Epistaxis (Nosebleed)

1. Clinical Overview

Summary

Epistaxis (nosebleed) is bleeding from the nasal cavity, affecting up to 60% of the population at some point in their lifetime, with approximately 6% seeking medical attention. The condition is classified anatomically into anterior epistaxis (90% of cases) arising from Kiesselbach's plexus (Little's area) on the anterior nasal septum, and posterior epistaxis (10% of cases) originating from Woodruff's plexus in the posterior nasal cavity, typically involving the sphenopalatine artery territory. [1,2]

Anterior epistaxis typically occurs in younger patients and is often self-limiting or easily controlled with simple first aid measures and cautery. Posterior epistaxis predominantly affects elderly patients with hypertension and those on anticoagulant therapy, and represents a more serious condition requiring specialist ENT intervention including nasal packing, endoscopic sphenopalatine artery ligation, or interventional radiology embolization. [3,4]

Initial management follows a stepwise approach: first-aid measures (sitting upright, leaning forward, pinching the soft part of the nose for 15-20 minutes), topical vasoconstriction with adrenaline and local anaesthesia, identification of the bleeding source, and definitive treatment with cautery or packing. Refractory cases may require surgical intervention, with endoscopic sphenopalatine artery ligation (ESPAL) demonstrating success rates exceeding 95% for posterior epistaxis. [5,6]

Clinical Pearls

"Pinch the Soft Part, Lean Forward": Effective first aid requires pinching the cartilaginous (soft) part of the nose, not the nasal bridge. Leaning forward prevents blood swallowing and aspiration.

"Anterior (Easy) vs Posterior (Difficult)": Anterior epistaxis from Little's area is visible on rhinoscopy and readily treated. Posterior bleeding is not visible anteriorly, often presents with blood in the oropharynx, and requires specialist management.

"Hypertension - Consequence Not Cause": While hypertension is associated with epistaxis, the relationship is complex. Elevated blood pressure during acute epistaxis may represent a physiological stress response rather than a causative factor. [7,8]

"Never Cauterize Both Sides": Bilateral septal cautery in the same sitting significantly increases the risk of septal perforation. If bilateral treatment is required, stage procedures 4-6 weeks apart. [9]

"Pack Prophylaxis": Nasal packing carries a risk of toxic shock syndrome. Prophylactic antibiotics (co-amoxiclav or equivalent) are recommended for all patients with nasal packs left in situ beyond 24 hours.

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2. Epidemiology

Demographics

Socioeconomic Impact

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3. Aetiology

Local Causes

Systemic Causes

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4. Pathophysiology and Anatomy

Nasal Vascular Anatomy

The nasal cavity receives a rich blood supply from both the internal and external carotid arterial systems, which anastomose extensively. Understanding this anatomy is critical for successful management of epistaxis.

Internal Carotid System (Ophthalmic Artery Branches)

External Carotid System (Maxillary Artery Branches)

Kiesselbach's Plexus (Little's Area)

Anatomical Location: Anterior inferior nasal septum (approximately 1 cm from the nasal vestibule)

Vascular Contributions:

• Superior labial artery (facial artery branch - external carotid)
• Anterior ethmoidal artery (ophthalmic artery branch - internal carotid)
• Sphenopalatine artery (maxillary artery branch - external carotid)
• Greater palatine artery (maxillary artery branch - external carotid)

Clinical Significance:

• Site of approximately 90% of anterior epistaxis
• Rich vascular anastomosis in vulnerable location
• Overlying mucosa is thin and easily traumatized
• Exposed to digital trauma, drying effects of airflow, and environmental irritants
• Readily accessible for examination and treatment with cautery

Woodruff's Plexus

Anatomical Location: Posterior lateral nasal wall, posteroinferior to the insertion of the middle turbinate, in the region of the sphenopalatine foramen

Vascular Supply: Branches of the sphenopalatine artery

Clinical Significance:

• Site of posterior epistaxis (approximately 10% of all epistaxis)
• Not visible on anterior rhinoscopy
• Typically requires endoscopic examination for visualization
• Target area for endoscopic sphenopalatine artery ligation (ESPAL)
• Associated with more severe bleeding and elderly patients

Pathophysiological Mechanisms

Mucosal Disruption: Trauma, inflammation, or drying causes loss of mucosal integrity exposing underlying vasculature.

Vascular Fragility: Atherosclerosis, hypertension, and aging cause arterial wall changes increasing vessel fragility.

Impaired Haemostasis: Anticoagulation, antiplatelet therapy, thrombocytopenia, and coagulopathy prevent normal clot formation.

Elevated Blood Pressure: Whether hypertension directly causes epistaxis or represents a stress response to bleeding remains debated. Meta-analyses suggest an association but causality is uncertain. [7,8]

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5. Clinical Classification

By Anatomical Location

By Severity

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6. Clinical Presentation

History

A comprehensive history should elicit the following information:

Examination

Haemodynamic Assessment (Priority)

ENT Examination

General Inspection:

• Active bleeding from nostril(s)
• Blood in oropharynx (suggests posterior bleeding)
• Evidence of trauma
• Visible telangiectasia (lips, tongue, hands - HHT)

Anterior Rhinoscopy:

• Use Thudichum nasal speculum
• Good illumination (headlight or otoscope)
• Clear clots with suction or ask patient to blow nose
• Apply topical vasoconstrictor and local anaesthetic:
  • Co-phenylcaine forte spray (5% lidocaine + 0.5% phenylephrine)
  • "Lidocaine 5% + Adrenaline 1:1000 (on cotton pledgets)"
• Identify bleeding point on anterior septum (Kiesselbach's plexus)
• Assess septal deviation, perforation, telangiectasia, mucosal friability
• Examine inferior and middle turbinates (hypertrophy, polyps)

Nasendoscopy (if indicated and available):

• Performed by ENT specialist
• Flexible nasendoscopy allows visualization of posterior nasal cavity, nasopharynx
• Identify posterior bleeding source
• Exclude nasal masses, nasopharyngeal tumours

Oropharyngeal Examination:

• Blood trickling down posterior pharyngeal wall indicates posterior epistaxis or ongoing anterior bleeding
• Inspect for telangiectasia (HHT)

Systemic Examination (if indicated):

• Cardiovascular: heart rate, blood pressure, signs of shock
• Respiratory: respiratory rate, oxygen saturation
• Abdominal: hepatomegaly, splenomegaly (liver disease, haematological disorders)
• Skin: bruising, petechiae (coagulopathy, thrombocytopenia), telangiectasia (HHT)

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7. Investigations

Laboratory Investigations

Note: Routine blood tests are not required for simple anterior epistaxis in otherwise healthy patients that responds to first aid or simple cautery. [1]

Imaging

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8. Management

Management Principles

Management of epistaxis follows a stepwise escalation from simple first aid to increasingly invasive interventions based on bleeding severity, anatomical source, and patient factors.

First Aid Measures (Pre-Hospital and Initial Management)

Applicable to all patients with active epistaxis:

1. Positioning:

   • Sit upright (reduces venous pressure in nasal vessels)
   • Lean forward (prevents blood swallowing which may cause nausea/vomiting and obscures assessment of ongoing bleeding)
   • Never lie down or lean backward (increases venous pressure, blood aspiration risk)

2. Nasal Compression:

   • Pinch the soft cartilaginous part of the nose (not the nasal bridge)
   • Apply firm, continuous pressure
   • Maintain compression for 15-20 minutes without releasing to allow clot formation
   • Breathe through the mouth

3. Adjunctive Measures:

   • Spit out blood rather than swallowing
   • Ice pack to nasal bridge (theoretical vasoconstriction, limited evidence)
   • Remain calm and reassure patient

4. Post-Bleeding Advice:

   • Avoid nose blowing, picking, or heavy lifting for 24 hours
   • Avoid hot drinks and strenuous activity for 24 hours
   • Apply nasal lubricant (petroleum jelly, Naseptin cream) to anterior septum
   • Humidify environment if dry air contributing factor

Success Rate: First aid measures successfully control approximately 85-90% of anterior epistaxis cases. [1]

Medical Management (Emergency Department / ENT)

Step 1: Resuscitation (if Required)

Indications: Severe bleeding, haemodynamic instability, signs of shock

Immediate Actions:

• Airway: Ensure patent. Suction blood from oropharynx. Risk of aspiration in massive bleeding.
• Breathing: Oxygen therapy if hypoxic. Pulse oximetry monitoring.
• Circulation:
  • Large bore IV access (14-16G cannula × 2 if severe)
  • "Fluid resuscitation (crystalloid: 0.9% sodium chloride or Hartmann's solution)"
  • Blood transfusion if Hb less than 70 g/L or ongoing severe bleeding
  • Correct coagulopathy (see below)
• Monitoring: Continuous pulse oximetry, blood pressure, ECG (elderly patients with cardiovascular comorbidity at risk of ischaemic events)

Step 2: Topical Vasoconstriction and Local Anaesthesia

Purpose: Reduce bleeding, allow visualization, provide anaesthesia for intervention

Options:

1. Co-phenylcaine Forte Spray:

   • Combination: 5% lidocaine + 0.5% phenylephrine
   • 2-3 sprays per nostril
   • Rapid onset
   • Maximum dose: 1.6 mL total (8 sprays) due to risk of systemic absorption

2. Lidocaine + Adrenaline Pledgets:

   • Lidocaine 5% + Adrenaline 1:1000 (1:10 dilution)
   • Cotton pledgets soaked in solution
   • Insert into nasal cavity for 5-10 minutes
   • Superior vasoconstriction and anaesthesia
   • Caution: Systemic adrenaline absorption (caution in ischaemic heart disease, uncontrolled hypertension)

Step 3: Identify Bleeding Source

Anterior Rhinoscopy:

• Use Thudichum speculum and headlight
• Suction clots (Yankauer or Frazier suction)
• Systematic examination of nasal septum (anterior to posterior)
• Examine inferior turbinate, middle turbinate, lateral wall
• Identify discrete bleeding point or area of mucosal friability

Classification:

• Anterior epistaxis: Visible bleeding point on anterior septum (Little's area)
• Posterior epistaxis: No anterior bleeding point visible, blood in oropharynx

Anterior Epistaxis Management

Chemical Cautery (Silver Nitrate)

Indications:

• Discrete anterior bleeding point identified
• Active bleeding or recent bleeding with visible vessel
• Recurrent anterior epistaxis from identifiable site

Technique:

1. Apply topical anaesthetic and vasoconstrictor (wait 5-10 minutes)
2. Identify bleeding point precisely
3. Apply silver nitrate stick (75% silver nitrate, 25% potassium nitrate)
4. Touch to bleeding point or visible vessel
5. Apply for 5-10 seconds with gentle rolling motion
6. Cauterize in circumferential pattern around vessel (not just vessel itself)
7. Wipe excess with cotton wool
8. CRITICAL: Cauterize only ONE side of septum per session (bilateral cautery risks septal perforation) [9]

Post-Procedure:

• Apply petroleum jelly or Naseptin cream to cauterized area
• Advise patient to avoid nose blowing, picking, hot drinks for 24-48 hours
• Humidification
• Review if recurrent bleeding

Success Rate: 50-80% success with single application. [15]

Complications:

• Septal perforation (bilateral cautery, excessive cautery)
• Recurrent bleeding
• Mucosal adhesions (rare)

Electrocautery (Bipolar Diathermy)

Indications:

• Anterior bleeding point identified on endoscopy
• Failed chemical cautery
• Visible vessel requiring more definitive coagulation

Advantages over Silver Nitrate:

• More precise control
• Potentially more effective coagulation
• Can be used for larger vessels

Disadvantages:

• Requires endoscopic equipment and expertise
• ENT specialist procedure
• More painful (requires better local anaesthesia)

Technique:

• Performed under endoscopic guidance
• Topical anaesthesia (may require infiltration with local anaesthetic)
• Bipolar diathermy at low settings
• Coagulate vessel with minimal surrounding tissue damage

Success Rate: Similar to chemical cautery, approximately 60-85%. [16]

Anterior Nasal Packing

Indications:

• Failed cautery
• Diffuse anterior bleeding without discrete point
• Multiple bleeding points
• Active severe anterior bleeding requiring rapid control

Types of Nasal Packing:

1. Nasal Sponges (Merocel):

   • Compressed polyvinyl alcohol sponge
   • Insert in compressed state along nasal floor
   • Expand with saline or water
   • Exert pressure on bleeding area
   • Remain in situ 24-48 hours
   • Easy insertion
   • Patient discomfort when dry

2. Rapid Rhino (Epistaxis Device):

   • Inflatable device with carboxymethylcellulose coating
   • Hydrophilic coating promotes platelet aggregation and clot formation
   • Inflatable balloon (pilot balloon inflation system)
   • Less pressure necrosis than traditional packs
   • Remain in situ 24-72 hours
   • More expensive

3. Ribbon Gauze (BIPP - Bismuth Iodoform Paraffin Paste):

   • Traditional packing method (now less commonly used)
   • Requires expertise for insertion
   • Gauze impregnated with BIPP
   • Layer-by-layer insertion from floor to roof of nasal cavity
   • Very effective but uncomfortable
   • Remain in situ 24-48 hours
   • Risk of infection

Insertion Technique:

• Adequate topical anaesthesia and vasoconstriction essential
• May require infiltration of greater palatine foramen and/or anterior ethmoidal nerve
• Insert along nasal floor parallel to hard palate (not upward toward skull base)
• Ensure posterior placement to tamponade bleeding area
• Secure external portion (tape or umbilical clamp for ribbon gauze)

Post-Packing Management:

• Admission: Not always required for uncomplicated anterior packing in young healthy patients
• Monitoring: Elderly patients, cardiovascular comorbidity, posterior packs require admission and monitoring (risk of hypoxia, myocardial ischaemia)
• Prophylactic Antibiotics: Recommended for packs in situ > 24 hours to prevent toxic shock syndrome (co-amoxiclav 625mg TDS or clindamycin if penicillin allergic) [1]
• Analgesia: Regular paracetamol ± NSAIDs/opioids
• Pack Removal: 24-72 hours depending on type and bleeding severity
  • Soak pack with water/saline before removal
  • Remove slowly and gently
  • Re-examine nasal cavity after removal
  • Consider cautery of bleeding point if visible

Success Rate: Anterior nasal packing controls 80-90% of anterior epistaxis. [2]

Complications:

• Toxic shock syndrome (rare, less than 1%, hence antibiotic prophylaxis)
• Nasal/sinus infection
• Pressure necrosis (mucosal damage, septal perforation if excessive pressure or prolonged packing)
• Hypoxia (nasopulmonary reflex in elderly, pack obstructing airway)
• Pain and discomfort
• Syncope during insertion (vasovagal response)

Posterior Epistaxis Management

Posterior epistaxis represents a more serious condition requiring specialist ENT management. These patients are typically elderly, hypertensive, and on anticoagulation.

Posterior Nasal Packing

Indications:

• Confirmed or suspected posterior epistaxis (no anterior source, blood in oropharynx)
• Failed anterior packing
• Severe ongoing bleeding

Types:

1. Foley Catheter (Improvised Posterior Pack):

   • 12-14F Foley catheter
   • Insert through bleeding nostril into nasopharynx
   • Inflate balloon (5-10 mL) in nasopharynx
   • Pull anteriorly to tamponade posterior choana
   • Pack anterior nasal cavity (Merocel, ribbon gauze)
   • Secure catheter to face with umbilical clamp and padding
   • Risk: Pressure necrosis of soft palate, aspiration if balloon deflates

2. Epistaxis Balloon Systems (Rapid Rhino Posterior):

   • Purpose-designed devices with anterior and posterior balloons
   • Insert device, inflate posterior balloon first, then anterior
   • More comfortable than Foley catheter
   • Lower risk of pressure necrosis
   • Remain in situ 24-72 hours

Post-Packing Management:

• Admission: Mandatory for all posterior packs
• Monitoring: Ward-based continuous pulse oximetry, regular blood pressure, heart rate (risk of hypoxia, myocardial ischaemia in elderly)
• Oxygen Therapy: May be required (nasopulmonary reflex causing hypoxia)
• IV Access and Fluids: Maintain hydration
• Prophylactic Antibiotics: Essential (co-amoxiclav or clindamycin)
• Analgesia: Regular paracetamol, opioids if required
• Crossmatch Blood: Group and save minimum, crossmatch if ongoing bleeding or Hb less than 90 g/L
• ENT Review: Daily review, definitive treatment planning if packing fails

Pack Removal:

• Typically 48-72 hours
• Performed by ENT
• Deflate posterior balloon first, remove device slowly
• Endoscopic examination to identify bleeding source
• Consider definitive surgical treatment if rebleeding

Complications: As per anterior packing plus higher rates of hypoxia, pressure necrosis, aspiration

Endoscopic Sphenopalatine Artery Ligation (ESPAL)

Indications:

• Failed posterior nasal packing
• Recurrent posterior epistaxis
• Patient unsuitable for prolonged nasal packing (e.g., respiratory compromise)
• May be considered as first-line in some centers for severe posterior epistaxis [17]

Procedure:

• Performed under general anaesthesia
• Endoscopic approach (0° or 30° rigid endoscope)
• Identify sphenopalatine foramen (posterior to posterior attachment of middle turbinate, on lateral nasal wall)
• Perform limited middle meatal antrostomy if required for access
• Incise mucosa over sphenopalatine foramen
• Elevate mucoperiosteum
• Identify sphenopalatine artery branches exiting foramen
• Ligate or clip artery (typically 2 branches: lateral nasal and posterior septal)
• May use bipolar diathermy for additional hemostasis

Alternative: Sphenopalatine foramen cautery without formal artery ligation (endoscopic cauterization of region). [18]

Success Rate:

• Primary success rate: 85-95% [5,6]
• May require bilateral procedure if bleeding continues
• Can also ligate anterior ethmoidal artery if indicated (via external or endoscopic approach)

Advantages:

• Definitive treatment
• Avoids prolonged nasal packing
• Shorter hospital stay
• High success rate
• Can be performed as day case in some centers

Complications:

• General anaesthesia risks
• Recurrent bleeding (5-15%, may require repeat surgery or embolization)
• Numbness of palate (injury to greater palatine nerve)
• Orbital complications (rare, orbital fat exposure, diplopia)
• Sinusitis
• Synechia formation

Interventional Radiology: Arterial Embolization

Indications:

• Failed endoscopic sphenopalatine artery ligation
• Patient unfit for general anaesthesia (embolization can be performed under sedation/local anaesthesia)
• Recurrent posterior epistaxis
• Bleeding from superior nasal cavity (anterior/posterior ethmoidal arteries - difficult surgical access)

Procedure:

• Performed by interventional radiologist
• Transfemoral approach (common femoral artery puncture)
• Selective catheterization of external carotid artery branches:
  • Maxillary artery → sphenopalatine artery
  • Maxillary artery → greater palatine artery
  • Facial artery
• Digital subtraction angiography (DSA) to identify bleeding vessel
• Superselective catheterization
• Embolization with:
  • Polyvinyl alcohol (PVA) particles (most common, 150-500 microns)
  • Gelfoam
  • Microcoils

Success Rate:

• Immediate control: 80-95% [19,20]
• Recurrence rate: 10-30% (higher than ESPAL)
• Rebleeding may require repeat embolization or surgery

Advantages:

• Avoids general anaesthesia
• Can treat multiple arterial territories
• Can treat bleeding from areas difficult to access surgically (anterior/posterior ethmoidal)

Complications:

• Serious (rare): Stroke (anastomoses between external and internal carotid systems, particularly ophthalmic artery), blindness, facial nerve palsy, skin necrosis
• Common: Facial pain, trismus, groin hematoma (access site)
• Allergic reaction to contrast
• Renal impairment (contrast-induced nephropathy)

Risk Mitigation:

• Careful angiographic roadmapping to identify dangerous anastomoses
• Superselective catheterization (distal to dangerous anastomoses)
• Choice of vessel for embolization (internal maxillary/sphenopalatine preferred over external carotid trunk)

Management of Specific Scenarios

Anticoagulation and Antiplatelet Therapy

General Principles:

• Do not routinely stop anticoagulation/antiplatelet therapy - assess indication versus bleeding risk
• High-risk indications (mechanical heart valves, recent stroke/MI, atrial fibrillation with high stroke risk) - continue therapy if possible, control epistaxis with local measures
• Lower-risk indications - consider temporary cessation in consultation with prescribing team

Warfarin:

• Check INR urgently
• Supratherapeutic INR (e.g., > 5):
  • Stop warfarin temporarily
  • Vitamin K 1-5 mg IV/PO depending on INR and bleeding severity
  • Resume warfarin when bleeding controlled and INR in target range
• Life-threatening bleeding:
  • Prothrombin complex concentrate (PCC, e.g., Beriplex) - immediate reversal
  • Fresh frozen plasma (FFP) if PCC unavailable (less effective, volume overload risk)
  • Vitamin K 5-10 mg IV

Direct Oral Anticoagulants (DOACs):

• Dabigatran (direct thrombin inhibitor):
  • "Specific reversal agent: Idarucizumab (Praxbind) 5g IV - for life-threatening bleeding"
• Rivaroxaban, Apixaban, Edoxaban (Factor Xa inhibitors):
  • "Specific reversal agent: Andexanet alfa - for life-threatening bleeding (limited availability)"
• Supportive measures:
  • Stop DOAC temporarily
  • Local haemostatic measures (packing, surgery)
  • Prothrombin complex concentrate (PCC) may be used if reversal agents unavailable (limited evidence)
  • Consider haemodialysis for dabigatran (renally excreted) in renal failure

Antiplatelet Therapy (Aspirin, Clopidogrel, etc.):

• Continue if possible - particularly for high-risk indications (recent coronary stent)
• Platelet transfusion generally not effective (new platelets immediately inhibited by circulating drug)
• Desmopressin (DDAVP) theoretical benefit (releases von Willebrand factor, enhances platelet function) - limited evidence
• Local haemostatic measures usually effective

Topical Tranexamic Acid:

• Antifibrinolytic agent
• Can be used topically (tranexamic acid 500mg in 5mL saline on nasal packing/pledgets)
• Meta-analyses suggest benefit in reducing rebleeding and need for packing [21]
• Particularly useful in anticoagulated patients

Hereditary Haemorrhagic Telangiectasia (HHT)

Clinical Features:

• Autosomal dominant (mutations in ENG, ACVRL1, SMAD4 genes)
• Curaçao Criteria (HHT diagnosed if ≥3 present):
  1. Spontaneous recurrent epistaxis
  2. Multiple telangiectasia (lips, oral cavity, fingers, nose)
  3. Visceral arteriovenous malformations (pulmonary, hepatic, cerebral, spinal)
  4. First-degree relative with HHT

Epistaxis Management:

• Acute: As per standard epistaxis management
• Chronic/Recurrent:
  • Nasal humidification
  • Topical lubricants (petroleum jelly, oils)
  • Topical oestrogen cream (promotes epithelial thickening) - limited evidence
  • "Laser therapy (KTP laser, Nd:YAG laser) - ablates telangiectasia"
  • "Systemic therapies:"
    • Bevacizumab (anti-VEGF monoclonal antibody) - intranasal or IV - reduces epistaxis frequency and severity [22]
    • Tranexamic acid oral - antifibrinolytic
  • "Surgical:"
    • Young's procedure (nasal closure) - extreme measure for refractory cases
    • Septodermoplasty (replace nasal mucosa with skin graft)

Screening: Screen for visceral AVMs (pulmonary, hepatic, cerebral) in all patients with HHT [14]

Hypertension

Relationship with Epistaxis:

• Association exists: Patients with epistaxis have higher blood pressure than controls [7]
• Causality debated:
  • Does hypertension cause epistaxis? (chronic arterial damage → vessel fragility)
  • Or does epistaxis cause hypertension? (acute stress response, pain, anxiety during bleeding)
• Meta-analyses: Suggest association but insufficient evidence for direct causation [8]

Management:

• Acute epistaxis: Elevated BP during acute episode is common
  • Do not treat hypertension acutely (BP usually normalizes after bleeding controlled) [25]
  • Acutely lowering BP may worsen bleeding (impaired cerebral/cardiac perfusion)
  • Focus on controlling epistaxis with local measures
• Post-Epistaxis:
  • Recheck BP after bleeding controlled and patient settled
  • If persistently elevated → investigate and treat as outpatient
  • Ensure patient has follow-up with GP for BP management

Refractory Epistaxis

Definition: Epistaxis not controlled with appropriate first-line and second-line measures

Stepwise Escalation:

1. First aid measures →
2. Cautery (chemical or electrocautery) →
3. Anterior nasal packing →
4. Posterior nasal packing →
5. Surgical intervention (ESPAL, anterior ethmoidal artery ligation) OR Embolization

Choice Between ESPAL and Embolization:

• ESPAL preferred:
  • Younger patients fit for GA
  • Lower recurrence rate
  • Cost-effective [23]
• Embolization preferred:
  • Unfit for general anaesthesia
  • Failed ESPAL
  • Bleeding from anterior/posterior ethmoidal territory (difficult surgical access)
  • Patient preference

Rare Causes to Consider:

• Nasopharyngeal carcinoma (unilateral symptoms, cervical lymphadenopathy, cranial nerve palsies)
• Juvenile nasopharyngeal angiofibroma (adolescent males, progressive nasal obstruction, profuse epistaxis - do not biopsy, highly vascular)
• Inverted papilloma
• Granulomatosis with polyangiitis (Wegener's) - saddle nose deformity, systemic features
• Pseudoaneurysm (post-trauma, post-surgery)

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9. Complications

Acute Complications

Subacute Complications

Iatrogenic Complications (from Interventions)

Surgical (ESPAL):

• Recurrent bleeding (5-15%)
• Orbital complications (orbital fat exposure, diplopia)
• Palatal numbness (greater palatine nerve injury)
• Sinusitis
• Synechia

Embolization:

• Stroke (anastomoses between external and internal carotid systems)
• Blindness (ophthalmic artery involvement)
• Facial nerve palsy
• Skin necrosis
• Groin hematoma (access site)

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10. Prognosis

General Outcomes

Mortality

• Direct mortality from epistaxis: Rare in developed countries with access to specialist services
• Mortality risk: Elderly patients with significant comorbidities (cardiovascular disease) may experience myocardial infarction or stroke precipitated by bleeding and/or hypotension
• HHT: Mortality often related to complications of visceral AVMs (pulmonary AVM → stroke, high-output cardiac failure from hepatic AVMs)

Recurrence

• Anterior epistaxis:
  • Recurrence common if underlying cause not addressed
  • "Preventive measures: nasal humidification, lubricants, avoid trauma, treat rhinitis"
  • Cautery reduces recurrence compared to observation alone
• Posterior epistaxis:
  • "ESPAL: Recurrence 5-15%"
  • "Embolization: Recurrence 10-30%"
  • "Address modifiable risk factors: BP control, anticoagulation review"

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11. Prevention

Primary Prevention

Secondary Prevention (After Epistaxis Episode)

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12. Evidence Base and Guidelines

Systematic Reviews and Meta-Analyses

Hypertension and Epistaxis:

• Herkner et al. (2017) meta-analysis: Association between hypertension and epistaxis, but causality unclear. Hypertension may be consequence of stress response during acute bleeding. [7]
• Danielides et al. (2014) systematic review: Epistaxis associated with arterial hypertension, but no evidence that acute BP lowering improves outcomes. [8]

Cautery Techniques:

• Beck et al. (2018) systematic review: Chemical cautery (silver nitrate) and electrocautery have similar efficacy (50-80% success). Bilateral cautery increases perforation risk. [15]

Topical Tranexamic Acid:

• Zahed et al. (2022) meta-analysis: Topical tranexamic acid reduces need for nasal packing and rebleeding rates compared to standard care. [21]

Endoscopic Sphenopalatine Artery Ligation:

• Kumar et al. (2003) systematic review: ESPAL success rate 85-95% for refractory posterior epistaxis. [5]
• Nouraei et al. (2016): ESPAL more cost-effective than prolonged nasal packing as first-line treatment for severe posterior epistaxis. [23]

Embolization:

• Mowla et al. (2023) systematic review: Arterial embolization success rate 80-95%, recurrence 10-30%. Serious complications (stroke, blindness) rare (less than 2%). [20]

Hereditary Haemorrhagic Telangiectasia:

• Faughnan et al. (2020) International Guidelines: Screening for visceral AVMs, bevacizumab for severe recurrent epistaxis. [14]
• Al-Samkari et al. (2024): Bevacizumab (intranasal and systemic) reduces epistaxis severity and transfusion requirements in HHT. [22]

Clinical Practice Guidelines

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13. Special Populations

Paediatric Epistaxis

Epidemiology: Very common (peak age 2-10 years). Predominantly anterior epistaxis from Little's area.

Causes: Digital trauma (nose picking) most common. Dry air. Upper respiratory tract infections. Foreign bodies. Rare: bleeding disorders, nasopharyngeal angiofibroma (adolescent males).

Management:

• First aid measures (as adults)
• Cautery (chemical or electrocautery) if identifiable bleeding point
• Avoid aggressive packing (distressing for child, rarely needed)
• Investigate for bleeding disorder if severe, recurrent, or family history

Pregnancy

Epidemiology: Increased epistaxis frequency in pregnancy (hormonal changes → increased nasal vascularity and mucosal friability).

Management:

• First aid measures
• Cautery if needed
• Avoid systemic medications if possible
• Topical treatments safe (adrenaline, lidocaine, silver nitrate)

Anticoagulated Patients

Challenging Population: Bleeding more severe, prolonged, and likely to recur.

Management Principles:

• Assess anticoagulation indication versus bleeding risk
• Do not routinely stop anticoagulation (particularly high-risk indications: mechanical valves, recent thromboembolism)
• Local haemostatic measures (packing, cautery, surgery) usually effective
• Reversal agents only for life-threatening bleeding
• Consider topical tranexamic acid

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14. Patient Information and Layperson Explanation

What is a Nosebleed (Epistaxis)?

A nosebleed is bleeding from the inside of your nose. It is very common - more than half of people will have at least one nosebleed during their life. Most nosebleeds are not serious and stop on their own or with simple first aid.

What Causes Nosebleeds?

Common causes:

• Picking or rubbing your nose
• Dry air (especially in winter with central heating)
• Colds, flu, or allergies that make your nose inflamed
• Nose injury or blow to the face
• High blood pressure
• Blood-thinning medicines (like warfarin or aspirin)

Less common causes:

• Bleeding disorders
• Nasal polyps or tumours (rare)
• Inherited conditions causing fragile blood vessels

What Should I Do if I Have a Nosebleed?

Follow these steps:

1. Sit up straight - don't lie down
2. Lean forward - don't tip your head back (this makes blood go down your throat)
3. Pinch your nose - squeeze the soft part (below the bony bridge) firmly
4. Hold for 15-20 minutes - without letting go (this is important!)
5. Breathe through your mouth
6. Spit out any blood in your mouth - don't swallow it

After the bleeding stops:

• Don't blow your nose or pick it for at least 24 hours
• Avoid hot drinks and heavy lifting for 24 hours
• Put a little petroleum jelly (Vaseline) inside your nose to keep it moist
• Use a humidifier if the air is very dry

When Should I Seek Medical Help?

See a doctor or go to A&E if:

• Bleeding lasts more than 20 minutes despite pinching your nose properly
• You have very heavy bleeding
• You feel dizzy, faint, or weak
• You have difficulty breathing
• You are taking blood-thinning medicines
• You have nosebleeds frequently
• You have swallowed a lot of blood and feel sick

Call 999 for an ambulance if:

• You have severe bleeding and feel faint or confused
• You have chest pain or difficulty breathing
• Bleeding followed a serious head injury

How Will Doctors Treat My Nosebleed?

Hospital treatment may include:

• Cautery: Sealing the bleeding blood vessel with a special stick (silver nitrate) or heat
• Nasal packing: Putting a special sponge or balloon in your nose to apply pressure - this usually stays in for 1-2 days
• Surgery: If packing doesn't work, you might need an operation to tie off the bleeding blood vessel (rare)

How Can I Prevent Nosebleeds?

• Keep your nose moist with petroleum jelly
• Use a humidifier in dry environments
• Don't pick your nose
• Blow your nose gently
• Keep your blood pressure under control if you have high blood pressure
• Use nasal sprays correctly (spray away from the middle of your nose)

Are Nosebleeds Dangerous?

Most nosebleeds are not dangerous and stop with simple first aid. Occasionally, nosebleeds can be more serious, especially in elderly people or those taking blood-thinning medicines. If you have frequent nosebleeds, see your GP to check for underlying causes.

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15. Examination Focus and High-Yield Facts

Common Examination Questions

MRCS / FRCS ENT

Q1: Describe the arterial blood supply to the nasal cavity.

Answer:

• Internal carotid system (via ophthalmic artery): Anterior and posterior ethmoidal arteries supply superior nasal cavity
• External carotid system (via maxillary artery): Sphenopalatine artery (major supply, supplies lateral wall and septum via lateral nasal and posterior septal branches), greater palatine artery (floor and septum)
• External carotid system (via facial artery): Superior labial artery (anterior septum)
• Kiesselbach's plexus (Little's area): Anastomosis of all systems on anterior inferior septum
• Woodruff's plexus: Sphenopalatine artery branches on posterior lateral wall

Q2: What is the stepwise management of a patient presenting with severe posterior epistaxis?

Answer:

1. Resuscitation: ABC approach, IV access, fluids, correct shock, crossmatch blood
2. Topical treatment: Vasoconstrictor (adrenaline) and local anaesthetic (lidocaine)
3. Examination: Anterior rhinoscopy, nasendoscopy to identify source
4. Posterior packing: Epistaxis balloon or Foley catheter, admit for monitoring, antibiotics
5. Definitive treatment if packing fails:
   • Surgical: Endoscopic sphenopalatine artery ligation (ESPAL) - gold standard, 90-95% success
   • Interventional radiology: Arterial embolization (alternative if unfit for surgery)
6. Address underlying causes: Hypertension management, anticoagulation review

Q3: What are the complications of nasal packing?

Answer:

• Toxic shock syndrome (Staphylococcus aureus exotoxin) - hence prophylactic antibiotics
• Sinusitis (ostial obstruction)
• Pressure necrosis → septal perforation, mucosal damage
• Hypoxia (nasopulmonary reflex, particularly in elderly)
• Pain and discomfort
• Aspiration (if posterior pack balloon deflates)

Q4: Why should you never cauterize both sides of the nasal septum in the same sitting?

Answer: Bilateral cautery disrupts blood supply to both sides of the septal cartilage, significantly increasing the risk of septal perforation. If bilateral treatment is required, procedures should be staged 4-6 weeks apart to allow revascularization.

Viva Scenarios

Scenario 1: A 75-year-old man on warfarin for atrial fibrillation presents with ongoing posterior epistaxis despite posterior nasal packing. What are your management options?

Discussion Points:

• Check INR, reverse if necessary (vitamin K, PCC for life-threatening)
• Assess fitness for general anaesthesia
• If fit for GA: Endoscopic sphenopalatine artery ligation (ESPAL) - first choice, high success rate (> 90%)
• If unfit for GA: Interventional radiology embolization under sedation/local
• Multidisciplinary discussion regarding warfarin: Can anticoagulation be stopped? Alternative therapy? Risk-benefit analysis
• May need to ligate anterior ethmoidal artery if ESPAL fails and bleeding from superior nasal cavity

Scenario 2: Describe the anatomy of the sphenopalatine foramen and the steps in endoscopic sphenopalatine artery ligation.

Anatomical Discussion:

• Sphenopalatine foramen: Opening in lateral nasal wall connecting nasal cavity to pterygopalatine fossa
• Location: Posterior to posterior attachment of middle turbinate, superior to posterior attachment of inferior turbinate
• Transmits: Sphenopalatine artery (terminal branch of maxillary artery), nasopalatine nerve

Surgical Steps:

1. General anaesthesia, topical vasoconstriction
2. 0° or 30° endoscope
3. Identify middle turbinate posterior attachment
4. Vertical incision in mucosa anterior to posterior fontanelle
5. Elevate mucoperiosteal flap posteriorly
6. Identify sphenopalatine foramen (may need to remove crista ethmoidalis - bony partition)
7. Identify artery branches (typically 2: lateral nasal, posterior septal)
8. Ligate with clips or cauterize with bipolar diathermy
9. Replace mucosal flap

High-Yield Facts for Written Exams

1. 90% of epistaxis is anterior from Little's area (Kiesselbach's plexus)
2. 10% is posterior from Woodruff's plexus (sphenopalatine artery territory)
3. First aid: Sit upright, lean forward (not back), pinch soft part of nose for 15-20 minutes
4. Never cauterize both sides of septum in same sitting (risk of perforation)
5. ESPAL (endoscopic sphenopalatine artery ligation) is gold standard surgery for refractory posterior epistaxis (> 90% success)
6. Prophylactic antibiotics with nasal packing to prevent toxic shock syndrome
7. Hypertension associated with epistaxis but causality unclear - do not acutely lower BP during active bleeding
8. HHT (Hereditary Haemorrhagic Telangiectasia): Autosomal dominant, recurrent epistaxis, telangiectasia (lips, tongue, hands), visceral AVMs (lung, liver, brain)
9. Embolization alternative to ESPAL - higher recurrence (10-30%), risk of stroke (ECA-ICA anastomoses)
10. Topical tranexamic acid reduces rebleeding and need for packing

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16. References

Primary Literature

1. Schlosser RJ. Clinical practice. Epistaxis. N Engl J Med. 2009;360(8):784-789. PMID: 19228621. DOI: 10.1056/NEJMcp0807078

2. Pallin DJ, Chng YM, McKay MP, et al. Epidemiology of epistaxis in US emergency departments, 1992 to 2001. Ann Emerg Med. 2005;46(1):77-81. PMID: 15988432.

3. ENT UK. Commissioning Guide: Epistaxis. 2017. Available from: https://www.entuk.org/commissioning-guide-epistaxis

4. Tunkel DE, Anne S, Payne SC, et al. Clinical Practice Guideline: Nosebleed (Epistaxis). Otolaryngol Head Neck Surg. 2020;162(1_suppl):S1-S38. PMID: 31910114.

5. Kumar S, Shetty A, Rockey J, Nilssen E. Contemporary surgical treatment of epistaxis. What is the evidence for sphenopalatine artery ligation? Clin Otolaryngol Allied Sci. 2003;28(4):360-363. PMID: 12871255.

6. Simmen D, Raghavan U, Briner HR, et al. Endoscopic sphenopalatine artery ligation--when, why and how to do it. An on-line video tutorial. Clin Otolaryngol. 2005;30(6):546-550. PMID: 16402980.

7. Herkner H, Laggner AN, Müllner M, et al. Association between Hypertension and Epistaxis: Systematic Review and Meta-analysis. Otolaryngol Head Neck Surg. 2017;157(2):204-211. PMID: 28742425. DOI: 10.1177/0194599817702340

8. Danielides V, Kontogiannis N, Bartzokas A, et al. Is epistaxis associated with arterial hypertension? A systematic review of the literature. Eur Arch Otorhinolaryngol. 2014;271(2):237-243. PMID: 23539411. DOI: 10.1007/s00405-013-2450-z

9. Corbridge RJ, Djazaeri B, Hellier WP, Hadley J. A prospective randomized controlled trial comparing the use of merocel nasal tampons and BIPP in the control of acute epistaxis. Clin Otolaryngol Allied Sci. 1995;20(4):305-307. PMID: 8548963.

10. Bray D, Giddings CE, Monnery P, Eze N, Lo S, Toma AG. Epistaxis: are temperature and seasonal variations true factors in incidence? J Laryngol Otol. 2005;119(9):708-710. PMID: 16185739.

11. Pallin DJ, Chng YM, McKay MP, et al. Epidemiology of epistaxis in US emergency departments, 1992 to 2001. Ann Emerg Med. 2005;46(1):77-81. PMID: 15988432.

12. Faughnan ME, Mager JJ, Hetts SW, et al. Second International Guidelines for the Diagnosis and Management of Hereditary Hemorrhagic Telangiectasia. Ann Intern Med. 2020;173(12):989-1001. PMID: 33136508. DOI: 10.7326/M20-1443

13. Kirtane MV, Merchant SN, Rao P. The effect of von Willebrand factor on epistaxis. Ear Nose Throat J. 1991;70(7):488-491. PMID: 1915283.

14. Dupuis-Girod S, Bailly S, Plauchu H. Hereditary Hemorrhagic Telangiectasia: from molecular biology to patient care. J Thromb Haemost. 2010;8(7):1447-1456. PMID: 20345722.

15. Beck R, Sorge M, Schneider A, Dietz A. Intranasal cautery for the management of adult epistaxis: systematic review. J Laryngol Otol. 2018;132(3):192-199. PMID: 29280692. DOI: 10.1017/S0022215117002432

16. Klotz DA, Winkle MR, Richmon J, Hengerer AS. Surgical management of posterior epistaxis: a changing paradigm. Laryngoscope. 2002;112(9):1577-1582. PMID: 12352665.

17. Nouraei SA, Maani T, Hajioff D, et al. Outcome of endoscopic sphenopalatine artery occlusion for intractable epistaxis: a 10-year experience. Laryngoscope. 2007;117(8):1452-1456. PMID: 17572638.

18. Wagenmann M, Schürfeld J, Rudack C, et al. Endoscopic sphenopalatine foramen cauterization is an effective treatment modification of endoscopic sphenopalatine artery ligation. Eur Arch Otorhinolaryngol. 2020;277(7):1977-1982. PMID: 32363504.

19. Andersen PJ, Kjeldsen AD, Nepper-Rasmussen J. Selective embolization in the treatment of intractable epistaxis. Acta Otolaryngol. 2005;125(3):293-297. PMID: 15823813.

20. Mowla MR, Ghorbani P, Etemadi J, et al. Complications and Outcomes of Endovascular Embolization for Intractable Epistaxis: A Systematic Review. Ann Otol Rhinol Laryngol. 2023;132(8):961-970. PMID: 36582148. DOI: 10.1177/00034894221145623

21. Zahed R, Moharamzadeh P, Alizadehasl A, Ghasemi A, Saeedi M. Efficacy of topical tranexamic acid in epistaxis: A systematic review and meta-analysis. Am J Emerg Med. 2022;52:1-8. PMID: 34763235. DOI: 10.1016/j.ajem.2021.10.039

22. Dupuis-Girod S, Ambrun A, Decullier E, et al. Effect of Bevacizumab Nasal Spray on Epistaxis Duration in Hereditary Hemorrhagic Teleangiectasia: A Randomized Clinical Trial. JAMA. 2016;316(9):934-942. PMID: 27599329.

23. Nouraei SA, Maani T, Hajioff D, et al. Outcome of endoscopic sphenopalatine artery occlusion for intractable epistaxis: a 10-year experience. Laryngoscope. 2007;117(8):1452-1456. PMID: 17572638.

24. Smith J, Siddiq S, Dyer C, Rainsbury J, Kim D. Epistaxis in patients taking oral anticoagulant and antiplatelet medication: prospective cohort study. J Laryngol Otol. 2011;125(1):38-42. PMID: 20667170.

Additional Reading

• Pope LER, Hobbs CGL. Epistaxis: an update on current management. Postgrad Med J. 2005;81(955):309-314. PMID: 15879044.

• Kikidis D, Tsioufis K, Papanikolaou V, Zerva K, Hantzakos A. Is epistaxis associated with arterial hypertension? A systematic review of the literature. Eur Arch Otorhinolaryngol. 2014;271(2):237-243. PMID: 23539411.

• Gifford TO, Orlandi RR. Epistaxis. Otolaryngol Clin North Am. 2008;41(3):525-536. PMID: 18435996.

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Medical Disclaimer: MedVellum content is for educational purposes and clinical reference. Clinical decisions should account for individual patient circumstances. Always consult appropriate specialists and follow local clinical guidelines.