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Background

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 artery.
View Media Gallery

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.

Anatomy
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
ethmoidal artery exits the orbit through the posterior ethmoidal foramen, located 2-9 mm anterior
to the optic canal. The larger anterior ethmoidal artery leaves the orbit through the anterior
ethmoidal foramen (see the image below).

Nasal vascular anatomy


View Media Gallery

The anterior and posterior ethmoidal arteries cross the ethmoidal 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 Littles 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.

Pathophysiology

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 Littles area, where the Kiesselbach
plexus forms on the septum. [8, 9] The Kiesselbach plexus is where vessels from both the ICA
(anterior and posterior ethmoidal 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.

Etiology

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]

Trauma
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.

Drugs
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.

Inflammation
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.

Tumors
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.

Migraine
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]

Hypertension
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]

Epidemiology

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%).

Prognosis

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.

History

Controlling significant bleeding or hemodynamic instability should always take precedence over
obtaining a lengthy history.

Ask specific questions about the severity, frequency, duration, and laterality of the nosebleed.
Determine whether the bleed occurs after exercise or during sleep or is associated with a
migraine. Determine whether hematemesis or melena has occurred because posterior bleeding in
particular may present in this fashion.
Inquire about precipitating and aggravating factors and methods used to stop the bleeding. Most
nosebleeds are reported as spontaneous events and are frequently related to nose picking or other
trauma; therefore, investigate the various possibilities.

Foreign bodies inserted in the nose may also present with epistaxis, but bleeding may be less and
accompanied by foul or purulent discharge if the object has been retained for some time. A
unilateral nasal discharge suggests the presence of a foreign body.

Children easily can insert small batteries from electronic devices (eg, calculators, watches,
handheld video games) into their nostrils. Not only can local irritation and bleeding result, but
these can leak and cause a chemical alkali burn that may result in local tissue necrosis. Severe
complications (eg, nasal stenosis) can result from batteries. Removal is a priority; removing the
batteries within 4 hours of insertion is best.

In addition to obtaining a head and neck history with an emphasis on nasal symptoms, elicit a
general medical history concerning relevant medical conditions, current medications, and
smoking and drinking habits.

Inquire about previous epistaxis, hypertension, hepatic or other systemic disease, easy bruising,
or prolonged bleeding after minor surgical procedures. A history of frequent recurrent
nosebleeds, easy bruising, or other bleeding episodes should make the clinician suspicious of a
systemic cause and prompt a hematologic workup. Obtain any family history of bleeding
disorders or leukemia.

Children with severe epistaxis are more likely to have required nasal cauterization, an underlying
coagulopathy, a positive family history of bleeding, and anemia. Although unusual, children with
bleeding disorders (eg, von Willebrand disease) can occasionally have normal coagulation
profiles. More than 1 sample may be required to notice the abnormality due to biologic
variability throughout the day.

Use of medicationsespecially aspirin, NSAIDs, warfarin, heparin, ticlopidine, and


dipyridamoleshould be documented, as these not only predispose to epistaxis but make
treatment more difficult. Particularly in children, include investigation of suspicion of accidental
ingestion (eg, accidental ingestion of rat poison in toddlers).

Physical Examination

Before evaluating a patient with epistaxis, have sufficient illumination, adequate suction, all the
necessary topical medications, and cauterization and packing materials ready. Remove all
packings, even though bleeding may not be active. The importance of obtaining adequate
anesthesia and vasoconstriction if time permits cannot be overemphasized. A comfortable patient
tends to be more cooperative, allowing for better examination and more effective treatment.
Perform a thorough and methodical examination of the nasal cavity. Blowing the nose decreases
the effects of local fibrinolysis and removes clots, permitting a better examination. Application of
a vasoconstrictor (eg, 0.05% oxymetazoline) before the examination may reduce hemorrhage and
help to pinpoint the precise bleeding site. A topical anesthetic (eg, 4% aqueous lidocaine) reduces
pain associated with the examination and nasal packing. Clots are then suctioned out to permit a
thorough examination.

Gently insert a nasal speculum (see the image below) and spread the naris vertically. Begin the
examination with inspection, looking specifically for any obvious bleeding site on the septum
that may be amenable to direct pressure or cautery. This permits visualization of most anterior
bleeding sources. Anterior bleeds from the nasal septum are most common type, and the site can
frequently be identified if bleeding is active.

Nasal speculum.
View Media Gallery

If an anterior source cannot be visualized, if the hemorrhage is from both nares, or if constant
dripping of blood is seen in the posterior pharynx, the bleeding may be from a posterior site.
After placement of an anterior pack, and, if bleeding is noted in the pharynx with the anterior
pack in place, strongly consider a posterior bleed.

Massive epistaxis may be confused with hemoptysis or hematemesis. Blood dripping from the
posterior nasopharynx confirms a nasal source. Approximately 90% of nosebleeds can be
visualized in the anterior portion of the nasal cavity.

Fiberoptic endoscopy may be performed with a flexible or (preferably) rigid endoscope to


inspect the entire nasal cavity, including the nasopharynx. The rigid endoscope is preferred
because of its superior optics and its ability to allow endoscopic suction and cauterization.
Examine the skin for evidence of bruises or petechiae that may indicate an underlying
hematologic abnormality.

Assess vital signs. Although high blood pressure rarely, if ever, causes epistaxis on its own, it
may impede clotting. Check blood pressure, and complete a workup if high blood pressure is
present. Persistent tachycardia must be recognized as an early indicator of significant blood loss
requiring intravenous (IV) fluid replacement and, potentially, transfusion.

Complications
Complications of epistaxis may include the following:

Sinusitis

Septal hematoma/perforation

External nasal deformity

Mucosal pressure necrosis

Vasovagal episode

Balloon migration

Aspiration

Diagnostic Considerations
Recurrent epistaxis in children could be caused by a foreign body, especially if the nosebleeds
are accompanied by symptoms of unilateral nasal congestion and purulent rhinorrhea. Delayed
epistaxis in a trauma patient may signal the presence of a traumatic aneurysm.

Other conditions to be considered include the following:

Chemical irritants

Hepatic failure

Leukemia

Thrombocytopenia

Heparin toxicity
Ticlopidine toxicity

Dipyridamole toxicity

Trauma

Tumor

Differential Diagnoses
Allergic Rhinitis

Barotrauma

Cocaine Toxicity

Coumarin Plant Poisoning

Disseminated Intravascular Coagulation in Emergency Medicine

Emergent Treatment of Endometriosis

Nasal Foreign Bodies

Nonsteroidal Anti-inflammatory Drug (NSAID) Toxicity

Pediatric Osler-Weber-Rendu Syndrome

Rodenticide Toxicity

Salicylate Toxicity

Sinusitis Imaging

Type A Hemophilia

Type B Hemophilia

von Willebrand Disease

Warfarin and Superwarfarin Toxicity

Approach Considerations
For the most part, laboratory studies are not needed or helpful for first-time nosebleeds or
infrequent recurrences with a good history of nose picking or trauma to the nose. However, they
are recommended if major bleeding is present or if a coagulopathy is suspected.

Laboratory Tests

Laboratory tests to evaluate the patients condition and underlying medical problems may be
ordered depending on the clinical picture at the time of presentation. If the bleeding is minor and
not recurrent, then a laboratory evaluation may not be needed.

If a history of persistent heavy bleeding is present, obtain a hematocrit count and type and cross-
match. If a history of recurrent epistaxis, a platelet disorder, or neoplasia is present, obtain a
complete blood count (CBC) with differential. The bleeding time is an excellent screening test if
suspicion of a bleeding disorder is present. Obtain the international normalized ratio
(INR)/prothrombin time (PT) if the patient is taking warfarin or if liver disease is suspected.
Obtain the activated partial thromboplastin time (aPTT) as necessary.

Other Studies

Direct visualization with a good directed light source, a nasal speculum, and nasal suction should
be sufficient in most patients. However, computed tomography (CT) scanning, magnetic
resonance imaging (MRI) or both may be indicated to evaluate the surgical anatomy and to
determine the presence and extent of rhinosinusitis, foreign bodies, and neoplasms.
Nasopharyngoscopy may also be performed if a tumor is the suspected cause of bleeding.

Sinus films are rarely indicated for a nosebleed. Angiography is rarely indicated.

Approach Considerations
When medical attention is needed for epistaxis, it is usually because of the problem is either
recurrent or severe. Treatment depends on the clinical picture, the experience of the treating
physician, and the availability of ancillary services.

In most patients with epistaxis, the bleeding responds to cauterization, nasal packing, or both.
For those who have recurrent or severe bleeding for which medical therapy has failed, various
surgical options are available. After surgery or embolization, patients should be closely observed
for any complications or signs of rebleeding.

Medical approaches to the treatment of epistaxis may include the following:

Adequate pain control in patients with nasal packing, especially in those with posterior
packing (However, the need of adequate pain control has to be balanced with the concern
over hypoventilation in the patient with posterior pack.)

Oral and topical antibiotics to prevent rhinosinusitis and possibly toxic shock syndrome
Avoidance of aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs)

Medications to control underlying medical problems (eg, hypertension, vitamin K


deficiency) in consultation with other specialists

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

Manual Hemostasis

Initial treatment begins with direct pressure. The nostrils are squeezed together for 5-30 minutes
straight, without frequent peeking to see if the bleeding is controlled. Usually, 5-10 minutes is
sufficient.

Patients should keep their heads elevated but not hyperextended because hyperextension may
cause bleeding into the pharynx and possible aspiration. This maneuver works more than 90% of
the time.

If direct pressure is not sufficient, gauze moistened with epinephrine at a ratio of 1:10,000 or
phenylephrine (Neo-Synephrine) may be placed in the affected nostril to help vasoconstrict and
achieve hemostasis.

References
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. Garca Callejo FJ, Muoz Fernndez N, Achiques Martnez MT, Fras 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].

27. Wirsching KE, Haubner F, Khnel TS. Influence of temporary nasal occlusion (tNO) on
epistaxis frequency in patients with hereditary hemorrhagic telangiectasia (HHT). Eur
Arch Otorhinolaryngol. 2017 Jan 9. [Medline].

28. Contis A, Gensous N, Viallard JF, Goizet C, Leaute-Labreze C, Duffau P. Efficacy and
safety of propranolol for epistaxis in Hereditary Hemorrhagic Telangiectasia (HHT);
retrospective, then prospective study, in a total of 21 patients. Clin Otolaryngol. 2016
Dec 29. [Medline].

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