Epistaxis is defined as bleeding from the nostril, nasal cavity, or nasopharynx. Nosebleeds are due to the rupture of a blood vessel within the richly perfused nasal mucosa. Rupture may be spontaneous or initiated by trauma. Nosebleeds are rarely life threatening and are usually self-limited. Epistaxis is generally divided into anterior or posterior nosebleed, depending upon location in the nasal cavity.
Approximately 60% of the population will be affected by epistaxis at some point in time, with 6% requiring professional medical attention. The etiology of epistaxis is typically idiopathic (unknown), but it may also result from tumors, trauma, medication use, or after nasal/sinus surgery. Treatment of epistaxis may include the use of local pressure, vasoconstrictor nasal sprays, chemical or electric cautery, hemostatic agents, nasal packing, embolization, and surgical arterial ligation. There is no definitive protocol for the management of epistaxis and many factors including severity of the bleeding, use of anticoagulants, and other medical conditions can play a role in which treatment is utilized.
The nasal cavity is extremely vascular. Blood is supplied via both the internal and external carotid arterial systems. The major blood arteries in the nasal cavity include the anterior and posterior ethmoid arteries and the sphenopalatine arteries. Over 90% of nose bleeds occur in the anteroinferior nasal septum in an area known as Kiesselback’s plexus (named after Wilhelm Kiesselbach, a German otolaryngologist). Keisselbach’s plexus is located over the anterior nasal septum and is formed by anastomoses of 5 arteries:
- Anterior ethmoidal artery (from the ophthalmic artery) (Figure 1)
- Posterior ethmoidal artery (from the ophthalmic artery)
- Sphenopalatine artery (terminal branch of the maxillary artery) (Figure 2)
- Greater palatine artery (from the maxillary artery)
- Septal branch of the superior labial artery (from the facial artery)
Approximately 5% to 10% of epistaxis is estimated to arise from the posterior nasal cavity, in an area known as Woodruff’s plexus. Woodruff’s plexus is located over the posterior middle turbinate and is primarily made up of anastamoses of branches of the internal maxillary artery, namely, the posterior nasal, sphenopalatine, and ascending pharyngeal arteries. Posterior bleeds usually originate from the lateral wall and more rarely from the nasal septum.
Causes of epistaxis can be divided into local causes (eg, trauma, mucosal irritation, septal abnormality, inflammatory diseases, tumors), systemic causes (eg, blood dyscrasias, arteriosclerosis, hereditary hemorrhagic telangiectasia), and idiopathic (unknown) causes. Local trauma is the most common cause followed by facial trauma, foreign bodies, nasal or sinus infections, and prolonged inhalation of dry air. Tumors and vascular malformations are also possible causes of nose bleeds. Epistaxis is also associated with septal perforations (a hole in the dividing wall between the two sides of the nose).
Trauma to the lining of the nose and septum is a frequent cause of epistaxis. Nose picking and repeated irritation caused by the tips of nasal spray bottles commonly give rise to many anterior nose bleeds. Certainly, traumatic deformation and fractures of the nose and surrounding structures can cause bleeding. Another common cause of nosebleeds is due to infection and mucosal inflammation. Sinusitis, upper respiratory tract infections, and allergies can damage the respiratory epithelium to the point that it becomes friable and irritated. Additionaly, septal deviations, nasal fractures, and septal perforations can be a cause of irregular nasal airflow causing dryness and bleeding in some cases. Iatrogenic causes such as endoscopic sinus surgery, skull base surgery, and orbital surgery can also be a cause of severe epistaxis. Tumors of the nasal cavity, sinuses, and nasopharynx can also give rise to recurrent bleeding. In general recurrent unilateral epistaxis should be evaluated by endoscopy with or without imaging studies to screen for a tumor.
Hypertension, hereditary hemorrhagic telangiectasia, use of anticoagulants such as aspirin, clopidogrel, warfarin, and a variety of conditions causing vasculitis such as Wegener’s granulomatosis are common systemic factors associated with epistaxis. Epistaxis is also associated with blood dyscrasias, patients with lymphoproliforative disorders, immunodeficiency, and liver failure. Thrombocytopenia is associated with nasal bleeding. There can be spontaneous mucous membrane bleeding at platelet levels of 10-20,000. Platelet deficiency can also result from use of chemotherapy, antibiotics, malignancies, hypersplenism, and some drugs. Platelet dysfunction can occur in patients with liver failure, kidney failure, vitamin C deficiency and in patients taking aspirin and non-steroidal anti-inflammatory medications (like ibuprofen).
Clotting factor abnormalities can result in frequent, recurring epistaxis. Bleeding disorders such as Von Willabrand’s disease (most common), Factor VIII deficiency (Hemophilia A), Factor IX deficiency (Hemophilia B), and Factor XI deficiency are all common primary coagulopathies. Additionally, patients with recurrent nosebleeds should be questioned about the use of complementary and alternative medicines such as Ginkgo Biloba and Vitamin E, which may increase their risk of bleeding.
Direct pressure is usually effective for stopping epistaxis by applying pressure to Kiesselbach’s area on the anterior nasal septum. Nasal decongestants such as oxymetazoline (Afrin) or neosynephrine may also be used. Chemical cauterization with silver nitrate is also used for control of epistaxis unresponsive to local application of pressure. This can be done in the office with topical anesthesia. When these methods are not effective, anterior or posterior packing might be necessary. Packing can be absorbable or non-absorbable.
For complicated nose bleeds, another method of treatment is angiographic embolization of the internal maxillary artery. This procedure deploys a coil into the bleeding vessel to stop the flow of blood. It has a success rate of 71% to 95%, but the procedure carries risk of stroke, ophthalmoplegia, facial nerve palsy, and hematomas at the catheterization site. Also revascularization after embolization is not uncommon.
Direct surgical ligation is an alternative to embolization. Numerous approaches and techniques have been utilized and described. We generally employ an endoscopic approach for ligation of the sphenopalatine artery in the case of posterior epistaxis. In the case of refractory anterior epistaxis, we may use either endoscopic or open approaches.
In general, non-surgical treatments are effective for control of most cases of epistaxis. Nasal packing, chemical cautery, and use of nasal decongest sprays represent the first line of treatment for a majority of nasal bleeding. For recalcitrant epistaxis, embolization and surgical ligation is sometimes required. More recently, endoscopic approaches to the sphenopalatine artery and ethmoid arteries have been utilized with promising results.