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Pictorial Essay
Epistaxis: Vascular Anatomy, Origins, and Endovascular
Treatment
Elsie Koh 1, Vincent I. Frazzini, Nolan J. Kagetsu
M
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
B
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 Kiesselbach’s or Little’s 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. Luke’s–Roosevelt Hospital Center, 1000 Tenth Ave., New York, NY 10019. Address correspondence to E. Koh.
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Koh et al.
B
A
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 findings. 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 findings.
The presence of prominent ethmoidal
branches indicate that embolization of
ECA branches may fail to control the
epistaxis. Kiesselbach’s plexus, also known
as Little’s or Kiesselbach’s 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 ).
A
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B
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Angiography of Epistaxis
Treatment
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 inflatable balloon
packs tamponades more of the nasal fossa.
However, packing has a reported failure rate
of 26–52% [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 [2–4]. Alternatively, studies of posterior endoscopic
cauterization report success rates of 80–90%
[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-
A
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 superficial temporal arteries, to avoid
nontarget embolization. Injection should not
be performed too forcefully because reflux into
the ICA can occur [5]. Control angiography is
B
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 flow
to sphenopalatine branches (arrow ).
C
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Fig. 5.—14-year-old boy with nasal obstruction and epistaxis caused by juvenile angiofibroma.
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 angiofibroma.
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).
B
A
C
performed after embolization to assess the
results (Fig. 4C).
imal occlusion. Gelfoam powder may embolize too distally and cause necrosis or cranial
nerve palsy.
Embolic Materials
Failure of Embolization
Embolic materials frequently used for
treatment of epistaxis include Gelfoam (Upjohn, Kalamazoo, MI) pieces, polyvinyl alcohol particles (Figs. 4–6), platinum coils
(Figs. 7 and 8), or a combination of materials
[6]. Polyvinyl alcohol particles (149–250
µm) 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].
D
Selected Causes of Epistaxis
Spontaneous
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 angiofibroma 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
C
B
A
Fig. 6.—57-year-old woman with right-sided nasal mass and epistaxis caused by solitary fibrous 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.
D
A
B
C
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 identifies 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 angiofibroma 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 field, and result in a
more complete and uncomplicated resection.
A solitary fibrous tumor of the nasopharynx is a rare cause of epistaxis (Fig. 6). This
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Koh et al.
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).
A
A
B
B
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 angiofibromas, hemangiopericytomas, and fibrous histiocytomas [9].
Traumatic–Iatrogenic
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
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neck of the pseudoaneurysm was above the
arch of C1.
Summary
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
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1981;89:1001–1006
4. Schaitkin B, Strauss M, Houck JR. Epistaxis: medical versus surgical therapy—a comparison of efficacy, complications, and economic considerations.
Laryngoscope 1987;97:1392–1396
5. Vitek JJ. Idiopathic intractable epistaxis: endovascular therapy. Radiology 1991;181:113–116
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9. Zukerberg LR, Rosenberg AE, Randolph G, Pilch
BZ, Goodman ML. Solitary fibrous tumor of the nasal cavity and paranasal sinuses. Am J Surg Pathol
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