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Vascular anatomy of the nasal cavity is provided in Figure 239-1. The blood supply of the nasal cavity is provided by branches of the internal and external carotid arteries. The ophthalmic artery, supplied by the internal carotid, courses along with the optic nerve until it branches into the anterior and posterior ethmoidal arteries, which exit through foramina along the medial aspect of the orbit. The anterior ethmoidal artery runs along the roof of the ethmoid sinus until it traverses the cribriform plate to supply the anterior nasal septum. The external carotid system supplies the internal maxillary artery (IMA) and the superior labial artery (from the facial artery). The superior labial branch of the facial artery joins the anterior ethmoidal and terminal branch of the sphenopalatine artery (SPA) to form Kiesselbach plexus on the anterior nasal septum, which is the source of 90% of nosebleeds and can usually be visualized with anterior rhinoscopy. The most likely source for posterior bleeds is the SPA, which is a product of the external carotid system via a terminal division of the IMA and requires endoscopic or open surgical techniques to visualize.1,2

Figure 239-1.

Arterial blood supply to the nasal cavity. The most common site of nasal hemorrhage is at Little area, located on the nasal septum. The most common origin of posterior epistaxis is from the sphenopalatine artery.

Clinical Features and General Assessment

The causes of epistaxis are numerous. Local causes of bleeding may include digital trauma, a deviated septum, neoplasia, or chemical irritants such as inhaled corticosteroids or chronic nasal cannula oxygen use. Rhinosinusitis may be a contributing factor causing mucosal irritation and friable vasculature. Systemic factors may include chronic renal insufficiency, alcoholism, hypertension, vascular malformations such as hereditary hemorrhagic telangiectasia, or any kind of coagulopathy, including warfarin administration, von Willebrand disease, or hemophilia. Malignancy can produce bone marrow suppression either from infiltration or direct toxicity from chemotherapeutic regimens, leading to thrombocytopenia and difficult-to-control nosebleeds. Many authors believe that uncontrolled, severe hypertension in the acute setting prolongs hemorrhage and makes achieving hemostasis more difficult.1–3

A directed history and physical examination is usually sufficient to evaluate the source of acute epistaxis. Ask about prior or recurrent epistaxis, duration and severity of the current episode, and laterality. Ask specifically about NSAID, warfarin, heparin, or aspirin use. Alcohol or cocaine abuse, trauma, prior head and neck procedures, as well as a personal and family history of coagulopathy, should all be addressed. Chronic unilateral epistaxis with nasal obstruction may suggest neoplasia and warrant direct visualization with endoscopy.

Initial ED assessment for epistaxis begins with a rapid primary survey addressing potential airway or hemodynamic compromise. Obtain IV access in patients with severe bleeding, and request cross-matched blood if there is hemodynamic instability. Reversal of coagulopathy with blood ...

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