Medscape is available in 5 Language Editions – Choose your Edition here.



  • Author: Quoc A Nguyen, MD; Chief Editor: Arlen D Meyers, MD, MBA  more...
Updated: May 04, 2016


Epistaxis, or bleeding from the nose, is a common complaint.[1] It is rarely life threatening but may cause significant concern, especially among parents of small children.[2] Most nosebleeds are benign, self-limiting, and spontaneous, but some can be recurrent. Many uncommon causes are also noted.

Epistaxis can be divided into 2 categories, anterior bleeds and posterior bleeds, on the basis of the site where the bleeding originates (see the image below).

Posterior epistaxis from the left sphenopalatine a Posterior epistaxis from the left sphenopalatine artery.

The true prevalence of epistaxis is not known, because most episodes are self-limited and thus are not reported. When medical attention is needed, it is usually because of either the recurrent or severe nature of the problem. Treatment depends on the clinical picture, the experience of the treating physician, and the availability of ancillary services.[3, 4, 5, 6]

Also see Anterior Epistaxis Nasal Pack, Posterior Epistaxis Nasal Pack, and Surgery for Pediatric Epistaxis.



The nose has a rich vascular supply, with substantial contributions from the internal carotid artery (ICA) and the external carotid artery (ECA).

The ECA system supplies blood to the nose via the facial and internal maxillary arteries. The superior labial artery is one of the terminal branches of the facial artery. This artery subsequently contributes to the blood supply of the anterior nasal floor and anterior septum through a septal branch.

The internal maxillary artery enters the pterygomaxillary fossa and divides into 6 branches: posterior superior alveolar, descending palatine, infraorbital, sphenopalatine, pterygoid canal, and pharyngeal.

The descending palatine artery descends through the greater palatine canal and supplies the lateral nasal wall. It then returns to the nose via a branch in the incisive foramen to provide blood to the anterior septum. The sphenopalatine artery enters the nose near the posterior attachment of the middle turbinate to supply the lateral nasal wall. It also gives off a branch to provide blood supply to the septum.

The ICA contributes to nasal vascularity through the ophthalmic artery. This artery enters the bony orbit via the superior orbital fissure and divides into several branches. The posterior ethmoid artery exits the orbit through the posterior ethmoid foramen, located 2-9 mm anterior to the optic canal. The larger anterior ethmoid artery leaves the orbit through the anterior ethmoid foramen.

The anterior and posterior ethmoid arteries cross the ethmoid roof to enter the anterior cranial fossa and then descend into the nasal cavity through the cribriform plate. Here, they divide into lateral and septal branches to supply the lateral nasal wall and the septum.

The Kiesselbach plexus, or Little’s area, is an anastomotic network of vessels located on the anterior cartilaginous septum. It receives blood supply from both the ICA and the ECA.[7] Many of the arteries supplying the septum have anastomotic connections at this site.



Bleeding typically occurs when the mucosa is eroded and vessels become exposed and subsequently break.

More than 90% of bleeds occur anteriorly and arise from Little’s area, where the Kiesselbach plexus forms on the septum.[8, 9] The Kiesselbach plexus is where vessels from both the ICA (anterior and posterior ethmoid arteries) and the ECA (sphenopalatine and branches of the internal maxillary arteries) converge. These capillary or venous bleeds provide a constant ooze, rather than the profuse pumping of blood observed from an arterial origin. Anterior bleeding may also originate anterior to the inferior turbinate.

Posterior bleeds arise further back in the nasal cavity, are usually more profuse, and are often of arterial origin (eg, from branches of the sphenopalatine artery in the posterior nasal cavity or nasopharynx). A posterior source presents a greater risk of airway compromise, aspiration of blood, and greater difficulty controlling bleeding.



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 causes. Local trauma is the most common cause, followed by facial trauma, foreign bodies, nasal or sinus infections, and prolonged inhalation of dry air. Children usually present with epistaxis due to local irritation or recent upper respiratory infection (URI).

In a retrospective cohort study of 2405 patients with epistaxis (3666 total episodes), Purkey et al used multivariate analysis to identify a series of risk factors for nosebleeds. The likelihood of epistaxis was found to increase in patients with allergic rhinitis, chronic sinusitis, hypertension, hematologic malignancy, coagulopathy, or, as mentioned, hereditary hemorrhagic telangiectasia. The investigators also found increased nosebleeds in association with older age and colder weather.[10]


Self-induced trauma from repeated nasal picking can cause anterior septal mucosal ulceration and bleeding. This scenario is frequently observed in young children. Nasal foreign bodies that cause local trauma (eg, nasogastric and nasotracheal tubes) can be responsible for rare cases of epistaxis.

Acute facial and nasal trauma commonly leads to epistaxis. If the bleeding is from minor mucosal laceration, it is usually limited. However, extensive facial trauma can result in severe bleeding requiring nasal packing. In these patients, delayed epistaxis may signal the presence of a traumatic aneurysm.

Patients undergoing nasal surgery should be warned of the potential for epistaxis. As with nasal trauma, bleeding can range from minor (due to mucosal laceration) to severe (due to transection of a major vessel).

Dry weather

Low humidity may lead to mucosal irritation. Epistaxis is more prevalent in dry climates and during cold weather due to the dehumidification of the nasal mucosa by home heating systems.


Topical nasal drugs such as antihistamines and corticosteroids may cause mucosal irritation. Especially when applied directly to the nasal septum instead of the lateral walls, they may cause mild epistaxis. Medications such as nonsteroidal anti-inflammatory drugs (NSAIDs) are also frequently involved.

Septal abnormality

Septal deviations (deviated nasal septum) and spurs may disrupt the normal nasal airflow, leading to dryness and epistaxis. The bleeding sites are usually located anterior to the spurs in most patients. The edges of septal perforations frequently harbor crusting and are common sources of epistaxis.


Bacterial, viral, and allergic rhinosinusitis causes mucosal inflammation and may lead to epistaxis. Bleeding in these cases is usually minor and frequently manifests as blood-streaked nasal discharge.

Granulomatosis diseases such as sarcoidosis, Wegener granulomatosis, tuberculosis, syphilis, and rhinoscleroma often lead to crusting and friable mucosa and may be a cause of recurrent epistaxis.

Young infants with gastroesophageal reflux into the nose may have epistaxis secondary to inflammation.


Benign and malignant tumors can manifest as epistaxis. Affected patients may also present with signs and symptoms of nasal obstruction and rhinosinusitis, often unilateral.

Intranasal rhabdomyosarcoma, although rare, often begins in the nasal, orbital, or sinus area in children. Juvenile nasal angiofibroma in adolescent males may cause severe nasal bleeding as the initial symptom.

Blood dyscrasias

Congenital coagulopathies should be suspected in individuals with a positive family history, easy bruising, or prolonged bleeding from minor trauma or surgery. Examples of congenital bleeding disorders include hemophilia and von Willebrand disease.[7]

Acquired coagulopathies can be primary (due to the diseases) or secondary (due to their treatments). Among the more common acquired coagulopathies are thrombocytopenia and liver disease with its consequential reduction in coagulation factors. Even in the absence of liver disease, alcoholism has also been associated with coagulopathy and epistaxis. Oral anticoagulants predispose to epistaxis.

Vascular abnormalities

Arteriosclerotic vascular disease is considered a reason for the higher prevalence of epistaxis in elderly individuals.

Hereditary hemorrhagic telangiectasia (HHT; also known as Osler-Weber-Rendu syndrome) is an autosomal dominant disease associated with recurrent bleeding from vascular anomalies. The condition can affect vessels ranging from capillaries to arteries, leading to the formation of telangiectasias and arteriovenous malformations. Pathologic examination of these lesions reveals a lack of elastic or muscular tissue in the vessel wall. As a result, bleeding can occur easily from minor trauma and tends not to stop spontaneously.

Various organ systems such as the respiratory, gastrointestinal, and genitourinary systems may be involved. The epistaxis in these individuals is variable in severity but is almost universally recurrent.

Other vascular abnormalities that predispose to epistaxis include vascular neoplasms, aneurysms, and endometriosis.


Children with migraine headaches have a higher incidence of recurrent epistaxis than children without the disease.[11] The Kiesselbach plexus, which is part of the trigeminovascular system, has been implicated in the pathogenesis of migraine.[12]


The relationship between hypertension and epistaxis is often misunderstood. Patients with epistaxis commonly present with an elevated blood pressure. Epistaxis is more common in hypertensive patients, perhaps owing to vascular fragility from long-standing disease.

Hypertension, however, is rarely a direct cause of epistaxis. More commonly, epistaxis and the associated anxiety cause an acute elevation of blood pressure. Therapy, therefore, should be focused on controlling hemorrhage and reducing anxiety as primary means of blood pressure reduction.

A study by Sarhan and Algamal, which included 40 patients with epistaxis and 40 controls, reported that the number of attacks of epistaxis was higher in patients with a history of hypertension, but the investigators were unable to determine whether a definite link existed between nosebleeds and high blood pressure. They did find, however, that control of epistaxis was more difficult in hypertensive patients; patients whose systolic blood pressure was higher at presentation tended to need management with packing, balloon devices, or cauterization.[13]

Excessive coughing causing nasal venous hypertension may be observed in pertussis or cystic fibrosis.

Idiopathic causes

The cause of epistaxis is not always readily identifiable. Approximately 10% of patients with epistaxis have no identifiable causes even after a thorough evaluation.[14]



The frequency of epistaxis is difficult to determine because most episodes resolve with self-treatment and, therefore, are not reported.[15] However, when multiple sources are reviewed, the lifelong incidence of epistaxis in the general population is about 60%, with fewer than 10% seeking medical attention.[7, 16, 15]

The age distribution is bimodal, with peaks in young children (2-10 y) and older individuals (50-80 y). Epistaxis is unusual in infants in the absence of a coagulopathy or nasal pathology (eg, choanal atresia, neoplasm). Local trauma (eg, nose picking) does not occur until later in the toddler years. Older children and adolescents also have a less frequent incidence. Consider cocaine abuse in adolescent patients.

Prevalence of epistaxis tends to be higher in males (58%) than in females (42%).



For most of the general population, epistaxis is merely a nuisance. However, the problem can occasionally be life-threatening, especially in elderly patients and in those patients with underlying medical problems. Fortunately, mortality is rare and is usually due to complications from hypovolemia, with severe hemorrhage or underlying disease states.

Overall, the prognosis is good but variable; with proper treatment, it is excellent. When adequate supportive care is provided and underlying medical problems are controlled, most patients are unlikely to experience any rebleeding. Others may have minor recurrences that resolve spontaneously or with minimal self-treatment. A small percentage of patients may require repacking or more aggressive treatments.

Patients with epistaxis that occurs from dry membranes or minor trauma do well, with no long-term effects. Patients with HHT tend to have multiple recurrences regardless of the treatment modality. Patients with bleeding from a hematologic problem or cancer have a variable prognosis. Patients who have undergone nasal packing are subject to increased morbidity. Posterior packing can potentially cause airway compromise and respiratory depression. Packing in any location may lead to infection.


Patient Education

For patient education resources, see the Breaks, Fractures, and Dislocations Center, as well as Broken Nose.

The following precautions should be imparted to the patient:

  • Use nasal saline spray.
  • Avoid hard nose blowing or sneezing.
  • Sneeze with the mouth open.
  • Do not use nasal digital manipulation.
  • Avoid hot and spicy foods.
  • Avoid taking hot showers.
  • Avoid aspirin and other NSAIDs.

The following simple instructions for self-treatment for minor epistaxis should be provided:

  • Apply firm digital pressure for 5-10 minutes.
  • Use an ice pack.
  • Practice deep, relaxed breathing.
  • Use a topical vasoconstrictor.
Contributor Information and Disclosures

Quoc A Nguyen, MD Associate Clinical Professor, Director, Sinus and Allergy Center, Department of Otolaryngology-Head and Neck Surgery, University of California, Irvine, Medical Center

Quoc A Nguyen, MD is a member of the following medical societies: American Academy of Facial Plastic and Reconstructive Surgery, Phi Beta Kappa, American Academy of Otolaryngic Allergy, American Academy of Otolaryngology-Head and Neck Surgery, The Triological Society, American Rhinologic Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Ted L Tewfik, MD Professor of Otolaryngology-Head and Neck Surgery, Professor of Pediatric Surgery, McGill University Faculty of Medicine; Senior Staff, Montreal Children's Hospital, Montreal General Hospital, and Royal Victoria Hospital

Ted L Tewfik, MD is a member of the following medical societies: American Society of Pediatric Otolaryngology, Canadian Society of Otolaryngology-Head & Neck Surgery

Disclosure: Nothing to disclose.

Chief Editor

Arlen D Meyers, MD, MBA Professor of Otolaryngology, Dentistry, and Engineering, University of Colorado School of Medicine

Arlen D Meyers, MD, MBA is a member of the following medical societies: American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, American Head and Neck Society

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Cerescan;RxRevu;SymbiaAllergySolutions<br/>Received income in an amount equal to or greater than $250 from: Symbia<br/>Received from Allergy Solutions, Inc for board membership; Received honoraria from RxRevu for chief medical editor; Received salary from Medvoy for founder and president; Received consulting fee from Corvectra for senior medical advisor; Received ownership interest from Cerescan for consulting; Received consulting fee from Essiahealth for advisor; Received consulting fee from Carespan for advisor; Received consulting fee from Covidien for consulting.

Additional Contributors

Hassan H Ramadan, MD, MSc Professor and Vice-Chair, Department of Otolaryngology-Head and Neck Surgery, Professor, Department of Pediatrics, West Virginia University School of Medicine

Hassan H Ramadan, MD, MSc is a member of the following medical societies: American Academy of Otolaryngic Allergy, American Academy of Otolaryngology-Head and Neck Surgery, American College of Surgeons, American Rhinologic Society

Disclosure: Nothing to disclose.

  1. Traboulsi H, Alam E, Hadi U. Changing Trends in the Management of Epistaxis. Int J Otolaryngol. 2015. 2015:263987. [Medline]. [Full Text].

  2. Moreau S, De Rugy MG, Babin E, Courtheoux P, Valdazo A. Supraselective embolization in intractable epistaxis: review of 45 cases. Laryngoscope. 1998 Jun. 108(6):887-8. [Medline].

  3. Abelson TI. Epistaxis. Schaefer SD. Rhinology and Sinus Disease 1st ed. New York: Mosby; 1998. 43-50.

  4. Douglas R, Wormald PJ. Update on epistaxis. Curr Opin Otolaryngol Head Neck Surg. 2007 Jun. 15(3):180-3. [Medline].

  5. Emanuel JM. Epistaxis. Cummings CW. Otolaryngology-Head and Neck Surgery. 3rd ed. St. Louis: Mosby; 1998. 852-865.

  6. Pope LE, Hobbs CG. Epistaxis: an update on current management. Postgrad Med J. 2005 May. 81(955):309-14. [Medline]. [Full Text].

  7. Cummings CW. Epistaxis. Cummings. Otolaryngology: Head and Neck Surgery. 4th ed. Philadelphia, Pa: Elsevier, Mosby; 2005. Chap 40.

  8. Padgham N. Epistaxis: anatomical and clinical correlates. J Laryngol Otol. 1990 Apr. 104(4):308-11. [Medline].

  9. Guarisco JL, Graham HD 3rd. Epistaxis in children: causes, diagnosis, and treatment. Ear Nose Throat J. 1989 Jul. 68(7):522, 528-30, 532 passim. [Medline].

  10. Purkey MR, Seeskin Z, Chandra R. Seasonal variation and predictors of epistaxis. Laryngoscope. 2014 Mar 15. [Medline].

  11. Jarjour IT, Jarjour LK. Migraine and recurrent epistaxis in children. Pediatr Neurol. 2005 Aug. 33(2):94-7. [Medline].

  12. Knight YE, Goadsby PJ. The periaqueductal grey matter modulates trigeminovascular input: a role in migraine?. Neuroscience. 2001. 106(4):793-800. [Medline].

  13. Sarhan NA, Algamal AM. Relationship between epistaxis and hypertension: a cause and effect or coincidence?. J Saudi Heart Assoc. 2015 Apr. 27 (2):79-84. [Medline].

  14. Qureishi A, Burton MJ. Interventions for recurrent idiopathic epistaxis (nosebleeds) in children. Cochrane Database Syst Rev. 2012 Sep 12. 9:CD004461. [Medline].

  15. Gifford TO, Orlandi RR. Epistaxis. Otolaryngol Clin North Am. 2008 Jun. 41(3):525-36, viii. [Medline].

  16. Schlosser RJ. Clinical practice. Epistaxis. N Engl J Med. 2009 Feb 19. 360(8):784-9. [Medline].

  17. Durr DG. Endoscopic electrosurgical management of posterior epistaxis: shifting paradigm. J Otolaryngol. 2004 Aug. 33(4):211-6. [Medline].

  18. Newton E, Lasso A, Petrcich W, Kilty SJ. An outcomes analysis of anterior epistaxis management in the emergency department. J Otolaryngol Head Neck Surg. 2016 Apr 11. 45:24. [Medline]. [Full Text].

  19. Kundi NA, Raza M. Duration of nasal packs in the management of epistaxis. J Coll Physicians Surg Pak. 2015 Mar. 25 (3):202-5. [Medline].

  20. García Callejo FJ, Muñoz Fernández N, Achiques Martínez MT, Frías Moya-Angeler S, Montoro Elena MJ, Algarra JM. [Nasal packing in posterior epistaxis. Comparison of two methods]. Acta Otorrinolaringol Esp. 2010 May-Jun. 61(3):196-201. [Medline].

  21. Brinjikji W, Kallmes DF, Cloft HJ. Trends in Epistaxis Embolization in the United States: A Study of the Nationwide Inpatient Sample 2003-2010. J Vasc Interv Radiol. 2013 May 3. [Medline].

  22. Abdelkader M, Leong SC, White PS. Endoscopic control of the sphenopalatine artery for epistaxis: long-term results. J Laryngol Otol. 2007 Aug. 121(8):759-62. [Medline].

  23. Wormald PJ, Wee DT, van Hasselt CA. Endoscopic ligation of the sphenopalatine artery for refractory posterior epistaxis. Am J Rhinol. 2000;Jul-Aug. 14(4):261-264.

  24. Strong EB, Bell DA, Johnson LP, Jacobs JM. Intractable epistaxis: transantral ligation vs. embolization: efficacy review and cost analysis. Otolaryngol Head Neck Surg. 1995 Dec. 113(6):674-8. [Medline].

  25. Wang B, Zu QQ, Liu XL, et al. Transarterial embolization in the management of intractable epistaxis: the angiographic findings and results based on etiologies. Acta Otolaryngol. 2016 Apr 8. 1-5. [Medline].

  26. Alderman C, Corlett J, Cullis J. The treatment of recurrent epistaxis due to hereditary haemorrhagic telangiectasia with intranasal bevacizumab. Br J Haematol. 2013 May 14. [Medline].

Posterior epistaxis from the left sphenopalatine artery.
Resolved posterior epistaxis after endoscopic cauterization of the left sphenopalatine artery.
Nasal speculum.
Vaseline gauze packing.
Expandable (Merocel) packing (dry).
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.