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Surgical Management of

S e vere E p i s t axi s
a b,
Giant Lin, MD , Benjamin Bleier, MD *

KEYWORDS
 Epistaxis  Sphenopalatine artery ligation  Anterior ethmoid artery ligation
 Hemostasis  Endoscopic sinus surgery

KEY LEARNING POINTS

At the end of this article, the reader will:


 Be familiar with passive methods of bleeding management to optimize endoscopic
visualization.
 Understand the anatomy of the anterior ethmoid artery and surgical approaches to ligate
this artery.
 Understand the anatomy of the sphenopalatine artery (SPA) and the surgical steps in
endoscopic SPA ligation.
 Know the results of SPA ligation for control of primary epistaxis.

INTRODUCTION

The true incidence of spontaneous epistaxis is unknown, but it is estimated that 60%
of individuals experience epistaxis in their lifetime. Of these, 6% seek medical treat-
ment.1 No standard definition of severe epistaxis exists, but a reasonable definition
is any epistaxis that requires surgical intervention, extensive nasal packing, or blood
products. In one study,2 45% of patients hospitalized for epistaxis had systemic con-
ditions that can contribute to severe epistaxis. Although high-dose aspirin increases
bleeding risk and leads to higher chance of rebleeding after intervention for epistaxis,
low-dose aspirin (81 mg daily) increases epistaxis risk only slightly (19.1 vs 16.7% in
one study).3 Hypertension as a primary cause of severe epistaxis is controversial. If
possible, systemic conditions should be addressed along with surgical intervention
in severe cases of epistaxis.

PATIENT OPTIMIZATION

Many patients with severe epistaxis benefit from endoscopic intervention for control of
bleeding. However, active bleeding worsens endoscopic visualization. A few initial

a
Advocare Aroesty Ear, Nose, and Throat Associates, 400 Valley Road, Suite 105, Mount Arling-
ton, NJ 07856, USA; b Department of Otolaryngology, Harvard Medical School, Massachusetts
Eye and Ear Infirmary, 243 Charles Street, Boston, MA 02114, USA
* Corresponding author.
E-mail address: bleierb@gmail.com

Otolaryngol Clin N Am 49 (2016) 627–637


http://dx.doi.org/10.1016/j.otc.2016.01.003 oto.theclinics.com
0030-6665/16/$ – see front matter Ó 2016 Elsevier Inc. All rights reserved.
628 Lin & Bleier

Systemic causes of bleeding

 Alcohol
 Connective tissue disease
 Medications: aspirin, nonsteroidal anti-inflammatory drugs, clopidogrel,
warfarin, other antiplatelet or anticoagulant therapy
 Renal disease
 Liver failure
 Hematologic malignancies
 Vitamin C deficiency
 Vitamin K deficiency
 Idiopathic thrombocytopenic purpura
 Disseminated intravascular coagulation
 Genetic bleeding tendency (eg, von Willebrand disease, hemophilia, Bernard-
Soulier syndrome)
 Hereditary hemorrhagic telangiectasia
 Alternative medicinals (garlic, ginkgo, ginseng)

maneuvers help the surgeon decrease the blood loss encountered at surgery to more
accurately visualize, locate, and control the hemorrhage.

What are some nonsurgical methods of bleeding management?

 Head of bed elevation as part of endoscopic surgical setup


 Topical epinephrine and other decongestants
 Intranasal injections
 Greater palatine injection
 Warm saline irrigation
Anesthetic strategies
 Blood pressure control to decrease bleeding
 Consider use of clonidine as a premedication

Elevation of the head of bed increases venous return and thus decreases overall
bleeding in the surgical field. The optimal angle of head elevation is 15 to 20 .4
One study4 compared blood loss of sinus surgery performed at 5 , 10 , and 20 of
head elevation. Blood loss was 231 mL, 230 mL, and 135 mL, respectively.
Topical decongestants include epinephrine, cocaine, oxymetazoline, phenyleph-
rine, and Moffett solution (2 mL of 10% cocaine, 1 mL of 1:1000 epinephrine, and
2 mL of sodium bicarbonate). No randomized trials exist comparing one decongestant
with another in endoscopic sinus surgery. One study5 showed no difference in blood
loss between surgery performed using 1:100,000 and 1:200,000 epinephrine. The
1:1000 epinephrine causes particularly robust vasoconstriction and has been proven
to be safe assuming the use of proper safeguards to prevent inadvertent injection.6
Regardless of surgeon preference, topical decongestants are all effective in producing
vasoconstriction and improving surgical visualization.
Surgical Management of Severe Epistaxis 629

Selective injection of local anesthetic/decongestant in areas of bleeding is effective


in managing epistaxis. Injections can decrease local hydrostatic pressure and also
produce vasoconstriction. Greater palatine injection effectively decreases posterior
nasal blood supply. It can be performed before endoscopic evaluation of epistaxis
by bending a 25-gauge needle 45 , 25 mm from the needle tip.7 The needle is inserted
transorally into the greater palatine canal and the pterygopalatine fossa infiltrated with
1:100,000 epinephrine.
Warm saline irrigation at 49 C has been shown to decrease the rate of bleeding, but
endoscopic visualization improves only in longer surgical cases.8 However, warm sa-
line irrigation can be used to help identify the primary source of bleeding, which can
then be treated effectively.
Controlled, hypotensive anesthesia can decrease intraoperative blood loss and
improve visualization during surgery. One benefit may be decreased heart rate in addi-
tion to decreased blood pressure. Regardless of theoretic advantages, trials regarding
the true efficacy of total intravenous anesthesia have not been entirely conclusive or
convincing.9,10 This anesthetic technique remains controversial but can certainly be
added to the surgeon and anesthesiologist armamentarium.
A more recent development in efforts to decrease blood loss during endoscopic
sinus surgery is the use of clonidine as a premedication. Clonidine activates a2 recep-
tors within the central nervous system to decrease peripheral sympathetic tone. There
is also a1 agonist activity to a lesser extent, resulting in some peripheral vasoconstric-
tion within the mucosal bed.11,12 More studies are required to demonstrate the benefit
of this medication in endoscopic sinus surgery.

Surgical techniques

 Major vascular targets and techniques to control epistaxis


 Sphenopalatine artery (SPA)
 Anterior ethmoid artery (AEA)
 Posterior ethmoid artery (PEA)
 Vidian and pharyngeal artery
 Carotid artery
 Venous bleeding

Sphenopalatine artery ligation

 Sphenopalatine foramen (SPF) most commonly in the transition zone between


middle and superior meatus
 Accessory foramen in 10%
 SPA may exit in multiple branches through the foramen in 35% to 40%
 SPA is generally identified emerging from posterior to the endoscopic
landmark, crista ethmoidalis of the palatine bone
 Surgical clipping or diathermy or both?

ANATOMY

The SPA is a branch of the internal maxillary artery and is the major blood supply of the
posterior nasal cavity. Epistaxis from this arterial source is generally more severe than
630 Lin & Bleier

anterior epistaxis. The artery enters the nasal cavity from the pterygopalatine fossa via the
SPF. Knowledge of the anatomic variations of the SPA and SPF improves surgical results.
This article focuses on anatomy pertinent to endoscopic SPA ligation. Transantral ligation
of internal maxillary artery branches is of historical interest and is not discussed.
The SPF is located most frequently (87%) at the transitional zone between the supe-
rior and middle meatus.13 It is less frequently found in the superior meatus. The crista
ethmoidalis is a bony crest of the palatine bone that points to the SPF. The SPF lies
behind this crest and may rest above or straddle this bony crest.14 A single foramen
is usually encountered, but an accessory foramen exists in 10% of patients.14,15 Termi-
nal branches of the SPA include the posterior septal artery and the posterior lateral
nasal artery branches. The SPA exits the SPF as a single branch in 60% to 75%, as
two branches in 20% to 30%, and three or more branches in less than 10%.13,15,16

SURGICAL APPROACH FOR ENDOSCOPIC SPHENOPALATINE ARTERY LIGATION

The entry zone of the SPA within the nasal cavity is located approximately at the tail of
the middle turbinate. The mucosa just anterior to the middle turbinate tail is infiltrated
with local anesthetic (usually 1% lidocaine with 1:100,000 epinephrine). Next, the pos-
terior fontanelle of the maxillary sinus and the perpendicular plate of the palatine bone
are palpated. A standard maxillary antrostomy is optional for this procedure, but is
often valuable in defining the area of mucosal incision at the palatine bone behind
the antrostomy and back wall of the maxillary sinus. A vertical mucosal incision at
the orbital process of the palatine bone is made, and submucosal dissection proceeds
posteriorly to identify the crista ethmoidalis. The crista can be removed with Kerrison
rongeurs but this is not always necessary. SPA branches are identified by wide expo-
sure of soft tissue behind the crista ethmoidalis (Fig. 1). A ball-probed seeker is helpful
in this dissection because it can help define arterial branches with minimal trauma.
Awareness of the considerable variation in the number of arterial branches and thor-
ough dissection via wide exposure are critical. Arterial occlusion can be performed by
Ligaclips or bipolar electrocoagulation on all isolated arterial branches. The mucosa
previously elevated for this dissection is returned to original position.

EFFICACY OF SPHENOPALATINE ARTERY LIGATION

Success rate of SPA ligation for severe epistaxis ranges from 88% to 98%.17,18 One
report showed statistically better control of bleeding with a combination of surgical
clips and diathermy.18 Because of anatomic variations, it is possible to miss arterial

Fig. 1. Example of right SPA dissection before ligation. The arrow points to the SPA as it
exits the sphenopalatine foramen. SPA branches are identified by wide exposure of soft tis-
sue behind the crista ethmoidalis before ligation.
Surgical Management of Severe Epistaxis 631

branches during surgical dissection. One report suggests extending the dissection
medially and posteriorly toward the lower sphenoid rostrum to locate the posterior
septal branch because this artery may enter the nose through a separate foramen pos-
terior to the SPA. Another option to ensure that all pertinent vessels are addressed is to
follow the SPA laterally into the pterygopalatine fossa to ligate the vessel more prox-
imally before any branching occurs. Complications of SPA ligation are uncommon but
include rebleeding, sinusitis, and palatal/nasal numbness. Inferior turbinate necrosis
was reported in one case.19 Postoperative care for the procedure involves regular sa-
line rinse as per standard endoscopic sinus surgery.

ANTERIOR ETHMOID ARTERY LIGATION


Surgical Anatomy
The AEA is a branch of the ophthalmic artery that supplies mucosa of the anterior nasal
cavity before entering intracranially to form meningeal branches. The artery traverses
the ethmoid roof via a bony mesentery in 36% in one cadaveric study (Fig. 2).20 Other-
wise, the AEA is protected by the fovea ethmoidalis along the skull base. From an
endoscopic approach, the AEA is identified on average 17.5 mm from the axilla of
the middle turbinate.21 From an external, transorbital approach, the artery averages
24 mm from the anterior lacrimal crest.
Severe epistaxis from the AEA is less common than from the SPA. Possible causes
include spontaneous, postsinus surgery, and traumatic bleeding. When endoscopic
examination suggests an anterior source of intractable bleeding, AEA ligation can
be considered.
Approaches

Surgical approaches for AEA ligation

 Open approach
 Lynch incision
 Transcaruncular incision
 Endoscopic approach
 Transethmoid (direct)
 Transorbital

Fig. 2. Anatomy of the left AEA. The AEA in this example traverses the left ethmoid roof via
bony mesentery below the skull base. The image-guided frontal probe (bottom right image)
confirms the location of the artery.
632 Lin & Bleier

External approach: the Lynch incision


The Lynch incision is performed by making a curvilinear incision at a midpoint between
the medial canthus and the middle of the anterior nasal bone. A subperiosteal dissection
is performed, identifying the lacrimal crests without injuring the lacrimal apparatus. The
AEA is identified in the frontoethmoidal suture line, approximately 24 mm behind the
anterior lacrimal crest. Surgical clips or bipolar electrocautery can be used for ligation.

Transcaruncular approach
A transcaruncular approach provides access to the AEA while avoiding a transfacial
incision. This medial conjunctival incision along the semilunar fold avoids the lacrimal
drainage pathways by staying deep to the posterior fibers of the pretarsal orbicularis
muscle (Horner muscle). Dissection in a natural plane between Horner muscle and
the medial orbital septum exposes the posterior lacrimal crest, which is the attachment
of Horner muscle. Next, the periorbita along the posterior lacrimal crest is incised to
expose the medial orbital wall. Subperiosteal dissection then allows access to the
medial wall (Fig. 3A). The AEA is then ligated (Fig. 3B). The periorbita does not require
closure, whereas the caruncle and conjunctiva are closed using 6–0 resorbable sutures.

Endoscopic anterior ethmoid artery ligation

Endoscopic landmarks of AEA

 AEA runs posterior to the bulla lamella (posterior to frontal recess)


 AEA runs in posterolateral to anteromedial direction
 Can be found approximately 17.5 mm from the axilla of middle turbinate.

Fig. 3. Trancaruncular approach in a left orbit for control anterior ethmoid artery ligation.
The medial orbital wall is exposed (A) after incising periorbital along the posterior lacrimal
crest. The anterior ethmoid is identified and ligated (B). The arrow points to the surgical clip
applied to the artery.

Endoscopic ligation of the AEA begins with injections of local anesthetic and vasocon-
strictors into the middle turbinate axilla and maxillary line. A standard maxillary antros-
tomy is performed and anterior ethmoid air cells cleared to identify the lamina
papyracea and fovea ethmoidalis. An angled telescope aids in identification of the
AEA, which crosses the ethmoidal skull base in an anteromedial direction from orbit
Surgical Management of Severe Epistaxis 633

to cribiform plate. In cases where the AEA is easily identifiable in a bony mesentery,
direct clipping or bipolar cautery of the artery may be possible (Fig. 4).
A more reliable technique for AEA ligation involves partial removal of the medial
orbital wall. A small opening is made through the lamina papyracea just below the
area of the AEA. Care is taken to avoid penetrating the periorbita because prolapse
of orbital fat narrows the endoscopic corridor and makes positive identification of
the AEA difficult. After removal of a small piece of lamina papyracea, gentle retraction
of the orbit contents laterally helps identify the AEA. Elevation anterior and posterior to
the artery exposes the artery for endoscopic clip placement. No closure is necessary
for the endoscopic approach.

Efficacy of Anterior Ethmoid Artery Ligation


Objective data addressing the efficacy of AEA ligation alone in the treatment of severe
epistaxis are limited. Most reports on this topic are cadaveric feasibility studies, and
AEA ligation is often performed in conjunction with SPA ligation. One cadaveric study
showed that endoscopic clipping was successful in only 50% in cases with bony mes-
entery based on intraoperative computed tomography scan results.22 Another study
showed successful endoscopic AEA ligation in three patients with severe epistaxis.23
Possible complications include rebleeding, orbital injury, and skull base disruption.

POSTERIOR ETHMOID ARTERY LIGATION

PEA is also a branch of the ophthalmic artery. In an endoscopic study, the PEA is
14.9 mm behind the AEA and 8.1 mm in front of the anterior wall of the sphenoid
sinus.21 The artery is in front of the sphenoid rostrum in 98% of cases when present
but may be congenitally absent in up to 50% of patients.24 Ligation of the PEA is rarely
necessary or indicated in severe epistaxis.

VIDIAN AND PHARYNGEAL ARTERY CAUTERY

Bleeding from the vidian and pharyngeal arteries is exceptionally rare except in cases
of endonasal tumor resection and other transpterygoid skull base approaches. The
pharyngeal artery is a branch of the internal maxillary artery that enters the palatova-
ginal canal at the sphenoid floor. The vidian artery runs with the vidian nerve in the
vidian canal, which is located 3.78 mm lateral to the palatovaginal canal.25 This artery
can be controlled definitively with electrocautery (Fig. 5).

Fig. 4. The bipolar cautery is applied to the left anterior ethmoid artery (arrow).
634 Lin & Bleier

Fig. 5. This right vidian canal (arrow) is cauterized as part of a juvenile angiofibroma resec-
tion, in this case to decrease blood supply to the tumor from the internal carotid artery sys-
tem. S, sphenoid sinus.

CAROTID ARTERY BLEEDING

Carotid injury during endoscopic endosnasal skull base surgery is a feared complication,
with an incidence of 0.3%.26 Detailed management protocols are discussed elsewhere in
this issue (see Gardner PA, Snyderman CH, Fernandez-Miranda JC, et al: Management
of Major Vascular Injury During Endoscopic Endonasal Skull Base Surgery, in this issue).

MANAGEMENT OF VENOUS BLEEDING

Venous bleeding is typically encountered at the pterygopalatine venous plexus,


cavernous sinus, and basilar venous plexus during endoscopic skull base surgery.
These can be controlled via tamponade. In addition, application of gelatin-based

Fig. 6. In this example, venous bleeding in the pterytopalatine venous plexus is controlled
with a gelatin-based hemostatic agent.
Surgical Management of Severe Epistaxis 635

hemostatic agents provides excellent and rapid control of high-flow venous bleeding
(Fig. 6). A review of hemostatic agents available for this application is detailed else-
where in this issue (see Barham HP, Sacks R, Harvey RJ: Hemostatic Materials and
Devices, in this issue).

SUMMARY

Advances in endoscopic technique and instrumentation have improved the care of the
patient with severe epistaxis. Many patients with severe epistaxis benefit from endo-
scopic intervention for control of bleeding. The high success rate of SPA ligation
should decrease the need for long-term nasal packing for posterior epistaxis. Although
less common, intractable bleeding from the anterior nasal cavity may call for anterior
ethmoid ligation. Endoscopic approaches for AEA ligation are now possible, but
further studies are needed to assess outcomes.

Post-Test Questions (Correct answers are in italics)


1. Which of the listed medications below are both an a2 agonist and a weak a1
agonist?
a. Sevoflurane
b. Propofol
c. Clonidine
d. Sufentanil
2. In the transcaruncular approach, what is the immediate plane of dissection after
initial conjunctival incision?
a. Dissection just deep to Horner muscle
b. Dissection just superficial to Horner muscle
c. Subperiosteal dissection
d. Just medial to the medial rectus muscle in a posterior direction
3. Which bony structure is located immediately anterior to the SPF and is a critical
landmark for endoscopic SPA ligation?
a. Superior turbinate
b. Middle turbinate
c. Uncinate process
d. Crista ethmoidalis
4. An accessory SPF is found in what percentage of patients?
a. 5%
b. 10%
c. 20%
d. 30%
5. Which of the following reasons could explain intractable ipsilateral spontaneous
posterior epistaxis following SPA clipping (select one or more that apply)
a. Incomplete clipping of bleeding vessel, need for clipping and diathermy
b. Wrong vessel clipped because of multiple branches, need for further explo-
ration, and control of bleeding vessel
c. Bleeding from posterior nasal artery emerging from a separate accessory
foramen
d. Bleeding from vidian artery, need for further exploration and ligation of vidian
artery
636 Lin & Bleier

SUPPLEMENTARY DATA

Supplementary PDF slides related to this article can be found online at http://www.
oto.theclinics.com/.

REFERENCES

1. Viehweg TL, Roberson JB, Hudson JW. Epistaxis: diagnosis and treatment. J Oral
Maxillofac Surg 2006;64:511–8.
2. Awan MS, Iqbal M, Imam SZ. Epistaxis: when are coagulation studies justified?
Emerg Med J 2008;25:156–7.
3. Ridker PM, Manson JE, Gaziano JM, et al. Low-dose aspirin therapy for chronic
stable angina. A randomized, placebo-controlled clinical trial. Ann Intern Med
1991;114:835–9.
4. Gan EC, Habib AR, Rajwani A, et al. Five-degree, 10-degree, and 20-degree
reverse Trendelenburg position during functional endoscopic sinus surgery: a
double-blind randomized controlled trial. Int Forum Allergy Rhinol 2014;4:61–8.
5. Moshaver A, Lin D, Pinto R, et al. The hemostatic and hemodynamic effects of
epinephrine during endoscopic sinus surgery: a randomized clinical trial. Arch
Otolaryngol Head Neck Surg 2009;135:1005–9.
6. Orlandi RR, Warrier S, Sato S, et al. Concentrated topical epinephrine is safe in
endoscopic sinus surgery. Am J Rhinol Allergy 2010;24:140–2.
7. Douglas R, Wormald PJ. Pterygopalatine fossa infiltration through the greater pal-
atine foramen: where to bend the needle. Laryngoscope 2006;116:1255–7.
8. Gan EC, Alsaleh S, Manji J, et al. Hemostatic effect of hot saline irrigation during
functional endoscopic sinus surgery: a randomized controlled trial. Int Forum Al-
lergy Rhinol 2014;4(11):877–84.
9. DeConde AS, Thompson CF, Wu EC, et al. Systematic review and meta-analysis
of total intravenous anesthesia and endoscopic sinus surgery. Int Forum Allergy
Rhinol 2013;3:848–54.
10. Beule AG, Wilhelmi F, Kuhnel TS, et al. Propofol versus sevoflurane: bleeding in
endoscopic sinus surgery. Otolaryngol Head Neck Surg 2007;136:45–50.
11. Wawrzyniak K, Burduk PK, Cywinski JB, et al. Improved quality of surgical field
during endoscopic sinus surgery after clonidine premedication: a pilot study.
Int Forum Allergy Rhinol 2014;4:542–7.
12. Mohseni M, Ebneshahidi A. The effect of oral clonidine premedication on blood
loss and the quality of the surgical field during endoscopic sinus surgery: a
placebo-controlled clinical trial. J Anesth 2011;25:614–7.
13. Padua FG, Voegels RL. Severe posterior epistaxis-endoscopic surgical anatomy.
Laryngoscope 2008;118:156–61.
14. Wareing MJ, Padgham ND. Osteologic classification of the sphenopalatine fora-
men. Laryngoscope 1998;108:125–7.
15. Midilli R, Orhan M, Saylam CY, et al. Anatomic variations of sphenopalatine artery
and minimally invasive surgical cauterization procedure. Am J Rhinol Allergy
2009;23:e38–41.
16. Gras-Cabrerizo JR, Adema-Alcover JM, Gras-Albert JR, et al. Anatomical and
surgical study of the sphenopalatine artery branches. Eur Arch Otorhinolaryngol
2014;271:1947–51.
17. Kumar S, Shetty A, Rockey J, et al. Contemporary surgical treatment of epistaxis.
What is the evidence for sphenopalatine artery ligation? Clin Otolaryngol Allied
Sci 2003;28:360–3.
Surgical Management of Severe Epistaxis 637

18. Nouraei SA, Maani T, Hajioff D, et al. Outcome of endoscopic sphenopalatine ar-
tery occlusion for intractable epistaxis: a 10-year experience. Laryngoscope
2007;117:1452–6.
19. Moorthy R, Anand R, Prior M, et al. Inferior turbinate necrosis following endo-
scopic sphenopalatine artery ligation. Otolaryngol Head Neck Surg 2003;129:
159–60.
20. Floreani SR, Nair SB, Switajewski MC, et al. Endoscopic anterior ethmoidal artery
ligation: a cadaver study. Laryngoscope 2006;116:1263–7.
21. Han JK, Becker SS, Bomeli SR, et al. Endoscopic localization of the anterior and
posterior ethmoid arteries. Ann Otol Rhinol Laryngol 2008;117:931–5.
22. Solares CA, Luong A, Batra PS. Technical feasibility of transnasal endoscopic
anterior ethmoid artery ligation: assessment with intraoperative CT imaging. Am
J Rhinol Allergy 2009;23:619–21.
23. Pletcher SD, Metson R. Endoscopic ligation of the anterior ethmoid artery. Laryn-
goscope 2007;117:378–81.
24. Bleier BS, Healy DY Jr, Chhabra N, et al. Compartmental endoscopic surgical
anatomy of the medial intraconal orbital space. Int Forum Allergy Rhinol 2014;
4:587–91.
25. Herzallah IR, Amin S, El-Hariri MA, et al. Endoscopic identification of the pharyn-
geal (palatovaginal) canal: an overlooked area. J Neurol Surg B Skull Base 2012;
73:352–7.
26. Gardner PA, Tormenti MJ, Pant H, et al. Carotid artery injury during endoscopic
endonasal skull base surgery: incidence and outcomes. Neurosurgery 2013;
73:261–9 [discussion: 269–70].

SUGGESTED READINGS

Kumar S, Shetty A, Rockey J, et al. Contemporary surgical treatment of epistaxis.


What is the evidence for sphenopalatine artery ligation? Clinical otolaryngology
and allied sciences 2003;28:360–3.
Nouraei SA, Maani T, Hajioff D, et al. Outcome of endoscopic sphenopalatine artery
occlusion for intractable epistaxis: a 10-year experience. The Laryngoscope
2007;117:1452–6.

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