Epistaxis

Epistaxis is the medical term for nosebleed, which is a common presenting complaint in the emergency room. The most common site of bleeding is the Kiesselbach plexus, where the vessels supplying the nasal mucosa anastomose with each other. Bleeding from this region causes blood to flow out through the nostrils (anterior epistaxis). Rarely, epistaxis may not be apparent because blood runs down the throat (posterior epistaxis). The most common causes of epistaxis include nose picking, foreign body in the nasal cavity, and a dry nose. Usually, the bleeding stops on its own, but severe epistaxis may occur with hypertension, bleeding disorders, and/or following severe traumatic injury. Hereditary hemorrhagic telangiectasia, which is an autosomal dominant vasculopathy characterized by telangiectasia on the skin and mucosa, is another cause of recurrent epistaxis. Immediate measures to control epistaxis include elevation of the upper body, application of ice packs, and nose pinching. If bleeding does not subside, the nasal cavity must be packed and the patient must be 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)
  • 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
  • Wegener granulomatosis
  • 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 measures ^[7]
  • Begin fluid resuscitation if the patient is hemodynamically unstable.
  • Keep the patient calm .
  • Elevate the patient's upper body and bend their head forward .
  • Apply cold packs and sustained, direct pressure by pinching the nose at the nostrils for 5–10 minutes in order to occlude the bleeding vessel.
  • Apply topical vasoconstrictors (e.g., oxymetazoline, phenylephrine).
• If epistaxis continues after 10–15 minutes ^[8]
  • First-line: cauterization of the bleeding vessel using silver nitrate or electrocautery
  • Second-line: nasal packing using gauze impregnated with petrolatum and antibiotics (for Staphylococcus aureus coverage). ^[3]
    • Anterior nasal packing: used for anterior epistaxis
    • Posterior nasal packing: used for posterior epistaxis; can be performed by using conventional ribbon gauze or a Foley catheter
• If epistaxis persists: arterial embolization or endoscopic ligation of the bleeding vessel
  • Anterior ethmoidal artery for anterior epistaxis
  • Sphenopalatine artery for posterior epistaxis

Nasal packs can cause toxic shock syndrome if left in place for more than 24 hours.

• 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 ^[9]
  • Recurrent epistaxis
  • Telangiectasia involving the skin and mucous membranes (including GI tract)
  • Cyanosis
• Diagnosis ^[10]
  • Diagnostic criteria for HHT (Curaçao criteria)
    • Epistaxis
    • Teleangiectasias
    • Family history of HHT
    • Signs of visceral involvement (e.g., pulmonary, gastrointestinal, cerebral)
  • 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