Jeffrey D. Suh MD
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 divided into 2 categories,based on the site of bleeding, anterior or posterior,.
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 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.
Figure 1: Endoscopic View of the Anterior Ethmoid Artery. Image courtesy of Drs. Alexander Chiu, MD and James N. Palmer, MD.
Figure 2: Endoscopic View of the Nasal Septal Artery. Legend: ST: Septum, NS: Nasal Septum, *: Nasal Septal Branch of the Sphenopalatine Artery. Image courtesy of Dr. Vijay Ramakrishnan, MD.
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 alsoimportant causes of nose bleeds. Epistaxis is also associated with septal perforations.
Trauma to the turbinate mucosa 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 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 after 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 NSAIDs.
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. Nasal decongestants such as oxymetazoline or neosynephrine may also be used. Chemical cauterization with silver nitrate is also used for control of epistaxis unresponsive to local application of pressure. 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. 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. The traditional approach for ligation of the anterior and posterior ethmoids artery is via a Lynch incision, but other approaches have been described, including a trancaruncular approach. The traditional way to ligate the internal maxillary artery in the pterygopalatine fossa is through a Caldwell-Luc. Transantral ligation of the internal maxillary artery was described in 1965 by Chandler and Serrins, and has a reported failure rate of 10% to 15%. More recently, Budrovich and Saetti described endoscopic ligation of the SPA in 1992 (Figure 3). It has been proposed as a more ideal treatment as it ligates the major arterial supply to the nasal cavity at a distal point, and therefore minimizes the risk of refractory bleeding from collateral circulation and spares the patient from a transoral incision. A review found a 92% to 100% success rate with endoscopic SPA ligation. Failures of this technique are attributed to the failure to identify all branches of the SPA, or the significant dissection that may be required in a patient with suboptimal coagulation properties.
Figure 3: Endoscopic view of a left sphenopalatine artery (arrow) that is being ligated with a surgical clip. Image courtesy of Dr. Kevin C. Welch.
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.
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