AJR 2000; 174:845-851
© American Roentgen Ray Society
Epistaxis
Vascular Anatomy, Origins, and Endovascular Treatment
Elsie Koh1,
Vincent I. Frazzini and
Nolan J. Kagetsu
1
All authors: Department of Radiology, St. Luke'sRoosevelt Hospital
Center, 1000 Tenth Ave., New York, NY 10019.
Received December 8, 1998;
accepted after revision August 26, 1999.
Address correspondence to E. Koh.
Introduction
Most 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 embolization 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.
1A,1B).
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 branches supply the nasal septum (Figs.
2A and
2B).

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Fig. 1A. Arterial anatomy of medial and lateral nasal wall. Ant. = anterior,
Post. = posterior, a. = artery. Drawing of medial nasal wall shows blood
supply of nasal septum. Note Kiesselbach's or Little's area, where most
anterior epistaxis occurs.
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Fig. 2A. 63-year-old woman with epistaxis refractory to nasal packing.
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).
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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. Embolization 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).

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Fig. 3A. 48-year-old man with epistaxis refractory to nasal packing.
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).
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Fig. 3B. 48-year-old man with epistaxis refractory to nasal packing. 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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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
[2,3,4].
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. Digital 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.
4A,4B,4C).
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
performed after embolization to assess the results
(Fig. 4C).

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Fig. 4A. 85-year old woman with refractory idiopathic epistaxis. Angiograms
show internal maxillary artery embolization. Mid arterial phase left external
carotid artery injection angiogram in anteroposterior (A) and lateral
(B) projections shows hypervascular sphenopalatine artery branches
(arrows).
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Fig. 4B. 85-year old woman with refractory idiopathic epistaxis. Angiograms
show internal maxillary artery embolization. Mid arterial phase left external
carotid artery injection angiogram in anteroposterior (A) and lateral
(B) projections shows hypervascular sphenopalatine artery branches
(arrows).
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Fig. 4C. 85-year old woman with refractory idiopathic epistaxis. Angiograms
show internal maxillary artery embolization. Lateral projection after
embolization shows successful obliteration of flow to sphenopalatine branches
(arrow).
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Embolic Materials
Embolic materials frequently used for treatment of epistaxis include
Gelfoam (Upjohn, Kalamazoo, MI) pieces, polyvinyl alcohol particles (Figs.
4A,4B,4C,5A,5B,5C,5D,6A,6B,6C,6D),
platinum coils (Figs.
7A,7B,7C
and
8A,8B),
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 proximal occlusion. Gelfoam powder may
embolize too distally and cause necrosis or cranial nerve palsy.

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Fig. 5A. 14-year-old boy with nasal obstruction and epistaxis caused by
juvenile angiofibroma. 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.
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Fig. 5B. 14-year-old boy with nasal obstruction and epistaxis caused by
juvenile angiofibroma. 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.
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Fig. 5C. 14-year-old boy with nasal obstruction and epistaxis caused by
juvenile angiofibroma. 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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Fig. 5D. 14-year-old boy with nasal obstruction and epistaxis caused by
juvenile angiofibroma. 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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Fig. 6A. 57-year-old woman with right-sided nasal mass and epistaxis caused
by solitary fibrous tumor. Conventional spin-echo T1-weighted sagittal MR
image after gadolinium administration shows peripheral enhancement
(arrow).
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Fig. 6C. 57-year-old woman with right-sided nasal mass and epistaxis caused
by solitary fibrous tumor. Mid to late arterial phase right external carotid
artery arteriogram in lateral projection shows peripheral vascularity.
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Fig. 6D. 57-year-old woman with right-sided nasal mass and epistaxis caused
by solitary fibrous tumor. Peripheral vascularity shown in C is
completely obliterated after distal internal maxillary artery
embolization.
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Fig. 7A. 32-year-old pregnant woman with epistaxis after gunshot wound. 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).
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Fig. 7B. 32-year-old pregnant woman with epistaxis after gunshort wound. 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).
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Fig. 7C. 32-year-old pregnant woman with epistaxis after gunshot wound.
Lateral projection of left external carotid angiogram shows hemostasis after
embolization of distal external carotid artery with platinum coil.
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Fig. 8A. 74-year-old man who presented to emergency department with epistaxis
refractory to nasal packing and internal carotid artery (ICA) pseudoaneurysm.
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. 8B. 75-year-old man who presented to emergency department with epistaxis
refractory to nasal packing and internal carotid artery (ICA) pseudoaneurysm.
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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Failure of Embolization
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].
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.
4A,4B,4C).
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
exclusively 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 supply of a juvenile angiofibroma can arise from ICA
or ECA branches (Fig.
5A,5B,5C,5D).
Angiography and embolization before surgery can reduce surgical blood loss,
improve visualization 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.
6A,6B,6C,6D).
This spindle cell tumor has pathologic features similar to those of
angiofibromas, hemangiopericytomas, and fibrous histiocytomas
[9].
Traumatic-latrogenic
Occasionally, active bleeding can be visualized as extravasation of
contrast material, particularly after trauma (Fig.
7A,7B,7C)
or surgery. Active extravasation from a posterior lateral branch of the
sphenopalatine artery may occur after functional endoscopic sinus surgery
(Fig.
9A,9B,9C).
Epistaxis with active extravasation was also seen in a patient with an ICA
pseudoaneurysm (Fig.
8A,8B).
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 neck of the pseudoaneurysm was above the arch of C1.

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Fig. 9A. 37-year-old man with sinusitis who presented with epistaxis after
functional endoscopic sinus surgery. Left external carotid artery arteriograms
in anteroposterior (A) and lateral (B) projections show active
extravasation (arrows).
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Fig. 9B. 37-year-old man with sinusitis who presented with epistaxis after
functional endoscopic sinus surgery. Left external carotid artery arteriograms
in anteroposterior (A) and lateral (B) projections show active
extravasation (arrows).
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Fig. 9C. 37-year-old man with sinusitis who presented with epistaxis after
functional endoscopic sinus surgery. Superselective angiogram in
anteroposterior projection shows extravasation (arrow) from
sphenopalatine branches more clearly than A and B.
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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.
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