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Pictorial Essay
Epistaxis: Vascular Anatomy, Origins, and Endovascular Treatment
Elsie Koh 1, Vincent I. Frazzini, Nolan J. Kagetsu
ost cases of epistaxis occur in the anterior septal area, a location readily accessible and treatable by cautery or anterior nasal packing. However, posterior epistaxis often requires more aggressive measures including posterior nasal packing and endoscopic cauterization. Epistaxis refractory to initial treatment attempts, often cases of posterior epistaxis, can be successfully treated by endovascular em-

bolization techniques. The vascular anatomy, endovascular treatment options, and spectrum of causes of epistaxis will be reviewed.
Arterial Anatomy

The arterial supply to the nasal fossa is complex and involves branches from both the external (ECA) and internal (ICA) carotid arteries [1] (Fig. 1). The ECA contributes most

of its supply via the internal maxillary (sphenopalatine and greater palatine branches) and facial arteries. The ophthalmic artery, usually a branch of the ICA, can supply the nasal fossa via the anterior and posterior ethmoidal arteries. The sphenopalatine artery serves as the major supply to the nasal fossa via the lateral and medial branches. The lateral branches supply the inferior, middle, and superior turbinates; the medial or septal

A
Fig. 1.Arterial anatomy of medial and lateral nasal wall. Ant. = anterior, Post. = posterior, a. = artery. A, Drawing of medial nasal wall shows blood supply of nasal septum. Note Kiesselbachs or Littles area, where most anterior epistaxis occurs. B, Drawing shows blood supply of lateral nasal wall.
Received December 8, 1998; accepted after revision August 26, 1999
1

All authors: Department of Radiology, St. LukesRoosevelt Hospital Center, 1000 Tenth Ave., New York, NY 10019. Address correspondence to E. Koh.

AJR 2000;174:845851 0361803X/00/1743845 American Roentgen Ray Society

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Fig. 2.63-year-old woman with epistaxis refractory to nasal packing. A, Anteroposterior angiogram shows injection in right distal internal maxillary artery. Medial or septal branches supply septum (straight arrow ), and lateral branches supply turbinates (curved arrow ). B, Angiogram in lateral projection shows branches of sphenopalatine artery (arrows ).

branches supply the nasal septum (Figs. 2A and 2B). The terminal branch of the greater palatine artery enters the incisive foramen and supplies the inferior nasal septum, where it anastomoses with medial branches of the sphenopalatine artery. The superior labial artery, arising from the facial artery, also supplies the medial wall of the nasal vestibule via a septal branch. This branch is rarely seen on angiograms with normal ndings. Emboliza-

tion of the facial artery should be performed with caution because of the potential risk of necrosis of the nasal ala with occlusion of the alar artery, the terminal branch of the facial artery. The anterior and posterior ethmoidal branches of the ophthalmic artery, usually a branch of the ICA, pass through the cribriform plate to anastomose with the nasal branches of the sphenopalatine artery (Figs. 3A and 3B). These vessels are rarely

seen on angiograms with normal ndings. The presence of prominent ethmoidal branches indicate that embolization of ECA branches may fail to control the epistaxis. Kiesselbachs plexus, also known as Littles or Kiesselbachs area, is a localized region of mucosa of the anteroinferior nasal septum. It is supplied by branches of the sphenopalatine, greater palatine, and facial arteries and is the site of most anterior epistaxis (Fig. 1A).

Fig. 3.48-year-old man with epistaxis refractory to nasal packing. A, Anteroposterior angiogram shows injection in right internal carotid artery. Note prominent ethmoidal arteries (thin arrows ), branches of ophthalmic artery. Ethmoidal arteries are typically not seen under normal circumstances, and abnormal hypervascularity of nasal septum is shown distally (thick arrow ). B, Delayed anteroposterior angiogram shows early venous drainage via facial vein (curved arrow ). Abnormal hypervascularity of nasal septum is shown distally (thick arrow ).

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Angiography of Epistaxis
Treatment

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Initial treatment attempts may include chemical or electric cautery of distal branches and the bleeding site [2]. When cautery is unsuccessful, nasal packing may be necessary. The relatively high failure rate of anterior nasal packing for superior and posterior epistaxis is not surprising because the posterior extent of an anterior nasal packing is limited and may not tamponade the posterior turbinates. More aggressive use of posterior packing with inatable balloon packs tamponades more of the nasal fossa. However, packing has a reported failure rate of 2652% [3, 4]. In addition, posterior nasal packing has caused severe complications such as alar and septal necrosis, aspiration,

sinusitis, exacerbation of sleep obstructive apnea, and pack-induced hypoxia [24]. Alternatively, studies of posterior endoscopic cauterization report success rates of 8090% [2]. Studying endovascular therapy for idiopathic intractable epistaxis in 30 patients, Vitek [5] found an 87% success rate after embolization of the internal maxillary artery and a 97% success rate (with a 3% complication rate) after embolization of the internal and facial arteries. Because interventional neuroradiology is increasingly available, embolization has become an option when initial treatment fails. The protocol should include evaluation of the ICA to determine if the ICA or its branches are the source of bleeding. Dig-

ital subtraction angiography with road mapping is used to selectively guide the catheter to the region of interest that is typically the distal portion of the internal maxillary artery (Fig. 4). One must identify potentially dangerous anastomoses to the carotid siphon (such as the artery of the foramen rotundum) and ophthalmic artery to avoid the complications of stroke or blindness. The microcatheter is routinely advanced distal to branches with high potential for dangerous anastomosis collaterals, such as the middle meningeal, accessory meningeal, and supercial temporal arteries, to avoid nontarget embolization. Injection should not be performed too forcefully because reux into the ICA can occur [5]. Control angiography is

Fig. 4.85-year old woman with refractory idiopathic epistaxis. Angiograms show internal maxillary artery embolization. A and B, Mid arterial phase left external carotid artery injection angiogram in anteroposterior (A) and lateral (B) projections shows hypervascular sphenopalatine artery branches (arrows ). C, Lateral projection after embolization shows successful obliteration of ow to sphenopalatine branches (arrow ).

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Fig. 5.14-year-old boy with nasal obstruction and epistaxis caused by juvenile angiobroma. A and B, Early (A) and late (B) arterial phase right internal maxillary artery (IMA) injection angiograms in lateral projection before embolization show marked vascularity of juvenile angiobroma. C and D, Early arterial phase right IMA angiograms after embolization show marked reduction of vascularity (C). However, note persistent supply of tumor by mandibular branch of internal carotid artery (arrow, D).

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performed after embolization to assess the results (Fig. 4C).

Embolic Materials

imal occlusion. Gelfoam powder may embolize too distally and cause necrosis or cranial nerve palsy.
Failure of Embolization

Selected Causes of Epistaxis

Spontaneous

Embolic materials frequently used for treatment of epistaxis include Gelfoam (Upjohn, Kalamazoo, MI) pieces, polyvinyl alcohol particles (Figs. 46), platinum coils (Figs. 7 and 8), or a combination of materials [6]. Polyvinyl alcohol particles (149250 m) are typically used. Platinum coils and Gelfoam pieces can be used to achieve proximal occlusion quickly. However, collateral formation and bleeding can occur after prox848

Failure of endovascular treatment of epistaxis is often related to continued bleeding from the ethmoidal branches of the ophthalmic artery (Fig. 3A). Embolization of these branches is contraindicated because ophthalmic artery embolization carries a high risk of blindness. However, the surgeon can ligate the ethmoidal vessels as they perforate the medial wall of the orbit [2].

The idiopathic or spontaneous form of epistaxis is the most common cause, often related to cigarette use, hypertension, and atherosclerotic disease (Fig. 4). Although hypervascularity is commonly seen, angiographic demonstration of the bleeding point (extravasation) is rare [7].
Primary Neoplasms

Juvenile angiobroma is the most common benign tumor arising from the nasopharynx and comprises 0.5% of all head and neck neoplasms [8]. It occurs almost exAJR:174, March 2000

Angiography of Epistaxis

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Fig. 6.57-year-old woman with right-sided nasal mass and epistaxis caused by solitary brous tumor. A, Conventional spin-echo T1-weighted sagittal MR image after gadolinium administration shows peripheral enhancement (arrow ). B, Mass is of low signal intensity (arrow ) on T2-weighted MR sequence. C, Mid to late arterial phase right external carotid artery arteriogram in lateral projection shows peripheral vascularity. D, Peripheral vascularity shown in C is completely obliterated after distal internal maxillary artery embolization.

Fig. 7.32-year-old pregnant woman with epistaxis after gunshot wound. A and B, Left common carotid arteriogram in anteroposterior projection (A) and left external carotid arteriogram in lateral projection (B) show active extravasation of contrast material from sphenopalatine artery (arrows ). C, Lateral projection of left external carotid angiogram shows hemostasis after embolization of distal external carotid artery with platinum coil.

clusively in boys. Cross-sectional imaging usually identies the mass with bowing or erosion of adjacent bony structures within the nasal cavity or nasopharynx. The arterial
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supply of a juvenile angiobroma can arise from ICA or ECA branches (Fig. 5). Angiography and embolization before surgery can reduce surgical blood loss, improve visual-

ization of the surgical eld, and result in a more complete and uncomplicated resection. A solitary brous tumor of the nasopharynx is a rare cause of epistaxis (Fig. 6). This
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Fig. 8.75-year-old man who presented to emergency department with epistaxis refractory to nasal packing and internal carotid artery (ICA) pseudoaneurysm. A and B, Left common carotid artery angiograms in anteroposterior (A) and lateral (B) projections show large pseudoaneurysm with extravasation of contrast material (straight arrows, B). Narrowing of ICA above and below pseudoaneurysm may result from spasm or prior dissection (open arrows). Multiple embolization coils were placed in aneurysm dome (curved arrow, B).

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Fig. 9.37-year-old man with sinusitis who presented with epistaxis after functional endoscopic sinus surgery. A and B, Left external carotid artery arteriograms in anteroposterior (A) and lateral (B) projections show active extravasation (arrows). C, Superselective angiogram in anteroposterior projection shows extravasation (arrow ) from sphenopalatine branches more clearly than A and B.

C
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Angiography of Epistaxis spindle cell tumor has pathologic features similar to those of angiobromas, hemangiopericytomas, and brous histiocytomas [9].
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neck of the pseudoaneurysm was above the arch of C1.

Summary

Occasionally, active bleeding can be visualized as extravasation of contrast material, particularly after trauma (Fig. 7) or surgery. Active extravasation from a posterior lateral branch of the sphenopalatine artery may occur after functional endoscopic sinus surgery (Fig. 9). Epistaxis with active extravasation was also seen in a patient with an ICA pseudoaneurysm (Fig. 8). This patient who presented to the emergency department with epistaxis refractory to nasal packing and an ICA pseudoaneurysm was not a surgical candidate because the

Embolization can play an important role in controlling epistaxis. However, one must be careful to avoid nontarget embolization via the dangerous anastomoses between the ECA branches, the carotid siphon, and ophthalmic arteries.
References
1. Osborn A. The nasal arteries. AJR 1978;130:8997 2. Emanuel JM. Epistaxis. In: Cummings CW, Fredrickson JM, Harker LA, Krause CJ, Richardson MA, Schuller DE, eds. Otolaryagology head and neck surgery, 3rd ed. St. Louis: Mosby, 1998:852865 3. Wang L, Vogel DH. Posterior epistaxis: comparison of treatment. Otolaryngol Head Neck Surg

1981;89:10011006 4. Schaitkin B, Strauss M, Houck JR. Epistaxis: medical versus surgical therapya comparison of efcacy, complications, and economic considerations. Laryngoscope 1987;97:13921396 5. Vitek JJ. Idiopathic intractable epistaxis: endovascular therapy. Radiology 1991;181:113116 6. Kagetsu NJ, Berenstein A, Choi IS. Interventional radiology of the extracranial head and neck. Cardiovasc Intervent Radiol 1991;14:325333 7. Lasjaunias P, Marsot-Dupuch K, Doyon D. The radio-anatomical basis of arterial embolization for epistaxis. J Neuroradiol 1979;6:4553 8. Davis KR. Embolization of epistaxis and juvenile nasopharyngeal angiobromas. AJNR 1986;7:953962 9. Zukerberg LR, Rosenberg AE, Randolph G, Pilch BZ, Goodman ML. Solitary brous tumor of the nasal cavity and paranasal sinuses. Am J Surg Pathol 1991;15:126130

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