Acute GI Bleeding – Primary Care Interface

📋 Key Information Summary

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Acute gastrointestinal (GI) bleeding is a common emergency presentation with significant mortality in patients aged ≥65 years; approximately 15,000 hospital admissions per year in Australia.
Upper GI bleeding (above the ligament of Treitz) accounts for the majority of acute presentations, with peptic ulcer disease (40–50%), varices (10–15%), and erosive oesophagitis among the leading causes.
Red flag features requiring emergent hospital transfer include haemodynamic instability (systolic BP <90 mmHg, HR >100 bpm), syncope, frank haematemesis, melaena, and brisk haematochezia.
Orthostatic hypotension (systolic drop ≥20 mmHg or diastolic drop ≥10 mmHg on standing) is an early and sensitive sign of significant volume depletion — assess before supine vitals normalise.
Immediate primary care actions: secure IV access (two large-bore cannulae, 16–18G), commence crystalloid resuscitation (0.9% sodium chloride), and arrange urgent transfer to the nearest ED with endoscopy capability.
Assess and document all anticoagulant and antiplatelet agents (warfarin, DOACs, clopidogrel, aspirin, ticagrelor); these significantly increase bleeding severity and influence management timing.
Patients on warfarin with active GI bleeding require urgent INR testing and may need prothrombin complex concentrate (PCC) and IV vitamin K at the receiving hospital.
DOACs (apixaban, rivaroxaban, dabigatran) should be withheld immediately; specific reversal agents (idarucizumab for dabigatran, andexanet alfa for factor Xa inhibitors) are available at tertiary centres.
A structured clinical handover using ISBAR (Introduction, Situation, Background, Assessment, Recommendation) improves communication with the receiving emergency team and reduces adverse events.
Do not delay transfer for investigations beyond basic bloods — time to definitive haemostasis (endoscopy/interventional radiology) is the key determinant of patient outcomes.
Aboriginal and Torres Strait Islander Australians experience higher rates of H. pylori infection and peptic ulcer disease; ensure culturally safe communication and involve Aboriginal health workers where possible.
Elderly patients and those with significant comorbidities (cardiac, renal, hepatic disease) are at highest risk of adverse outcomes and require lower thresholds for transfer and aggressive resuscitation.

Introduction & Australian Epidemiology

Acute gastrointestinal (GI) bleeding encompasses any bleeding from the oesophagus to the anus that presents as an emergency requiring urgent assessment and management. In the Australian primary care setting, the general practitioner's role is to rapidly identify the severity of bleeding, initiate resuscitation, stabilise the patient, and facilitate timely transfer to a facility capable of definitive management — typically via endoscopy or interventional radiology.

GI bleeding is classified anatomically as upper GI (proximal to the ligament of Treitz) or lower GI (distal to the ligament of Treitz). Upper GI bleeding accounts for approximately 70–80% of acute presentations and carries a higher mortality rate (6–10%) compared with lower GI bleeding (2–4%). In Australia, acute upper GI bleeding results in an estimated 15,000 hospital admissions annually, with peptic ulcer disease remaining the single most common aetiology.

Epidemiological Feature	Australian Data
Annual hospital admissions (acute GI bleed)	~15,000 (AIHW data)
In-hospital mortality (upper GI bleed)	6–10% overall; up to 20% in patients aged ≥80 years
Most common cause — upper GI	Peptic ulcer disease (40–50%)
Most common cause — lower GI	Diverticular disease (30–40%)
Median age at presentation	65–70 years
Proportion on anticoagulants/antiplatelets	30–40% of admissions
Re-bleeding rate (peptic ulcer)	10–20% without definitive treatment
ATSI over-representation	1.5–2× age-adjusted rate vs non-Indigenous Australians

Key risk factors in the Australian population include increasing age, chronic NSAID or aspirin use, Helicobacter pylori infection (prevalence 15–30% in the general Australian population, higher in ATSI communities), cirrhosis with portal hypertension, and anticoagulant or antiplatelet therapy. The widespread use of direct oral anticoagulants (DOACs) for atrial fibrillation has contributed to an increasing proportion of GI bleeds related to anticoagulation.

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Clinical responsibility in primary care: The GP's primary role is recognition of severity, initiation of resuscitation, and expeditious transfer. Do not delay transfer for non-essential investigations. Definitive haemostasis is achieved in hospital — time to endoscopy is the key prognostic factor.

Red Flag Features

Rapid identification of red flag features is the most critical step in primary care assessment of acute GI bleeding. These features indicate significant haemorrhage or haemodynamic compromise and mandate immediate resuscitation and emergency transfer. The absence of visible blood (melaena may be occult to the patient) does not exclude significant GI bleeding.

Lower Risk

Minor Bleeding — Consider Urgent Outpatient Review

Small volume haematemesis (coffee grounds), trace melaena, stable vitals, no syncope, no anticoagulant use, Hb >100 g/L, age <60, no significant comorbidities

Setting: Arrange urgent outpatient gastroenterology within 24–48 hours; same-day if possible

High Risk

Significant Bleeding — Urgent Transfer Required

Recurrent haematemesis, ongoing melaena, HR 90–100 bpm, SBP 90–100 mmHg, mild postural symptoms, Hb 80–100 g/L, on antiplatelet therapy

Setting: Urgent transfer to ED — call 000 or arrange immediate medical transfer

Critical

Life-Threatening Bleeding — Emergent Transfer

Frank haematemesis with clots, brisk haematochezia, syncope/presyncope, HR >100 bpm, SBP <90 mmHg, ongoing active bleeding, on anticoagulants

Setting: Call 000 immediately; commence resuscitation in clinic; requires tertiary centre with 24-hour endoscopy

Hemodynamic Instability

Haemodynamic instability is the single most important red flag. In primary care, assess:

Heart rate >100 bpm: Tachycardia is an early compensatory response to hypovolaemia and may precede hypotension by 30–60 minutes.
Systolic blood pressure <90 mmHg: Indicates decompensated haemorrhagic shock; by this stage, estimated blood loss is typically >1,500 mL (Class III haemorrhage).
Cool peripheries, pallor, diaphoresis: Clinical signs of poor peripheral perfusion consistent with Class II–III haemorrhage.
Altered mental status: Agitation, confusion, or obtundation indicate cerebral hypoperfusion and Class III–IV haemorrhage — this is a medical emergency.

Syncope and Pre-Syncope

Syncope in the context of GI bleeding indicates significant volume loss (>1,000–1,500 mL) and is an independent predictor of severe haemorrhage. Even a single episode of presyncope (lightheadedness on standing, visual dimming) warrants urgent transfer. Patients who present after a syncopal episode — even if now haemodynamically stable — should be considered high risk, as they may re-bleed unpredictably.

Orthostatic Hypotension

Orthostatic (postural) hypotension is one of the earliest and most sensitive indicators of intravascular volume depletion. It may be detected before supine blood pressure falls below the normal range. Measure as follows:

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Orthostatic assessment technique: Measure BP and HR after 5 minutes supine, then at 1 minute and 3 minutes after standing. Positive if: Systolic drop ≥20 mmHg OR diastolic drop ≥10 mmHg OR HR increase ≥20 bpm. Positive orthostasis implies ≥15% blood volume loss (~750 mL in a 70 kg adult).

Melaena

Melaena — black, tarry, foul-smelling stools — indicates upper GI bleeding (typically proximal to the ileum) with blood in transit for ≥14 hours. A single melaena stool may represent 100–200 mL of blood loss; copious or ongoing melaena indicates a significant and potentially ongoing bleed. Importantly, melaena may persist for 3–5 days after a self-limited bleed, so the clinical context (vital signs, haemoglobin trend) is more important than stool colour alone.

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Pitfall: Melaena can be mistaken for iron supplement–related dark stools or bismuth (De-Nol®) stools. If in doubt, perform a rectal examination and test stool with a faecal occult blood test (FOBT). Iron and bismuth cause dark but formed stools; true melaena is black, sticky, and has a characteristic odour.

Haematemesis

Haematemesis (vomiting of blood) is the hallmark of upper GI bleeding. It may present as:

Coffee-ground vomitus: Dark brown-black granular material indicating partially digested blood — suggests slower or intermittent upper GI bleeding.
Frank haematemesis: Fresh red blood or blood clots — indicates rapid, high-volume upper GI bleeding and is a more urgent presentation.

The volume of haematemesis is a poor guide to total blood loss, as significant volumes may pool in the stomach before being vomited. Always assess haemodynamic status rather than relying on the volume of visible blood.

Brisk Haematochezia

Haematochezia — passage of bright red or maroon blood per rectum — is most commonly associated with lower GI bleeding (diverticular disease, angiodysplasia, colorectal neoplasm). However, brisk haematochezia (large-volume passage of red blood with clots) can occur with massive upper GI bleeding when rapid transit overwhelms the capacity for digestion. A rapid upper GI source must be excluded in any patient with brisk haematochezia and haemodynamic instability.

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Key distinction: Brisk haematochezia + haemodynamic instability = assume upper GI source until proven otherwise. These patients require emergent transfer to a centre with both upper and lower endoscopy capability.

Summary of Red Flag Features

Red Flag	Clinical Significance	Action
SBP <90 mmHg	Class III–IV haemorrhage (>1,500 mL loss)	Call 000, commence IV resuscitation
HR >100 bpm	Compensated to decompensated shock	Urgent transfer, IV access
Syncope / presyncope	Significant volume loss, high-risk feature	Urgent transfer irrespective of current vitals
Orthostatic hypotension	Early volume depletion (≥15% blood loss)	Transfer for observation, IV fluids
Frank haematemesis	Active upper GI haemorrhage	Urgent transfer, nil by mouth
Ongoing melaena	Continued upper GI blood loss	Transfer, monitor Hb trend
Brisk haematochezia	Potentially massive upper or lower GI bleed	Emergent transfer to tertiary centre
On anticoagulants/antiplatelets	Increased severity, delayed haemostasis	Withhold agents, transfer with medication list
Age ≥65 years	Higher mortality, reduced physiological reserve	Lower threshold for transfer
Known cirrhosis / liver disease	Variceal bleeding risk — highest mortality	Emergent transfer to tertiary centre with hepatology

Immediate Actions in Primary Care

When a patient presents to a general practice with suspected acute GI bleeding, the GP has a narrow window of opportunity to stabilise the patient before transfer. The following actions should be undertaken in a structured, time-critical manner. Do not delay transfer for non-essential investigations.

1

Secure Airway & Assess Breathing

Position patient supine (or recovery position if vomiting). Suction available. High-flow oxygen if SpO₂ <94% or signs of shock. Assess respiratory rate, depth, and work of breathing.

2

Establish IV Access

Insert two large-bore IV cannulae (16–18 gauge, antecubital fossa preferred). If difficult access, consider external jugular vein. Send bloods from first cannula.

3

Blood Collection

FBC, UEC, LFTs, coagulation profile (INR, APTT, fibrinogen), GXM (group and crossmatch — request 2–4 units), blood gas if available. Label and send with patient.

4

Commence Fluid Resuscitation

0.9% sodium chloride (normal saline) 500–1,000 mL IV bolus over 15–30 minutes. Repeat based on clinical response. Avoid over-resuscitation — target SBP ≥90 mmHg (permissive hypotension until haemostasis in suspected variceal bleed).

5

Withhold Anticoagulants & Antiplatelets

Cease all anticoagulant and antiplatelet agents immediately. Document exact last dose and time. Do NOT administer reversal agents in primary care — this occurs at the receiving hospital.

6

Continuous Monitoring

Vital signs (HR, BP, SpO₂) every 5–10 minutes. Urine output if catheterised. Record mental status (GCS). Document all findings with timestamps.

7

Arrange Urgent Transfer

Call 000 for ambulance with paramedics briefed on active GI bleeding. Provide written clinical handover (ISBAR). Transfer to nearest facility with 24-hour endoscopy capability.

Fluid Resuscitation — Detail

Crystalloid resuscitation with 0.9% sodium chloride is the first-line fluid in primary care for acute GI bleeding. The following guidance applies:

Fluid	Volume	Rate	Notes
0.9% sodium chloride (first-line)	500–1,000 mL bolus	Over 15–30 min	Repeat ×1–2 as needed; target SBP ≥90 mmHg
Hartmann's solution (alternative)	500–1,000 mL bolus	Over 15–30 min	Acceptable alternative if NS unavailable
Packed red blood cells	As per transfusion protocol	N/A in primary care	Commence at receiving hospital; GXM essential

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Permissive hypotension in variceal bleeding: If known or suspected cirrhosis with variceal bleeding, avoid aggressive fluid resuscitation. Target SBP 80–90 mmHg rather than normotension, as over-resuscitation can increase portal pressure and worsen variceal haemorrhage. This distinction should be communicated to the receiving team.

Medications That May Be Considered at Receiving Hospital

While the primary care role does not include administering definitive pharmacotherapy, awareness of the agents used at the receiving hospital helps with pre-transfer communication and anticipatory management.

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Pantoprazole

Somac® · Proton pump inhibitor

Adult dose (suspected upper GI bleed) 80 mg IV bolus, then 8 mg/hr infusion for 72 hours (at receiving hospital)

Paediatric dose 1 mg/kg IV BD (max 40 mg BD); specialist guidance recommended

Route IV infusion

Renal adjustment No adjustment required

PBS status ✔ PBS General Benefit

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Tranexamic Acid

Cyklokapron® · Antifibrinolytic

Adult dose 1 g IV over 10 minutes; may repeat once. Evidence for GI bleeding is evolving (HALT-IT trial — use with caution)

Paediatric dose 15 mg/kg IV (max 1 g); specialist guidance

Route IV slow injection or infusion

Renal adjustment Reduce dose if eGFR <30 mL/min; avoid if eGFR <15

PBS status ✔ PBS General Benefit

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Vitamin K (Phytomenadione)

Konakion MM® · Reversal of warfarin effect

Adult dose 5–10 mg IV slow injection (diluted); for warfarin-related bleeding with INR >4.0

Paediatric dose 0.3–1 mg IV; specialist guidance

Route IV (slow injection over 20 min via syringe pump) or oral

Renal adjustment No adjustment required

PBS status ✔ PBS General Benefit

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Idarucizumab

Praxbind® · Specific dabigatran reversal agent

Adult dose 5 g IV (2 × 2.5 g boluses no more than 15 min apart)

Indication Life-threatening or uncontrolled bleeding in patients on dabigatran

Route IV bolus

Availability Tertiary hospital blood bank; not for primary care use

PBS status ⚠ PBS Authority Required — Hospital only

Nil by Mouth (NBM) Status

All patients with active GI bleeding should be made nil by mouth from the point of assessment. This is essential for:

Safety in case of emergency endoscopy or surgical intervention
Prevention of aspiration if the patient deteriorates or requires sedation
Reducing gastric acid production and potential re-bleeding stimulus

If the patient is on essential oral medications (e.g., antiepileptics), discuss with the receiving team regarding IV conversion.

Communication with the Receiving Team

Effective communication between primary care and the receiving emergency or gastroenterology team is a critical determinant of patient outcomes. A structured handover reduces information loss, prevents errors in medication management, and ensures the receiving team can initiate definitive management without delay.

ISBAR Framework for Clinical Handover

The ISBAR (Introduction, Situation, Background, Assessment, Recommendation) framework is endorsed by the Australian Commission on Safety and Quality in Health Care (ACSQHC) and should be used for all clinical handovers.

I

Introduction

"This is Dr [Name], GP at [Practice], calling about [Patient Name], [age]-year-old [sex]."

S

Situation

"I am referring this patient for emergency assessment of acute GI bleeding — [haematemesis / melaena / haematochezia]. The patient is [stable / haemodynamically compromised]."

B

Background

Relevant medical history: liver disease, previous GI bleeding, peptic ulcer disease, GI malignancy. Current medications — especially anticoagulants/antiplatelets with last dose. Allergies. Recent procedures.

A

Assessment

Current vitals (HR, BP, SpO₂, RR, temperature), orthostatic changes, GCS, estimated blood loss, Hb result (if available), current IV access and fluids administered.

R

Recommendation

"I recommend urgent assessment for upper GI endoscopy. The patient requires 2–4 unit GXM. I have withheld [warfarin/DOAC/antiplatelet]. ETA of ambulance is [time]. Is there anything you need from me before transfer?"

Critical Information to Provide

Medication List — Anticoagulants and Antiplatelets

The medication list is arguably the single most important piece of information for the receiving team. Provide precise details for all anticoagulant and antiplatelet agents:

Medication Class	Common Agents in Australia	Critical Information to Communicate
Warfarin	Coumadin®, Marevan®	Last dose, most recent INR, indication (AF, VTE, mechanical valve)
DOACs — Factor Xa inhibitors	Rivaroxaban (Xarelto®), Apixaban (Eliquis®), Edoxaban (Lixiana®)	Last dose (hours ago), dose, renal function (eGFR), indication
DOACs — Direct thrombin inhibitor	Dabigatran (Pradaxa®)	Last dose, renal function — dabigatran is 80% renally cleared, reversal with idarucizumab available
Aspirin	Cartia®, aspirin 100 mg	Dose, indication (primary vs secondary prevention), last dose
Clopidogrel	Plavix®, Iscover®	Dose, last dose, recent PCI/stent (critical — may affect timing of cessation)
Ticagrelor	Brilinta®	Dose, last dose, recent ACS or stent — discuss with cardiology if <12 months post-ACS
Dual antiplatelet therapy (DAPT)	Aspirin + clopidogrel or ticagrelor	Duration remaining, date and type of stent/intervention
LMWH	Enoxaparin (Clexane®)	Dose, last dose, indication (treatment vs prophylaxis)

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Do NOT restart anticoagulants/antiplatelets in primary care. The decision to resume or bridge anticoagulation is made by the receiving team in consultation with the relevant specialist (cardiology, haematology, gastroenterology). This is especially critical for patients with mechanical heart valves or recent (<12 months) coronary stents.

Comorbidities

The following comorbidities significantly impact the management and prognosis of acute GI bleeding and should be communicated to the receiving team:

Chronic liver disease / cirrhosis: High risk of variceal bleeding, coagulopathy, and hepatic decompensation. Communicate known Child-Pugh or MELD score if available.
Chronic kidney disease (CKD): Impaired platelet function (uraemic bleeding diathesis), altered drug clearance, higher bleeding risk. Provide most recent eGFR and creatinine.
Ischaemic heart disease / recent ACS: Affects decision-making regarding antiplatelet resumption and permissive hypotension targets.
Atrial fibrillation: Explains anticoagulant use; risk of thromboembolism if anticoagulation withheld for prolonged period.
Previous GI surgery: Altered anatomy may affect endoscopy approach or indicate afferent loop bleeding (Billroth II).
Known GI malignancy or polyps: May indicate neoplastic source of bleeding.
Diabetes mellitus: Increased infection risk, impaired wound healing, potential for HbA1c-related perioperative issues.

Prior GI History

Previous episodes of GI bleeding — dates, cause, and management (endoscopic therapy, surgery)
Known peptic ulcer disease, H. pylori status, eradication history
Previous gastroscopy or colonoscopy findings and dates
History of oesophageal varices or portal hypertensive gastropathy
Inflammatory bowel disease (Crohn's disease, ulcerative colitis) and current flare status
Known diverticular disease

Vitals and Estimated Blood Loss

Provide a serial record of vital signs with timestamps. This enables the receiving team to assess trajectory (improving vs deteriorating):

Parameter	What to Record	Method
Heart rate	Rate, rhythm, regularity	Manual or automated BP cuff
Blood pressure	Supine + standing (at 1 min and 3 min)	Automated sphygmomanometer
Oxygen saturation	SpO₂ on room air (or O₂ if administered)	Pulse oximetry
Respiratory rate	Breaths per minute	Observed count over 30 seconds × 2
Mental status	GCS (Eye + Verbal + Motor)	Standardised GCS assessment
Temperature	Core temperature	Tympanic or axillary
Estimated blood loss	Volume of haematemesis / melaena / haematochezia	Clinical estimation (pints, cups); photograph if possible
Urine output	Volume per hour (if catheterised)	Hourly measurement; oliguria (<0.5 mL/kg/hr) indicates inadequate perfusion

Haemoglobin and Laboratory Results

If point-of-care or rapid pathology is available at the practice, include the following in your handover:

Haemoglobin: Note that Hb may be normal in the first 1–2 hours of acute bleeding (haemodilution has not yet occurred). A normal Hb does not exclude significant haemorrhage.
INR / APTT: Critical if the patient is on anticoagulants. An INR >4.0 in a warfarinised patient with active bleeding warrants urgent reversal.
Urea: Elevated urea with normal creatinine may suggest upper GI bleeding (digested blood protein absorption).
Crossmatch status: Advise whether GXM has been collected and sent, or if it needs to be done at the receiving hospital.

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Documentation tip: Send a printed or faxed clinical summary with the patient, including: presenting complaint, vital sign trends, medications ceased, IV fluids administered, bloods collected, and relevant comorbidities. This supplements verbal handover and serves as a medico-legal record.

Handover Checklist

Item	Provided?
Patient identification (name, DOB, address, Medicare number)	☐
Presenting complaint and onset / duration	☐
Type of bleeding (haematemesis / melaena / haematochezia)	☐
Estimated volume and duration of bleeding	☐
Vital signs with timestamps (including orthostatic measurements)	☐
Full medication list — especially anticoagulants and antiplatelets with last dose	☐
Relevant comorbidities (liver disease, CKD, IHD, AF)	☐
Prior GI history (previous bleeds, endoscopy findings, H. pylori status)	☐
Allergies	☐
Interventions commenced (IV access size, fluids given, medications ceased)	☐
Blood results (Hb, INR, UEC if available)	☐
GXM collected and sent? Yes / No	☐
Specialist notification (hepatologist if cirrhosis, cardiologist if recent stent)	☐

Special Populations

👴 Elderly Patients (≥65 years)

Higher mortality: In-hospital mortality for upper GI bleeding increases from ~3% in patients <60 years to ~15–20% in patients ≥80 years. Reduced physiological reserve and polypharmacy contribute.

Atypical presentation: Elderly patients may present with isolated syncope, confusion, or falls rather than classic GI bleeding symptoms. Maintain a low threshold for rectal examination.

Medication review: Elderly patients are disproportionately represented among users of NSAIDs (including over-the-counter ibuprofen), aspirin, and anticoagulants. Comprehensive medication reconciliation is essential.

Frailty assessment: Consider clinical frailty score; very frail patients may benefit from conservative management rather than aggressive intervention — discuss goals of care with patient/family.

Fluid resuscitation: Start at 500 mL bolus rather than 1 L; assess for signs of fluid overload (pulmonary oedema) — elderly patients with cardiac comorbidities are at risk.

🫘 Renal Impairment

Uraemic platelet dysfunction: CKD stage 4–5 (eGFR <30) impairs platelet adhesion and aggregation, increasing bleeding risk independent of anticoagulation.

Dose adjustments: Dabigatran (Pradaxa®) is contraindicated if eGFR <30 mL/min. DOAC dose reductions required for apixaban and rivaroxaban at specific renal thresholds.

Tranexamic acid: Reduce dose if eGFR <30 mL/min; avoid if eGFR <15 mL/min due to accumulation and seizure risk.

Document most recent eGFR and creatinine in handover. If not available within 3 months, communicate this to the receiving team.

🫁 Hepatic Impairment / Cirrhosis

Variceal bleeding: Cirrhotic patients presenting with haematemesis should be presumed to have variceal bleeding until proven otherwise. Mortality is 15–20% per episode.

Coagulopathy: Deranged INR, low platelets (thrombocytopaenia of chronic liver disease), and reduced fibrinogen synthesis — these compound bleeding risk.

Permissive hypotension: Target SBP 80–90 mmHg to avoid increasing portal pressure. Communicate this target clearly to the receiving team.

Transfer destination: Ideally transfer to a centre with hepatology / interventional radiology capability for TIPS (transjugular intrahepatic portosystemic shunt) if needed.

PPI: Pantoprazole 80 mg IV bolus may be considered if transfer is delayed >30 minutes (administered by paramedics or in clinic if qualified). No hepatic dose adjustment required.

🛡️ Immunocompromised Patients

CMV colitis: In immunocompromised patients (post-transplant, HIV with low CD4), cytomegalovirus (CMV) colitis may cause lower GI bleeding. This is a consideration for the receiving team, not for primary care management.

Atypical presentations: Blunted inflammatory response may mask signs of haemodynamic compromise. Tachycardia may be absent in patients on beta-blockers.

Drug interactions: Immunosuppressant medications (tacrolimus, cyclosporine) have important interactions with PPIs and antifungals used in hospital management.

Document all immunosuppressive medications and transplant status in the handover communication.

👶 Paediatric Patients

Different aetiology: Paediatric GI bleeding has a different differential — Meckel's diverticulum, intussusception, juvenile polyps, milk protein allergy (infants), and oesophageal varices (biliary atresia).

Haemodynamic assessment: Children compensate well and decompensate abruptly. Tachycardia is the earliest sign. Hypotension is a late and ominous finding.

Weight-based fluid resuscitation: 20 mL/kg bolus of 0.9% sodium chloride; may repeat up to 3 times. Use Broselow tape or weight estimation for paediatric dosing.

Transfer: All paediatric GI bleeds should be transferred to a paediatric facility with paediatric gastroenterology and endoscopy capability.

Paediatric dosing: Pantoprazole 1 mg/kg IV BD (max 40 mg BD); Tranexamic acid 15 mg/kg IV (max 1 g); Normal saline 20 mL/kg bolus.

🤰 Pregnancy

Causes: Hyperemesis-related Mallory-Weiss tear (most common), peptic ulcer disease, varices (portal hypertension in pregnancy), and placental abruption (third trimester — differential for haemodynamic instability).

Physiological changes: Increased blood volume (up to 50% increase) may mask early blood loss. Resting tachycardia is normal in pregnancy (HR up to 100 bpm).

Left lateral tilt: Position the patient in left lateral tilt (≥15°) to avoid aortocaval compression, especially in the third trimester.

Transfer: Transfer to a facility with both obstetric and gastroenterology capabilities. Fetal monitoring should be initiated at the receiving hospital.

PPI safety in pregnancy: Pantoprazole (Category B3) is generally considered safe. Tranexamic acid should be used with caution and only if benefits outweigh risks — discuss with haematology.

Aboriginal and Torres Strait Islander Health Considerations

Aboriginal and Torres Strait Islander Health

Higher burden of GI disease

Aboriginal and Torres Strait Islander Australians experience 1.5–2 times the age-adjusted rate of hospitalisation for GI bleeding compared with non-Indigenous Australians. Helicobacter pylori infection prevalence is significantly higher (50–80% in remote communities vs 15–30% in the general population), driving increased rates of peptic ulcer disease.

Remote and rural access barriers

Patients in remote communities may be hours from the nearest facility with endoscopy capability. Royal Flying Doctor Service (RFDS) retrieval may be required. Primary care clinicians in these settings should have advanced resuscitation skills and IV access capability. Ensure satellite phone or HF radio communication with retrieval services is functioning.

Chronic disease comorbidity

Higher prevalence of chronic kidney disease, rheumatic heart disease (relevant to anticoagulation decisions), diabetes, and chronic liver disease — all of which increase GI bleeding risk and complicate management. These comorbidities should be systematically documented in the handover.

Cultural safety in assessment

Rectal examination and discussion of melaena/haematochezia may cause embarrassment. Involve an Aboriginal health worker or practitioner (AHW/AHP) to facilitate culturally safe communication. Use clear, non-judgemental language. Where possible, ensure same-gender clinician for intimate examinations, or have an AHW present.

NSAID and aspirin access

Over-the-counter NSAIDs (ibuprofen, diclofenac) are widely available and commonly used in remote communities for musculoskeletal pain. Long-term NSAID use without PPI cover is a significant and preventable cause of GI bleeding. Primary care interventions include education about NSAID risks, H. pylori testing and eradication, and PPI co-prescription for high-risk patients.

H. pylori screening and eradication

Consider H. pylori testing (urea breath test or stool antigen) for all Aboriginal and Torres Strait Islander patients presenting with dyspepsia, epigastric pain, or a history of peptic ulcer disease. Eradication therapy (triple therapy: PPI + amoxicillin 1 g BD + clarithromycin 500 BD for 7 days, or PPI + amoxicillin 1 g BD + metronidazole 400 BD for 7 days where clarithromycin resistance is a concern) reduces re-bleeding risk by 50–70%.

Alcohol-related liver disease

Chronic liver disease and alcohol-related hepatitis are disproportionately prevalent and may present as GI bleeding with underlying varices or coagulopathy. Ask about alcohol use non-judgementally and communicate alcohol history to the receiving team. Brief intervention and referral to Aboriginal Community Controlled Health Organisation (ACCHO) services for alcohol support.

Follow-up and continuity of care

After hospital discharge, patients returning to remote communities may face challenges in attending follow-up gastroenterology appointments. Coordinate with the receiving hospital to arrange telehealth follow-up where possible. Ensure discharge summaries reach the community health centre. AHWs can support medication adherence (PPI, H. pylori eradication completion) and monitoring for re-bleeding symptoms.

Investigations in Primary Care

Investigations in primary care should be limited to those that are immediately available and will not delay transfer. The primary care role is to initiate, not complete, the diagnostic workup.

Essential Full Blood Count (FBC) Haemoglobin may be normal in the first 1–2 hours (haemodilution lag). A low Hb confirms significant blood loss but a normal Hb does not exclude it. MCV may indicate chronic iron deficiency (microcytosis) suggesting chronic/intermittent GI blood loss. MBS Item: 65070.

Essential Urea, Electrolytes, Creatinine (UEC) Elevated urea with normal creatinine may suggest upper GI bleeding (digested blood). Creatinine/eGFR is critical for DOAC dosing decisions. MBS Item: 66500.

Essential Coagulation Profile (INR, APTT) INR is essential for warfarinised patients. APTT is prolonged with heparin and dabigatran. MBS Item: 65140.

Essential Group and Crossmatch (GXM) Request 2–4 units packed red blood cells. Collect and send with patient to receiving hospital. Crossmatch takes 30–60 minutes — early collection facilitates faster transfusion. MBS Item: 13700.

If Available Blood Gas / Point-of-Care Lactate Elevated lactate (>2 mmol/L) indicates tissue hypoperfusion and is a marker of shock severity. Base deficit correlates with blood loss volume. Available in many GP practices with point-of-care devices.

If Available Liver Function Tests (LFTs) Deranged LFTs suggest underlying liver disease — important for predicting variceal bleeding risk and coagulopathy. MBS Item: 66551.

If Available Stool for Faecal Occult Blood Test (FOBT) Useful when melaena is suspected but the clinical picture is uncertain (e.g., iron supplements, bismuth). Positive test confirms GI blood.

At Receiving Hospital Upper GI Endoscopy (Gastroscopy) Gold standard for upper GI bleeding diagnosis and treatment. Should be performed within 24 hours for high-risk patients, and within 12 hours for those with variceal bleeding or haemodynamic instability. Not available in primary care — arrange via transfer.

At Receiving Hospital Colonoscopy For lower GI bleeding investigation. May be performed after adequate bowel preparation, though urgent colonoscopy is sometimes warranted for brisk haematochezia. Arranged at receiving hospital.

Specialist CT Angiography / Interventional Radiology For ongoing GI bleeding where endoscopy has failed or is not feasible. Catheter-directed embolisation can achieve haemostasis. Available at tertiary centres with interventional radiology services.

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Do not delay transfer for investigations. If basic bloods cannot be drawn within 15 minutes, or if the patient is critically unstable, commence resuscitation and arrange transfer immediately. Bloods can be collected by paramedics en route or at the receiving hospital.

Quick Reference — Primary Care Action Summary

Haemodynamically unstable GI bleed

Two large-bore IV (16–18G) + 0.9% NaCl 1 L bolus

Call 000 immediately

GXM 2–4 units; cease all anticoagulants; NBM; continuous monitoring

Stable + melaena (high-risk features)

One large-bore IV (16–18G) + 0.9% NaCl 500 mL

Urgent transfer within 30 min

FBC, UEC, coags, GXM; cease anticoagulants; orthostatic assessment

Minor haematemesis — stable, no red flags

IV access if available; consider oral PPI

Same-day or 24-hour gastroenterology review

FBC, UEC, coags; medication review; H. pylori consideration

Known cirrhosis + GI bleed

Two large-bore IV + cautious fluids (SBP target 80–90)

Emergent transfer to tertiary centre

Permissive hypotension; hepatology referral; GXM 4 units

On warfarin + active bleeding

Cease warfarin; IV access; FBC + INR + GXM

Urgent transfer — reversal at hospital

Vitamin K 5–10 mg IV + PCC at receiving hospital if INR >4.0

On DOAC + active bleeding

Cease DOAC; IV access; FBC + UEC + coags + GXM

Urgent transfer

Reversal at hospital: idarucizumab (dabigatran) or andexanet alfa (FXa inhibitors)

📚 References

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