Epistaxis

Epistaxis is the medical term for a nosebleed, which is a common presenting concern in the emergency room. The most common site of bleeding is the Kiesselbach plexus, where the vessels supplying the nasal mucosa anastomose, resulting in bleeding from the nostrils (anterior epistaxis). Posterior epistaxis is less common and may not be clinically apparent because blood may flow down the throat. The most common causes of epistaxis include nose picking, a foreign body in the nasal cavity, and a dry nose. Usually, bleeding is self-limited, but severe epistaxis may occur in patients with posterior bleeding sites, systemic conditions such as hypertension or bleeding disorders, and/or following traumatic injury. Hereditary hemorrhagic telangiectasia, which is an autosomal dominant vasculopathy characterized by telangiectasia on the skin and mucosa, may cause recurrent epistaxis. Immediate measures to control epistaxis include elevating the patient's head and tilting it forward and pinching the nose. For continued bleeding from an anterior site, local hemostatic measures (i.e., vasoconstrictors and nasal cautery) are used. If hemostasis cannot be achieved with these measures, the nasal cavity must be packed and the patient referred to an ENT surgeon.

In most cases, the exact cause of epistaxis remains unknown (idiopathic epistaxis). While a single episode of epistaxis usually does not require any investigation, recurrent epistaxis must be investigated for an underlying cause (e.g., a bleeding disorder).

Local causes ^[1][2]

• Nasal irritation
  • Nose picking (most common cause)
  • Foreign intranasal body
  • Dry nose (rhinitis sicca)
  • CPAP therapy
  • Excessive nose blowing
  • Intranasal drug use (e.g., cocaine, topical corticosteroids)
• Vascular malformations
  • Hereditary hemorrhagic telangiectasia (HHT)
  • Nasal hemangioma
• Inflammatory/granulomatous disorders
  • Allergic rhinitis
  • Bacterial sinusitis
  • Rhinosporidiosis
• Craniofacial trauma
  • Blunt trauma (e.g., a fist punch to the nose)
  • Nasal and septal fractures
  • Zygomatic, maxillary, or frontal bone fracture
  • Basal skull fractures
• Nasal septal defects
  • Deviated nasal septum
  • Septal spurs
  • Septal perforation
• Tumors of the nasopharynx and/or paranasal sinuses
  • Juvenile nasopharyngeal angiofibroma
  • Squamous cell carcinoma

Systemic causes ^[1][3]

• Bleeding disorders
  • Von Willebrand disease
  • Severe thrombocytopenia; (e.g., ITP, leukemia, dengue)
  • Hemophilia
  • Anticoagulant and/or aspirin therapy
• Vascular causes
  • Hypertension
  • Granulomatosis with polyangiitis
  • Carotid artery aneurysm

Posterior epistaxis may be a sign of life-threatening hemorrhages.

To remember the vessels that form the Kiesselbach plexus, think of LEGS: Labial (superior), Ethmoidal (anterior), Greater palatine, and Sphenopalatine arteries.

Immediate management ^[7][8][9]

• Use standard precautions to avoid exposure to body fluids.
• Stabilize patients using the ABCDE approach, including:
  • Difficult airway management in patients with signs of airway compromise
  • Immediate hemodynamic support for hemorrhagic shock
• Keep the patient's head elevated and tilted forward.
• Control bleeding by applying uninterrupted, bilateral pressure.
  • Clear the nose of blood clots.
  • Pinch the nasal ala against the nasal septum for 15–20 minutes.
  • Consider concurrent use of a topical vasoconstrictor (e.g., oxymetazoline ). ^[7]
• Perform anterior rhinoscopy to identify the source of bleeding.

Management of ongoing bleeding ^[7][8][9]

• For anterior epistaxis with the bleeding site identified, consider:
  • Topical vasoconstrictors (e.g., oxymetazoline, phenylephrine)
  • Nasal cautery: chemical cautery (e.g., using a silver nitrate stick) or electrocautery
• If bleeding persists or the bleeding site cannot be identified, place nasal packing.
  • Perform anterior nasal packing, e.g., with a nasal tampon, ribbon gauze, or absorbable packing.
  • If unsuccessful, consult ENT and perform posterior packing, e.g., with a nasal balloon or Foley catheter.
• For refractory or recurrent bleeding, consider arterial embolization or endoscopic ligation of the bleeding vessel, i.e.:
  • Anterior ethmoidal artery for anterior epistaxis
  • Sphenopalatine artery for posterior epistaxis

Anterior nasal packing is not sufficient to control posterior epistaxis.

Consult otolaryngology for refractory or recurrent bleeding despite nasal cautery and packing. ^[8]

Supportive treatment

• Topical anesthesia (e.g., 2% lidocaine) and analgesia as needed ^[7]
• Consider prophylactic antibiotics for patients who require packing. ^[8]
• Consider anticoagulant reversal after specialist consultation for patients with posterior and/or severe epistaxis. ^[10]

For patients on anticoagulants or antiplatelets, initiate local treatments prior to withholding or reversing anticoagulants unless there is life-threatening epistaxis. ^[8][9]

In rare cases, retained nasal packing can cause toxic shock syndrome. ^[11]

Disposition ^[7][8][9]

• Anterior epistaxis
  • Consider discharge after observation if hemostasis is successful.
  • Counsel patients on preventative measures and return precautions.
  • Arrange follow-up and ensure packing removal within 48–72 hours if discharging with nonresorbable packing.
• Posterior epistaxis
  • Admit patients with posterior packing for monitoring.
  • Consider ICU admission for patients with hemodynamic instability.

• ABCDE approach
• Bilateral pressure for 15–20 minutes
• Bleeding site identified: topical vasoconstrictors and/or cautery
• Persistent bleeding or unclear bleeding site: nasal packing
• Nasal packing unsuccessful: ENT consult
• Analgesia and local anesthesia as needed
• Anterior epistaxis: Discharge if hemostasis is successful.
• Posterior epistaxis: Admit for monitoring.

• Definition: a hereditary, systemic vasculopathy characterized by telangiectasia on the skin and mucosa, particularly in the area of the face (nose, lips, tongue)
• Pattern of inheritance: : autosomal dominant
• Pathophysiology: mutations in genes which code for TGF-β receptors (e.g., endoglin or ALK-1) → structural defects in the vessel wall → postcapillary venous pooling → formation of small and large arteriovenous shunts
• Clinical features ^[12]
  • Recurrent epistaxis
  • Telangiectasia
  • Cyanosis
• Diagnosis ^[13]
  • Diagnostic criteria for HHT (Curaçao criteria)
    • Epistaxis
    • Telangiectasias involving the skin and mucous membranes
    • Family history of HHT
    • Signs of visceral involvement (e.g., pulmonary, gastrointestinal, cerebral arteriovenous malformations or telangiectases)
  • Genetic testing
• Management
  • For epistaxis management, see “Treatment” section above.
  • Skin telangiectasia can be treated by laser therapy or by injection of sclerosing agents.
  • Embolization is used to treat large pulmonary and hepatic AV fistulas.
• Complications
  • High-output cardiac failure
  • Paradoxical emboli → brain abscess and/or stroke
  • Chronic GI bleeding and/or hematuria → anemia