Posterior epistaxis is a medical emergency β bleeding from sphenopalatine or ethmoidal arteries, difficult to control with simple pressure. Blood flows down throat (patient swallows/vomits blood). Requires ENT packing or interventional radiology (arterial embolisation). Can cause airway obstruction or aspiration.
Massive haemorrhage (>1 litre blood loss) causes hypovolaemic shock. Elderly patients on anticoagulants are highest risk. Requires IV access, resuscitation, transfusion, urgent ENT/interventional radiology. Death from epistaxis is rare but occurs (40 deaths/year UK, mostly elderly anticoagulated patients).
Unilateral bleeds with obstruction = nasal malignancy until proven otherwise. Squamous cell carcinoma, adenoid cystic carcinoma, melanoma all present with unilateral bleeding + obstruction. Delay = advanced disease, poor prognosis. 2WW referral mandatory.
Correct first aid technique is critical β 90% of anterior nosebleeds stop with proper pressure (pinch soft part 10-15 minutes). Many "refractory" bleeds are actually inadequate pressure (pinching bony bridge, insufficient duration, looking up to check bleeding = releasing pressure). Education on technique prevents ED attendances.
Anticoagulation increases bleeding risk 2-3 fold but is rarely sole cause of epistaxis. Nosebleed in anticoagulated patient = identify bleeding site (usually Little's area), control bleed, check INR (reverse if supratherapeutic), but do NOT routinely stop anticoagulation (thrombotic risk > bleeding risk).
Bilateral bleeding suggests systemic cause β coagulopathy, thrombocytopenia, or posterior source. Unilateral bleeding suggests local pathology (Little's area trauma, tumour, vascular malformation). Laterality directs investigation.
Anterior vs posterior distinction is critical β determines management site (home vs hospital). Anterior bleeds managed in primary care with pressure Β± cautery. Posterior bleeds require ENT packing or interventional radiology in hospital. Missing posterior bleed = massive haemorrhage, aspiration, death.
Primary epistaxis is diagnosis of exclusion β only diagnosed after excluding systemic causes (anticoagulation, blood dyscrasia, hypertension, malignancy). Young healthy patient with unilateral bleeding = likely primary. Elderly patient on warfarin with bilateral bleeding = secondary until proven otherwise.
HHT prevalence 1 in 5000 β underdiagnosed. Think of HHT in anyone with recurrent epistaxis starting in childhood. CuraΓ§ao criteria (need 3 of 4): epistaxis, telangiectasia, visceral AVMs, family history. Diagnosis important because pulmonary AVMs cause stroke risk (paradoxical embolism) β treatable with coil embolisation.
Identifying bleeding site enables targeted cautery β silver nitrate stick applied to visible vessel at Little's area stops 95% recurrent anterior bleeds. Blind cautery without identifying site is ineffective and risks septal perforation. If site not visible, ENT nasoendoscopy needed.
Hypertension does NOT cause epistaxis directly but worsens bleeding once started (higher arterial pressure = harder to achieve haemostasis). Posterior bleeds are more common in hypertensives (atherosclerotic vessel fragility). Do NOT aggressively lower BP during acute bleed (impairs clot formation) β control after bleeding stopped.
Septal perforation causes: cocaine (vasoconstriction β ischaemic necrosis), chronic intranasal steroid misuse (spray aimed at septum not turbinates), Wegener's granulomatosis (ANCA-associated vasculitis), trauma (repeated cautery). Large perforations whistle, crust, bleed recurrently.
FBC and clotting find bleeding disorders in <5% of epistaxis patients. Reserve for those with clinical features suggesting systemic cause (easy bruising, petechiae, bleeding gums, family history). Routine testing in healthy children with single nosebleed is low yield and unnecessary.
INR monitoring in warfarin patients β target INR 2-3 for most indications. INR >4 increases bleeding risk 5-fold. Supratherapeutic INR + epistaxis = withhold warfarin 1-2 doses, recheck INR, restart when <3.5. If INR >8 or uncontrolled bleeding = vitamin K 1-2 mg PO. Do NOT routinely stop warfarin (stroke risk > bleeding risk).
Nasoendoscopy is gold standard for visualising entire nasal cavity and nasopharynx. Identifies posterior bleeding points, tumours, AVMs not visible on anterior rhinoscopy. Flexible scope passed via nostril under local anaesthetic (co-phenylcaine spray). ENT procedure, not primary care.
Posterior epistaxis requires hospital admission β cannot be controlled with simple pressure. Requires ENT packing (anterior + posterior packs, or Foley catheter balloon tamponade), or interventional radiology (sphenopalatine artery embolisation). 10-15% of admissions require embolisation. Delay = massive blood loss, aspiration, death.
Unilateral symptoms = malignancy until proven otherwise. Squamous cell carcinoma, adenocarcinoma, esthesioneuroblastoma all present with unilateral bleeding + obstruction. 2WW nasoendoscopy + biopsy. 5-year survival 60% if early, <20% if advanced. Delay = metastasis.
Most anterior bleeds managed in primary care β 90% stop with pressure, 95% of recurrent bleeds resolve with silver nitrate cautery. Only refer if: no visible source (needs nasoendoscopy), recurrent despite cautery (may need diathermy/laser), or red flags. Unnecessary ENT referrals burden limited capacity.
Pinching soft part of nose compresses Little's area (anterior inferior septum where 90% bleeds originate). Pinching bony bridge does nothing β no vessels there. Forward-leaning position prevents blood swallowing (causes nausea, obscures volume assessment). 15 minutes continuous pressure allows platelet plug formation.
Silver nitrate cautery is highly effective (95% success) when bleeding point visible. Chemical cauterisation coagulates vessel and surrounding tissue, seals bleeding point. Bilateral cautery risks septal perforation (devascularisation β ischaemic necrosis). Wait 6 weeks before cauterising opposite side if needed.
Stopping anticoagulation is harmful β stroke risk in AF patient off warfarin is 5%/year. Epistaxis in anticoagulated patient warrants investigation (identify source, cautery), INR check (reverse if supratherapeutic), but NOT routine cessation. Discuss with cardiologist before stopping DOACs/warfarin long-term.
Naseptin reduces recurrence 70% in studies β antibacterial (chlorhexidine + neomycin) eradicates S. aureus (found in 60% recurrent epistaxis patients), while emollient base moisturises fragile mucosa. 10-day course sufficient. Longer use risks resistance. Peanut allergy contraindication because contains arachis (peanut) oil.
Humidification prevents drying β nasal mucosa needs 40-50% humidity. Winter central heating drops humidity to 20-30%, drying mucosa, causing crusting, cracking, bleeding. Bedroom humidifier or bowl of water on radiator restores physiological humidity. Simple, cheap, effective.
Correct steroid spray technique prevents iatrogenic epistaxis β aim spray AWAY from septum (toward outer wall/turbinates). Spraying directly at septum causes chemical thinning, ulceration, perforation, recurrent bleeding. Right hand for left nostril, left hand for right nostril achieves correct angle.
Post-cautery follow-up ensures healing and identifies treatment failure. Silver nitrate creates black eschar (coagulated tissue) which falls off in 7-10 days, revealing healed pink mucosa underneath. If re-bleeding occurs = either incomplete cautery (missed bleeding point) or new bleeding site. Re-examine and re-cauterise if source visible.
Chronic blood loss causes iron-deficiency anaemia β even small frequent nosebleeds (teaspoon daily) = 5-10ml/day = 150-300ml/month. Check FBC if >4 weeks recurrent bleeds. Treat with ferrous sulphate 200mg BD, but also identify and treat bleeding source (cautery, Naseptin).
HHT requires specialist centre input β not managed in primary care. Screen for visceral AVMs (pulmonary with bubble echo, cerebral with MRI brain, hepatic with USS liver). Pulmonary AVMs cause paradoxical emboli (stroke risk 30% lifetime) β treatable with coil embolisation. Bevacizumab (anti-VEGF) reduces epistaxis severity in severe HHT.