Etiology
Approximately 90% of epistaxis is caused by bleeding originating from blood vessels in Little's area, located at the anterior inferior septum.[3]
This area contains a confluence of vessels from the main arterial supply of the nose (sphenopalatine artery, anterior and posterior ethmoid arteries, greater palatine artery and superior labial artery) called the Kiesselbach plexus.[3][10]
Posterior epistaxis originates from the posterior nasal cavity or nasopharynx, most commonly from the posterior or anterior ethmoid arteries or the sphenopalatine artery.[1][2][3][10]
Vessels may bleed due to:
Mucosal compromise
Impairment of vasoconstriction and inadequate activation of the clotting mechanism.
Neoplasm represents an atypical and, if located in a paranasal sinus, elusive cause of nosebleed and includes:
Sinus tumors, malignant: squamous cell carcinoma (SCC), sinonasal undifferentiated carcinoma (SNUC), adenocarcinoma, adenoid cystic carcinoma, melanoma, lymphoma.
The most common malignancies to present with epistaxis are mucosal melanoma and SCC.[11]
Sinus tumors, benign: juvenile nasopharyngeal angiofibroma (JNA), inverted papilloma, choanal antral polyp.
The most common benign neoplasm to present with epistaxis is JNA; a rare nasopharyngeal tumor of adolescent men that can produce significant unilateral hemorrhage in the presence of nasal obstruction.[5][12][13]
Adults with nosebleed often have elevated blood pressure (BP), although difficulty exists in determining whether hypertension is a causative factor or whether the elevated BP is secondary to anxiety. Conclusive proof is lacking.[5][14][15][16] A Korean population cohort study of more than 70,000 people found that those with hypertension appeared to have an increased risk of epistaxis, had more emergency department visits, and required more posterior nasal packing procedures than people without hypertension.[17]
Whether atherosclerotic change, secondary to hypertension, increases vessel fragility is also debated. In the manner that elevated BP impairs intraoperative surgical hemostasis, it may be reasonably inferred that it would similarly prolong and worsen active nasal bleeding.[14][15]
Pathophysiology
The physiologic demands of the nose require a robust blood supply. Loss of mucosal integrity, for any reason, exposes underlying vessels, which may be violated and bleed.
Vasoconstriction and activation of the clotting mechanism normally regains hemostasis. Impairment of these processes may prolong bleeding.
Classification
Commonly used classification according to site of bleeding source
Anterior epistaxis:
Accounts for approximately 90% of nosebleeds.
Usually originates from the Kiesselbach plexus (also known as Little’s area), a rich vascular anastomosis located at the anterior nasal septum; comprised of branches from anterior ethmoid, greater palatine, superior labial, and sphenopalatine arteries.
Posterior epistaxis:
Originates from the posterior nasal cavity, usually branches of sphenopalatine or from an area known as Woodruff’s plexus (a confluence of vessels posterior to the inferior turbinate) or nasopharynx.[1][2]
Posterior nasal and nasopharyngeal vessels often have a larger caliber and may produce more aggressive bleeding.
Commonly used classification according to cause of bleeding
Minor vessel bleeding due to erosion or injury to mucosa resulting in blood vessel exposure.
Trauma with vessel laceration in atypical areas of the nose, such as lateral nasal wall with nasal fracture.
Neoplasm causing bleeding. The diagnosis should be considered when epistaxis occurs without a typical anterior or posterior source or occurs in the setting of nasal obstruction.
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