EENT · PANCE / PANRE

Epistaxis

Nasal bleeding categorized as anterior (most common, Kiesselbach plexus) or posterior (Woodruff plexus, more severe).

Also known as: epistaxis, nosebleed, anterior epistaxis, posterior epistaxis

Overview

Bleeding from the nasal cavity. Anterior epistaxis (~90%) originates from Kiesselbach plexus on the anteroinferior nasal septum (Little's area). Posterior epistaxis arises from Woodruff plexus (sphenopalatine artery branches) on the lateral nasal wall — typically heavier, harder to control, and more common in older patients.

Epidemiology

Lifetime prevalence ~60%; only ~10% seek medical attention. Bimodal age distribution: peaks in children <10 (anterior) and adults >50 (anterior and posterior). Increased incidence in dry winter months.

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Question 1EENTMedium
A 10-year-old male has profuse nosebleed from the right nostril after picking his nose. Direct pressure for 15 minutes stops the bleeding. Which of the following is the most common source of anterior epistaxis bleeding?
  • ACribriform plate
  • BKiesselbach plexus
  • CSphenopalatine artery
  • DInferior turbinate
Reveal answer & full explanation
Correct answer: B — Kiesselbach plexus
  • ACribriform plate
  • BKiesselbach plexus
  • CSphenopalatine artery
  • DInferior turbinate

Why Kiesselbach plexus is correct

  • 90% of epistaxis is anterior; the Kiesselbach plexus (also called Little area) on the anteroinferior nasal septum is the most common source
  • Four arteries converge at this plexus: the superior labial, anterior ethmoid, sphenopalatine, and greater palatine arteries (the posterior ethmoid supplies the posterosuperior septum, not Kiesselbach)
  • Anterior epistaxis is common in children due to digital trauma and dry air

Why the others are wrong

  • Cribriform plate — not a vascular plexus and not a common bleeding source for epistaxis
  • Sphenopalatine artery — the sphenopalatine artery is the primary source of posterior epistaxis, which accounts for only 10% of cases, is more severe, more common in adults with hypertension (HTN), and requires posterior packing or balloon and ear, nose, and throat (ENT) consultation; the Woodruff plexus is also a posterior source
  • Inferior turbinate — not the classic named site of anterior epistaxis; the anteroinferior septum (Kiesselbach plexus) is the canonical answer

Additional high-yield points

  • Treatment of anterior epistaxis: direct compression (squeeze soft part of nose for 10-15 min, lean forward), topical vasoconstrictor (oxymetazoline), silver nitrate cautery if a visible bleeding source is identified
  • Always evaluate for hypertension, anticoagulation, and bleeding diatheses
  • Hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu): recurrent epistaxis + telangiectasias + arteriovenous malformations (AVMs)
Question 2EENTEasy
A 9-year-old boy is brought to the clinic in January for recurrent nosebleeds over the past several weeks. The bleeding is always from the right nostril, lasts a few minutes, and stops with gentle pressure. His mother notes he frequently inserts his finger into his nose, and the home has forced-air heating. He takes no medications and has no family history of bleeding disorders. Vital signs are normal. Anterior rhinoscopy shows excoriated mucosa over the anterior nasal septum without active bleeding. Which of the following is the most likely cause of this patient's epistaxis?
  • ADigital nasal trauma
  • BSystemic hypertension
  • Cvon Willebrand disease
  • DDaily aspirin therapy
Reveal answer & full explanation
Correct answer: A — Digital nasal trauma
  • ADigital nasal trauma
  • BSystemic hypertension
  • Cvon Willebrand disease
  • DDaily aspirin therapy

Why Digital nasal trauma is correct

  • Anterior epistaxis (~90% of cases) arises from the Kiesselbach plexus on the anteroinferior septum (Little's area), and recurrent nose picking is the leading local risk factor, especially in children under 10.
  • This patient has the classic profile: a young child, unilateral recurrent low-volume bleeding, documented finger insertion, dry forced-air winter heating, and excoriated anterior septal mucosa on exam — all pointing to local digital trauma as the dominant cause.

Why the others are wrong

  • Systemic hypertension — an association with the severity/duration of a bleed once it starts, not an initiating cause; it is also implausible in a normotensive 9-year-old with normal vital signs.
  • Daily aspirin therapy — antiplatelet agents increase bleeding tendency and recurrence, but this child takes no medications, so it does not apply here.
  • von Willebrand disease — the most common inherited bleeding disorder, but it typically causes bleeding from multiple sites, easy bruising, and a positive family history; none are present, making it a far weaker explanation than a local cause.
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Risk factors

  • Local: digital trauma (nose picking), dry air, nasal foreign body, intranasal medications (corticosteroids, cocaine), septal deformity or perforation, nasal/sinus surgery, tumors (juvenile nasopharyngeal angiofibroma in adolescent males)
  • Systemic: hypertension (association with severity, not cause), anticoagulants and antiplatelets, inherited bleeding disorders (von Willebrand disease, hemophilia), thrombocytopenia, liver disease/uremia, hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu), aspirin/NSAID use, alcohol
  • Vascular malformations and tumors as red-flag etiologies

Pathophysiology

Mucosal disruption exposes submucosal vessels. Anterior bleeds arise from anastomotic vessels of Kiesselbach plexus (anterior ethmoidal, sphenopalatine, greater palatine, and superior labial arteries). Posterior bleeds come from larger branches of the sphenopalatine artery (Woodruff plexus), often arterial and brisk.

Clinical presentation

Symptoms

  • Active bleeding from one or both nostrils (unilateral typical of anterior)
  • Blood dripping into posterior pharynx — suggests posterior source
  • Sensation of nasal fullness or pooling
  • Lightheadedness, syncope, or shock if substantial blood loss
  • Recurrent low-volume bleeding may suggest HHT or tumor

Signs / physical exam

  • Visualization of bleeding source on anterior rhinoscopy with nasal speculum
  • Blood in posterior pharynx without anterior source visible → suspect posterior bleed
  • Hypertension, tachycardia, hypotension if significant loss
  • Telangiectases on lips, tongue (HHT)
  • Bruising, petechiae (coagulopathy)

Classic findings

Anterior: visible bleeding from Kiesselbach plexus on anterior septum. Posterior: blood pooling in posterior pharynx without anterior source after good visualization.

Differential diagnosis

  • Hemoptysis — Blood from lower airway with cough; frothy, bright red; chest pathology; do not confuse with posterior epistaxis dripping into pharynx
  • Hematemesis — Vomited blood; coffee-ground or bright red; GI source; swallowed posterior epistaxis can mimic
  • Nasal foreign body — Unilateral foul purulent discharge ± blood, often in a young child
  • Sinonasal tumor — Unilateral persistent or recurrent bleeding, nasal obstruction, mass on endoscopy or imaging
  • Juvenile nasopharyngeal angiofibroma — Adolescent male with recurrent unilateral severe epistaxis and obstruction; vascular mass; biopsy contraindicated, image and refer ENT
  • Hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu) — Recurrent epistaxis + telangiectases on lips/tongue/fingertips + family history + AVMs (pulmonary, hepatic, cerebral)
  • Coagulopathy — Bleeding from multiple sites, easy bruising; check CBC, PT/INR, aPTT, vWF

Diagnostic workup

Labs

  • Most anterior epistaxis: none required
  • CBC for significant or recurrent bleeding
  • PT/INR if on warfarin; aPTT if on heparin; consider DOAC levels if available
  • Type and crossmatch for substantial blood loss
  • vWF antigen and ristocetin cofactor if recurrent without local cause, or family history of bleeding

Imaging

  • Not routine for typical anterior epistaxis
  • CT or angiography if recurrent, refractory, or tumor/AVM suspected
  • Nasal endoscopy (ENT) for posterior or recurrent bleeding to identify source

Diagnostic algorithm

flowchart TD
  A[Active epistaxis] --> B[ABCs<br/>lean forward<br/>pinch soft nose 10-15 min]
  B --> C{Bleeding stopped?}
  C -->|Yes| D[Identify source<br/>discharge with home care]
  C -->|No| E[Topical vasoconstrictor<br/>oxymetazoline pledget]
  E --> F{Anterior source<br/>identified?}
  F -->|Yes, focal| G[Silver nitrate cautery<br/>one side septum only]
  F -->|Diffuse or persistent| H[Anterior packing<br/>Merocel / Rapid Rhino<br/>24-72 h]
  F -->|No anterior source| I[POSTERIOR bleed]
  I --> J[Posterior balloon pack<br/>or Foley<br/>ADMIT with monitoring]
  J --> K[ENT consult<br/>endoscopic cautery<br/>SPA ligation<br/>or IR embolization]
  G --> L[Discharge with<br/>saline gel + humidifier]
  H --> M{Re-bleed at 24-72 h?}
  M -->|Yes| K
  M -->|No| L
Stepwise management of anterior vs posterior epistaxis.

Treatment

First-line

  • ABCs first — assess airway, hemodynamics; gown and PPE
  • Patient leans FORWARD (not back) and pinches the soft cartilaginous portion of the nose firmly × 10-15 minutes continuously
  • Apply topical vasoconstrictor — oxymetazoline spray, phenylephrine, or cocaine 4% — onto cotton pledget or directly
  • Identify bleeding source with good lighting and headlamp after clot removal/suction
  • Silver nitrate cautery (chemical) for visible anterior bleeding source — cauterize one side of septum only to prevent septal perforation
  • Anterior nasal packing (e.g., Merocel, Rapid Rhino, nasal tampon, or ribbon gauze with petrolatum) if continued bleeding — leave 24-72 h
  • Patients with anterior packing may not require prophylactic antibiotics in most guidelines (AAO-HNS 2020), but selectively used for immunocompromised, valve, or prolonged packing

Second-line / adjunct

  • Posterior epistaxis: posterior pack (Foley balloon catheter or commercial double-balloon device) — ADMIT and monitor (risk of nasovagal reflex, hypoxia, dysrhythmia, pressure necrosis)
  • ENT consultation for posterior packing, endoscopic cautery, or arterial ligation (sphenopalatine artery)
  • Interventional radiology embolization for refractory posterior epistaxis or for those who are poor surgical candidates
  • Reverse anticoagulation as appropriate (vitamin K for warfarin, andexanet/idarucizumab/PCC for DOACs) only if bleeding is life-threatening and after risk-benefit weighing
  • Treat hypertension if very severely elevated, but BP control is not first-line therapy for the bleed
  • Prevention: humidification, saline gel/spray, petrolatum to nares, avoid digital trauma; for HHT — bevacizumab nasal spray or systemic, laser photocoagulation

Complications

  • Hypovolemic shock with substantial blood loss
  • Aspiration of blood
  • Septal hematoma → septal perforation or saddle nose if not drained
  • Septal perforation from bilateral cautery
  • Pressure necrosis or toxic shock syndrome from prolonged packing
  • Nasovagal reflex with posterior packing (bradycardia, hypotension)
  • Vascular complications from embolization (stroke, blindness)

PANCE pearls

  • LEAN FORWARD — leaning back causes blood to be swallowed (nausea, vomiting, aspiration) and obscures volume estimation.
  • Pinch the SOFT cartilaginous portion of the nose (not the bony bridge) for 10-15 minutes continuously.
  • Cauterize ONLY one side of the septum at a time and avoid both sides at the same visit — bilateral cautery risks septal perforation.
  • Posterior epistaxis = admit and monitor on telemetry; high risk of hemodynamic instability and nasovagal events.
  • In an adolescent male with recurrent unilateral epistaxis + nasal obstruction — suspect juvenile nasopharyngeal angiofibroma. Image first; biopsy can cause catastrophic bleeding.
  • Septal hematoma after trauma must be drained urgently or it causes cartilage necrosis (saddle-nose).

References

  • AAO-HNS 2020 — Tunkel DE et al. Clinical Practice Guideline: Nosebleed (Epistaxis). Otolaryngol Head Neck Surg 2020;162(1S):S1-S38
  • AAFP — Krulewitz NA, Fix ML. Epistaxis. Emerg Med Clin North Am 2019;37(1):29-39

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