, cardiopulmonary resuscitation.

Clinical Presentation

Classic presentation: haematemesis preceded by an episode of forceful vomiting or retching — the "herald vomit" of non-bloody emesis followed by bloody emesis.
Approximately 80–90% of Mallory-Weiss tears cease bleeding spontaneously.
Patients may present with melaena if the bleeding rate is slow.
Haemodynamic instability is uncommon but may occur with large tears or concurrent coagulopathy.
The diagnosis is confirmed at upper GI endoscopy, which shows one or more linear mucosal tears at or just below the GEJ.

Management

Resuscitation and stabilisation

IV access, fluid resuscitation, crossmatch. Correct any coagulopathy. Most patients are haemodynamically stable.

Supportive care

NPO initially, IV fluids, antiemetics (ondansetron 4 mg IV) to prevent further vomiting. PPI therapy (pantoprazole 40 mg PO BD or IV).

Endoscopy

Upper GI endoscopy within 24 hours for diagnosis and to exclude other causes. Active bleeding at endoscopy can be managed with injection therapy (adrenaline 1:10,000), haemoclip application, or thermal coagulation.

Interventional radiology / Surgery

For refractory bleeding: transarterial embolisation (TAE) via interventional radiology. Surgical ligation is rarely needed.

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Prognosis: Mallory-Weiss tears have an excellent prognosis. Rebleeding occurs in only 3–7% of cases. Most patients can be discharged within 24–48 hours once stable and tolerating oral intake.

Oesophageal Varices

Oesophageal varices are dilated submucosal veins in the distal oesophagus that develop as a consequence of portal hypertension, most commonly due to cirrhosis. Variceal haemorrhage is a life-threatening emergency with a mortality rate of 15–20% per episode, and up to 30–40% of patients with large varices will bleed within 2 years of diagnosis without prophylactic treatment.

Pathophysiology

Portal hypertension (hepatic venous pressure gradient [HVPG] ≥10 mmHg) leads to the formation of portosystemic collaterals. Oesophageal varices develop when portal pressure exceeds 12 mmHg. Variceal wall tension increases as the varix enlarges, and when the wall tension exceeds the wall strength, rupture and haemorrhage occur. Key factors determining rupture risk include the size of the varix, the portal pressure gradient, and the thickness of the variceal wall.

Causes of Portal Hypertension Leading to Varices

Category	Causes
Pre-hepatic	Portal vein thrombosis, splenic vein thrombosis, splenomegaly
Intra-hepatic (most common)	Alcoholic cirrhosis, hepatitis B/C cirrhosis, non-alcoholic steatohepatitis (NASH) cirrhosis, autoimmune hepatitis, primary biliary cholangitis, haemochromatosis, Wilson disease, alpha-1 antitrypsin deficiency
Post-hepatic	Budd-Chiari syndrome, constrictive pericarditis, severe right heart failure

Acute Variceal Haemorrhage — Emergency Management

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Variceal bleeding is a medical emergency with 15–20% mortality per episode. Initiate resuscitation and pharmacological therapy simultaneously. Do not wait for endoscopy to commence vasoactive drugs and antibiotics.

Immediate Resuscitation (Minutes 0–30)

IV access: Two large-bore (16G or 18G) peripheral IV cannulae.
Blood transfusion: Crossmatch 4 units packed red blood cells (PRBCs). Transfuse to maintain Hb 70–90 g/L — avoid over-transfusion as this can increase portal pressure and worsen bleeding.
Restrictive transfusion strategy: Evidence supports a target Hb of 70 g/L (trigger) in the absence of ischaemic heart disease.
Correct coagulopathy: Platelets if <50 × 10⁹/L; fresh frozen plasma (FFP) or prothrombin complex concentrate (PCC) if INR >1.5 with active bleeding; IV vitamin K 10 mg.
ICU/HDU admission for haemodynamically unstable patients.

Pharmacological Therapy (Commence Immediately)

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Terlipressin

Glypressin® · Vasoconstrictor analogue of vasopressin

Adult dose 2 mg IV bolus, then 1–2 mg IV every 4–6 hours for up to 72 hours (reduce to 1 mg once bleeding controlled)

Mechanism Splanchnic vasoconstriction → reduces portal blood flow and portal pressure

Key cautions Contraindicated in ischaemic heart disease, peripheral vascular disease, sepsis. Monitor for hyponatraemia and ischaemic complications.

PBS status ⚑ Authority Required

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Octreotide

Sandostatin® · Somatostatin analogue (alternative to terlipressin)

Adult dose 50 µg IV bolus, then 50 µg/hr continuous IV infusion for 5 days

When to use Alternative to terlipressin when terlipressin is unavailable or contraindicated (e.g., significant cardiovascular disease)

PBS status ⚑ Authority Required

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Ceftriaxone

Rocephin® · 3rd-generation cephalosporin

Adult dose 1 g IV daily for 5–7 days

Indication Prophylactic antibiotics reduce rebleeding and mortality in cirrhotic patients with variceal haemorrhage. Commence at presentation.

Penicillin allergy alternative Ciprofloxacin 400 mg IV BD or fluoroquinolone PO if tolerating oral

PBS status ✔ PBS General Benefit (IV)

Endoscopic Therapy

Emergency endoscopy within 12 hours of presentation (after haemodynamic stabilisation).
Endoscopic variceal ligation (EVL / banding): First-line endoscopic treatment for oesophageal varices. Rubber bands are applied to varices starting at the GEJ, achieving haemostasis in >90% of cases.
Endoscopic sclerotherapy: Injection of sclerosant (e.g., sodium tetradecyl sulphate, ethanolamine) into or adjacent to varices. Used when EVL is technically difficult.
Repeat banding every 2–4 weeks until variceal eradication is achieved.

Refractory Bleeding — Rescue Therapies

Sengstaken-Blakemore tube (SBT): Balloon tamponade as a temporising measure. Requires ICU monitoring, NG suction above proximal balloon. Maximum tamponade time 24 hours. Definitive therapy must be planned.
Transjugular intrahepatic portosystemic shunt (TIPS): Recommended for patients who fail two endoscopic and pharmacological treatments. Reduces portal pressure by creating a shunt between the hepatic and portal veins. Available at major tertiary centres in Australia.
Self-expandable metal stent (SEMS / Danis stent): An alternative to SBT for refractory oesophageal variceal bleeding, with lower complication rates. Can be deployed endoscopically and left in situ for up to 14 days.

Primary Prophylaxis — Preventing First Variceal Bleed

Screening: All patients with cirrhosis should undergo screening upper GI endoscopy at diagnosis. If no varices are found, repeat in 2–3 years (compensated cirrhosis) or annually (decompensated cirrhosis).
Non-selective beta-blockers (NSBB): Carvedilol (6.25–12.5 mg PO daily) or propranolol (20–40 mg PO BD, titrate to resting HR 55–60 bpm) — recommended for medium/large varices and small varices with red wale signs.
EVL: Alternative for patients who are intolerant or have contraindications to NSBB.

Secondary Prophylaxis — Preventing Rebleeding

Combination therapy: NSBB + EVL (standard of care for secondary prophylaxis).
TIPS: Consider early TIPS (within 72 hours) for high-risk patients (Child-Pugh C 10–13 or Child-Pugh B with active bleeding at endoscopy).
Liver transplant assessment should be considered for all patients with decompensated cirrhosis.

Drug-Associated GI Bleeding

Medications are a leading contributing factor in upper GI bleeding, both through direct mucosal injury and through impairment of haemostasis. A careful medication history is essential in every patient presenting with haematemesis or melaena.

Drug Classes Implicated in Upper GI Bleeding

Drug Class	Mechanism	Risk Magnitude	Risk Reduction Strategy
NSAIDs (ibuprofen, naproxen, diclofenac, meloxicam, celecoxib)	COX-1 inhibition → ↓ prostaglandin-mediated mucosal protection; direct topical mucosal injury	RR 2–6× vs non-users. Highest in first month and with higher doses.	PPI co-prescription; use lowest effective dose for shortest duration; prefer celecoxib (COX-2 selective) in high-risk patients.
Aspirin (low-dose 100–300 mg)	Irreversible COX-1 inhibition → ↓ thromboxane A₂ → impaired platelet aggregation; mucosal injury	RR 2–4× vs non-users	PPI co-prescription (e.g., pantoprazole 20–40 mg PO daily) for all patients with additional risk factors.
Dual antiplatelet therapy (DAPT) (aspirin + clopidogrel/ticagrelor/prasugrel)	Additive antiplatelet effects; combined with direct mucosal injury from aspirin	RR 5–9× vs aspirin alone	PPI co-prescription mandatory. Minimise DAPT duration per current ACS/PCI guidelines.
Warfarin	Inhibits vitamin K-dependent clotting factors; does not cause GI injury directly but worsens bleeding from pre-existing lesions	RR 2–3× vs non-users; increased with INR >3.0	Maintain INR 2.0–3.0; PPI co-prescription in high-risk patients; consider DOAC if INR control is poor.
DOACs (apixaban, rivaroxaban, dabigatran, edoxaban)	Direct inhibition of Factor Xa or thrombin; GI bleeding risk varies by agent	Dabigatran and rivaroxaban have higher GI bleeding rates than warfarin in trials; apixaban similar or lower	Dose adjustment for renal impairment; PPI co-prescription in high-risk patients; avoid concurrent NSAIDs.
Corticosteroids	Impair mucosal healing; increase susceptibility to NSAID-related GI injury when co-prescribed	RR 1.5–2× (alone); RR 15× when combined with NSAIDs	Avoid concurrent NSAIDs. PPI if on corticosteroids + any additional risk factor.
SSRIs	Impair platelet serotonin uptake → ↓ platelet aggregation	RR 1.5–2×; synergistic with NSAIDs/aspirin	PPI co-prescription when combined with NSAIDs or aspirin.

PPI Gastroprotection — Australian Recommendations

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Pantoprazole

Somac® · Proton pump inhibitor

Gastroprotection dose 20–40 mg PO daily, 30 minutes before breakfast

Acute UGI bleed dose 80 mg IV bolus then 8 mg/hr IV infusion for 72 hours (pre-endoscopy Forrest I–III ulcers)

Renal adjustment No adjustment required

PBS status ✔ PBS General Benefit

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Esomeprazole

Nexium® · Proton pump inhibitor

Gastroprotection dose 20 mg PO daily

Acute UGI bleed dose 80 mg IV bolus then 8 mg/hr IV infusion for 72 hours

PBS status ✔ PBS General Benefit

Antiplatelet/Anticoagulant Management During Active Bleeding

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Do not abruptly cease antiplatelet agents in patients with recent coronary stents (<12 months) without cardiology consultation. Premature cessation of DAPT carries a high risk of stent thrombosis and myocardial infarction. A multidisciplinary decision involving gastroenterology and cardiology is essential.

Aspirin for secondary cardiovascular prophylaxis: Cease temporarily in active major bleeding; restart as soon as clinically safe (ideally within 3–5 days, after endoscopy and haemostasis confirmed).
Warfarin: Cease and reverse with IV vitamin K 10 mg + PCC (dose per INR: 25 IU/kg for INR 2–4, 35 IU/kg for INR 4–6, 50 IU/kg for INR >6). FFP is an alternative if PCC unavailable.
Dabigatran: Reversal with idarucizumab (Praxbind®) 5 g IV. Available in Australian emergency departments. ⚑ Authority Required
Apixaban / Rivaroxaban: Reversal with andexanet alfa (Ondexxya®) — limited availability in Australia; consult haematology. PCC 50 IU/kg as alternative. ✘ Specialist only
Clopidogrel / Ticagrelor / Prasugrel: Cease; platelet transfusion may be considered for life-threatening bleeding (limited evidence of benefit). Desmopressin 0.3 µg/kg IV may be considered.

Clinical Presentation & Diagnostic Criteria

Presenting Features

Haematemesis: Vomiting of fresh (bright red) blood indicates active or recent high-volume upper GI bleeding. "Coffee-ground" vomitus represents altered blood that has been acted upon by gastric acid.
Melaena: Black, tarry, offensive-smelling stools indicate digested blood from the upper GI tract (typically proximal to the ligament of Treitz). A single melaena stool may represent 50–100 mL of blood loss.
Haematochezia: Passage of bright red blood per rectum may occasionally originate from a very brisk upper GI bleed (10–15% of severe UGI bleeds present this way).
Syncope or presyncope: May indicate significant hypovolaemia.
Abdominal pain: Epigastric pain may suggest peptic ulcer disease; absence of pain does not exclude significant bleeding.
Signs of chronic liver disease: Spider naevi, palmar erythema, gynaecomastia, ascites, splenomegaly — suggest variceal aetiology.
History of vomiting/retching prior to haematemesis: Classic for Mallory-Weiss tear.

Clinical Assessment

Vital signs: Heart rate, blood pressure (including postural drop), respiratory rate, oxygen saturation, temperature, GCS.
Haemodynamic assessment: Tachycardia >100 bpm and/or systolic BP <100 mmHg suggest significant blood loss (>1,000 mL or >20% circulating volume).
Digital rectal examination: Essential to confirm melaena and assess stool colour.
Nasogastric aspirate: Blood in the NG aspirate confirms upper GI source; absence of blood does not exclude it. Not routinely recommended but may help guide triage decisions.
Signs of liver disease: Stigmata of chronic liver disease, hepatomegaly, splenomegaly, ascites, jaundice.

Laboratory Investigations

Essential Full blood count (FBC) Haemoglobin may be normal initially due to haemoconcentration; repeat in 4–6 hours. Thrombocytopenia suggests chronic liver disease or DIC.

Essential Coagulation studies (INR, APTT, fibrinogen) Elevated INR in liver disease or anticoagulant use. Correct if actively bleeding.

Essential Group and screen / Crossmatch Crossmatch at least 2–4 units PRBCs for all actively bleeding patients.

Essential Urea, creatinine, electrolytes (U&E) Elevated urea disproportionate to creatinine suggests upper GI bleed (digested blood protein absorption). Also assess renal function for drug dosing.

Essential Liver function tests (LFTs) Deranged in chronic liver disease; albumin, bilirubin, ALT, AST, ALP, GGT.

Available Venous blood gas (VBG) Lactate >2 mmol/L suggests significant tissue hypoperfusion and need for aggressive resuscitation. Base deficit correlates with severity.

Available Blood type ABO and Rh typing. Essential if transfusion anticipated.

Available Helicobacter pylori testing Urea breath test, stool antigen, or biopsy at endoscopy. All patients with peptic ulcer bleeding should be tested. MBS item 69487 (urea breath test).

Investigations

Upper GI Endoscopy (OGD)

Upper GI endoscopy (oesophagogastroduodenoscopy) is the gold-standard diagnostic and therapeutic investigation for upper GI bleeding. It allows direct visualisation of the bleeding source, risk classification, and immediate haemostatic intervention.

Timing — non-variceal bleeding: Within 24 hours of presentation for all patients with significant upper GI bleeding (Glasgow-Blatchford Score ≥1).
Timing — variceal bleeding: Emergency endoscopy within 12 hours, after initial resuscitation and vasoactive drug administration.
Pre-endoscopy PPI: IV high-dose PPI (pantoprazole 80 mg bolus then 8 mg/hr) should be commenced before endoscopy in suspected non-variceal upper GI bleeding — downstages high-risk stigmata at endoscopy.
Erythromycin prokinetic: IV erythromycin 250 mg over 30 minutes, 30–120 minutes before endoscopy, improves gastric mucosal visualisation by promoting gastric emptying. Particularly useful when large volumes of blood or clot are expected.
MBS item numbers: OGD — MBS item 30473 (diagnostic), 30475 (with therapeutic intervention such as injection, clipping, or banding).

Forrest Classification of Peptic Ulcers

Forrest Class	Description	Rebleed Risk	Treatment
Ia	Spurting haemorrhage	90%	Endoscopic haemostasis mandatory
Ib	Oozing haemorrhage	50%	Endoscopic haemostasis mandatory
IIa	Non-bleeding visible vessel	50%	Endoscopic haemostasis mandatory
IIb	Adherent clot	30%	Consider endoscopic treatment (clot removal + haemostasis)
IIc	Flat pigmented spot (haematin)	10%	Medical therapy (PPI); no endoscopic intervention required
III	Clean-based ulcer	<5%	Medical therapy only; may be safe for early discharge

Endoscopic Haemostasis Techniques

Injection therapy: Adrenaline (epinephrine) 1:10,000 dilution injected in 4 quadrants around the bleeding vessel. Used in combination with a second modality (thermal or mechanical).
Thermal coagulation: Bipolar electrocoagulation or heater probe applied to the bleeding vessel after adrenaline injection.
Mechanical haemostasis: Through-the-scope haemoclips. Effective for visible vessels and active bleeding. Preferred for patients on anticoagulants.
Combination therapy (injection + thermal or clip) is superior to injection alone for high-risk ulcers.

Second-Line and Adjunctive Investigations

Available CT angiography (CTA) For ongoing or recurrent bleeding when endoscopy is non-diagnostic or not feasible. Detects active contrast extravasation at rates >0.5 mL/min. Available at most metropolitan hospitals.

Referral Interventional angiography ± embolisation For ongoing bleeding after failed endoscopic therapy. Transarterial embolisation (TAE) performed by interventional radiology. Available at major tertiary centres.

Available Capsule endoscopy For obscure GI bleeding when upper and lower endoscopy are non-diagnostic. MBS item 30634.

Referral Push enteroscopy / double-balloon enteroscopy For suspected small bowel bleeding source. Available at specialist centres.

Specialist Meckel's scan (Tc-99m pertechnetate) Rarely indicated in upper GI bleeding; useful for suspected Meckel's diverticulum in younger patients presenting with significant GI haemorrhage.

Risk Stratification

Glasgow-Blatchford Score (GBS)

The Glasgow-Blatchford Score is the preferred pre-endoscopy risk stratification tool for upper GI bleeding, as recommended by NICE and the Australian Clinical Practice Guidelines. It identifies low-risk patients (GBS 0–1) who may be suitable for outpatient management without endoscopy.

Parameter	Finding	Score
Blood urea (mmol/L)	6.5–7.9	2
	8.0–9.9	3
	10.0–24.9	4
≥25.0		6
Haemoglobin (g/L) — Men	120–129	1
Haemoglobin (g/L) — Men	100–119	3
<100		6
Haemoglobin (g/L) — Women	100–119	1
Haemoglobin (g/L) — Women	<100	6
Systolic BP (mmHg)	100–109	1
	90–99	2
	<90	3
Heart rate ≥100 bpm	Yes	1
Melaena	Yes	1
Syncope	Yes	2
Hepatic disease	Yes	2
Cardiac failure	Yes	2

Low Risk

GBS 0–1

Very low risk of intervention or death (<1%). Suitable for outpatient investigation and management. No endoscopy required acutely.

Setting: GP / Outpatient endoscopy

Moderate Risk

GBS 2–6

Moderate risk of needing intervention. Endoscopy within 24 hours. Observation in ED or short-stay unit. IV PPI if high-risk features.

Setting: Hospital ward / Short-stay unit

High Risk

GBS ≥7

High risk of needing intervention (>50%) and mortality (>10%). Urgent endoscopy, ICU/HDU consideration. Aggressive resuscitation. Transfusion as needed.

Setting: ICU / HDU

Post-Endoscopy Risk Scores

AIMS65 score: Predicts in-hospital mortality. Points for: Albumin <30 g/L, INR >1.5, Mental status altered, Systolic BP ≤90 mmHg, age ≥65 years. Score ≥2 = high mortality risk.
Rockall score (full): Combines clinical and endoscopic findings. Score ≥5 indicates high risk of rebleeding and mortality.

Management — Empirical & Directed Therapy

Initial Resuscitation

Airway

Protect airway in obtunded patients with massive haematemesis. Consider early intubation (RSI) if GCS <8 or active large-volume haematemesis with aspiration risk.

Breathing

Supplemental O₂ to maintain SpO₂ ≥94%. Monitor respiratory rate.

Circulation

Two large-bore IV cannulae. Crystalloid bolus (Hartmann's solution 500 mL) for hypotension. Crossmatch 2–4 units PRBCs. Target Hb ≥70 g/L (restrictive strategy). Correct coagulopathy.

Disability

Assess GCS. Check blood glucose. Hepatic encephalopathy may present in cirrhotic patients with variceal bleeding.

Exposure

Full examination: signs of chronic liver disease, stigmata of bleeding, abdominal signs. Insert urinary catheter for UO monitoring (target ≥0.5 mL/kg/hr).

Pharmacological Management — Quick Reference

Suspected peptic ulcer bleeding

Pantoprazole 80 mg IV bolus → 8 mg/hr infusion

72 hours, then 40 mg PO BD

Commence pre-endoscopy

Suspected variceal bleeding

Terlipressin 2 mg IV → 1–2 mg Q4-6h + Ceftriaxone 1 g IV daily

Up to 5 days (vasoactive); 5–7 days (antibiotic)

Commence immediately; do NOT wait for endoscopy

Warfarin-related bleeding

Vitamin K 10 mg IV + PCC per INR

Vitamin K single dose; PCC single dose

FFP if PCC unavailable (slower onset)

Dabigatran-related bleeding

Idarucizumab (Praxbind®) 5 g IV

Single dose

Available in Australian EDs; Authority Required

H. pylori Eradication — Post-Ulcer Bleeding

H. pylori eradication significantly reduces rebleeding rates from peptic ulcers (from ~20% to ~2%). All patients with peptic ulcer bleeding should be tested for H. pylori and treated if positive.

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Standard Triple Therapy (First-Line)

PPI + Amoxicillin + Clarithromycin

Regimen PPI (e.g., pantoprazole 40 mg PO BD) + amoxicillin 1 g PO BD + clarithromycin 500 mg PO BD for 14 days

Penicillin allergy Replace amoxicillin with metronidazole 400 mg PO BD

PBS status ✔ PBS General Benefit (Authority Required for H. pylori)

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Bismuth Quadruple Therapy (Second-Line / Salvage)

PPI + Bismuth + Metronidazole + Tetracycline

Regimen PPI (pantoprazole 40 mg PO BD) + bismuth subsalicylate/subcitrate 120 mg PO QID + metronidazole 400 mg PO TDS + tetracycline 500 mg PO QID for 14 days

Indication First-line treatment failure; clarithromycin resistance areas; prior macrolide exposure

PBS status ⚑ Authority Required

⚠️

Test of cure: Confirm H. pylori eradication with a urea breath test (UBT) or stool antigen test at least 4 weeks after completing eradication therapy and at least 2 weeks after stopping PPI therapy. MBS item 69487.

Monitoring

Inpatient Monitoring

0–6 hours

Continuous cardiac monitoring, hourly vital signs, fluid balance chart, repeat FBC at 4–6 hours (initial Hb may be deceptively normal). IV PPI infusion commenced if indicated. Transfusion as needed.

6–24 hours

Upper GI endoscopy performed. Post-endoscopy monitoring for signs of rebleeding. Adjust management based on Forrest classification and endoscopic findings.

24–72 hours

Monitor FBC 12–24 hourly. Transition IV PPI to oral once tolerating. Commence H. pylori eradication if positive and tolerating oral intake. Monitor for rebleeding (further haematemesis, melaena, tachycardia, falling Hb).

72 hours – discharge

IV PPI converted to oral PPI at 72 hours. Discharge criteria: haemodynamically stable >24 hours, tolerating oral diet, stable Hb, no further bleeding. Arrange follow-up endoscopy if indicated (e.g., gastric ulcer — repeat OGD at 8–12 weeks to exclude malignancy).

Signs of Rebleeding

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Rebleeding occurs in 10–15% of non-variceal and 20–30% of variceal bleeds. Indicators include: recurrent haematemesis or fresh melaena, tachycardia (HR >100), hypotension (SBP <100), dropping Hb despite transfusion, rising urea, and haemodynamic instability. Urgent repeat endoscopy is required; surgery or interventional radiology if endoscopic therapy fails again.

Outpatient Follow-Up

Peptic ulcer: Continue PPI for 4–8 weeks (duodenal ulcer) or 8–12 weeks (gastric ulcer). Repeat OGD for gastric ulcer to confirm healing and exclude malignancy.
H. pylori eradication: Test of cure at ≥4 weeks post-treatment.
NSAIDs/aspirin: Review necessity. If ongoing NSAID required, switch to COX-2 selective + PPI. If aspirin for secondary prevention, restart as soon as safe with PPI co-prescription.
Oesophageal varices: Repeat EVL every 2–4 weeks until eradication. Long-term NSBB. Hepatology/GP shared care. Surveillance endoscopy as per guidelines.
Alcohol counselling: Referral to drug and alcohol services for patients with alcohol-related bleeding. Brief intervention and consideration of pharmacotherapy (naltrexone, acamprosate).

Special Populations

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Pregnancy

General considerations: Upper GI bleeding in pregnancy is uncommon but may be associated with hyperemesis gravidarum (Mallory-Weiss), pre-eclampsia/HELLP syndrome, or peptic ulcer disease.

PPI use: Pantoprazole and omeprazole are considered safe in pregnancy (Category B1/A). Avoid lansoprazole and rabeprazole (limited data).

Endoscopy: Safe in pregnancy when clinically indicated. Left lateral positioning to avoid aortocaval compression. Fetal monitoring. Use lowest effective sedation doses.

Avoid: Terlipressin (uterine contractions). Octreotide if possible. Tranexamic acid relatively contraindicated.

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Paediatrics

Common causes: Oesophagitis (reflux, eosinophilic), Mallory-Weiss tear, peptic ulcer disease, oesophageal varices (biliary atresia, portal vein thrombosis), swallowed blood (neonatal), Meckel's diverticulum, NSAID ingestion.

Resuscitation: Use paediatric advanced life support (PALS) fluid bolus of 10 mL/kg crystalloid. Transfusion target Hb ≥70 g/L (per kg dosing for PRBC: 10 mL/kg raises Hb by ~20 g/L).

PPI dosing: Pantoprazole: 1–2 mg/kg/day PO/IV once daily (max 40 mg/day). Omeprazole: 1–2 mg/kg/day PO once daily.

Endoscopy: Paediatric gastroscope required. General anaesthesia usually required. Available at tertiary paediatric centres (e.g., RCH Melbourne, CHW Sydney, QCH Brisbane).

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Elderly (≥65 years)

Key concerns: Higher mortality (5–15%). Comorbidities (IHD, CKD, CVA). Polypharmacy (NSAIDs, aspirin, anticoagulants). Atypical presentation — may present with syncope, confusion, or falls rather than haematemesis.

Transfusion: Restrictive strategy (Hb target 70 g/L) unless symptomatic ischaemic heart disease — then liberal strategy (Hb target 80–90 g/L) may be appropriate.

Medication review: Review all anticoagulants and antiplatelets. Consider risk-benefit of continuing vs ceasing. Multidisciplinary input (geriatrics, cardiology, gastroenterology).

Endoscopy: Age alone is not a contraindication. Assess procedural risk (ASA score). Conscious sedation with monitoring preferred.

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Renal Impairment

Dialysis patients: Increased GI bleeding risk due to uraemic platelet dysfunction, heparinisation during dialysis, and higher prevalence of angiodysplasia.

PPI: No dose adjustment required for pantoprazole or omeprazole in renal impairment. Safe in dialysis.

Terlipressin: Use with caution in severe CKD. Monitor for hyponatraemia.

Anticoagulant adjustment: DOACs require dose reduction in CKD (eGFR <30 mL/min). Dabigatran is renally cleared — contraindicated if eGFR <30. Apixaban: reduce dose if ≥2 of (age ≥80, weight ≤60 kg, Cr ≥133 µmol/L).

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Hepatic Impairment

Child-Pugh score: Assess severity of liver disease. Child-Pugh C carries highest mortality from variceal bleeding (~30–40%).

Coagulopathy: Correct with vitamin K, FFP, or PCC. Monitor INR closely. Thromboelastography (TEG/ROTEM) may guide transfusion at centres where available.

Encephalopathy: Lactulose 30 mL PO/NG TDS, titrate to 2–3 soft stools daily. Rifaximin 550 mg PO BD as adjunct. Avoid sedation if possible.

Hepatology referral: Early involvement of hepatology/gastroenterology. Consider transplant assessment for decompensated cirrhosis.

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Immunocompromised

Key considerations: HIV, transplant recipients, chemotherapy patients, and those on immunosuppressants (e.g., post-organ transplant). CMV oesophagitis/gastritis, Kaposi sarcoma, and lymphoma may present with GI bleeding.

Infection risk: Broaden antibiotic prophylaxis as clinically indicated. Endoscopy may reveal opportunistic causes (CMV ulcers, fungal oesophagitis).

Drug interactions: Clarithromycin interacts with tacrolimus, cyclosporine, and many antiretrovirals. Azithromycin may be preferred for H. pylori in these patients. Consult infectious diseases/pharmacy.

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 upper gastrointestinal bleeding compared with the non-Indigenous population. This is driven by higher rates of Helicobacter pylori infection, peptic ulcer disease, alcohol-related liver disease, hepatitis B, and chronic kidney disease. Culturally safe, trauma-informed care is essential throughout the patient journey.

H. pylori prevalence

H. pylori infection rates in Aboriginal and Torres Strait Islander communities range from 30–70% in some remote communities, compared with 15–20% in non-Indigenous Australians. This contributes to higher rates of peptic ulcer disease, gastritis, and upper GI bleeding. Community-wide screening and eradication programs have been piloted in some regions (e.g., Northern Territory) with promising results.

Liver disease burden

Alcohol-related liver disease and chronic hepatitis B infection are significantly more prevalent in Indigenous Australians, leading to higher rates of cirrhosis and variceal bleeding. Hepatitis B vaccination coverage has improved but remains suboptimal in some remote communities. The AIHW reports that liver disease is the fifth leading cause of death for Aboriginal and Torres Strait Islander people.

Geographic access to endoscopy

Many remote and very remote communities in the NT, WA, and QLD have limited or no access to endoscopy services. Patients may require aeromedical retrieval (Royal Flying Doctor Service) for emergency endoscopy at a tertiary centre. This introduces delays in definitive management. Training and supporting Indigenous health practitioners in acute GI assessment is critical.

NSAID and analgesic use

Over-the-counter access to NSAIDs and the historical burden of analgesic nephropathy contribute to GI mucosal injury in some communities. Education about safe analgesic use and PPI co-prescription when NSAIDs are necessary is important.

Cultural safety and communication

Health literacy levels vary. Use plain language, involve Aboriginal and Torres Strait Islander health workers/interpreters, and acknowledge the role of family and community in decision-making. Avoid assumptions about alcohol use. Ask about and respect Sorry Business and cultural obligations that may affect hospital attendance and follow-up.

Multidisciplinary and community-based care

Aboriginal Community Controlled Health Organisations (ACCHOs) play a central role in follow-up care, H. pylori eradication completion, and chronic disease management. Shared care models between ACCHOs and hospital gastroenterology services improve outcomes. The Close the Gap PBS Co-payment Measure supports medication access.

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Actionable recommendation: All Aboriginal and Torres Strait Islander patients presenting with upper GI bleeding should be tested for H. pylori, hepatitis B surface antigen, and have liver disease screening (FIB-4 score, liver ultrasound if indicated). Ensure follow-up is coordinated through the patient's primary healthcare service, including an ACCHO if preferred.

📚 References

1. Laine L, Barkun AN, Saltzman JR, et al. ACG Clinical Guideline: Upper Gastrointestinal and Ulcer Bleeding. Am J Gastroenterol. 2021;116(5):899–917.
2. National Institute for Health and Care Excellence (NICE). Acute upper gastrointestinal bleeding in over 16s: diagnosis and management. NICE guideline [CG141]. Updated June 2023.
3. de Franchis R, Bosch J, Garcia-Tsao G, et al. Baveno VII — Renewing consensus in portal hypertension. J Hepatol. 2022;76(4):959–974.
4. Blatchford O, Murray WR, Blatchford M. A risk score to predict need for treatment for upper-gastrointestinal haemorrhage. Lancet. 2000;356(9238):1318–1321.
5. Australian Institute of Health and Welfare (AIHW). Aboriginal and Torres Strait Islander Health Performance Framework: Summary report 2023. Canberra: AIHW; 2023.
6. Stanley AJ, Laine L, Dalton HR, et al. Comparison of risk scoring systems for patients presenting with upper gastrointestinal bleeding: international multicentre prospective study. BMJ. 2017;356:i6432.
7. Crooks CJ, West J, Card TR. Upper gastrointestinal haemorrhage and deprivation: a nationwide cohort study of health inequality in hospital admissions. Gut. 2012;61(4):514–520.
8. Gastroenterological Society of Australia (GESA). Clinical update: Management of acute upper gastrointestinal bleeding. Melbourne: GESA; 2019.
9. Vergara M, Bennett C, Calvet X, et al. Helicobacter pylori eradication for the prevention of peptic ulcer rebleeding. Cochrane Database Syst Rev. 2022;12:CD009398.
10. Mejia-Rivas M, Remes-Troche JM. Mallory-Weiss syndrome: a review of the literature. Curr Gastroenterol Rep. 2023;25(3):45–52.
11. Royal Australian College of General Practitioners (RACGP). Prescribing drugs of dependence in general practice: Part B — Benzodiazepines. Melbourne: RACGP; 2015. [Relevant for analgesic/NSAID prescribing guidance].
12. Australian Commission on Safety and Quality in Health Care (ACSQHC). National Safety and Quality Health Service Standards. 2nd ed. Sydney: ACSQHC; 2021.
13. Sung JJ, Chiu PW, Chan FKL, et al. Asia-Pacific working group consensus on non-variceal upper gastrointestinal bleeding: an update 2018. Gut. 2018;67(10):1757–1768.
14. RHDAustralia (ARF/RHD Australia). 10.6 — Peptic ulcer disease and Helicobacter pylori in Aboriginal and Torres Strait Islander communities. Darwin: Menzies School of Health Research; 2022.
15. Karaoui WR, El Khoury G, Hallit S, et al. Proton pump inhibitors for gastrointestinal bleeding prophylaxis in patients on antiplatelet therapy: a systematic review. Br J Clin Pharmacol. 2022;88(6):2634–2648.

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).