Clinical meaning
Epistaxis occurs from rupture of blood vessels within the richly vascular nasal mucosa. Anterior epistaxis (90% of cases) originates from Kiesselbach plexus (Little's area) on the anterior nasal septum, where branches of the anterior ethmoidal, sphenopalatine, greater palatine, and superior labial arteries anastomose. The thin mucosal layer over this vascular plexus is vulnerable to drying, trauma, and inflammation. Posterior epistaxis (10%) arises from branches of the sphenopalatine artery in the posterior nasal cavity and is more dangerous due to higher-pressure arterial bleeding that may not be visible anteriorly, instead flowing down the posterior pharynx causing aspiration risk. Hypertension contributes to epistaxis severity by increasing arterial pressure against weakened vessel walls, though it more commonly prolongs bleeding than initiates it. Coagulopathy from anticoagulant therapy, liver disease, or platelet disorders impairs clot formation at the bleeding site. Hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu syndrome) causes arteriovenous malformations in the nasal mucosa, leading to recurrent, difficult-to-control epistaxis.