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
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
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