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47
of epistaxis should always be considered in the differential diagnosis
(Table 47.1).
As it is more of a symptom rather than a single condition,
management principles surrounding epistaxis vary significantly,
although all require addressing the underlying cause of the bleeding.
Furthermore, despite its high incidence and multiple proposed
ways to treat it, epistaxis, in a nationwide study conducted in the
United Kingdom, is associated with a 13.9% recurrence rate and
3.4% mortality rate within 30 days of presentation.7
This highlights
the importance of familiarizing oneself with a systematic approach
to the problem. Over the past few decades, several guidelines or
protocols have been proposed to guide clinicians on optimal
treatment of this common disorder.8-14
Understanding the possible
etiologies, vascular anatomy, and medical and surgical treatments,
both in terms of options and timing, is essential for optimizing
outcomes and is oftentimes life-saving. The American Academy
of Otolaryngology–Head and Neck Surgery is currently preparing
a Clinical Practice Guideline for epistaxis, which will be published
in June 2019.
ANATOMY
The nasal cavity and paranasal sinuses have an intensely rich blood
supply from both the internal and external carotid arteries (Box
47.1, Fig. 47.1). There is an extremely rich network of vascular
anastomoses between the left and right sides and among the various
terminal tributaries. Broadly speaking, epistaxis is divided into
anterior and posterior sources of bleeding. Anterior epistaxis accounts
for the vast majority (>90%) of cases and typically originates from
the Kiesselbach plexus (Little area) on the anterior nasal septum,
which is a confluence of distal branches from the anterior ethmoidal
artery, sphenopalatine artery, greater palatine artery, and superior
labial artery (Fig. 47.2). Due to its anterior location, the Kiesselbach
plexus is subject to frequent turbulent airflow, which causes local
mucosal drying and increased fragility when irritated. Nasal septal
deviations may further worsen turbulent airflow and contribute
to anterior epistaxis in this location as well.
Posterior epistaxis typically arises from branches of the spheno-
palatine artery. A prominent network of arteries can often be
visualized posterior to the inferior turbinate root and the horizontal
part of the middle turbinate and is coined the Woodruff plexus
(Fig. 47.3). This area is made up of branches of the sphenopalatine
artery and ascending pharyngeal artery and is implicated as a
common source of posterior epistaxis. The maxillary artery
(formerly referred to as the internal maxillary artery), which is a
terminal branch of the external carotid artery, divides into its
own terminal branches, the sphenopalatine, descending palatine,
infraorbital, and posterior superior alveolar arteries, as it courses
through the pterygopalatine fossa from a lateral to medial direction.
The sphenopalatine artery enters the nasal cavity through the
sphenopalatine foramen and, at this point, exhibits a highly variable
branching pattern (Fig. 47.4).15,16
In most cases, there are two
clinically important branches—the posterior septal and posterior
lateral nasal branches. The posterior septal branch courses from
lateral to medial across the superior choana below the natural
ostium of the sphenoid sinus. It is the named artery supplying the
pedicled vascularized nasoseptal flap and is not uncommonly injured
when extending the sphenoidotomy inferiorly.17
The posterior
lateral nasal branch further divides into tributaries, which supply
KEY POINTS
• Epistaxis is a common otorhinolaryngologic complaint
encountered by multiple medical disciplines and is the
most common otorhinolaryngologic emergency.
• The vascular anatomy of the nose is extremely rich, with
bilateral supply from both the external and internal
carotid systems.
• Initial assessment should include evaluating the ABCs
and identifying any underlying causes that predispose to
bleeding.
• Identifying the site of bleeding allows for direct source
control, often with cautery or hemostatic agents.
• Conservative measures for control of epistaxis include
holding pressure, topical vasoconstrictor use, and, in
some cases, gentle nasal inspiration.
• Although effective in cases when the source of bleeding
cannot be found, nasal packing is uncomfortable, causes
trauma to the nasal mucosa, and can be costly.
• Endoscopic sphenopalatine artery ligation is a safe and
effective means to control epistaxis while avoiding the
need for posterior nasal packing.
• Depending on anatomy, bleeding from the anterior
ethmoidal artery can be controlled either endoscopically
or via a transorbital approach.
• Refractory epistaxis due to nasal tumors, facial trauma,
or carotid injury, or for preoperative vascular control,
may be suited for interventional radiologic embolization.
• Hereditary hemorrhagic telangiectasia is an autosomal
dominant vascular disorder, which presents with
recurrent epistaxis. Options for surgical treatment
include laser photocoagulation or cauterization of nasal
telangiectasias, septodermoplasty, or nasal closure.
Epistaxis, conventionally known as nosebleeds, is the most common
otorhinolaryngologic emergency. More than 60% of the population
is affected at some point in time, with 6% requiring medical
attention.1
It is a condition encountered by multiple specialties—
primary care physicians, emergency physicians, otolaryngologists,
hematologist/oncologists, and geneticists, to name a few. In fact,
approximately 1 in 200 visits to the emergency department is
centered on acute management of epistaxis.2
There is a bimodal
distribution for peak incidence, with children younger than 10
years of age and adults older than 35 years of age being most
commonly afflicted.3
Furthermore, epistaxis tends to be more
common among men, and more visits tend to occur in the winter.4
A possible explanation in variation between men and women is
that estrogen appears to have a protective effect on the nasal
vasculature,5
and the winter season, especially in less humid
geographic reasons, tends to irritate the nasal mucosa and increase
the risk of bleeding.6
The vast majority of cases are due to local
mucosal trauma either from digital trauma (nose picking), vigorous
nose blowing, or cold, dry climate exposure. However, rarer causes
47 Epistaxis
Edward C. Kuan, James N. Palmer
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47
CHAPTER 47 Epistaxis 733.e1
Keywords
Epistaxis
packing
hemostasis
sphenopalatine
anterior ethmoidal
embolization
hereditary hemorrhagic telangiectasia
Abstract
Epistaxis is the most common otorhinolaryngologic emergency.
Conservative measures are efficacious in the vast majority of cases,
and successful hemostasis is dependent on identification of the
source of bleeding. Nasal packing controls most cases of epistaxis
but is uncomfortable and may worsen nasal trauma. Operative
ligation of the sphenopalatine artery is a safe and effective way
to treat refractory epistaxis, whereas embolization may be reserved
for specific cases.
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734 PART IV Sinus, Rhinology, and Allergy/Immunology
the superior, middle, and inferior turbinates. These branches are
encountered during turbinate reduction or resection procedures
and are located in the posterolateral root of each structure. The
descending palatine artery travels inferiorly into the greater palatine
canal and becomes the greater and lesser palatine arteries within
the hard and soft palate, respectively. Tributaries of the greater
palatine artery then travel anteriorly and reenter the nose through
the incisive foramen, providing vascular supply to the anterior
inferior septum and the nasal floor.
The internal carotid artery supplies the nasal cavity through
the ophthalmic artery branches. The anterior and posterior
ethmoidal arteries branch from the ophthalmic artery within the
medial orbit and travel from lateral to medial (and from posterior
to anterior) via the anterior and posterior ethmoidal foramina
within the anterior skull base, respectively. In approximately 30%
of patients, there is also a middle ethmoidal artery located between
the two, although it tends to be unilateral and positioned within
the skull base.18,19
Although the posterior ethmoidal arteries are
almost always located within the skull base, the anterior ethmoidal
arteries are “low-lying,” or located below the skull base, in up to
25% of cases.20-22
Epistaxis arising from the anterior or posterior
ethmoidal arteries requires disruption of the vessel within a
mesentery below the skull base or within its bony canal and typically
happens only following skull base trauma or surgical dissection.
MANAGEMENT
Initial Considerations
Prior to evaluation of any patient with epistaxis, the otorhinolar-
yngologist must consider possible underlying conditions that may
complicate management. For instance, antiplatelet agent (e.g.,
aspirin, clopidogrel, and nonsteroidal antiinflammatory drugs) use,
anticoagulant (e.g., warfarin, enoxaparin, and heparin) use, herbal
supplement (e.g., ginger, gingko biloba, and ginseng) use, systemic
coagulopathy (e.g., liver cirrhosis), uremia (e.g., renal failure),
thrombocytopenia (e.g., chemotherapy and hematologic malignan-
cies), and other predisposing bleeding disorders (e.g., von
Willebrand disease and hemophilia) are all factors that may make
control of intranasal hemorrhage much more challenging, and
successful control is likely only possible through addressing the
underlying causes (Table 47.2). Arterial hypertension is thought
to have some association with epistaxis, although there is conflicting
data. A systematic review and meta-analysis found that the presence
of hypertension conferred more than 50% risk of epistaxis.23
Evidence suggesting a link is based on increased long-term wear
and tear and atherosclerotic changes to small vessel walls due to
increased hemodynamic pressures,24-27
whereas evidence against
a link proposes that hypertension may in fact be a byproduct of
epistaxis-induced anxiety.28,29
In either case, it seems that epistaxis
control is more challenging in hypertensive patients, and, as a
principle,29
attaining good blood pressure control may assist in
mitigating the incidence and severity of epistaxis.
During the initial assessment, attention should be paid to
the “ABCs” —namely, assessing vital signs, cardiovascular status,
and circulatory volume as a result of blood loss. Large-volume
epistaxis can cause aspiration of blood, and for those patients
with poor pulmonary reserve, endotracheal intubation may be
necessary for stabilization in the short term. An attempt should
be made to determine the side, amount, timing, frequency,
and duration of blood loss. Intravenous access, preferably with
large-bore needles for those patients with large volume loss,
for fluid resuscitation should be obtained. The earliest clinical
sign of acute blood loss is tachycardia. Orthostatic hypotension
may be present early as well. Dry mucous membranes, mucosal
pallor, and hypotension are all later signs and portend significant
blood loss. For those patients where large volume or ongoing
blood loss is apparent, a complete blood count with hemoglobin/
TABLE 47.1 Differential Diagnosis of Epistaxis
General Etiology Specific Disorders
Primary mucosal Mucosal irritation (e.g., cold, dry weather)—
generally spontaneous
Continuous positive airway pressure
Nasal cannula
Septal deviation
Septal perforation
General systemic Hypertension
Arteriosclerosis
Hereditary hemorrhagic telangiectasias (Fig. 47.5)
Thrombocytopenia—primary, drug-induced,
leukemia/lymphoma
Antiplatelet/anticoagulation agent use
Chronic liver disease, cirrhosis
Chronic kidney disease
Trauma Digital manipulation
Nose blowing
Facial or skull base fractures (e.g., anterior
ethmoidal arteries)
Foreign body
Piercings
Chemical injury
Iatrogenic Postoperative from nasal, septal, or sinus surgery
(Fig. 47.6)
Nasogastric tube placement
Nasal packing
Drugs Topical nasal steroids
Saline sprays
Cocaine abuse
Infectious Viral, bacterial, and fungal rhinosinusitis
Inflammatory Granulomatosis with polyangiitis (Wegener)
Sarcoidosis
Eosinophilic granulomatosis with polyangiitis
(Churg-Strauss)
Neoplastic Hemangioma (Fig. 47.7)
Pyogenic granuloma (Fig. 47.8)
Papilloma—inverted, squamous
Juvenile angiofibroma (Fig. 47.9)
Malignancy—carcinomas, sarcomas, and
lymphomas
Hematologic Hemophilia
Von Willebrand disease
BOX 47.1 Vascular Supply of the Nasal Cavity
External Carotid Artery Internal Carotid Artery
Internal maxillary artery* Ophthalmic artery*
Sphenopalatine artery Anterior ethmoidal artery
Posterior septal branch Middle ethmoidal artery
(variable)
Posterior lateral nasal branches
Superior turbinate Posterior ethmoidal artery
Middle turbinate
Inferior turbinate
Descending palatine artery*
Greater palatine artery
Facial artery*
Superior labial artery
Ascending pharyngeal artery
Vidian artery (can be from internal
carotid)
*Indicates branches that do not directly supply the nasal cavity.
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47
CHAPTER 47 Epistaxis 735
Kiesselbach plexus
or Little area
Sphenopalatine
foramen
Maxillary a.
Internal
carotid a.
Ophthalmic a.
Posterior
ethmoidal a.
Anterior
ethmoidal a.
Septal branch of
sphenopalatine a.
Kiesselbach
plexus or
Little area
Anterior ethmoidal a.
Posterior
ethmoidal a.
Internal
carotid a.
Maxillary a.
Sphenopalatine a.
Woodruff area
Posterior
ethmoidal a.
Anterior ethmoidal a.
Ophthalmic a.
A
B
Fig. 47.1 (A) Vascular anatomy of the lateral nasal wall (left) and nasal septum (right). (B) Diagram depicting
tributaries supplying the nasal cavity as they branch from the main trunks arising from the face and neck.
a., artery. (From Chiu AG, Palmer JN, Adappa ND (eds): Atlas of Endoscopic Sinus and Skull Base Surgery,
ed 2, Philadelphia: Elsevier, 2013.)
Fig. 47.2 Kiesselbach plexus as seen on the anterior right nasal
septum during nasal endoscopy. (From Chiu AG, Palmer JN, Adappa
ND (eds): Atlas of Endoscopic Sinus and Skull Base Surgery, ed 2,
Philadelphia: Elsevier, 2013.)
Middle
turbinate
Inferior
turbinate
Choana
Fig. 47.3 Woodruff plexus as seen on the posterior left lateral nasal
wall during nasal endoscopy. (From Chiu AG, Palmer JN, Adappa ND
(eds): Atlas of Endoscopic Sinus and Skull Base Surgery, ed 2,
Philadelphia: Elsevier, 2013.)
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736 PART IV Sinus, Rhinology, and Allergy/Immunology
recommend patients to use these measures more frequently during
colder weather, due to the elevated risk of epistaxis.
Conservative Measures
In general, most cases of anterior epistaxis can be controlled with
firm pressure applied to the soft tissue/cartilaginous portion of
the anterior nose for 15 to 20 minutes while the head is tilted
forward (i.e., chin to chest) in the upright position. There are two
critical components of this management principle. The first is
“no peeking” or fighting the temptation to release pressure before
the allotted time is up to check if bleeding has ceased. Platelet
plugs take up to 20 minutes to form and may not be functional
hematocrit and blood typing should be obtained to determine the
need for transfusion. Updated guidelines recommend consider-
ation of transfusion at or below a hemoglobin level of 7 g/dL
(8 g/dL for patients with cardiovascular comorbidities or following
cardiac or orthopedic surgery) in adult patients who are otherwise
hemodynamically stable.30
Preventive Measures
Because many cases of recurrent epistaxis occur from trauma to
or mucosal irritation of the Kiesselbach plexus, topical moisturiza-
tion and nasal humidification are oftentimes a highly effective
strategy for preventing anterior epistaxis.31,32
Over-the-counter
moisturizing creams, jelly, or ointments can be applied to the
nasal vestibule multiple times per day to address the anterior nasal
cavity, and nasal saline sprays can be used in a similar fashion to
moisturize the middle or posterior areas of the nasal cavity. Patients
should be warned regarding direct fingernail or spray bottle tip
trauma, which will inevitably worsen bleeding. The authors
N = 2 N = 6 N = 18 N = 16 N = 6 N = 1 N = 6
N = 5 N = 1 N = 5 N = 1 N = 1 N = 2 N = 1
Fig. 47.4 Diagrams illustrating the highly variable anatomy of the
sphenopalatine artery as it enters the nasal cavity posterior to the
crista ethmoidalis. (Modified from Simmen D, Raghavan U, Manestar
M, et al: The anatomy of the sphenopalatine artery for the endoscopic
sinus surgeon. Am J Rhinol 20, 502–505, 2006.)
Fig. 47.5 Nasal endoscopy of the left nasal cavity in a patient with
hereditary hemorrhagic telangiectasia. Note the numerous mucosal
telangiectasias covering the inferior turbinate and nasal septal
mucosa.
Fig. 47.6 Bleeding from the middle turbinate branch of the left
sphenopalatine artery following middle turbinate resection.
Fig. 47.7 Hemangioma of the right nasal septum.
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47
CHAPTER 47 Epistaxis 737
to sniff several times per minute until the bleeding ceases.
Anecdotally, this is especially effective for patients presenting
with slow ooze epistaxis following nasal, septal, or sinus surgery,
because their nasal cavities tend to be more widely open fol-
lowing surgical treatment of sources of obstruction, thereby
introducing more laminar airflow. Sometimes a large clot forms
and occludes the nasal airway, which decreases the effectiveness
of this strategy, and gentle suctioning along the floor of nose
may be warranted.
A useful adjunct to epistaxis control is topical vasoconstrictor
use. Traditionally, cocaine has played a large role in sinonasal
hemostasis but is less frequently used nowadays due to its status
as a controlled substance and other potential adverse effects. Instead,
oxymetazoline, a selective α1-adrenergic receptor agonist and
α2-adrenergic receptor partial agonist, has become the most readily
available topical vasoconstrictor used in the management of
epistaxis. It has an outstanding safety profile with limited systemic
absorption and is relatively inexpensive.33
A common strategy is
to deliver oxymetazoline spray into the bleeding side(s) before
holding pressure with the head tilted forward. For the most part,
the vasoconstriction attained with topical agents is additive with
holding pressure in achieving hemostasis. However, the use of
oxymetazoline should be limited to 3 days or less to minimize the
risk of rhinitis medicamentosa. In addition, there is some evidence
suggesting that oral and/or topical tranexamic acid may help in
treating epistaxis.34
Greater Palatine Canal Injection
Prior to performing endoscopic sinus surgery, injection of the
greater palatine canal with lidocaine and diluted epinephrine has
been shown to improve the surgical field and intraoperative
hemostasis, especially when dissecting the posterior ethmoid cavity.35
The greater palatine canal leads superiorly to the sphenopalatine
foramen and, thus, exerts a hemostatic effect on the sphenopalatine
artery directly. Bharadwaj and Novotny reported a 90% posterior
epistaxis control rate in a cohort of 61 patients with this technique,
although 36% developed recurrent epistaxis and required an
if not allowed time to mature. The second is to have the patient
remain upright in the tilt-forward position (“chin-to-chest”) because
leaning the head back to prevent egress of blood out of the nares
may actually cause inadvertent swallowing (with subsequent
vomiting) and aspiration of blood. The patient should remain
calm during this time; sometimes an ice pack over the forehead
and/or face is helpful.
An alternative strategy for management of slow-rate epistaxis
is through gentle nasal inspiration, much like “sniffing,” of air.
The thought is that constant influx and efflux of air creates a
local drying effect over bleeding surfaces. Patients are asked
Fig. 47.8 Pyogenic granuloma of the left middle turbinate.
Fig. 47.9 Juvenile angiofibroma as seen through right-sided nasal
endoscopy.
TABLE 47.2 Predisposing Conditions That May Worsen Epistaxis and
Suggested Ways to Address the Underlying Cause
Predisposing Condition Management
Antiplatelet agents (e.g., aspirin,
clopidogrel, and NSAIDs)
Effect persists for up to 7–10 days
Hold medication, if possible
Platelet transfusion may help but
not completely
NSAIDs more readily reversible
with platelets
Anticoagulation (e.g., warfarin,
enoxaparin, and heparin)
Variable duration of effect based
on drug
Hold medication, if possible
Warfarin: FFP, vitamin K
Herbal supplements (e.g., ginger,
gingko biloba, and ginseng)
Variable duration of effect
Thrombocytopenia Platelet transfusion (goal
>50,000/µL for active bleeding,
>10,000/µL to prevent
spontaneous bleeding)
Liver cirrhosis Monitor PT/INR
FFP for acute bleeding
Renal failure and uremia Desmopressin
Hemodialysis
Von Willebrand disease Desmopressin (types 1 and 2A)
Factor VIII replacement
Hemophilia Factor replacement
FFP, Fresh frozen plasma; INR, international normalized ratio;
NSAID, nonsteroidal antiinflammatory drugs; PT, prothrombin time.
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738 PART IV Sinus, Rhinology, and Allergy/Immunology
anesthetized and decongested (e.g., with lidocaine and oxymetazo-
line), and local anesthesia (e.g., lidocaine with dilute epinephrine)
can be helpful. Usually, a setting of 15 W is sufficient for directed
control of even arterial bleeds, with minimal risk of causing col-
lateral mucosal trauma.
Alternatively, absorbable topical hemostatic materials may be
used at the bleeding site to promote platelet aggregation and local
activation of the coagulation pathway.This has the added advantage
of minimizing discomfort from cautery as well as avoiding mucosal
trauma as in the case of nasal packing. Some materials include
oxidized regenerated cellulose (Surgicel, Ethicon, Somerville, NJ),47
gelatin sponge (Gelfoam, Pfizer, New York City, NY), microfibrillar
collagen (Avitene, C. R. Bard, Murray Hill, NJ), fibrin glue (Tisseel,
Baxter, Deerfield, IL),48-50
and thrombin with gelatin matrix (Floseal,
Baxter, Deerfield, IL). Floseal, especially, has gained popularity
recently as a potent hemostatic agent that can be used for both
anterior and posterior epistaxis.51-54
In all cases the hemostatic
material is gently applied over the bleeding site and gentle pressure
should be exerted toward the bleeding surface to “push” the
hemostatic material into it.
In all cases where directed treatment is successful, a significant
advantage is that the patient may not require admission. Following
successful hemostasis, patients should be instructed to refrain from
blowing the nose for at least 1 week. The cauterized area will
form a scab, which should be left alone to slough off spontaneously,
leaving a healed surface behind. Patients may moisturize the nasal
cavities with saline sprays and creams to prevent buildup of crusts.
Nasal Packing
If the otorhinolaryngologist cannot identify the source of bleeding,
if bleeding is from multiple sources, if no specialized equipment
or expertise in endoscopic management is available, or if the patient
cannot tolerate extensive bedside nasal manipulation, then nasal
packing may be warranted as either a temporizing measure or
definitive management. A population-based epidemiologic study
of U.S. emergency departments identified lower socioeconomic
status, geography within the South or Midwest, nontrauma hospital
status, long-term anticoagulation, male gender, older age, and
winter season as risk factors associated with the use of nasal packing
as an initial form of management for epistaxis.55
A cost analysis
performed in the late 1990s found that nasal packing was overall
more or as cost effective as arterial ligation or embolization56
;
however, emergency department charges tend to be more costly
when nasal packing was performed.55
The first step in most cases is to place an anterior nasal pack.
These can be either absorbable or nonabsorbable and can generally
be inserted into the nasal cavity with bayonet forceps or manually,
with a nasal speculum to dilate the nares. Of importance is to
direct the nasal pack along the axis of the nasal floor inferiorly
and not superiorly toward the middle turbinate and skull base
(Fig. 47.10). Commonly used absorbable packing includes synthetic
polyurethane foam (Nasopore or Hemopore, Stryker, Kalamazoo,
MI) and hyaluronic acid (MeroGel, Medtronic, Minneapolis, MN).57
These materials tend to break down within a week of placement
and may be readily suctioned and debrided in the office setting.
However, the major disadvantages are that absorbable nasal packs
typically do not apply significant pressure and, thus, may not be
suited for controlling arterial bleeds, and there is a potential risk
for undue nasal mucosal trauma during placement. Nevertheless,
as compared with nonabsorbable packing, absorbable packing
appears to be better tolerated by patients, with improved reported
pain and satisfaction scores.58
Nonabsorbable packs (e.g., polyvinyl alcohol [Merocel,
Medtronic, Minneapolis, MN; Rhino Rocket, Summit Medical,
Berkeley Heights, NJ]) typically exert more pressure due to their
ability to absorb surrounding water and expand. Thus they may
even control high pressure arterial bleeds but must be removed
additional injection (with hemostasis afterwards).36
The injection
is performed by using a long 25-gauge syringe needle bent 1.5 cm
from the tip and advanced into the greater palatine canal located
just medial to the upper second molar. The needle must fall into
a space easily and should be aspirated to ensure that no epinephrine
is delivered intravascularly into the descending palatine vessels.
Then, 1 mL of diluted epinephrine is given and the degree of
epistaxis subsequently reassessed.
Examination With Source Identification
Identifying the source of bleeding in a patient with epistaxis is
essential for tailoring treatment.37,38
The otolaryngologist should
wear eye protection, gather towels and basins for the patient to
catch blood, and acquire a light source and suction device, with
multiple calibers of suctions, if possible. Intranasal blood and clots
should be gently suctioned with a small caliber (8, 10, or 12 French)
Frazier suction tip and the nose examined with either a headlight
or a rigid endoscope. Although it may provide excellent visualiza-
tion, the flexible nasolaryngoscope often requires two-hand use
and precludes simultaneous instrumentation of the bleeding site.
In addition, the oral cavity and oropharynx should be thoroughly
suctioned with a Yankauer suction tip to ensure clearing out all
blood that may potentially be swallowed or aspirated as well as
to check for continued posterior bleeding.
Address Coagulopathy
Correcting, or at least mitigating, any underlying cause of coagu-
lopathy is of essence in successful management of epistaxis (see
Table 47.2). In fact, according to a study by Jones et al., nearly
half of patients presenting with epistaxis had abnormal coagulation
studies.39
However, routine laboratory screening is not necessary
(and not cost effective) unless there is suggestive information
derived from the history, such as a positive bleeding history,
anticoagulant/antiplatelet agent use, or chronic liver disease.40
Long-term warfarin use is fairly common in patients presenting
with epistaxis, accounting for 8% of emergency department
admissions.41
For those patients who are supratherapeutic on
warfarin, reversal of the anticoagulation effect is indicated, although
patients who are within the designated therapeutic range may not
need to be reversed.42
Reversal of warfarin can be done by
administering fresh frozen plasma while stopping the warfarin.
Vitamin K has a slower onset of action and delays restarting warfarin
due to its longer half-life (effects up to 1 week after administration).
Patients with a history of alcohol use may be at increased risk for
recalcitrant epistaxis due to its effects in decreasing plasma
fibrinogen levels;43
thus this should be ascertained in the history.44,45
Directed Treatment—Cautery or Topical
Hemostatic Agents
Either chemical or electrical cautery may be used for local control
of epistaxis. Most commonly, silver nitrate sticks can be used to
apply chemical cautery to a prominent nasal mucosal vessel. The
technique is less effective when the vessel is actively bleeding, and
if this occurs, firm pressure with a pledget following application
of cautery may help.46
There is a theoretical risk of causing septal
perforation from cauterizing opposing sides of the nasal septal
mucosa in one sitting, and this should be avoided.
For actively bleeding patients, monopolar or bipolar electro-
cautery, preferably used in conjunction with a suction device, is
extremely effective in controlling the bleeding site, regardless of
whether it is venous or arterial. It may be used over sites of mucosal
oozing or an actively pumping artery. Although commonly per-
formed in the operating room under general anesthesia, electro-
cautery may be performed in the awake, office setting for patients
who can tolerate some discomfort. The nasal cavities should be
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47
CHAPTER 47 Epistaxis 739
anteriorly. This is followed by anterior packing, usually in the
form of long 1
2 - to 1-inch petrolatum gauze strips, to fill the
bilateral nasal cavities. The authors recommend two technical
modifications of significance—one is to tie the ends of the multiple
gauze strips together so that all gauze can be removed at the same
time without risk of foreign body retention and possible aspiration;
another is to start gauze placement with the ends outside of the
nose, working the ends in only after a substantial amount of gauze
has already been packed so that the ends would not inadvertently
fall down into the oropharynx. Equally important is securing the
balloon in place without undue pressure against the nasal alae,
and, thus, some form of padding, usually gauze or makeshift
after staying in place for 3 to 5 days.59
Due to continuous pressure
exerted across all nasal mucosal surfaces with increased absorption
of water from surrounding mucus, the extent of mucosal trauma
may be greater than that in the case of absorbable packs, which,
in some cases, may actually worsen bleeding. One way to decrease
mucosal trauma is to cover the nonabsorbable pack with a latex
glove finger and suture the ends, creating a so-called finger cot,
prior to placement (Fig. 47.11). Some nonabsorbable packs, such
as the Rapid Rhino (Arthrocare, Austin, TX), have built-in anterior
and/or posterior balloon cuffs that may be inflated with water to
provide additional pressure points based on the expected locations
of the bleeds.54,60,61
Prior to packing removal, the nasal packs should
be moistened with water or saline solution because packs tend to
dry out when left in place for several days.
For unilateral anterior nasal packs or even some cases of bilateral
nonabsorbable nasal packs, patients may not require admission
for monitoring. Nasal packing tends to be rather uncomfortable
for patients and may lead to further mucosal trauma in multiple
areas, hypoxia, pain, nasal dryness, epiphora from obstruction of
the nasolacrimal duct, eustachian tube dysfunction, and iatrogenic
sinusitis from blockage of natural ostia. Packing removal is also
uncomfortable and anxiety provoking. For these reasons, targeted
treatment of the source of bleeding should be attempted first
whenever possible.
The “gold standard” for nasal packing is placement of a posterior
nasopharyngeal pack (e.g., Foley catheter and tonsil sponges)
followed by anterior packing. This is usually indicated for posterior
arterial bleeds or epistaxis refractory to cautery and anterior packing.
Most popularly, the procedure involves the threading of a large-
diameter (i.e., 12 or 14 French) Foley balloon with a 30-cc balloon
through one nostril, into the nasopharynx, and inferiorly into the
oropharynx where the distal tip should be visible in the back of
the mouth (Fig. 47.12). Only when the distal tip is confirmed to
be in the oropharynx should the cuff be inflated with 5 to 10 mL
of water and pulled back to occlude the choana, which may
tamponade posterior bleeding or, at the very least, direct it
Fig. 47.10 From left to right, the figure demonstrates placement of nasal packing, a coronal CT scan, and a
sagittal CT scan of the sinuses. Proper placement of nasal packing should follow the axis of the floor of the
nose in a somewhat inferior vector (top). Improper placement tends to bias the operator superiorly, where the
packing may sit against the middle turbinate or other structures, causing discomfort and ineffective
hemostasis (bottom).
Fig. 47.11 Custom-made “finger cot” made using a 10-cm polyvinyl
alcohol (Merocel) covered with the middle finger of a latex glove and
secured in place with a 2-0 Prolene suture. The addition of the latex
glove is less traumatic during placement and removal of the packing.
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740 PART IV Sinus, Rhinology, and Allergy/Immunology
be given to performing local, directed treatment of bleeding sites,
if still present. Ultimately, nasal packing, although effective in
controlling epistaxis in most cases, is uncomfortable and often
requires inpatient hospital monitoring and may cause additional
undue nasal trauma.
Endoscopic Sphenopalatine Artery Ligation
Over the years, endoscopic sphenopalatine artery ligation (ESPAL)
has gained in prominence as a reliable, safe, and effective way to
control epistaxis refractory to conservative measures and as a
substitute to nasal packing.72-75
The procedure is usually performed
under general anesthesia. The initial step is to identify the crista
ethmoidalis, which is a small, medially oriented bone ridge anterior
or anteroinferior to the sphenopalatine foramen (Fig. 47.13). It
is posterior to the posterior wall of the maxillary sinus, superior
to the inferior border of the horizontal part of the middle turbinate,
anterior to the sphenoid face, and inferior to the retromaxillary
area of the posterior ethmoid cells. In 95% of cases, the spheno-
palatine foramen is located within 1 mm of the crista ethmoidalis.76
The mucosa may be incised anterior to it and elevated posteriorly
until the crista ethmoidalis is identified. The crista is then removed
with Kerrison rongeurs, which should expose the sphenopalatine
artery branches emerging from the foramina posteriorly. Oftentimes,
a blunt probe can be placed behind the branches and dissected
medially and laterally to isolate them one by one for ligation.
Numerous techniques exist for arterial ligation, including clip
placement, bipolar electrocautery, or monopolar electrocautery,
and are dependent on surgeon preference. Once hemostasis has
been confirmed, the flap may then be replaced and a small amount
of dissolvable hemostatic material (e.g., Avitene or Surgicel) is
placed over the dissected area. No postoperative nasal packing is
indicated. Patients may be monitored overnight for any recurrent
bleeding, and a nasal saline spray may be started 1 to 2 days after
the procedure.
A purported reason for recurrent epistaxis following ESPAL
is failure to identify and clip all branches of the sphenopalatine
artery as it enters the nasal cavity. The various tributaries of the
sphenopalatine artery may branch at any point between the
pterygopalatine fossa and the nasal cavity, forming numerous
foramina. Therefore, although the anatomy is highly variable, a
meaningful search for multiple branches should be attempted.16
ESPAL is highly effective in long-term epistaxis control
(>90%).77
In an early series, initial control rates were 87%, with
no complications encountered.72
In comparison with nasal packing,
one series involving 537 patients reported that posterior nasal
packing achieved hemostasis in 62% of cases, whereas surgical
management was successful in 97% of cases.78
Furthermore, a
cost analysis revealed that ESPAL tended to be much more cost-
saving than posterior nasal packing, even if the duration of posterior
packing was decreased to 2 days,79
and another study noted
decreased length of stay when compared with nasal packing (3
days versus 6 days).80
The most common complaints include nasal
crusting and nasopalatal paresthesia, both of which are usually
transient.
Endoscopic Maxillary Artery Ligation
One alternative means to circumvent dissection and individual
control of all sphenopalatine tributaries is to attain proximal control
through maxillary artery ligation (Fig. 47.14).81,82
Exposure of this
large-caliber vessel involves a maxillary antrostomy with exposure
of the posterior wall of the maxillary sinus. The mucosa overlying
the posterior wall is removed and the underlying bone widely
drilled or removed with Kerrison rongeurs. Deep to the bone is
the periosteum of the pterygopalatine fossa, which should be
preserved while the bone is still being removed. The periosteum
can be electrocauterized to expose the pterygopalatine fossa fat.
modification of the proximal balloon itself, is recommended.62-65
Nasal alar necrosis can occur with mismanagement of the nasal
balloon and is notoriously difficult to reconstruct.66,67
Finally,
patients with posterior balloon nasal packing should be monitored
with continuous pulse oximetry and telemetry, with consideration
of intensive care unit admission for those patients with preexisting
cardiac or pulmonary comorbidities.68
Another theoretical concern
for justifying cardiac monitoring is activation of the nasocardiac
reflex in certain sensitive individuals, where continuous nasal
stimulation may produce a reflexive bradycardia.69
Despite this,
a systematic review did not find that respiratory complications
are more prevalent among patients with nasal packing.70
There is some debate regarding the necessity of prophylactic
systemic antibiotics for patients with nasal packing. The traditional
teaching is that nasal packing acts like a tampon within a rich
bacterial culture medium (blood and mucus), thereby risking
opportunistic sinusitis and potentially leading to Staphylococcus-
mediated toxic shock syndrome. Thus systemic antibiotics with
antistaphylococcal coverage are generally considered prophylacti-
cally for patients with nasal packing. However, a systematic review
evaluating adverse events in 990 patients across six studies found
no cases of toxic shock syndrome when prophylactic antibiotics
were not used.71
Although unlikely to occur in this population,
the dangers of toxic shock syndrome most likely outweigh the
risks of developing antibiotic resistance, and the authors would
recommend a short course (1 to 2 weeks) of clindamycin and/or
trimethoprim-sulfamethoxazole while nasal packing is in place.
Resolution of acute epistaxis is confirmed by direct examination
of both the anterior nares and the oropharynx (run down from
above). Nasal packing should be left in place to allow for the
formation of a mature clot at the sites of bleeding. Usually, this
will take anywhere between 1 and 5 days. It may be more comfort-
able to moisten the packing prior to removal, and patients should
use a nasal saline spray starting 1 to 2 days following no further
bleeding. Once packing is removed, nasal endoscopy or headlight
examination should be reattempted to evaluate for any residual
bleeding. Equally important is to assess trauma to the nasal mucosa,
which often may stir up additional bleeding. Consideration should
Fig. 47.12 Critical view of the Foley balloon tip in the oropharynx
when placing posterior packing. Proper placement should be
confirmed prior to inflating the balloon.
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47
CHAPTER 47 Epistaxis 741
The maxillary artery travels from lateral to medial and can often
be seen as a pulsatile structure once the fat is exposed. A blunt
probe can be used to isolate the main trunk and dissect both
medially and laterally to accommodate clip placement. Two clips
should be placed proximally over the entire circumference of the
vessel and one distally; bipolar electrocautery is applied between
the clips and the artery transected. Dissolvable hemostatic material
is placed over the field and the patient monitored overnight. Nasal
saline sprays may be started 1 to 2 days postoperatively.
Reported outcomes for maxillary artery ligation are comparable
with those achieved for ESPAL, although maxillary artery ligation
is frequently performed for skull base procedures, such as
transpterygoid approaches or resection of juvenile angiofibromas.75,81
Previously, maxillary artery ligation was performed via a transantral
approach (Caldwell-Luc). Although this provides excellent instru-
ment access and is still favored in many cases requiring extended
exposure, modified endoscopic approaches to the lateral maxillary
sinus and infratemporal fossa have precluded the absolute need
for open approaches.83,84
Due to more extensive dissection of the
pterygopalatine fossa, there is an increased risk to the surrounding
neural structures, including the vidian nerve (decreased lacrimation
and dry eyes), greater palatine nerve (palatal paresthesia), and
infraorbital nerve (cheek and nasal paresthesia).
Ligation of the External Carotid Artery
A last resort option for control of refractory, severe epistaxis is
ligation of the ipsilateral external carotid artery through a
transcervical approach.85,86
Due to more sophisticated endoscopic
techniques affording improved visualization and dissection, this
is no longer favored due to its more invasive nature without proven
additional benefit.
Anterior Ethmoidal Artery Ligation
An uncommon source of epistaxis is from the anterior eth-
moidal artery, which usually arises from skull base trauma (e.g.,
MT
U
MT
U
Fig. 47.13 Exposure of the left sphenopalatine artery (left, arrow) with subsequent bipolar electrocautery. The
crista ethmoidalis has been resected for access. MT, Middle turbinate; U, uncinate process. (From Chiu AG,
Palmer JN, Adappa ND (eds): Atlas of Endoscopic Sinus and Skull Base Surgery, ed 2, Philadelphia: Elsevier,
2013.)
Middle
turbinate
Crista
ethmoidalis
Sphenopalatine
foramen
Sphenopalatine a.
Internal
maxillary a.
Fig. 47.14 Schematic depicting the anatomy of the right maxillary
artery within the pterygopalatine fossa and the right sphenopalatine
artery as it exits the sphenopalatine foramen. Note the relationship to
the crista ethmoidalis. (From Chiu AG, Palmer JN, Adappa ND (eds):
Atlas of Endoscopic Sinus and Skull Base Surgery, ed 2, Philadelphia:
Elsevier, 2013.)
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742 PART IV Sinus, Rhinology, and Allergy/Immunology
suggests that the progressive distances between the anterior lacrimal
crest, anterior ethmoidal foramen, posterior ethmoidal foramen,
and optic canal are 24, 12, and 6 mm, respectively. However, a
recent cadaveric study found that, although the distances are
relatively consistent, the number of foramina is not, and otorhi-
nolaryngologists should be aware of the possibility of multiple
branches.91,92
The incision may be closed with fast-absorbing gut
sutures and treated with erythromycin ophthalmic ointment for
several days postoperatively.
Embolization
Cerebral angiography with transarterial embolization by inter-
ventional radiologists is an effective option for treatment of
recalcitrant epistaxis, with reported success in 75% to 92% of
cases (Fig. 47.16).93-95
Advantages include avoiding the need for
general anesthesia and use in poor surgical candidates. However,
inadvertent embolization of nontarget vessels or migration of
embolic materials has been associated with blindness (ophthalmic
artery), cerebrovascular accident (internal carotid artery), and other
complications related to vascular infarction. Other possible
complications include hematoma formation at the puncture site
(e.g., femoral artery) and acute kidney injury due to iodinated
contrast material administration. According to a systematic review
evaluating surgical versus interventional radiologic treatment of
adult epistaxis, stroke was reported in 1.1% to 1.5% of cases.95
The maxillary artery is the most commonly selected target vessel
for embolization in patients with epistaxis. Other external carotid
system tributaries may also be embolized, but embolization is not
recommended for the internal carotid system due to the risk of
stroke and/or blindness. From an economic perspective, emboliza-
tion appears to be more costly than surgical management.96,97
There are certain specific indications for when embolization
is a more desired option than surgical management of epistaxis.
First, embolization is effective for control of epistaxis due to
nasopharyngeal carcinoma98-100
and other tumors of the sinonasal
tract. Because most cases are now surgically resectable, this is an
effective strategy to obliterate tumor-feeding vessels without
violating the external surface. Second, preoperative embolization
is helpful for vascular tumors, especially juvenile angiofibromas,
prior to surgical resection and has been shown to decrease
intraoperative blood loss due to devascularization of the tumor.101-104
In fact, in some cases, decreased vascularity actually slightly
decreases the size of the tumor, thereby improving surgical access.
Third, in cases of craniofacial trauma with distorted anatomy and
mobile bone fragments, embolization is potentially helpful in
controlling oronasal hemorrhage.105,106
Finally, epistaxis from the
carotid artery, either through iatrogenic carotid injury during
endoscopic sinus or skull base surgery or blowout from other
external causes, is best managed definitively with local control at
the site of intranasal bleeding following by interventional radiologic
treatment.107-110
PEDIATRIC EPISTAXIS
Unless there is an unusual underlying cause (e.g., coagulopathy
and tumor), epistaxis in children invariably self-resolves with
conservative management. Digital trauma is extremely common
in this population and is a frequent cause of self-limiting anterior
epistaxis. Moisturizing the anterior nares and nasal mucosal
humidification remain effective strategies in this cohort.111
In
cooperative children, the addition of silver nitrate cautery has
been shown to be highly effective in addressing prominent septal
vessels.112,113
Young children who present with recurrent severe
epistaxis should be screened for bleeding disorders such as
hemophilia or von Willebrand disease. Juvenile angiofibroma
should be part of the differential diagnosis for any adolescent
male complaining of unilateral nasal obstruction and epistaxis.
naso-orbito-ethmoidal fractures) or iatrogenic injury (e.g.,
endoscopic sinus or skull base surgery). The artery has a rather
variable location but can always be found between the second and
third lamella.87
The risk of injury to the anterior ethmoidal artery
is higher when it is dehiscent from the skull base. Risk factors
for low-lying anterior ethmoidal arteries include the presence of
a supraorbital ethmoid air cell, high Keros classification (deeper
olfactory fossa), and increased distance between the anterior wall
of the frontal sinus to the skull base.22
If the anterior ethmoidal
artery is transected more medially, the likely outcome is epistaxis
that is unlikely to stop without surgical intervention (due to its
superior location in the nasal cavity). If transected more laterally,
the proximal stump may retract into the orbit and produce a
retrobulbar hematoma, which is a surgical emergency requiring
immediate orbital decompression. In performing anterior skull base
surgery (e.g., transcribriform and transplanum approaches), the
anterior and posterior ethmoidal arteries are often prophylactically
ligated for tumor resection.
Endoscopic ligation of the anterior ethmoidal artery begins
with a complete ethmoidectomy and defining the ethmoid skull
base.20,88
If the anterior ethmoidal artery is located within a bony
canal, it may need to be gently drilled to expose the vessel;
otherwise, a curette may be used to manipulate the bone fragments
off the vessel (Fig. 47.15). Clips may be applied if the vessel is
isolated, although bipolar electrocautery on a low setting is equally
effective in achieving hemostasis. The artery does not need to be
transected following cauterization unless purposeful skull base
entry is desired.
Alternatively, the ethmoidal arteries may be ligated through
an open, transorbital approach. The Lynch incision is a straight-
forward approach to the anatomy in this area, although it has the
potential disadvantage of leaving a visible scar. The precaruncular
or transcaruncular approach is a newer, scarless technique, which
offers excellent exposure to the anterior and posterior ethmoidal
arteries within their bony foramina.89,90
The lacrimal caruncle is
incised (transcaruncular) or an incision made anterior to it
(precaruncular), with dissection carried through the superior and
inferior conjunctival folds. Horner muscle is identified and left
undissected, and the periorbita posterior to its insertion is incised
vertically to expose the lamina papyracea. Blunt elevation posteriorly
will reveal the ethmoidal neurovascular foramina sequentially,
which may be ligated and divided. Traditional anatomic teaching
Frontal sinus
Septum
Orbit
Anterior
ethmoidal artery
Fig. 47.15 Endoscopic view of the left anterior ethmoidal artery. The
bony canal is being drilled in preparation for bipolar electrocautery.
(From Chiu AG, Palmer JN, Adappa ND (eds): Atlas of Endoscopic
Sinus and Skull Base Surgery, ed 2, Philadelphia: Elsevier, 2013.)
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47
CHAPTER 47 Epistaxis 743
to septal perforations, although many HHT patients usually present
with perforations secondary to repeated bouts of nasal packing.
Less commonly performed surgical treatments for HHT-related
epistaxis include septodermoplasty and nasal closure.137
Septoder-
moplasty involves removing the septal and nasal floor mucosa
(which harbor telangiectasias), leaving the underlying perichondrium
intact, and replacing it with a split-thickness skin graft (Fig.
47.17).127,138,139
Nasal closure, or Lund modified Young’s procedure,
Hereditary Hemorrhagic Telangiectasia
(Osler-Weber-Rendu)
Hereditary hemorrhagic telangiectasia (HHT, Osler-Weber-Rendu)
is an autosomal dominant multisystem vascular disorder that causes
variable cutaneous and mucosal telangiectasia formation as well
as arteriovenous malformations in the lungs, brain, and liver.
Epistaxis from nasal telangiectasias is the most common complaint
in HHT patients, afflicting more than 90% of individuals. With
progression of the disease over time, patients present with repeated
epistaxis of varying severity and frequency, with significant negative
impact on quality of life.114-116
These patients are also prone to
receiving repeated transfusions due to their epistaxis. Coordination
of multidisciplinary care among otorhinolaryngologists, geneticists,
interventional radiologists, and other specialists is of critical
importance in the long-term care of these patients.117
Conservative measures apply for most cases of HHT-related
epistaxis. Nasal humidification and avoidance of trauma (i.e.,
minimize nasal packing) prevent inadvertent trauma to telangi-
ectasias.118
Hormonal therapy with antiestrogen agents (e.g.,
tamoxifen) have been explored for their antiendothelial effects,
with promise demonstrated in some studies.119-121
Intranasal beva-
cizumab, an antivascular endothelial growth factor A monoclonal
antibody, has recently been explored for use in HHT-related
epistaxis. However, at this point, the current evidence is conflicting
with regard to its efficacy.122-126
With respect to surgical treatments, the most widely performed
procedure is cauterization and/or laser photocoagulation of nasal
telangiectasias.127-132
T
o achieve submucosal ablation of blood vessels
while attempting to spare the mucosa, the potassium titanyl
phosphate (KTP) laser is commonly used. Outcomes following
laser treatments are variable but generally will decrease the severity
and frequency of epistaxis over the course of months to years,
with corresponding improvement in the quality of life of patients.133
Other thermal instruments, such as the bipolar electrocautery and
coblator, are also effective adjuncts to laser treatment and may be
more effective when telangiectasias are actively bleeding.134-136
It
is important to note that bilateral thermal treatments may lead
A B
Fig. 47.16 Preembolization (A) and postembolization (B) cerebral angiography of a left-sided juvenile
angiofibroma. Notice the tumor blush (dotted arrows) fed by the left sphenopalatine/maxillary artery (solid
arrow) disappear in this successful embolization. (From Chiu AG, Palmer JN, Adappa ND (eds): Atlas of
Endoscopic Sinus and Skull Base Surgery, ed 2, Philadelphia: Elsevier, 2013.)
Fig. 47.17 Septodermoplasty. Split-thickness skin grafts are
harvested and secured over septal perichondrium. (From Palmer JN,
Chiu AG, Adappa ND (eds): Atlas of Endoscopic Sinus and Skull Base
Surgery, ed 1.)
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744 PART IV Sinus, Rhinology, and Allergy/Immunology
produces complete cessation of bleeding when there is complete
cessation of airflow through the nose and is reserved for the most
severe cases that have failed other treatments.140-142
SUMMARY
Epistaxis is the most common otorhinolaryngologic emergency,
and an algorithm for management is presented (Fig. 47.18).
Conservative measures are efficacious in the vast majority of cases,
ABCs
Fluid resuscitation
Establish intravenous access
Complete blood count, type and screen
Control hypertension
Treat any underlying cause predisposing
to bleeding
Suction clots
Examine nose with headlamp or rigid
endoscopy to identify source of
bleeding
Source identified
Bipolar electrocautery, silver nitrate
cautery, or topical hemostatic agent
Hemostasis achieved
Nasal humidification, nasal saline sprays,
nasal creams to anterior nares
Facial trauma
Nasopharyngeal carcinoma or other
sinonasal tumor
Carotid injury
Angiography and embolization
Endoscopic sphenopalatine artery ligation
Evaluate all possible areas for bleeding
Consider possibility of multiple branches
If rebleed with packing in or after packing
removed
Nasal packing − dissolvable vs. non-
dissolvable, anterior vs. posterior,
minimize nasal trauma
Consider prophylactic antibiotics
Keep packing in 1-5 days depending on
severity of bleed
Source not identified or unable to control
Fig. 47.18 Algorithm for managing epistaxis when conservative measures have failed. The decision branching
point between nasal packing and endoscopic sphenopalatine artery ligation is important to discuss with the
patient.
and successful hemostasis is dependent on identification of the
source of bleeding. Nasal packing controls most cases of epistaxis
but is uncomfortable and may worsen nasal trauma. Operative
ligation of the sphenopalatine artery is a safe and effective way
to treat refractory epistaxis, whereas embolization may be reserved
for specific cases.
For a complete list of references, visit ExpertConsult.com.
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47
CHAPTER 47 Epistaxis 744.e1
27. Elwany S, Ibrahim AA, Soliman AI, et al: The significance of ath-
erosclerosis in hypertensive patients with epistaxis, J Laryngol Otol
1–4, 2018.
28. Kikidis D, Tsioufis K, Papanikolaou V, et al: Is epistaxis associated
with arterial hypertension? A systematic review of the literature, Eur
Arch Otorhinolaryngol 271:237–243, 2014.
29. Sarhan NA,Algamal AM: Relationship between epistaxis and hyperten-
sion: a cause and effect or coincidence?, J Saudi Heart Assoc 27:79–84,
2015.
30. Carson JL, Guyatt G, Heddle NM, et al: Clinical practice guidelines
from the AABB: red blood cell transfusion thresholds and storage,
JAMA 316:2025–2035, 2016.
31. Murthy P, Nilssen EL, Rao S, et al: A randomised clinical trial of
antiseptic nasal carrier cream and silver nitrate cautery in the treatment
of recurrent anterior epistaxis, Clin Otolaryngol Allied Sci 24:228–231,
1999.
32. London SD, Lindsey WH: A reliable medical treatment for recurrent
mild anterior epistaxis, Laryngoscope 109:1535–1537, 1999.
33. Higgins TS, Hwang PH, Kingdom TT, et al: Systematic review of
topical vasoconstrictors in endoscopic sinus surgery, Laryngoscope
121:422–432, 2011.
34. Kamhieh Y, Fox H: Tranexamic acid in epistaxis: a systematic review,
Clin Otolaryngol 41:771–776, 2016.
35. Eloy JA, Kovalerchik O, Bublik M, et al: Effect of greater palatine
canal injection on estimated blood loss during endoscopic sinus
surgery, Am J Otolaryngol 35:1–4, 2014.
36. Bharadwaj VK, Novotny GM: Greater palatine canal injection: an
alternative to the posterior nasal packing and arterial ligation in
epistaxis, J Otolaryngol 15:94–100, 1986.
37. Chiu TW, McGarry GW: Prospective clinical study of bleeding sites
in idiopathic adult posterior epistaxis, Otolaryngol Head Neck Surg
137:390–393, 2007.
38. Thornton MA, Mahesh BN, Lang J: Posterior epistaxis: identification
of common bleeding sites, Laryngoscope 115:588–590, 2005.
39. Jones GL, Browning S, Phillipps J: The value of coagulation profiles
in epistaxis management, Int J Clin Pract 57:577–578, 2003.
40. Awan MS, Iqbal M, Imam SZ: Epistaxis: when are coagulation studies
justified?, Emerg Med J 25:156–157, 2008.
41. Thaha MA, Nilssen EL, Holland S, et al: Routine coagulation screen-
ing in the management of emergency admission for epistaxis–is it
necessary?, J Laryngol Otol 114:38–40, 2000.
42. Srinivasan V, Patel H, John DG, et al: Warfarin and epistaxis: should
warfarin always be discontinued?, Clin Otolaryngol Allied Sci 22:542–544,
1997.
43. Dimmitt SB, Rakic V, Puddey IB, et al: The effects of alcohol on
coagulation and fibrinolytic factors: a controlled trial, Blood Coagul
Fibrinolysis 9:39–45, 1998.
44. McGarry GW, Gatehouse S, Hinnie J: Relation between alcohol
and nose bleeds, BMJ 309:640, 1994.
45. McGarry GW, Gatehouse S, Vernham G: Idiopathic epistaxis,
haemostasis and alcohol, Clin Otolaryngol Allied Sci 20:174–177, 1995.
46. Barr GD: Silver nitrate cautery and epistaxis, Arch Emerg Med 6:233,
1989.
47. Bhatnagar RK, Berry S: Selective surgicel packing for the treatment
of posterior epistaxis, Ear Nose Throat J 83:633–634, 2004.
48. Vaiman M, Segal S, Eviatar E: Fibrin glue treatment for epistaxis,
Rhinology 40:88–91, 2002.
49. Walshe P: The use of fibrin glue to arrest epistaxis in the presence
of a coagulopathy, Laryngoscope 112:1126–1128, 2002.
50. Walshe P, Harkin C, Murphy S, et al: The use of fibrin glue in refrac-
tory coagulopathic epistaxis, Clin Otolaryngol Allied Sci 26:284–285,
2001.
51. Khan MK, Reda El Badawey M, Powell J, et al: The utility of FloSeal
haemostatic agent in the management of epistaxis, J Laryngol Otol
129:353–357, 2015.
52. Mathiasen RA, Cruz RM: Prospective, randomized, controlled clinical
trial of a novel matrix hemostatic sealant in patients with acute anterior
epistaxis, Laryngoscope 115:899–902, 2005.
53. Wakelam OC, Dimitriadis PA, Stephens J: The use of FloSeal
haemostatic sealant in the management of epistaxis: a prospective
clinical study and literature review, Ann R Coll Surg Engl 99:28–30,
2017.
54. Iqbal IZ, Jones GH, Dawe N, et al: Intranasal packs and haemostatic
agents for the management of adult epistaxis: systematic review,
J Laryngol Otol 131:1065–1092, 2017.
REFERENCES
1. Tomkinson A, Roblin DG, Flanagan P, et al: Patterns of hospital
attendance with epistaxis, Rhinology 35:129–131, 1997.
2. Pallin DJ, Chng YM, McKay MP, et al: Epidemiology of epistaxis in
US emergency departments, 1992 to 2001, Ann Emerg Med 46:77–81,
2005.
3. Walker TW, Macfarlane TV, McGarry GW: The epidemiology
and chronobiology of epistaxis: an investigation of Scottish hospital
admissions 1995-2004, Clin Otolaryngol 32:361–365, 2007.
4. Chaaban MR, Zhang D, Resto V, et al: Demographic, seasonal, and
geographic differences in emergency department visits for epistaxis,
Otolaryngol Head Neck Surg 156:81–86, 2017.
5. Ross CS, Pruthi RK, Schmidt KA, et al: Intranasal oestrogen cream
for the prevention of epistaxis in patients with bleeding disorders,
Haemophilia 17:164, 2011.
6. Comelli I, Vincenti V, Benatti M, et al: Influence of air temperature
variations on incidence of epistaxis, Am J Rhinol Allergy 29:e175–e181,
2015.
7. Integrate, National ENTTRN: Epistaxis 2016: national audit of
management, J Laryngol Otol 131:1131–1141, 2017.
8. Bequignon E, Verillaud B, Robard L, et al: Guidelines of the French
Society of Otorhinolaryngology (SFORL). First-line treatment of epi-
staxis in adults, Eur Ann Otorhinolaryngol Head Neck Dis 134:185–189,
2017.
9. Bertrand B, Eloy P, Rombaux P, et al: Guidelines to the management
of epistaxis, B-ENT Suppl 1:27–41, quiz 42–43, 2005.
10. Daudia A, Jaiswal V, Jones NS: Guidelines for the management of
idiopathic epistaxis in adults: how we do it, Clin Otolaryngol 33:618–620,
2008.
11. Verillaud B, Robard L, Michel J, et al: Guidelines of the French Society
of Otorhinolaryngology (SFORL). Second-line treatment of epistaxis
in adults, Eur Ann Otorhinolaryngol Head Neck Dis 134:191–193, 2017.
12. Leung RM, Smith TL, Rudmik L: Developing a laddered algorithm
for the management of intractable epistaxis: a risk analysis, JAMA
Otolaryngol Head Neck Surg 141:405–409, 2015.
13. Shargorodsky J, Bleier BS, Holbrook EH, et al: Outcomes analysis
in epistaxis management: development of a therapeutic algorithm,
Otolaryngol Head Neck Surg 149:390–398, 2013.
14. Vosler PS, Kass JI, Wang EW, et al: Successful Implementation of
a Clinical Care Pathway for Management of Epistaxis at a Tertiary
Care Center, Otolaryngol Head Neck Surg 155:879–885, 2016.
15. Gras-Cabrerizo JR,Adema-Alcover JM, Gras-Albert JR, et al: Anatomi-
cal and surgical study of the sphenopalatine artery branches, Eur
Arch Otorhinolaryngol 271:1947–1951, 2014.
16. Simmen DB, Raghavan U, Briner HR, et al: The anatomy of the
sphenopalatine artery for the endoscopic sinus surgeon, Am J Rhinol
20:502–505, 2006.
17. Hadad G, Bassagasteguy L, Carrau RL, et al: A novel reconstructive
technique after endoscopic expanded endonasal approaches: vascular
pedicle nasoseptal flap, Laryngoscope 116:1882–1886, 2006.
18. Mason E, Solares CA, Carrau RL, et al: Computed tomographic
exploration of the middle ethmoidal artery, J Neurol Surg B Skull
Base 76:372–378, 2015.
19. Wang L, Youseef A, Al Qahtani AA, et al: Endoscopic anatomy of the
middle ethmoidal artery, Int Forum Allergy Rhinol 4:164–168, 2014.
20. Floreani SR, Nair SB, Switajewski MC, et al: Endoscopic anterior
ethmoidal artery ligation: a cadaver study, Laryngoscope 116:1263–1267,
2006.
21. Poteet PS, Cox MD, Wang RA, et al: Analysis of the Relationship
between the Location of the Anterior Ethmoid Artery and Keros
Classification, Otolaryngol Head Neck Surg 157:320–324, 2017.
22. Sjogren PP, Waghela R, Ashby S, et al: International Frontal Sinus
Anatomy Classification and anatomic predictors of low-lying anterior
ethmoidal arteries, Am J Rhinol Allergy 31:174–176, 2017.
23. Min HJ, Kang H, Choi GJ, et al: Association between hypertension
and epistaxis: systematic review and meta-analysis, Otolaryngol Head
Neck Surg 157:921–927, 2017.
24. Herkner H, Havel C, Mullner M, et al: Active epistaxis at ED
presentation is associated with arterial hypertension, Am J Emerg
Med 20:92–95, 2002.
25. Terakura M, Fujisaki R, Suda T, et al: Relationship between blood
pressure and persistent epistaxis at the emergency department: a
retrospective study, J Am Soc Hypertens 6:291–295, 2012.
26. Abrich V, Brozek A, Boyle TR, et al: Risk factors for recurrent
spontaneous epistaxis, Mayo Clin Proc 89:1636–1643, 2014.
Descargado para ALEX LARA (ua.alexlara@uniandes.edu.ec) en Regional Autonomous University of the Andes de ClinicalKey.es por Elsevier en diciembre 04,
2022. Para uso personal exclusivamente. No se permiten otros usos sin autorización. Copyright ©2022. Elsevier Inc. Todos los derechos reservados.
PART IV Sinus, Rhinology, and Allergy/Immunology
744.e2
82. Piastro K, Scagnelli R, Gildener-Leapman N, et al: Outcomes of
sphenopalatine and internal maxillary artery ligation inside the
pterygopalatine fossa for posterior epistaxis, Rhinology 2018.
83. Harvey RJ, Sheehan PO, Debnath NI, et al: Transseptal approach
for extended endoscopic resections of the maxilla and infratemporal
fossa, Am J Rhinol Allergy 23:426–432, 2009.
84. Upadhyay S, Dolci RL, Buohliqah L, et al: Endoscopic endonasal
anterior maxillotomy, Laryngoscope 125:2668–2671, 2015.
85. Hassard AD, Kirkpatrick DA, Wong FS: Ligation of the external
carotid and anterior ethmoidal arteries for severe or unusual epistaxis
resulting from facial fractures, Can J Surg 29:447–449, 1986.
86. Waldron J, Stafford N: Ligation of the external carotid artery for
severe epistaxis, J Otolaryngol 21:249–251, 1992.
87. Simmen D, Raghavan U, Briner HR, et al: The surgeon’s view of
the anterior ethmoid artery, Clin Otolaryngol 31:187–191, 2006.
88. Woolford TJ, Jones NS: Endoscopic ligation of anterior ethmoidal
artery in treatment of epistaxis, J Laryngol Otol 114:858–860, 2000.
89. Cornelis MM, Lubbe DE: Pre-caruncular approach to the medial
orbit and landmarks for anterior ethmoidal artery ligation: a cadaveric
study, Clin Otolaryngol 41:777–781, 2016.
90. Morera E, Artigas C, Ferran L, et al: Transcaruncular electrocoagula-
tion of anterior ethmoidal artery for the treatment of severe epistaxis,
Laryngoscope 121:446–450, 2011.
91. Shaheen OH: Arterial epistaxis, J Laryngol Otol 89:17–34, 1975.
92. Abed SF, Shams P, Shen S, et al: A cadaveric study of ethmoidal
foramina variation and its surgical significance in Caucasians, Br J
Ophthalmol 96:118–121, 2012.
93. Moreau S, De Rugy MG, Babin E, et al: Supraselective embolization
in intractable epistaxis: review of 45 cases, Laryngoscope 108:887–888,
1998.
94. Cohen JE, Moscovici S, Gomori JM, et al: Selective endovascular
embolization for refractory idiopathic epistaxis is a safe and effective
therapeutic option: technique, complications, and outcomes, J Clin
Neurosci 19:687–690, 2012.
95. Swords C, Patel A, Smith ME, et al: Surgical and interventional
radiological management of adult epistaxis: systematic review,
J Laryngol Otol 131:1108–1130, 2017.
96. Miller TR, Stevens ES, Orlandi RR: Economic analysis of the treat-
ment of posterior epistaxis, Am J Rhinol 19:79–82, 2005.
97. Rudmik L, Leung R: Cost-effectiveness analysis of endoscopic
sphenopalatine artery ligation vs arterial embolization for intractable
epistaxis, JAMA Otolaryngol Head Neck Surg 140:802–808, 2014.
98. He CC, Si YF, Xie YA, et al: Management of intractable epistaxis in
patients who received radiation therapy for nasopharyngeal carcinoma,
Eur Arch Otorhinolaryngol 270:2763–2767, 2013.
99. Mok JS, Marshall JN, Chan M, et al: Percutaneous embolization to
control intractable epistaxis in nasopharyngeal carcinoma, Head Neck
21:211–216, 1999.
100. Wong GK, Chan KK, Yu SC, et al: Treatment of profuse epistaxis
in patients irradiated for nasopharyngeal carcinoma, ANZ J Surg
77:270–274, 2007.
101. Ballah D, Rabinowitz D, Vossough A, et al: Preoperative angiography
and external carotid artery embolization of juvenile nasopharyngeal
angiofibromas in a tertiary referral paediatric centre, Clin Radiol
68:1097–1106, 2013.
102. Elhammady MS, Johnson JN, Peterson EC, et al: Preoperative
embolization of juvenile nasopharyngeal angiofibromas: transarterial
versus direct tumoral puncture, World Neurosurg 76:328–334, discussion
263–265, 2011.
103. Gao M, Gemmete JJ, Chaudhary N, et al: A comparison of par-
ticulate and onyx embolization in preoperative devascularization of
juvenile nasopharyngeal angiofibromas, Neuroradiology 55:1089–1096,
2013.
104. Lutz J, Holtmannspotter M, Flatz W, et al: Preoperative emboliza-
tion to improve the surgical management and outcome of juvenile
nasopharyngeal angiofibroma (JNA) in a single center: 10-year
experience, Clin Neuroradiol 26:405–413, 2016.
105. Komiyama M, Nishikawa M, Kan M, et al: Endovascular treatment
of intractable oronasal bleeding associated with severe craniofacial
injury, J Trauma 44:330–334, 1998.
106. Liao CC, Hsu YP, Chen CT, et al: Transarterial embolization for
intractable oronasal hemorrhage associated with craniofacial trauma:
evaluation of prognostic factors, J Trauma 63:827–830, 2007.
107. Adeel M, Ikram M: Post-traumatic pseudoaneurysm of internal carotid
artery: a cause of intractable epistaxis, BMJ Case Rep 2012:2012.
55. Sethi RKV, Kozin ED, Abt NB, et al: Treatment disparities in the
management of epistaxis in United States emergency departments,
Laryngoscope 128:356–362, 2018.
56. Goddard JC, Reiter ER: Inpatient management of epistaxis: outcomes
and cost, Otolaryngol Head Neck Surg 132:707–712, 2005.
57. Yan M, Zheng D, Li Y, et al: Biodegradable nasal packings for
endoscopic sinonasal surgery: a systematic review and meta-analysis,
PLoS ONE 9:e115458, 2014.
58. Wang J, Cai C, Wang S: Merocel versus Nasopore for nasal packing:
a meta-analysis of randomized controlled trials, PLoS ONE 9:e93959,
2014.
59. Pringle MB, Beasley P, Brightwell AP: The use of Merocel nasal
packs in the treatment of epistaxis, J Laryngol Otol 110:543–546,
1996.
60. Gudziol V, Mewes T, Mann WJ: Rapid Rhino: a new pneumatic
nasal tamponade for posterior epistaxis, Otolaryngol Head Neck Surg
132:152–155, 2005.
61. Badran K, Malik TH, Belloso A, et al: Randomized controlled trial
comparing Merocel and RapidRhino packing in the management of
anterior epistaxis, Clin Otolaryngol 30:333–337, 2005.
62. Ho EC, Mansell NJ: How we do it: a practical approach to Foley
catheter posterior nasal packing, Clin Otolaryngol Allied Sci 29:754–757,
2004.
63. Ismail H, Buckland JR, Harries PG: The prevention of alar necrosis
in Foley catheter fixation in posterior epistaxis, Ann R Coll Surg Engl
86:307, 2004.
64. Judd O, Gaskin J: Securing the posterior nasal pack; a technique to
prevent alar necrosis, Ann R Coll Surg Engl 91:713–714, 2009.
65. Thomas L, Karagama YG, Watson C: Avoiding alar necrosis with
post-nasal packs, J Laryngol Otol 119:727–728, 2005.
66. Civelek B, Kargi AE, Sensoz O, et al: Rare complication of nasal
packing: alar region necrosis, Otolaryngol Head Neck Surg 123:656–657,
2000.
67. Vermeeren L, Derks W, Fokkens W, et al: Complications of balloon
packing in epistaxis, Eur Arch Otorhinolaryngol 272:3077–3081, 2015.
68. Corrales CE, Goode RL: Should patients with posterior nasal packing
require ICU admission?, Laryngoscope 123:2928–2929, 2013.
69. Baxandall ML, Thorn JL: The nasocardiac reflex, Anaesthesia
43:480–481, 1988.
70. Rotenberg B, Tam S: Respiratory complications from nasal packing:
systematic review, J Otolaryngol Head Neck Surg 39:606–614, 2010.
71. Lange JL, Peeden EH, Stringer SP: Are prophylactic systemic
antibiotics necessary with nasal packing? A systematic review, Am J
Rhinol Allergy 31:240–247, 2017.
72. Snyderman CH, Goldman SA, Carrau RL, et al: Endoscopic sphe-
nopalatine artery ligation is an effective method of treatment for
posterior epistaxis, Am J Rhinol 13:137–140, 1999.
73. Wormald PJ, Wee DT, van Hasselt CA: Endoscopic ligation of the
sphenopalatine artery for refractory posterior epistaxis, Am J Rhinol
14:261–264, 2000.
74. 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 28:360–363, 2003.
75. Seno S, Arikata M, Sakurai H, et al: Endoscopic ligation of the
sphenopalatine artery and the maxillary artery for the treatment
of intractable posterior epistaxis, Am J Rhinol Allergy 23:197–199,
2009.
76. Bolger WE, Borgie RC, Melder P: The role of the crista ethmoidalis
in endoscopic sphenopalatine artery ligation, Am J Rhinol 13:81–86,
1999.
77. Abdelkader M, Leong SC, White PS: Endoscopic control of the
sphenopalatine artery for epistaxis: long-term results, J Laryngol Otol
121:759–762, 2007.
78. Soyka MB, Nikolaou G, Rufibach K, et al: On the effectiveness
of treatment options in epistaxis: an analysis of 678 interventions,
Rhinology 49:474–478, 2011.
79. Dedhia RC, Desai SS, Smith KJ, et al: Cost-effectiveness of endoscopic
sphenopalatine artery ligation versus nasal packing as first-line treat-
ment for posterior epistaxis, Int Forum Allergy Rhinol 3:563–566, 2013.
80. McDermott AM, O’Cathain E, Carey BW, et al: Sphenopalatine
artery ligation for epistaxis: factors influencing outcome and impact
of timing of surgery, Otolaryngol Head Neck Surg 154:547–552, 2016.
81. Pritikin JB, Caldarelli DD, Panje WR: Endoscopic ligation of the
internal maxillary artery for treatment of intractable posterior epistaxis,
Ann Otol Rhinol Laryngol 107:85–91, 1998.
Descargado para ALEX LARA (ua.alexlara@uniandes.edu.ec) en Regional Autonomous University of the Andes de ClinicalKey.es por Elsevier en diciembre 04,
2022. Para uso personal exclusivamente. No se permiten otros usos sin autorización. Copyright ©2022. Elsevier Inc. Todos los derechos reservados.
47
CHAPTER 47 Epistaxis 744.e3
126. Whitehead KJ, Sautter NB, McWilliams JP, et al: Effect of topical
intranasal therapy on epistaxis frequency in patients with hereditary
hemorrhagic telangiectasia: a randomized clinical trial, JAMA 316:
943–951, 2016.
127. Harvey RJ, Kanagalingam J, Lund VJ: The impact of septodermoplasty
and potassium-titanyl-phosphate (KTP) laser therapy in the treatment
of hereditary hemorrhagic telangiectasia-related epistaxis, Am J Rhinol
22:182–187, 2008.
128. Jorgensen G, Lange B, Wanscher JH, et al: Efficiency of laser treat-
ment in patients with hereditary hemorrhagic telangiectasia, Eur Arch
Otorhinolaryngol 268:1765–1770, 2011.
129. Poje G, Kavanagh MM: Hereditary hemorrhagic telangiectasia-laser
treatment of epistaxis, Ear Nose Throat J 96:E10–E14, 2017.
130. Sautter NB, Smith TL: Treatment of hereditary hemorrhagic
telangiectasia-related epistaxis, Otolaryngol Clin North Am 49:639–654,
2016.
131. Werner A, Baumler W, Zietz S, et al: Hereditary haemorrhagic
telangiectasia treated by pulsed neodymium:yttrium-aluminium-garnet
(Nd:YAG) laser (1,064 nm), Lasers Med Sci 23:385–391, 2008.
132. Fiorella ML, Lillo L, Fiorella R: Diode laser in the treatment of
epistaxis in patients with hereditary haemorrhagic telangiectasia, Acta
Otorhinolaryngol Ital 32:164–169, 2012.
133. Kuan EC, Peng KA, Thompson CF, et al: Sinonasal quality of life
outcomes following laser treatment of epistaxis related to hereditary
hemorrhagic telangiectasia, Lasers Med Sci 32:527–531, 2017.
134. Dabiri J, Fakhoury R, Choufani G, et al: Cauterization for epistaxis
in hereditary hemorrhagic telangiectasia, B-ENT 12:9–16, 2016.
135. Ghaheri BA, Fong KJ, Hwang PH: The utility of bipolar electrocautery
in hereditary hemorrhagic telangiectasia, Otolaryngol Head Neck Surg
134:1006–1009, 2006.
136. Poetker DM: Endoscopic-guided coblation treatment of nasal
telangiectasias in hereditary hemorrhagic telangiectasia: “How I do
it”, Am J Rhinol Allergy 31:205–206, 2017.
137. Lund VJ, Howard DJ: A treatment algorithm for the management
of epistaxis in hereditary hemorrhagic telangiectasia, Am J Rhinol
13:319–322, 1999.
138. Bastianelli M, Kilty SJ: Technique modifications for septodermoplasty:
an illustrative case, J Otolaryngol Head Neck Surg 44:59, 2015.
139. Geisthoff UW, Fiorella ML, Fiorella R: Treatment of recurrent
epistaxis in HHT, Curr Pharm Des 12:1237–1242, 2006.
140. Hitchings AE, Lennox PA, Lund VJ, et al: The effect of treatment
for epistaxis secondary to hereditary hemorrhagic telangiectasia, Am
J Rhinol 19:75–78, 2005.
141. Lund VJ, Darby Y, Rimmer J, et al: Nasal closure for severe hereditary
haemorrhagic telangiectasia in 100 patients. The Lund modification
of the Young’s procedure: a 22-year experience, Rhinology 55:135–141,
2017.
142. Lund VJ, Howard DJ: Closure of the nasal cavities in the treatment
of refractory hereditary haemorrhagic telangiectasia, J Laryngol Otol
111:30–33, 1997.
108. Pepper JP, Wadhwa AK, Tsai F, et al: Cavernous carotid injury during
functional endoscopic sinus surgery: case presentations and guidelines
for optimal management, Am J Rhinol 21:105–109, 2007.
109. Snyderman CH, Pant H: Endoscopic management of vascular sinonasal
tumors, including angiofibroma, Otolaryngol Clin North Am 49:791–807,
2016.
110. Valentine R, Wormald PJ: Carotid artery injury after endonasal
surgery, Otolaryngol Clin North Am 44:1059–1079, 2011.
111. Ruddy J, Proops DW, Pearman K, et al: Management of epistaxis in
children, Int J Pediatr Otorhinolaryngol 21:139–142, 1991.
112. Qureishi A, Burton MJ: Interventions for recurrent idiopathic epistaxis
(nosebleeds) in children, Cochrane Database Syst Rev (9):CD004461,
2012.
113. Calder N, Kang S, Fraser L, et al: A double-blind randomized
controlled trial of management of recurrent nosebleeds in children,
Otolaryngol Head Neck Surg 140:670–674, 2009.
114. Geisthoff UW, Heckmann K, D’Amelio R, et al: Health-related
quality of life in hereditary hemorrhagic telangiectasia, Otolaryngol
Head Neck Surg 136:726–733, discussion 34–35, 2007.
115. Lennox PA, Hitchings AE, Lund VJ, et al: The SF-36 health status
questionnaire in assessing patients with epistaxis secondary to
hereditary hemorrhagic telangiectasia, Am J Rhinol 19:71–74, 2005.
116. Merlo CA, Yin LX, Hoag JB, et al: The effects of epistaxis on
health-related quality of life in patients with hereditary hemorrhagic
telangiectasia, Int Forum Allergy Rhinol 4:921–925, 2014.
117. Thompson CF, Suh JD, McWilliams J, et al: Initial experience of a
hereditary hemorrhagic telangiectasia center of excellence, Ear Nose
Throat J 96:E33–E36, 2017.
118. Silva BM, Hosman AE, Devlin HL, et al: Lifestyle and dietary influ-
ences on nosebleed severity in hereditary hemorrhagic telangiectasia,
Laryngoscope 123:1092–1099, 2013.
119. Jameson JJ, Cave DR: Hormonal and antihormonal therapy for epistaxis
in hereditary hemorrhagic telangiectasia, Laryngoscope 114:705–709,
2004.
120. Yaniv E, Preis M, Hadar T, et al: Antiestrogen therapy for hereditary
hemorrhagic telangiectasia: a double-blind placebo-controlled clinical
trial, Laryngoscope 119:284–288, 2009.
121. Yaniv E, Preis M, Shevro J, et al: Anti-estrogen therapy for hereditary
hemorrhagic telangiectasia—a long-term clinical trial, Rhinology
49:214–216, 2011.
122. Chin CJ: Is bevacizumab effective for reducing epistaxis in hereditary
hemorrhagic telangiectasia?, Laryngoscope 127:289–290, 2017.
123. Dheyauldeen S, Ostertun Geirdal A, Osnes T, et al: Bevacizumab in
hereditary hemorrhagic telangiectasia-associated epistaxis: effectiveness
of an injection protocol based on the vascular anatomy of the nose,
Laryngoscope 122:1210–1214, 2012.
124. Steineger J, Osnes T, Heimdal K, et al: Long-term experience with
intranasal bevacizumab therapy, Laryngoscope 2018.
125. Stokes P, Rimmer J: Intranasal bevacizumab in the treatment of
HHT—related epistaxis: a systematic review, Rhinology 2017.
Descargado para ALEX LARA (ua.alexlara@uniandes.edu.ec) en Regional Autonomous University of the Andes de ClinicalKey.es por Elsevier en diciembre 04,
2022. Para uso personal exclusivamente. No se permiten otros usos sin autorización. Copyright ©2022. Elsevier Inc. Todos los derechos reservados.

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CAP 47. Epistaxis.pdf

  • 1. 733 47 of epistaxis should always be considered in the differential diagnosis (Table 47.1). As it is more of a symptom rather than a single condition, management principles surrounding epistaxis vary significantly, although all require addressing the underlying cause of the bleeding. Furthermore, despite its high incidence and multiple proposed ways to treat it, epistaxis, in a nationwide study conducted in the United Kingdom, is associated with a 13.9% recurrence rate and 3.4% mortality rate within 30 days of presentation.7 This highlights the importance of familiarizing oneself with a systematic approach to the problem. Over the past few decades, several guidelines or protocols have been proposed to guide clinicians on optimal treatment of this common disorder.8-14 Understanding the possible etiologies, vascular anatomy, and medical and surgical treatments, both in terms of options and timing, is essential for optimizing outcomes and is oftentimes life-saving. The American Academy of Otolaryngology–Head and Neck Surgery is currently preparing a Clinical Practice Guideline for epistaxis, which will be published in June 2019. ANATOMY The nasal cavity and paranasal sinuses have an intensely rich blood supply from both the internal and external carotid arteries (Box 47.1, Fig. 47.1). There is an extremely rich network of vascular anastomoses between the left and right sides and among the various terminal tributaries. Broadly speaking, epistaxis is divided into anterior and posterior sources of bleeding. Anterior epistaxis accounts for the vast majority (>90%) of cases and typically originates from the Kiesselbach plexus (Little area) on the anterior nasal septum, which is a confluence of distal branches from the anterior ethmoidal artery, sphenopalatine artery, greater palatine artery, and superior labial artery (Fig. 47.2). Due to its anterior location, the Kiesselbach plexus is subject to frequent turbulent airflow, which causes local mucosal drying and increased fragility when irritated. Nasal septal deviations may further worsen turbulent airflow and contribute to anterior epistaxis in this location as well. Posterior epistaxis typically arises from branches of the spheno- palatine artery. A prominent network of arteries can often be visualized posterior to the inferior turbinate root and the horizontal part of the middle turbinate and is coined the Woodruff plexus (Fig. 47.3). This area is made up of branches of the sphenopalatine artery and ascending pharyngeal artery and is implicated as a common source of posterior epistaxis. The maxillary artery (formerly referred to as the internal maxillary artery), which is a terminal branch of the external carotid artery, divides into its own terminal branches, the sphenopalatine, descending palatine, infraorbital, and posterior superior alveolar arteries, as it courses through the pterygopalatine fossa from a lateral to medial direction. The sphenopalatine artery enters the nasal cavity through the sphenopalatine foramen and, at this point, exhibits a highly variable branching pattern (Fig. 47.4).15,16 In most cases, there are two clinically important branches—the posterior septal and posterior lateral nasal branches. The posterior septal branch courses from lateral to medial across the superior choana below the natural ostium of the sphenoid sinus. It is the named artery supplying the pedicled vascularized nasoseptal flap and is not uncommonly injured when extending the sphenoidotomy inferiorly.17 The posterior lateral nasal branch further divides into tributaries, which supply KEY POINTS • Epistaxis is a common otorhinolaryngologic complaint encountered by multiple medical disciplines and is the most common otorhinolaryngologic emergency. • The vascular anatomy of the nose is extremely rich, with bilateral supply from both the external and internal carotid systems. • Initial assessment should include evaluating the ABCs and identifying any underlying causes that predispose to bleeding. • Identifying the site of bleeding allows for direct source control, often with cautery or hemostatic agents. • Conservative measures for control of epistaxis include holding pressure, topical vasoconstrictor use, and, in some cases, gentle nasal inspiration. • Although effective in cases when the source of bleeding cannot be found, nasal packing is uncomfortable, causes trauma to the nasal mucosa, and can be costly. • Endoscopic sphenopalatine artery ligation is a safe and effective means to control epistaxis while avoiding the need for posterior nasal packing. • Depending on anatomy, bleeding from the anterior ethmoidal artery can be controlled either endoscopically or via a transorbital approach. • Refractory epistaxis due to nasal tumors, facial trauma, or carotid injury, or for preoperative vascular control, may be suited for interventional radiologic embolization. • Hereditary hemorrhagic telangiectasia is an autosomal dominant vascular disorder, which presents with recurrent epistaxis. Options for surgical treatment include laser photocoagulation or cauterization of nasal telangiectasias, septodermoplasty, or nasal closure. Epistaxis, conventionally known as nosebleeds, is the most common otorhinolaryngologic emergency. More than 60% of the population is affected at some point in time, with 6% requiring medical attention.1 It is a condition encountered by multiple specialties— primary care physicians, emergency physicians, otolaryngologists, hematologist/oncologists, and geneticists, to name a few. In fact, approximately 1 in 200 visits to the emergency department is centered on acute management of epistaxis.2 There is a bimodal distribution for peak incidence, with children younger than 10 years of age and adults older than 35 years of age being most commonly afflicted.3 Furthermore, epistaxis tends to be more common among men, and more visits tend to occur in the winter.4 A possible explanation in variation between men and women is that estrogen appears to have a protective effect on the nasal vasculature,5 and the winter season, especially in less humid geographic reasons, tends to irritate the nasal mucosa and increase the risk of bleeding.6 The vast majority of cases are due to local mucosal trauma either from digital trauma (nose picking), vigorous nose blowing, or cold, dry climate exposure. However, rarer causes 47 Epistaxis Edward C. Kuan, James N. Palmer Descargado para ALEX LARA (ua.alexlara@uniandes.edu.ec) en Regional Autonomous University of the Andes de ClinicalKey.es por Elsevier en diciembre 04, 2022. Para uso personal exclusivamente. No se permiten otros usos sin autorización. Copyright ©2022. Elsevier Inc. Todos los derechos reservados.
  • 2. 47 CHAPTER 47 Epistaxis 733.e1 Keywords Epistaxis packing hemostasis sphenopalatine anterior ethmoidal embolization hereditary hemorrhagic telangiectasia Abstract Epistaxis is the most common otorhinolaryngologic emergency. Conservative measures are efficacious in the vast majority of cases, and successful hemostasis is dependent on identification of the source of bleeding. Nasal packing controls most cases of epistaxis but is uncomfortable and may worsen nasal trauma. Operative ligation of the sphenopalatine artery is a safe and effective way to treat refractory epistaxis, whereas embolization may be reserved for specific cases. Descargado para ALEX LARA (ua.alexlara@uniandes.edu.ec) en Regional Autonomous University of the Andes de ClinicalKey.es por Elsevier en diciembre 04, 2022. Para uso personal exclusivamente. No se permiten otros usos sin autorización. Copyright ©2022. Elsevier Inc. Todos los derechos reservados.
  • 3. 734 PART IV Sinus, Rhinology, and Allergy/Immunology the superior, middle, and inferior turbinates. These branches are encountered during turbinate reduction or resection procedures and are located in the posterolateral root of each structure. The descending palatine artery travels inferiorly into the greater palatine canal and becomes the greater and lesser palatine arteries within the hard and soft palate, respectively. Tributaries of the greater palatine artery then travel anteriorly and reenter the nose through the incisive foramen, providing vascular supply to the anterior inferior septum and the nasal floor. The internal carotid artery supplies the nasal cavity through the ophthalmic artery branches. The anterior and posterior ethmoidal arteries branch from the ophthalmic artery within the medial orbit and travel from lateral to medial (and from posterior to anterior) via the anterior and posterior ethmoidal foramina within the anterior skull base, respectively. In approximately 30% of patients, there is also a middle ethmoidal artery located between the two, although it tends to be unilateral and positioned within the skull base.18,19 Although the posterior ethmoidal arteries are almost always located within the skull base, the anterior ethmoidal arteries are “low-lying,” or located below the skull base, in up to 25% of cases.20-22 Epistaxis arising from the anterior or posterior ethmoidal arteries requires disruption of the vessel within a mesentery below the skull base or within its bony canal and typically happens only following skull base trauma or surgical dissection. MANAGEMENT Initial Considerations Prior to evaluation of any patient with epistaxis, the otorhinolar- yngologist must consider possible underlying conditions that may complicate management. For instance, antiplatelet agent (e.g., aspirin, clopidogrel, and nonsteroidal antiinflammatory drugs) use, anticoagulant (e.g., warfarin, enoxaparin, and heparin) use, herbal supplement (e.g., ginger, gingko biloba, and ginseng) use, systemic coagulopathy (e.g., liver cirrhosis), uremia (e.g., renal failure), thrombocytopenia (e.g., chemotherapy and hematologic malignan- cies), and other predisposing bleeding disorders (e.g., von Willebrand disease and hemophilia) are all factors that may make control of intranasal hemorrhage much more challenging, and successful control is likely only possible through addressing the underlying causes (Table 47.2). Arterial hypertension is thought to have some association with epistaxis, although there is conflicting data. A systematic review and meta-analysis found that the presence of hypertension conferred more than 50% risk of epistaxis.23 Evidence suggesting a link is based on increased long-term wear and tear and atherosclerotic changes to small vessel walls due to increased hemodynamic pressures,24-27 whereas evidence against a link proposes that hypertension may in fact be a byproduct of epistaxis-induced anxiety.28,29 In either case, it seems that epistaxis control is more challenging in hypertensive patients, and, as a principle,29 attaining good blood pressure control may assist in mitigating the incidence and severity of epistaxis. During the initial assessment, attention should be paid to the “ABCs” —namely, assessing vital signs, cardiovascular status, and circulatory volume as a result of blood loss. Large-volume epistaxis can cause aspiration of blood, and for those patients with poor pulmonary reserve, endotracheal intubation may be necessary for stabilization in the short term. An attempt should be made to determine the side, amount, timing, frequency, and duration of blood loss. Intravenous access, preferably with large-bore needles for those patients with large volume loss, for fluid resuscitation should be obtained. The earliest clinical sign of acute blood loss is tachycardia. Orthostatic hypotension may be present early as well. Dry mucous membranes, mucosal pallor, and hypotension are all later signs and portend significant blood loss. For those patients where large volume or ongoing blood loss is apparent, a complete blood count with hemoglobin/ TABLE 47.1 Differential Diagnosis of Epistaxis General Etiology Specific Disorders Primary mucosal Mucosal irritation (e.g., cold, dry weather)— generally spontaneous Continuous positive airway pressure Nasal cannula Septal deviation Septal perforation General systemic Hypertension Arteriosclerosis Hereditary hemorrhagic telangiectasias (Fig. 47.5) Thrombocytopenia—primary, drug-induced, leukemia/lymphoma Antiplatelet/anticoagulation agent use Chronic liver disease, cirrhosis Chronic kidney disease Trauma Digital manipulation Nose blowing Facial or skull base fractures (e.g., anterior ethmoidal arteries) Foreign body Piercings Chemical injury Iatrogenic Postoperative from nasal, septal, or sinus surgery (Fig. 47.6) Nasogastric tube placement Nasal packing Drugs Topical nasal steroids Saline sprays Cocaine abuse Infectious Viral, bacterial, and fungal rhinosinusitis Inflammatory Granulomatosis with polyangiitis (Wegener) Sarcoidosis Eosinophilic granulomatosis with polyangiitis (Churg-Strauss) Neoplastic Hemangioma (Fig. 47.7) Pyogenic granuloma (Fig. 47.8) Papilloma—inverted, squamous Juvenile angiofibroma (Fig. 47.9) Malignancy—carcinomas, sarcomas, and lymphomas Hematologic Hemophilia Von Willebrand disease BOX 47.1 Vascular Supply of the Nasal Cavity External Carotid Artery Internal Carotid Artery Internal maxillary artery* Ophthalmic artery* Sphenopalatine artery Anterior ethmoidal artery Posterior septal branch Middle ethmoidal artery (variable) Posterior lateral nasal branches Superior turbinate Posterior ethmoidal artery Middle turbinate Inferior turbinate Descending palatine artery* Greater palatine artery Facial artery* Superior labial artery Ascending pharyngeal artery Vidian artery (can be from internal carotid) *Indicates branches that do not directly supply the nasal cavity. Descargado para ALEX LARA (ua.alexlara@uniandes.edu.ec) en Regional Autonomous University of the Andes de ClinicalKey.es por Elsevier en diciembre 04, 2022. Para uso personal exclusivamente. No se permiten otros usos sin autorización. Copyright ©2022. Elsevier Inc. Todos los derechos reservados.
  • 4. 47 CHAPTER 47 Epistaxis 735 Kiesselbach plexus or Little area Sphenopalatine foramen Maxillary a. Internal carotid a. Ophthalmic a. Posterior ethmoidal a. Anterior ethmoidal a. Septal branch of sphenopalatine a. Kiesselbach plexus or Little area Anterior ethmoidal a. Posterior ethmoidal a. Internal carotid a. Maxillary a. Sphenopalatine a. Woodruff area Posterior ethmoidal a. Anterior ethmoidal a. Ophthalmic a. A B Fig. 47.1 (A) Vascular anatomy of the lateral nasal wall (left) and nasal septum (right). (B) Diagram depicting tributaries supplying the nasal cavity as they branch from the main trunks arising from the face and neck. a., artery. (From Chiu AG, Palmer JN, Adappa ND (eds): Atlas of Endoscopic Sinus and Skull Base Surgery, ed 2, Philadelphia: Elsevier, 2013.) Fig. 47.2 Kiesselbach plexus as seen on the anterior right nasal septum during nasal endoscopy. (From Chiu AG, Palmer JN, Adappa ND (eds): Atlas of Endoscopic Sinus and Skull Base Surgery, ed 2, Philadelphia: Elsevier, 2013.) Middle turbinate Inferior turbinate Choana Fig. 47.3 Woodruff plexus as seen on the posterior left lateral nasal wall during nasal endoscopy. (From Chiu AG, Palmer JN, Adappa ND (eds): Atlas of Endoscopic Sinus and Skull Base Surgery, ed 2, Philadelphia: Elsevier, 2013.) Descargado para ALEX LARA (ua.alexlara@uniandes.edu.ec) en Regional Autonomous University of the Andes de ClinicalKey.es por Elsevier en diciembre 04, 2022. Para uso personal exclusivamente. No se permiten otros usos sin autorización. Copyright ©2022. Elsevier Inc. Todos los derechos reservados.
  • 5. 736 PART IV Sinus, Rhinology, and Allergy/Immunology recommend patients to use these measures more frequently during colder weather, due to the elevated risk of epistaxis. Conservative Measures In general, most cases of anterior epistaxis can be controlled with firm pressure applied to the soft tissue/cartilaginous portion of the anterior nose for 15 to 20 minutes while the head is tilted forward (i.e., chin to chest) in the upright position. There are two critical components of this management principle. The first is “no peeking” or fighting the temptation to release pressure before the allotted time is up to check if bleeding has ceased. Platelet plugs take up to 20 minutes to form and may not be functional hematocrit and blood typing should be obtained to determine the need for transfusion. Updated guidelines recommend consider- ation of transfusion at or below a hemoglobin level of 7 g/dL (8 g/dL for patients with cardiovascular comorbidities or following cardiac or orthopedic surgery) in adult patients who are otherwise hemodynamically stable.30 Preventive Measures Because many cases of recurrent epistaxis occur from trauma to or mucosal irritation of the Kiesselbach plexus, topical moisturiza- tion and nasal humidification are oftentimes a highly effective strategy for preventing anterior epistaxis.31,32 Over-the-counter moisturizing creams, jelly, or ointments can be applied to the nasal vestibule multiple times per day to address the anterior nasal cavity, and nasal saline sprays can be used in a similar fashion to moisturize the middle or posterior areas of the nasal cavity. Patients should be warned regarding direct fingernail or spray bottle tip trauma, which will inevitably worsen bleeding. The authors N = 2 N = 6 N = 18 N = 16 N = 6 N = 1 N = 6 N = 5 N = 1 N = 5 N = 1 N = 1 N = 2 N = 1 Fig. 47.4 Diagrams illustrating the highly variable anatomy of the sphenopalatine artery as it enters the nasal cavity posterior to the crista ethmoidalis. (Modified from Simmen D, Raghavan U, Manestar M, et al: The anatomy of the sphenopalatine artery for the endoscopic sinus surgeon. Am J Rhinol 20, 502–505, 2006.) Fig. 47.5 Nasal endoscopy of the left nasal cavity in a patient with hereditary hemorrhagic telangiectasia. Note the numerous mucosal telangiectasias covering the inferior turbinate and nasal septal mucosa. Fig. 47.6 Bleeding from the middle turbinate branch of the left sphenopalatine artery following middle turbinate resection. Fig. 47.7 Hemangioma of the right nasal septum. Descargado para ALEX LARA (ua.alexlara@uniandes.edu.ec) en Regional Autonomous University of the Andes de ClinicalKey.es por Elsevier en diciembre 04, 2022. Para uso personal exclusivamente. No se permiten otros usos sin autorización. Copyright ©2022. Elsevier Inc. Todos los derechos reservados.
  • 6. 47 CHAPTER 47 Epistaxis 737 to sniff several times per minute until the bleeding ceases. Anecdotally, this is especially effective for patients presenting with slow ooze epistaxis following nasal, septal, or sinus surgery, because their nasal cavities tend to be more widely open fol- lowing surgical treatment of sources of obstruction, thereby introducing more laminar airflow. Sometimes a large clot forms and occludes the nasal airway, which decreases the effectiveness of this strategy, and gentle suctioning along the floor of nose may be warranted. A useful adjunct to epistaxis control is topical vasoconstrictor use. Traditionally, cocaine has played a large role in sinonasal hemostasis but is less frequently used nowadays due to its status as a controlled substance and other potential adverse effects. Instead, oxymetazoline, a selective α1-adrenergic receptor agonist and α2-adrenergic receptor partial agonist, has become the most readily available topical vasoconstrictor used in the management of epistaxis. It has an outstanding safety profile with limited systemic absorption and is relatively inexpensive.33 A common strategy is to deliver oxymetazoline spray into the bleeding side(s) before holding pressure with the head tilted forward. For the most part, the vasoconstriction attained with topical agents is additive with holding pressure in achieving hemostasis. However, the use of oxymetazoline should be limited to 3 days or less to minimize the risk of rhinitis medicamentosa. In addition, there is some evidence suggesting that oral and/or topical tranexamic acid may help in treating epistaxis.34 Greater Palatine Canal Injection Prior to performing endoscopic sinus surgery, injection of the greater palatine canal with lidocaine and diluted epinephrine has been shown to improve the surgical field and intraoperative hemostasis, especially when dissecting the posterior ethmoid cavity.35 The greater palatine canal leads superiorly to the sphenopalatine foramen and, thus, exerts a hemostatic effect on the sphenopalatine artery directly. Bharadwaj and Novotny reported a 90% posterior epistaxis control rate in a cohort of 61 patients with this technique, although 36% developed recurrent epistaxis and required an if not allowed time to mature. The second is to have the patient remain upright in the tilt-forward position (“chin-to-chest”) because leaning the head back to prevent egress of blood out of the nares may actually cause inadvertent swallowing (with subsequent vomiting) and aspiration of blood. The patient should remain calm during this time; sometimes an ice pack over the forehead and/or face is helpful. An alternative strategy for management of slow-rate epistaxis is through gentle nasal inspiration, much like “sniffing,” of air. The thought is that constant influx and efflux of air creates a local drying effect over bleeding surfaces. Patients are asked Fig. 47.8 Pyogenic granuloma of the left middle turbinate. Fig. 47.9 Juvenile angiofibroma as seen through right-sided nasal endoscopy. TABLE 47.2 Predisposing Conditions That May Worsen Epistaxis and Suggested Ways to Address the Underlying Cause Predisposing Condition Management Antiplatelet agents (e.g., aspirin, clopidogrel, and NSAIDs) Effect persists for up to 7–10 days Hold medication, if possible Platelet transfusion may help but not completely NSAIDs more readily reversible with platelets Anticoagulation (e.g., warfarin, enoxaparin, and heparin) Variable duration of effect based on drug Hold medication, if possible Warfarin: FFP, vitamin K Herbal supplements (e.g., ginger, gingko biloba, and ginseng) Variable duration of effect Thrombocytopenia Platelet transfusion (goal >50,000/µL for active bleeding, >10,000/µL to prevent spontaneous bleeding) Liver cirrhosis Monitor PT/INR FFP for acute bleeding Renal failure and uremia Desmopressin Hemodialysis Von Willebrand disease Desmopressin (types 1 and 2A) Factor VIII replacement Hemophilia Factor replacement FFP, Fresh frozen plasma; INR, international normalized ratio; NSAID, nonsteroidal antiinflammatory drugs; PT, prothrombin time. Descargado para ALEX LARA (ua.alexlara@uniandes.edu.ec) en Regional Autonomous University of the Andes de ClinicalKey.es por Elsevier en diciembre 04, 2022. Para uso personal exclusivamente. No se permiten otros usos sin autorización. Copyright ©2022. Elsevier Inc. Todos los derechos reservados.
  • 7. 738 PART IV Sinus, Rhinology, and Allergy/Immunology anesthetized and decongested (e.g., with lidocaine and oxymetazo- line), and local anesthesia (e.g., lidocaine with dilute epinephrine) can be helpful. Usually, a setting of 15 W is sufficient for directed control of even arterial bleeds, with minimal risk of causing col- lateral mucosal trauma. Alternatively, absorbable topical hemostatic materials may be used at the bleeding site to promote platelet aggregation and local activation of the coagulation pathway.This has the added advantage of minimizing discomfort from cautery as well as avoiding mucosal trauma as in the case of nasal packing. Some materials include oxidized regenerated cellulose (Surgicel, Ethicon, Somerville, NJ),47 gelatin sponge (Gelfoam, Pfizer, New York City, NY), microfibrillar collagen (Avitene, C. R. Bard, Murray Hill, NJ), fibrin glue (Tisseel, Baxter, Deerfield, IL),48-50 and thrombin with gelatin matrix (Floseal, Baxter, Deerfield, IL). Floseal, especially, has gained popularity recently as a potent hemostatic agent that can be used for both anterior and posterior epistaxis.51-54 In all cases the hemostatic material is gently applied over the bleeding site and gentle pressure should be exerted toward the bleeding surface to “push” the hemostatic material into it. In all cases where directed treatment is successful, a significant advantage is that the patient may not require admission. Following successful hemostasis, patients should be instructed to refrain from blowing the nose for at least 1 week. The cauterized area will form a scab, which should be left alone to slough off spontaneously, leaving a healed surface behind. Patients may moisturize the nasal cavities with saline sprays and creams to prevent buildup of crusts. Nasal Packing If the otorhinolaryngologist cannot identify the source of bleeding, if bleeding is from multiple sources, if no specialized equipment or expertise in endoscopic management is available, or if the patient cannot tolerate extensive bedside nasal manipulation, then nasal packing may be warranted as either a temporizing measure or definitive management. A population-based epidemiologic study of U.S. emergency departments identified lower socioeconomic status, geography within the South or Midwest, nontrauma hospital status, long-term anticoagulation, male gender, older age, and winter season as risk factors associated with the use of nasal packing as an initial form of management for epistaxis.55 A cost analysis performed in the late 1990s found that nasal packing was overall more or as cost effective as arterial ligation or embolization56 ; however, emergency department charges tend to be more costly when nasal packing was performed.55 The first step in most cases is to place an anterior nasal pack. These can be either absorbable or nonabsorbable and can generally be inserted into the nasal cavity with bayonet forceps or manually, with a nasal speculum to dilate the nares. Of importance is to direct the nasal pack along the axis of the nasal floor inferiorly and not superiorly toward the middle turbinate and skull base (Fig. 47.10). Commonly used absorbable packing includes synthetic polyurethane foam (Nasopore or Hemopore, Stryker, Kalamazoo, MI) and hyaluronic acid (MeroGel, Medtronic, Minneapolis, MN).57 These materials tend to break down within a week of placement and may be readily suctioned and debrided in the office setting. However, the major disadvantages are that absorbable nasal packs typically do not apply significant pressure and, thus, may not be suited for controlling arterial bleeds, and there is a potential risk for undue nasal mucosal trauma during placement. Nevertheless, as compared with nonabsorbable packing, absorbable packing appears to be better tolerated by patients, with improved reported pain and satisfaction scores.58 Nonabsorbable packs (e.g., polyvinyl alcohol [Merocel, Medtronic, Minneapolis, MN; Rhino Rocket, Summit Medical, Berkeley Heights, NJ]) typically exert more pressure due to their ability to absorb surrounding water and expand. Thus they may even control high pressure arterial bleeds but must be removed additional injection (with hemostasis afterwards).36 The injection is performed by using a long 25-gauge syringe needle bent 1.5 cm from the tip and advanced into the greater palatine canal located just medial to the upper second molar. The needle must fall into a space easily and should be aspirated to ensure that no epinephrine is delivered intravascularly into the descending palatine vessels. Then, 1 mL of diluted epinephrine is given and the degree of epistaxis subsequently reassessed. Examination With Source Identification Identifying the source of bleeding in a patient with epistaxis is essential for tailoring treatment.37,38 The otolaryngologist should wear eye protection, gather towels and basins for the patient to catch blood, and acquire a light source and suction device, with multiple calibers of suctions, if possible. Intranasal blood and clots should be gently suctioned with a small caliber (8, 10, or 12 French) Frazier suction tip and the nose examined with either a headlight or a rigid endoscope. Although it may provide excellent visualiza- tion, the flexible nasolaryngoscope often requires two-hand use and precludes simultaneous instrumentation of the bleeding site. In addition, the oral cavity and oropharynx should be thoroughly suctioned with a Yankauer suction tip to ensure clearing out all blood that may potentially be swallowed or aspirated as well as to check for continued posterior bleeding. Address Coagulopathy Correcting, or at least mitigating, any underlying cause of coagu- lopathy is of essence in successful management of epistaxis (see Table 47.2). In fact, according to a study by Jones et al., nearly half of patients presenting with epistaxis had abnormal coagulation studies.39 However, routine laboratory screening is not necessary (and not cost effective) unless there is suggestive information derived from the history, such as a positive bleeding history, anticoagulant/antiplatelet agent use, or chronic liver disease.40 Long-term warfarin use is fairly common in patients presenting with epistaxis, accounting for 8% of emergency department admissions.41 For those patients who are supratherapeutic on warfarin, reversal of the anticoagulation effect is indicated, although patients who are within the designated therapeutic range may not need to be reversed.42 Reversal of warfarin can be done by administering fresh frozen plasma while stopping the warfarin. Vitamin K has a slower onset of action and delays restarting warfarin due to its longer half-life (effects up to 1 week after administration). Patients with a history of alcohol use may be at increased risk for recalcitrant epistaxis due to its effects in decreasing plasma fibrinogen levels;43 thus this should be ascertained in the history.44,45 Directed Treatment—Cautery or Topical Hemostatic Agents Either chemical or electrical cautery may be used for local control of epistaxis. Most commonly, silver nitrate sticks can be used to apply chemical cautery to a prominent nasal mucosal vessel. The technique is less effective when the vessel is actively bleeding, and if this occurs, firm pressure with a pledget following application of cautery may help.46 There is a theoretical risk of causing septal perforation from cauterizing opposing sides of the nasal septal mucosa in one sitting, and this should be avoided. For actively bleeding patients, monopolar or bipolar electro- cautery, preferably used in conjunction with a suction device, is extremely effective in controlling the bleeding site, regardless of whether it is venous or arterial. It may be used over sites of mucosal oozing or an actively pumping artery. Although commonly per- formed in the operating room under general anesthesia, electro- cautery may be performed in the awake, office setting for patients who can tolerate some discomfort. The nasal cavities should be Descargado para ALEX LARA (ua.alexlara@uniandes.edu.ec) en Regional Autonomous University of the Andes de ClinicalKey.es por Elsevier en diciembre 04, 2022. Para uso personal exclusivamente. No se permiten otros usos sin autorización. Copyright ©2022. Elsevier Inc. Todos los derechos reservados.
  • 8. 47 CHAPTER 47 Epistaxis 739 anteriorly. This is followed by anterior packing, usually in the form of long 1 2 - to 1-inch petrolatum gauze strips, to fill the bilateral nasal cavities. The authors recommend two technical modifications of significance—one is to tie the ends of the multiple gauze strips together so that all gauze can be removed at the same time without risk of foreign body retention and possible aspiration; another is to start gauze placement with the ends outside of the nose, working the ends in only after a substantial amount of gauze has already been packed so that the ends would not inadvertently fall down into the oropharynx. Equally important is securing the balloon in place without undue pressure against the nasal alae, and, thus, some form of padding, usually gauze or makeshift after staying in place for 3 to 5 days.59 Due to continuous pressure exerted across all nasal mucosal surfaces with increased absorption of water from surrounding mucus, the extent of mucosal trauma may be greater than that in the case of absorbable packs, which, in some cases, may actually worsen bleeding. One way to decrease mucosal trauma is to cover the nonabsorbable pack with a latex glove finger and suture the ends, creating a so-called finger cot, prior to placement (Fig. 47.11). Some nonabsorbable packs, such as the Rapid Rhino (Arthrocare, Austin, TX), have built-in anterior and/or posterior balloon cuffs that may be inflated with water to provide additional pressure points based on the expected locations of the bleeds.54,60,61 Prior to packing removal, the nasal packs should be moistened with water or saline solution because packs tend to dry out when left in place for several days. For unilateral anterior nasal packs or even some cases of bilateral nonabsorbable nasal packs, patients may not require admission for monitoring. Nasal packing tends to be rather uncomfortable for patients and may lead to further mucosal trauma in multiple areas, hypoxia, pain, nasal dryness, epiphora from obstruction of the nasolacrimal duct, eustachian tube dysfunction, and iatrogenic sinusitis from blockage of natural ostia. Packing removal is also uncomfortable and anxiety provoking. For these reasons, targeted treatment of the source of bleeding should be attempted first whenever possible. The “gold standard” for nasal packing is placement of a posterior nasopharyngeal pack (e.g., Foley catheter and tonsil sponges) followed by anterior packing. This is usually indicated for posterior arterial bleeds or epistaxis refractory to cautery and anterior packing. Most popularly, the procedure involves the threading of a large- diameter (i.e., 12 or 14 French) Foley balloon with a 30-cc balloon through one nostril, into the nasopharynx, and inferiorly into the oropharynx where the distal tip should be visible in the back of the mouth (Fig. 47.12). Only when the distal tip is confirmed to be in the oropharynx should the cuff be inflated with 5 to 10 mL of water and pulled back to occlude the choana, which may tamponade posterior bleeding or, at the very least, direct it Fig. 47.10 From left to right, the figure demonstrates placement of nasal packing, a coronal CT scan, and a sagittal CT scan of the sinuses. Proper placement of nasal packing should follow the axis of the floor of the nose in a somewhat inferior vector (top). Improper placement tends to bias the operator superiorly, where the packing may sit against the middle turbinate or other structures, causing discomfort and ineffective hemostasis (bottom). Fig. 47.11 Custom-made “finger cot” made using a 10-cm polyvinyl alcohol (Merocel) covered with the middle finger of a latex glove and secured in place with a 2-0 Prolene suture. The addition of the latex glove is less traumatic during placement and removal of the packing. Descargado para ALEX LARA (ua.alexlara@uniandes.edu.ec) en Regional Autonomous University of the Andes de ClinicalKey.es por Elsevier en diciembre 04, 2022. Para uso personal exclusivamente. No se permiten otros usos sin autorización. Copyright ©2022. Elsevier Inc. Todos los derechos reservados.
  • 9. 740 PART IV Sinus, Rhinology, and Allergy/Immunology be given to performing local, directed treatment of bleeding sites, if still present. Ultimately, nasal packing, although effective in controlling epistaxis in most cases, is uncomfortable and often requires inpatient hospital monitoring and may cause additional undue nasal trauma. Endoscopic Sphenopalatine Artery Ligation Over the years, endoscopic sphenopalatine artery ligation (ESPAL) has gained in prominence as a reliable, safe, and effective way to control epistaxis refractory to conservative measures and as a substitute to nasal packing.72-75 The procedure is usually performed under general anesthesia. The initial step is to identify the crista ethmoidalis, which is a small, medially oriented bone ridge anterior or anteroinferior to the sphenopalatine foramen (Fig. 47.13). It is posterior to the posterior wall of the maxillary sinus, superior to the inferior border of the horizontal part of the middle turbinate, anterior to the sphenoid face, and inferior to the retromaxillary area of the posterior ethmoid cells. In 95% of cases, the spheno- palatine foramen is located within 1 mm of the crista ethmoidalis.76 The mucosa may be incised anterior to it and elevated posteriorly until the crista ethmoidalis is identified. The crista is then removed with Kerrison rongeurs, which should expose the sphenopalatine artery branches emerging from the foramina posteriorly. Oftentimes, a blunt probe can be placed behind the branches and dissected medially and laterally to isolate them one by one for ligation. Numerous techniques exist for arterial ligation, including clip placement, bipolar electrocautery, or monopolar electrocautery, and are dependent on surgeon preference. Once hemostasis has been confirmed, the flap may then be replaced and a small amount of dissolvable hemostatic material (e.g., Avitene or Surgicel) is placed over the dissected area. No postoperative nasal packing is indicated. Patients may be monitored overnight for any recurrent bleeding, and a nasal saline spray may be started 1 to 2 days after the procedure. A purported reason for recurrent epistaxis following ESPAL is failure to identify and clip all branches of the sphenopalatine artery as it enters the nasal cavity. The various tributaries of the sphenopalatine artery may branch at any point between the pterygopalatine fossa and the nasal cavity, forming numerous foramina. Therefore, although the anatomy is highly variable, a meaningful search for multiple branches should be attempted.16 ESPAL is highly effective in long-term epistaxis control (>90%).77 In an early series, initial control rates were 87%, with no complications encountered.72 In comparison with nasal packing, one series involving 537 patients reported that posterior nasal packing achieved hemostasis in 62% of cases, whereas surgical management was successful in 97% of cases.78 Furthermore, a cost analysis revealed that ESPAL tended to be much more cost- saving than posterior nasal packing, even if the duration of posterior packing was decreased to 2 days,79 and another study noted decreased length of stay when compared with nasal packing (3 days versus 6 days).80 The most common complaints include nasal crusting and nasopalatal paresthesia, both of which are usually transient. Endoscopic Maxillary Artery Ligation One alternative means to circumvent dissection and individual control of all sphenopalatine tributaries is to attain proximal control through maxillary artery ligation (Fig. 47.14).81,82 Exposure of this large-caliber vessel involves a maxillary antrostomy with exposure of the posterior wall of the maxillary sinus. The mucosa overlying the posterior wall is removed and the underlying bone widely drilled or removed with Kerrison rongeurs. Deep to the bone is the periosteum of the pterygopalatine fossa, which should be preserved while the bone is still being removed. The periosteum can be electrocauterized to expose the pterygopalatine fossa fat. modification of the proximal balloon itself, is recommended.62-65 Nasal alar necrosis can occur with mismanagement of the nasal balloon and is notoriously difficult to reconstruct.66,67 Finally, patients with posterior balloon nasal packing should be monitored with continuous pulse oximetry and telemetry, with consideration of intensive care unit admission for those patients with preexisting cardiac or pulmonary comorbidities.68 Another theoretical concern for justifying cardiac monitoring is activation of the nasocardiac reflex in certain sensitive individuals, where continuous nasal stimulation may produce a reflexive bradycardia.69 Despite this, a systematic review did not find that respiratory complications are more prevalent among patients with nasal packing.70 There is some debate regarding the necessity of prophylactic systemic antibiotics for patients with nasal packing. The traditional teaching is that nasal packing acts like a tampon within a rich bacterial culture medium (blood and mucus), thereby risking opportunistic sinusitis and potentially leading to Staphylococcus- mediated toxic shock syndrome. Thus systemic antibiotics with antistaphylococcal coverage are generally considered prophylacti- cally for patients with nasal packing. However, a systematic review evaluating adverse events in 990 patients across six studies found no cases of toxic shock syndrome when prophylactic antibiotics were not used.71 Although unlikely to occur in this population, the dangers of toxic shock syndrome most likely outweigh the risks of developing antibiotic resistance, and the authors would recommend a short course (1 to 2 weeks) of clindamycin and/or trimethoprim-sulfamethoxazole while nasal packing is in place. Resolution of acute epistaxis is confirmed by direct examination of both the anterior nares and the oropharynx (run down from above). Nasal packing should be left in place to allow for the formation of a mature clot at the sites of bleeding. Usually, this will take anywhere between 1 and 5 days. It may be more comfort- able to moisten the packing prior to removal, and patients should use a nasal saline spray starting 1 to 2 days following no further bleeding. Once packing is removed, nasal endoscopy or headlight examination should be reattempted to evaluate for any residual bleeding. Equally important is to assess trauma to the nasal mucosa, which often may stir up additional bleeding. Consideration should Fig. 47.12 Critical view of the Foley balloon tip in the oropharynx when placing posterior packing. Proper placement should be confirmed prior to inflating the balloon. Descargado para ALEX LARA (ua.alexlara@uniandes.edu.ec) en Regional Autonomous University of the Andes de ClinicalKey.es por Elsevier en diciembre 04, 2022. Para uso personal exclusivamente. No se permiten otros usos sin autorización. Copyright ©2022. Elsevier Inc. Todos los derechos reservados.
  • 10. 47 CHAPTER 47 Epistaxis 741 The maxillary artery travels from lateral to medial and can often be seen as a pulsatile structure once the fat is exposed. A blunt probe can be used to isolate the main trunk and dissect both medially and laterally to accommodate clip placement. Two clips should be placed proximally over the entire circumference of the vessel and one distally; bipolar electrocautery is applied between the clips and the artery transected. Dissolvable hemostatic material is placed over the field and the patient monitored overnight. Nasal saline sprays may be started 1 to 2 days postoperatively. Reported outcomes for maxillary artery ligation are comparable with those achieved for ESPAL, although maxillary artery ligation is frequently performed for skull base procedures, such as transpterygoid approaches or resection of juvenile angiofibromas.75,81 Previously, maxillary artery ligation was performed via a transantral approach (Caldwell-Luc). Although this provides excellent instru- ment access and is still favored in many cases requiring extended exposure, modified endoscopic approaches to the lateral maxillary sinus and infratemporal fossa have precluded the absolute need for open approaches.83,84 Due to more extensive dissection of the pterygopalatine fossa, there is an increased risk to the surrounding neural structures, including the vidian nerve (decreased lacrimation and dry eyes), greater palatine nerve (palatal paresthesia), and infraorbital nerve (cheek and nasal paresthesia). Ligation of the External Carotid Artery A last resort option for control of refractory, severe epistaxis is ligation of the ipsilateral external carotid artery through a transcervical approach.85,86 Due to more sophisticated endoscopic techniques affording improved visualization and dissection, this is no longer favored due to its more invasive nature without proven additional benefit. Anterior Ethmoidal Artery Ligation An uncommon source of epistaxis is from the anterior eth- moidal artery, which usually arises from skull base trauma (e.g., MT U MT U Fig. 47.13 Exposure of the left sphenopalatine artery (left, arrow) with subsequent bipolar electrocautery. The crista ethmoidalis has been resected for access. MT, Middle turbinate; U, uncinate process. (From Chiu AG, Palmer JN, Adappa ND (eds): Atlas of Endoscopic Sinus and Skull Base Surgery, ed 2, Philadelphia: Elsevier, 2013.) Middle turbinate Crista ethmoidalis Sphenopalatine foramen Sphenopalatine a. Internal maxillary a. Fig. 47.14 Schematic depicting the anatomy of the right maxillary artery within the pterygopalatine fossa and the right sphenopalatine artery as it exits the sphenopalatine foramen. Note the relationship to the crista ethmoidalis. (From Chiu AG, Palmer JN, Adappa ND (eds): Atlas of Endoscopic Sinus and Skull Base Surgery, ed 2, Philadelphia: Elsevier, 2013.) Descargado para ALEX LARA (ua.alexlara@uniandes.edu.ec) en Regional Autonomous University of the Andes de ClinicalKey.es por Elsevier en diciembre 04, 2022. Para uso personal exclusivamente. No se permiten otros usos sin autorización. Copyright ©2022. Elsevier Inc. Todos los derechos reservados.
  • 11. 742 PART IV Sinus, Rhinology, and Allergy/Immunology suggests that the progressive distances between the anterior lacrimal crest, anterior ethmoidal foramen, posterior ethmoidal foramen, and optic canal are 24, 12, and 6 mm, respectively. However, a recent cadaveric study found that, although the distances are relatively consistent, the number of foramina is not, and otorhi- nolaryngologists should be aware of the possibility of multiple branches.91,92 The incision may be closed with fast-absorbing gut sutures and treated with erythromycin ophthalmic ointment for several days postoperatively. Embolization Cerebral angiography with transarterial embolization by inter- ventional radiologists is an effective option for treatment of recalcitrant epistaxis, with reported success in 75% to 92% of cases (Fig. 47.16).93-95 Advantages include avoiding the need for general anesthesia and use in poor surgical candidates. However, inadvertent embolization of nontarget vessels or migration of embolic materials has been associated with blindness (ophthalmic artery), cerebrovascular accident (internal carotid artery), and other complications related to vascular infarction. Other possible complications include hematoma formation at the puncture site (e.g., femoral artery) and acute kidney injury due to iodinated contrast material administration. According to a systematic review evaluating surgical versus interventional radiologic treatment of adult epistaxis, stroke was reported in 1.1% to 1.5% of cases.95 The maxillary artery is the most commonly selected target vessel for embolization in patients with epistaxis. Other external carotid system tributaries may also be embolized, but embolization is not recommended for the internal carotid system due to the risk of stroke and/or blindness. From an economic perspective, emboliza- tion appears to be more costly than surgical management.96,97 There are certain specific indications for when embolization is a more desired option than surgical management of epistaxis. First, embolization is effective for control of epistaxis due to nasopharyngeal carcinoma98-100 and other tumors of the sinonasal tract. Because most cases are now surgically resectable, this is an effective strategy to obliterate tumor-feeding vessels without violating the external surface. Second, preoperative embolization is helpful for vascular tumors, especially juvenile angiofibromas, prior to surgical resection and has been shown to decrease intraoperative blood loss due to devascularization of the tumor.101-104 In fact, in some cases, decreased vascularity actually slightly decreases the size of the tumor, thereby improving surgical access. Third, in cases of craniofacial trauma with distorted anatomy and mobile bone fragments, embolization is potentially helpful in controlling oronasal hemorrhage.105,106 Finally, epistaxis from the carotid artery, either through iatrogenic carotid injury during endoscopic sinus or skull base surgery or blowout from other external causes, is best managed definitively with local control at the site of intranasal bleeding following by interventional radiologic treatment.107-110 PEDIATRIC EPISTAXIS Unless there is an unusual underlying cause (e.g., coagulopathy and tumor), epistaxis in children invariably self-resolves with conservative management. Digital trauma is extremely common in this population and is a frequent cause of self-limiting anterior epistaxis. Moisturizing the anterior nares and nasal mucosal humidification remain effective strategies in this cohort.111 In cooperative children, the addition of silver nitrate cautery has been shown to be highly effective in addressing prominent septal vessels.112,113 Young children who present with recurrent severe epistaxis should be screened for bleeding disorders such as hemophilia or von Willebrand disease. Juvenile angiofibroma should be part of the differential diagnosis for any adolescent male complaining of unilateral nasal obstruction and epistaxis. naso-orbito-ethmoidal fractures) or iatrogenic injury (e.g., endoscopic sinus or skull base surgery). The artery has a rather variable location but can always be found between the second and third lamella.87 The risk of injury to the anterior ethmoidal artery is higher when it is dehiscent from the skull base. Risk factors for low-lying anterior ethmoidal arteries include the presence of a supraorbital ethmoid air cell, high Keros classification (deeper olfactory fossa), and increased distance between the anterior wall of the frontal sinus to the skull base.22 If the anterior ethmoidal artery is transected more medially, the likely outcome is epistaxis that is unlikely to stop without surgical intervention (due to its superior location in the nasal cavity). If transected more laterally, the proximal stump may retract into the orbit and produce a retrobulbar hematoma, which is a surgical emergency requiring immediate orbital decompression. In performing anterior skull base surgery (e.g., transcribriform and transplanum approaches), the anterior and posterior ethmoidal arteries are often prophylactically ligated for tumor resection. Endoscopic ligation of the anterior ethmoidal artery begins with a complete ethmoidectomy and defining the ethmoid skull base.20,88 If the anterior ethmoidal artery is located within a bony canal, it may need to be gently drilled to expose the vessel; otherwise, a curette may be used to manipulate the bone fragments off the vessel (Fig. 47.15). Clips may be applied if the vessel is isolated, although bipolar electrocautery on a low setting is equally effective in achieving hemostasis. The artery does not need to be transected following cauterization unless purposeful skull base entry is desired. Alternatively, the ethmoidal arteries may be ligated through an open, transorbital approach. The Lynch incision is a straight- forward approach to the anatomy in this area, although it has the potential disadvantage of leaving a visible scar. The precaruncular or transcaruncular approach is a newer, scarless technique, which offers excellent exposure to the anterior and posterior ethmoidal arteries within their bony foramina.89,90 The lacrimal caruncle is incised (transcaruncular) or an incision made anterior to it (precaruncular), with dissection carried through the superior and inferior conjunctival folds. Horner muscle is identified and left undissected, and the periorbita posterior to its insertion is incised vertically to expose the lamina papyracea. Blunt elevation posteriorly will reveal the ethmoidal neurovascular foramina sequentially, which may be ligated and divided. Traditional anatomic teaching Frontal sinus Septum Orbit Anterior ethmoidal artery Fig. 47.15 Endoscopic view of the left anterior ethmoidal artery. The bony canal is being drilled in preparation for bipolar electrocautery. (From Chiu AG, Palmer JN, Adappa ND (eds): Atlas of Endoscopic Sinus and Skull Base Surgery, ed 2, Philadelphia: Elsevier, 2013.) Descargado para ALEX LARA (ua.alexlara@uniandes.edu.ec) en Regional Autonomous University of the Andes de ClinicalKey.es por Elsevier en diciembre 04, 2022. Para uso personal exclusivamente. No se permiten otros usos sin autorización. Copyright ©2022. Elsevier Inc. Todos los derechos reservados.
  • 12. 47 CHAPTER 47 Epistaxis 743 to septal perforations, although many HHT patients usually present with perforations secondary to repeated bouts of nasal packing. Less commonly performed surgical treatments for HHT-related epistaxis include septodermoplasty and nasal closure.137 Septoder- moplasty involves removing the septal and nasal floor mucosa (which harbor telangiectasias), leaving the underlying perichondrium intact, and replacing it with a split-thickness skin graft (Fig. 47.17).127,138,139 Nasal closure, or Lund modified Young’s procedure, Hereditary Hemorrhagic Telangiectasia (Osler-Weber-Rendu) Hereditary hemorrhagic telangiectasia (HHT, Osler-Weber-Rendu) is an autosomal dominant multisystem vascular disorder that causes variable cutaneous and mucosal telangiectasia formation as well as arteriovenous malformations in the lungs, brain, and liver. Epistaxis from nasal telangiectasias is the most common complaint in HHT patients, afflicting more than 90% of individuals. With progression of the disease over time, patients present with repeated epistaxis of varying severity and frequency, with significant negative impact on quality of life.114-116 These patients are also prone to receiving repeated transfusions due to their epistaxis. Coordination of multidisciplinary care among otorhinolaryngologists, geneticists, interventional radiologists, and other specialists is of critical importance in the long-term care of these patients.117 Conservative measures apply for most cases of HHT-related epistaxis. Nasal humidification and avoidance of trauma (i.e., minimize nasal packing) prevent inadvertent trauma to telangi- ectasias.118 Hormonal therapy with antiestrogen agents (e.g., tamoxifen) have been explored for their antiendothelial effects, with promise demonstrated in some studies.119-121 Intranasal beva- cizumab, an antivascular endothelial growth factor A monoclonal antibody, has recently been explored for use in HHT-related epistaxis. However, at this point, the current evidence is conflicting with regard to its efficacy.122-126 With respect to surgical treatments, the most widely performed procedure is cauterization and/or laser photocoagulation of nasal telangiectasias.127-132 T o achieve submucosal ablation of blood vessels while attempting to spare the mucosa, the potassium titanyl phosphate (KTP) laser is commonly used. Outcomes following laser treatments are variable but generally will decrease the severity and frequency of epistaxis over the course of months to years, with corresponding improvement in the quality of life of patients.133 Other thermal instruments, such as the bipolar electrocautery and coblator, are also effective adjuncts to laser treatment and may be more effective when telangiectasias are actively bleeding.134-136 It is important to note that bilateral thermal treatments may lead A B Fig. 47.16 Preembolization (A) and postembolization (B) cerebral angiography of a left-sided juvenile angiofibroma. Notice the tumor blush (dotted arrows) fed by the left sphenopalatine/maxillary artery (solid arrow) disappear in this successful embolization. (From Chiu AG, Palmer JN, Adappa ND (eds): Atlas of Endoscopic Sinus and Skull Base Surgery, ed 2, Philadelphia: Elsevier, 2013.) Fig. 47.17 Septodermoplasty. Split-thickness skin grafts are harvested and secured over septal perichondrium. (From Palmer JN, Chiu AG, Adappa ND (eds): Atlas of Endoscopic Sinus and Skull Base Surgery, ed 1.) Descargado para ALEX LARA (ua.alexlara@uniandes.edu.ec) en Regional Autonomous University of the Andes de ClinicalKey.es por Elsevier en diciembre 04, 2022. Para uso personal exclusivamente. No se permiten otros usos sin autorización. Copyright ©2022. Elsevier Inc. Todos los derechos reservados.
  • 13. 744 PART IV Sinus, Rhinology, and Allergy/Immunology produces complete cessation of bleeding when there is complete cessation of airflow through the nose and is reserved for the most severe cases that have failed other treatments.140-142 SUMMARY Epistaxis is the most common otorhinolaryngologic emergency, and an algorithm for management is presented (Fig. 47.18). Conservative measures are efficacious in the vast majority of cases, ABCs Fluid resuscitation Establish intravenous access Complete blood count, type and screen Control hypertension Treat any underlying cause predisposing to bleeding Suction clots Examine nose with headlamp or rigid endoscopy to identify source of bleeding Source identified Bipolar electrocautery, silver nitrate cautery, or topical hemostatic agent Hemostasis achieved Nasal humidification, nasal saline sprays, nasal creams to anterior nares Facial trauma Nasopharyngeal carcinoma or other sinonasal tumor Carotid injury Angiography and embolization Endoscopic sphenopalatine artery ligation Evaluate all possible areas for bleeding Consider possibility of multiple branches If rebleed with packing in or after packing removed Nasal packing − dissolvable vs. non- dissolvable, anterior vs. posterior, minimize nasal trauma Consider prophylactic antibiotics Keep packing in 1-5 days depending on severity of bleed Source not identified or unable to control Fig. 47.18 Algorithm for managing epistaxis when conservative measures have failed. The decision branching point between nasal packing and endoscopic sphenopalatine artery ligation is important to discuss with the patient. and successful hemostasis is dependent on identification of the source of bleeding. Nasal packing controls most cases of epistaxis but is uncomfortable and may worsen nasal trauma. Operative ligation of the sphenopalatine artery is a safe and effective way to treat refractory epistaxis, whereas embolization may be reserved for specific cases. For a complete list of references, visit ExpertConsult.com. Descargado para ALEX LARA (ua.alexlara@uniandes.edu.ec) en Regional Autonomous University of the Andes de ClinicalKey.es por Elsevier en diciembre 04, 2022. Para uso personal exclusivamente. No se permiten otros usos sin autorización. Copyright ©2022. Elsevier Inc. Todos los derechos reservados.
  • 14. 47 CHAPTER 47 Epistaxis 744.e1 27. Elwany S, Ibrahim AA, Soliman AI, et al: The significance of ath- erosclerosis in hypertensive patients with epistaxis, J Laryngol Otol 1–4, 2018. 28. Kikidis D, Tsioufis K, Papanikolaou V, et al: Is epistaxis associated with arterial hypertension? A systematic review of the literature, Eur Arch Otorhinolaryngol 271:237–243, 2014. 29. Sarhan NA,Algamal AM: Relationship between epistaxis and hyperten- sion: a cause and effect or coincidence?, J Saudi Heart Assoc 27:79–84, 2015. 30. Carson JL, Guyatt G, Heddle NM, et al: Clinical practice guidelines from the AABB: red blood cell transfusion thresholds and storage, JAMA 316:2025–2035, 2016. 31. Murthy P, Nilssen EL, Rao S, et al: A randomised clinical trial of antiseptic nasal carrier cream and silver nitrate cautery in the treatment of recurrent anterior epistaxis, Clin Otolaryngol Allied Sci 24:228–231, 1999. 32. London SD, Lindsey WH: A reliable medical treatment for recurrent mild anterior epistaxis, Laryngoscope 109:1535–1537, 1999. 33. Higgins TS, Hwang PH, Kingdom TT, et al: Systematic review of topical vasoconstrictors in endoscopic sinus surgery, Laryngoscope 121:422–432, 2011. 34. Kamhieh Y, Fox H: Tranexamic acid in epistaxis: a systematic review, Clin Otolaryngol 41:771–776, 2016. 35. Eloy JA, Kovalerchik O, Bublik M, et al: Effect of greater palatine canal injection on estimated blood loss during endoscopic sinus surgery, Am J Otolaryngol 35:1–4, 2014. 36. Bharadwaj VK, Novotny GM: Greater palatine canal injection: an alternative to the posterior nasal packing and arterial ligation in epistaxis, J Otolaryngol 15:94–100, 1986. 37. Chiu TW, McGarry GW: Prospective clinical study of bleeding sites in idiopathic adult posterior epistaxis, Otolaryngol Head Neck Surg 137:390–393, 2007. 38. Thornton MA, Mahesh BN, Lang J: Posterior epistaxis: identification of common bleeding sites, Laryngoscope 115:588–590, 2005. 39. Jones GL, Browning S, Phillipps J: The value of coagulation profiles in epistaxis management, Int J Clin Pract 57:577–578, 2003. 40. Awan MS, Iqbal M, Imam SZ: Epistaxis: when are coagulation studies justified?, Emerg Med J 25:156–157, 2008. 41. Thaha MA, Nilssen EL, Holland S, et al: Routine coagulation screen- ing in the management of emergency admission for epistaxis–is it necessary?, J Laryngol Otol 114:38–40, 2000. 42. Srinivasan V, Patel H, John DG, et al: Warfarin and epistaxis: should warfarin always be discontinued?, Clin Otolaryngol Allied Sci 22:542–544, 1997. 43. Dimmitt SB, Rakic V, Puddey IB, et al: The effects of alcohol on coagulation and fibrinolytic factors: a controlled trial, Blood Coagul Fibrinolysis 9:39–45, 1998. 44. McGarry GW, Gatehouse S, Hinnie J: Relation between alcohol and nose bleeds, BMJ 309:640, 1994. 45. McGarry GW, Gatehouse S, Vernham G: Idiopathic epistaxis, haemostasis and alcohol, Clin Otolaryngol Allied Sci 20:174–177, 1995. 46. Barr GD: Silver nitrate cautery and epistaxis, Arch Emerg Med 6:233, 1989. 47. Bhatnagar RK, Berry S: Selective surgicel packing for the treatment of posterior epistaxis, Ear Nose Throat J 83:633–634, 2004. 48. Vaiman M, Segal S, Eviatar E: Fibrin glue treatment for epistaxis, Rhinology 40:88–91, 2002. 49. Walshe P: The use of fibrin glue to arrest epistaxis in the presence of a coagulopathy, Laryngoscope 112:1126–1128, 2002. 50. Walshe P, Harkin C, Murphy S, et al: The use of fibrin glue in refrac- tory coagulopathic epistaxis, Clin Otolaryngol Allied Sci 26:284–285, 2001. 51. Khan MK, Reda El Badawey M, Powell J, et al: The utility of FloSeal haemostatic agent in the management of epistaxis, J Laryngol Otol 129:353–357, 2015. 52. Mathiasen RA, Cruz RM: Prospective, randomized, controlled clinical trial of a novel matrix hemostatic sealant in patients with acute anterior epistaxis, Laryngoscope 115:899–902, 2005. 53. Wakelam OC, Dimitriadis PA, Stephens J: The use of FloSeal haemostatic sealant in the management of epistaxis: a prospective clinical study and literature review, Ann R Coll Surg Engl 99:28–30, 2017. 54. Iqbal IZ, Jones GH, Dawe N, et al: Intranasal packs and haemostatic agents for the management of adult epistaxis: systematic review, J Laryngol Otol 131:1065–1092, 2017. REFERENCES 1. Tomkinson A, Roblin DG, Flanagan P, et al: Patterns of hospital attendance with epistaxis, Rhinology 35:129–131, 1997. 2. Pallin DJ, Chng YM, McKay MP, et al: Epidemiology of epistaxis in US emergency departments, 1992 to 2001, Ann Emerg Med 46:77–81, 2005. 3. Walker TW, Macfarlane TV, McGarry GW: The epidemiology and chronobiology of epistaxis: an investigation of Scottish hospital admissions 1995-2004, Clin Otolaryngol 32:361–365, 2007. 4. Chaaban MR, Zhang D, Resto V, et al: Demographic, seasonal, and geographic differences in emergency department visits for epistaxis, Otolaryngol Head Neck Surg 156:81–86, 2017. 5. Ross CS, Pruthi RK, Schmidt KA, et al: Intranasal oestrogen cream for the prevention of epistaxis in patients with bleeding disorders, Haemophilia 17:164, 2011. 6. Comelli I, Vincenti V, Benatti M, et al: Influence of air temperature variations on incidence of epistaxis, Am J Rhinol Allergy 29:e175–e181, 2015. 7. Integrate, National ENTTRN: Epistaxis 2016: national audit of management, J Laryngol Otol 131:1131–1141, 2017. 8. Bequignon E, Verillaud B, Robard L, et al: Guidelines of the French Society of Otorhinolaryngology (SFORL). First-line treatment of epi- staxis in adults, Eur Ann Otorhinolaryngol Head Neck Dis 134:185–189, 2017. 9. Bertrand B, Eloy P, Rombaux P, et al: Guidelines to the management of epistaxis, B-ENT Suppl 1:27–41, quiz 42–43, 2005. 10. Daudia A, Jaiswal V, Jones NS: Guidelines for the management of idiopathic epistaxis in adults: how we do it, Clin Otolaryngol 33:618–620, 2008. 11. Verillaud B, Robard L, Michel J, et al: Guidelines of the French Society of Otorhinolaryngology (SFORL). Second-line treatment of epistaxis in adults, Eur Ann Otorhinolaryngol Head Neck Dis 134:191–193, 2017. 12. Leung RM, Smith TL, Rudmik L: Developing a laddered algorithm for the management of intractable epistaxis: a risk analysis, JAMA Otolaryngol Head Neck Surg 141:405–409, 2015. 13. Shargorodsky J, Bleier BS, Holbrook EH, et al: Outcomes analysis in epistaxis management: development of a therapeutic algorithm, Otolaryngol Head Neck Surg 149:390–398, 2013. 14. Vosler PS, Kass JI, Wang EW, et al: Successful Implementation of a Clinical Care Pathway for Management of Epistaxis at a Tertiary Care Center, Otolaryngol Head Neck Surg 155:879–885, 2016. 15. Gras-Cabrerizo JR,Adema-Alcover JM, Gras-Albert JR, et al: Anatomi- cal and surgical study of the sphenopalatine artery branches, Eur Arch Otorhinolaryngol 271:1947–1951, 2014. 16. Simmen DB, Raghavan U, Briner HR, et al: The anatomy of the sphenopalatine artery for the endoscopic sinus surgeon, Am J Rhinol 20:502–505, 2006. 17. Hadad G, Bassagasteguy L, Carrau RL, et al: A novel reconstructive technique after endoscopic expanded endonasal approaches: vascular pedicle nasoseptal flap, Laryngoscope 116:1882–1886, 2006. 18. Mason E, Solares CA, Carrau RL, et al: Computed tomographic exploration of the middle ethmoidal artery, J Neurol Surg B Skull Base 76:372–378, 2015. 19. Wang L, Youseef A, Al Qahtani AA, et al: Endoscopic anatomy of the middle ethmoidal artery, Int Forum Allergy Rhinol 4:164–168, 2014. 20. Floreani SR, Nair SB, Switajewski MC, et al: Endoscopic anterior ethmoidal artery ligation: a cadaver study, Laryngoscope 116:1263–1267, 2006. 21. Poteet PS, Cox MD, Wang RA, et al: Analysis of the Relationship between the Location of the Anterior Ethmoid Artery and Keros Classification, Otolaryngol Head Neck Surg 157:320–324, 2017. 22. Sjogren PP, Waghela R, Ashby S, et al: International Frontal Sinus Anatomy Classification and anatomic predictors of low-lying anterior ethmoidal arteries, Am J Rhinol Allergy 31:174–176, 2017. 23. Min HJ, Kang H, Choi GJ, et al: Association between hypertension and epistaxis: systematic review and meta-analysis, Otolaryngol Head Neck Surg 157:921–927, 2017. 24. Herkner H, Havel C, Mullner M, et al: Active epistaxis at ED presentation is associated with arterial hypertension, Am J Emerg Med 20:92–95, 2002. 25. Terakura M, Fujisaki R, Suda T, et al: Relationship between blood pressure and persistent epistaxis at the emergency department: a retrospective study, J Am Soc Hypertens 6:291–295, 2012. 26. Abrich V, Brozek A, Boyle TR, et al: Risk factors for recurrent spontaneous epistaxis, Mayo Clin Proc 89:1636–1643, 2014. Descargado para ALEX LARA (ua.alexlara@uniandes.edu.ec) en Regional Autonomous University of the Andes de ClinicalKey.es por Elsevier en diciembre 04, 2022. Para uso personal exclusivamente. No se permiten otros usos sin autorización. Copyright ©2022. Elsevier Inc. Todos los derechos reservados.
  • 15. PART IV Sinus, Rhinology, and Allergy/Immunology 744.e2 82. Piastro K, Scagnelli R, Gildener-Leapman N, et al: Outcomes of sphenopalatine and internal maxillary artery ligation inside the pterygopalatine fossa for posterior epistaxis, Rhinology 2018. 83. Harvey RJ, Sheehan PO, Debnath NI, et al: Transseptal approach for extended endoscopic resections of the maxilla and infratemporal fossa, Am J Rhinol Allergy 23:426–432, 2009. 84. Upadhyay S, Dolci RL, Buohliqah L, et al: Endoscopic endonasal anterior maxillotomy, Laryngoscope 125:2668–2671, 2015. 85. Hassard AD, Kirkpatrick DA, Wong FS: Ligation of the external carotid and anterior ethmoidal arteries for severe or unusual epistaxis resulting from facial fractures, Can J Surg 29:447–449, 1986. 86. Waldron J, Stafford N: Ligation of the external carotid artery for severe epistaxis, J Otolaryngol 21:249–251, 1992. 87. Simmen D, Raghavan U, Briner HR, et al: The surgeon’s view of the anterior ethmoid artery, Clin Otolaryngol 31:187–191, 2006. 88. Woolford TJ, Jones NS: Endoscopic ligation of anterior ethmoidal artery in treatment of epistaxis, J Laryngol Otol 114:858–860, 2000. 89. Cornelis MM, Lubbe DE: Pre-caruncular approach to the medial orbit and landmarks for anterior ethmoidal artery ligation: a cadaveric study, Clin Otolaryngol 41:777–781, 2016. 90. Morera E, Artigas C, Ferran L, et al: Transcaruncular electrocoagula- tion of anterior ethmoidal artery for the treatment of severe epistaxis, Laryngoscope 121:446–450, 2011. 91. Shaheen OH: Arterial epistaxis, J Laryngol Otol 89:17–34, 1975. 92. Abed SF, Shams P, Shen S, et al: A cadaveric study of ethmoidal foramina variation and its surgical significance in Caucasians, Br J Ophthalmol 96:118–121, 2012. 93. Moreau S, De Rugy MG, Babin E, et al: Supraselective embolization in intractable epistaxis: review of 45 cases, Laryngoscope 108:887–888, 1998. 94. Cohen JE, Moscovici S, Gomori JM, et al: Selective endovascular embolization for refractory idiopathic epistaxis is a safe and effective therapeutic option: technique, complications, and outcomes, J Clin Neurosci 19:687–690, 2012. 95. Swords C, Patel A, Smith ME, et al: Surgical and interventional radiological management of adult epistaxis: systematic review, J Laryngol Otol 131:1108–1130, 2017. 96. Miller TR, Stevens ES, Orlandi RR: Economic analysis of the treat- ment of posterior epistaxis, Am J Rhinol 19:79–82, 2005. 97. Rudmik L, Leung R: Cost-effectiveness analysis of endoscopic sphenopalatine artery ligation vs arterial embolization for intractable epistaxis, JAMA Otolaryngol Head Neck Surg 140:802–808, 2014. 98. He CC, Si YF, Xie YA, et al: Management of intractable epistaxis in patients who received radiation therapy for nasopharyngeal carcinoma, Eur Arch Otorhinolaryngol 270:2763–2767, 2013. 99. Mok JS, Marshall JN, Chan M, et al: Percutaneous embolization to control intractable epistaxis in nasopharyngeal carcinoma, Head Neck 21:211–216, 1999. 100. Wong GK, Chan KK, Yu SC, et al: Treatment of profuse epistaxis in patients irradiated for nasopharyngeal carcinoma, ANZ J Surg 77:270–274, 2007. 101. Ballah D, Rabinowitz D, Vossough A, et al: Preoperative angiography and external carotid artery embolization of juvenile nasopharyngeal angiofibromas in a tertiary referral paediatric centre, Clin Radiol 68:1097–1106, 2013. 102. Elhammady MS, Johnson JN, Peterson EC, et al: Preoperative embolization of juvenile nasopharyngeal angiofibromas: transarterial versus direct tumoral puncture, World Neurosurg 76:328–334, discussion 263–265, 2011. 103. Gao M, Gemmete JJ, Chaudhary N, et al: A comparison of par- ticulate and onyx embolization in preoperative devascularization of juvenile nasopharyngeal angiofibromas, Neuroradiology 55:1089–1096, 2013. 104. Lutz J, Holtmannspotter M, Flatz W, et al: Preoperative emboliza- tion to improve the surgical management and outcome of juvenile nasopharyngeal angiofibroma (JNA) in a single center: 10-year experience, Clin Neuroradiol 26:405–413, 2016. 105. Komiyama M, Nishikawa M, Kan M, et al: Endovascular treatment of intractable oronasal bleeding associated with severe craniofacial injury, J Trauma 44:330–334, 1998. 106. Liao CC, Hsu YP, Chen CT, et al: Transarterial embolization for intractable oronasal hemorrhage associated with craniofacial trauma: evaluation of prognostic factors, J Trauma 63:827–830, 2007. 107. Adeel M, Ikram M: Post-traumatic pseudoaneurysm of internal carotid artery: a cause of intractable epistaxis, BMJ Case Rep 2012:2012. 55. Sethi RKV, Kozin ED, Abt NB, et al: Treatment disparities in the management of epistaxis in United States emergency departments, Laryngoscope 128:356–362, 2018. 56. Goddard JC, Reiter ER: Inpatient management of epistaxis: outcomes and cost, Otolaryngol Head Neck Surg 132:707–712, 2005. 57. Yan M, Zheng D, Li Y, et al: Biodegradable nasal packings for endoscopic sinonasal surgery: a systematic review and meta-analysis, PLoS ONE 9:e115458, 2014. 58. Wang J, Cai C, Wang S: Merocel versus Nasopore for nasal packing: a meta-analysis of randomized controlled trials, PLoS ONE 9:e93959, 2014. 59. Pringle MB, Beasley P, Brightwell AP: The use of Merocel nasal packs in the treatment of epistaxis, J Laryngol Otol 110:543–546, 1996. 60. Gudziol V, Mewes T, Mann WJ: Rapid Rhino: a new pneumatic nasal tamponade for posterior epistaxis, Otolaryngol Head Neck Surg 132:152–155, 2005. 61. Badran K, Malik TH, Belloso A, et al: Randomized controlled trial comparing Merocel and RapidRhino packing in the management of anterior epistaxis, Clin Otolaryngol 30:333–337, 2005. 62. Ho EC, Mansell NJ: How we do it: a practical approach to Foley catheter posterior nasal packing, Clin Otolaryngol Allied Sci 29:754–757, 2004. 63. Ismail H, Buckland JR, Harries PG: The prevention of alar necrosis in Foley catheter fixation in posterior epistaxis, Ann R Coll Surg Engl 86:307, 2004. 64. Judd O, Gaskin J: Securing the posterior nasal pack; a technique to prevent alar necrosis, Ann R Coll Surg Engl 91:713–714, 2009. 65. Thomas L, Karagama YG, Watson C: Avoiding alar necrosis with post-nasal packs, J Laryngol Otol 119:727–728, 2005. 66. Civelek B, Kargi AE, Sensoz O, et al: Rare complication of nasal packing: alar region necrosis, Otolaryngol Head Neck Surg 123:656–657, 2000. 67. Vermeeren L, Derks W, Fokkens W, et al: Complications of balloon packing in epistaxis, Eur Arch Otorhinolaryngol 272:3077–3081, 2015. 68. Corrales CE, Goode RL: Should patients with posterior nasal packing require ICU admission?, Laryngoscope 123:2928–2929, 2013. 69. Baxandall ML, Thorn JL: The nasocardiac reflex, Anaesthesia 43:480–481, 1988. 70. Rotenberg B, Tam S: Respiratory complications from nasal packing: systematic review, J Otolaryngol Head Neck Surg 39:606–614, 2010. 71. Lange JL, Peeden EH, Stringer SP: Are prophylactic systemic antibiotics necessary with nasal packing? A systematic review, Am J Rhinol Allergy 31:240–247, 2017. 72. Snyderman CH, Goldman SA, Carrau RL, et al: Endoscopic sphe- nopalatine artery ligation is an effective method of treatment for posterior epistaxis, Am J Rhinol 13:137–140, 1999. 73. Wormald PJ, Wee DT, van Hasselt CA: Endoscopic ligation of the sphenopalatine artery for refractory posterior epistaxis, Am J Rhinol 14:261–264, 2000. 74. 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 28:360–363, 2003. 75. Seno S, Arikata M, Sakurai H, et al: Endoscopic ligation of the sphenopalatine artery and the maxillary artery for the treatment of intractable posterior epistaxis, Am J Rhinol Allergy 23:197–199, 2009. 76. Bolger WE, Borgie RC, Melder P: The role of the crista ethmoidalis in endoscopic sphenopalatine artery ligation, Am J Rhinol 13:81–86, 1999. 77. Abdelkader M, Leong SC, White PS: Endoscopic control of the sphenopalatine artery for epistaxis: long-term results, J Laryngol Otol 121:759–762, 2007. 78. Soyka MB, Nikolaou G, Rufibach K, et al: On the effectiveness of treatment options in epistaxis: an analysis of 678 interventions, Rhinology 49:474–478, 2011. 79. Dedhia RC, Desai SS, Smith KJ, et al: Cost-effectiveness of endoscopic sphenopalatine artery ligation versus nasal packing as first-line treat- ment for posterior epistaxis, Int Forum Allergy Rhinol 3:563–566, 2013. 80. McDermott AM, O’Cathain E, Carey BW, et al: Sphenopalatine artery ligation for epistaxis: factors influencing outcome and impact of timing of surgery, Otolaryngol Head Neck Surg 154:547–552, 2016. 81. Pritikin JB, Caldarelli DD, Panje WR: Endoscopic ligation of the internal maxillary artery for treatment of intractable posterior epistaxis, Ann Otol Rhinol Laryngol 107:85–91, 1998. Descargado para ALEX LARA (ua.alexlara@uniandes.edu.ec) en Regional Autonomous University of the Andes de ClinicalKey.es por Elsevier en diciembre 04, 2022. Para uso personal exclusivamente. No se permiten otros usos sin autorización. Copyright ©2022. Elsevier Inc. Todos los derechos reservados.
  • 16. 47 CHAPTER 47 Epistaxis 744.e3 126. Whitehead KJ, Sautter NB, McWilliams JP, et al: Effect of topical intranasal therapy on epistaxis frequency in patients with hereditary hemorrhagic telangiectasia: a randomized clinical trial, JAMA 316: 943–951, 2016. 127. Harvey RJ, Kanagalingam J, Lund VJ: The impact of septodermoplasty and potassium-titanyl-phosphate (KTP) laser therapy in the treatment of hereditary hemorrhagic telangiectasia-related epistaxis, Am J Rhinol 22:182–187, 2008. 128. Jorgensen G, Lange B, Wanscher JH, et al: Efficiency of laser treat- ment in patients with hereditary hemorrhagic telangiectasia, Eur Arch Otorhinolaryngol 268:1765–1770, 2011. 129. Poje G, Kavanagh MM: Hereditary hemorrhagic telangiectasia-laser treatment of epistaxis, Ear Nose Throat J 96:E10–E14, 2017. 130. Sautter NB, Smith TL: Treatment of hereditary hemorrhagic telangiectasia-related epistaxis, Otolaryngol Clin North Am 49:639–654, 2016. 131. Werner A, Baumler W, Zietz S, et al: Hereditary haemorrhagic telangiectasia treated by pulsed neodymium:yttrium-aluminium-garnet (Nd:YAG) laser (1,064 nm), Lasers Med Sci 23:385–391, 2008. 132. Fiorella ML, Lillo L, Fiorella R: Diode laser in the treatment of epistaxis in patients with hereditary haemorrhagic telangiectasia, Acta Otorhinolaryngol Ital 32:164–169, 2012. 133. Kuan EC, Peng KA, Thompson CF, et al: Sinonasal quality of life outcomes following laser treatment of epistaxis related to hereditary hemorrhagic telangiectasia, Lasers Med Sci 32:527–531, 2017. 134. Dabiri J, Fakhoury R, Choufani G, et al: Cauterization for epistaxis in hereditary hemorrhagic telangiectasia, B-ENT 12:9–16, 2016. 135. Ghaheri BA, Fong KJ, Hwang PH: The utility of bipolar electrocautery in hereditary hemorrhagic telangiectasia, Otolaryngol Head Neck Surg 134:1006–1009, 2006. 136. Poetker DM: Endoscopic-guided coblation treatment of nasal telangiectasias in hereditary hemorrhagic telangiectasia: “How I do it”, Am J Rhinol Allergy 31:205–206, 2017. 137. Lund VJ, Howard DJ: A treatment algorithm for the management of epistaxis in hereditary hemorrhagic telangiectasia, Am J Rhinol 13:319–322, 1999. 138. Bastianelli M, Kilty SJ: Technique modifications for septodermoplasty: an illustrative case, J Otolaryngol Head Neck Surg 44:59, 2015. 139. Geisthoff UW, Fiorella ML, Fiorella R: Treatment of recurrent epistaxis in HHT, Curr Pharm Des 12:1237–1242, 2006. 140. Hitchings AE, Lennox PA, Lund VJ, et al: The effect of treatment for epistaxis secondary to hereditary hemorrhagic telangiectasia, Am J Rhinol 19:75–78, 2005. 141. Lund VJ, Darby Y, Rimmer J, et al: Nasal closure for severe hereditary haemorrhagic telangiectasia in 100 patients. The Lund modification of the Young’s procedure: a 22-year experience, Rhinology 55:135–141, 2017. 142. Lund VJ, Howard DJ: Closure of the nasal cavities in the treatment of refractory hereditary haemorrhagic telangiectasia, J Laryngol Otol 111:30–33, 1997. 108. Pepper JP, Wadhwa AK, Tsai F, et al: Cavernous carotid injury during functional endoscopic sinus surgery: case presentations and guidelines for optimal management, Am J Rhinol 21:105–109, 2007. 109. Snyderman CH, Pant H: Endoscopic management of vascular sinonasal tumors, including angiofibroma, Otolaryngol Clin North Am 49:791–807, 2016. 110. Valentine R, Wormald PJ: Carotid artery injury after endonasal surgery, Otolaryngol Clin North Am 44:1059–1079, 2011. 111. Ruddy J, Proops DW, Pearman K, et al: Management of epistaxis in children, Int J Pediatr Otorhinolaryngol 21:139–142, 1991. 112. Qureishi A, Burton MJ: Interventions for recurrent idiopathic epistaxis (nosebleeds) in children, Cochrane Database Syst Rev (9):CD004461, 2012. 113. Calder N, Kang S, Fraser L, et al: A double-blind randomized controlled trial of management of recurrent nosebleeds in children, Otolaryngol Head Neck Surg 140:670–674, 2009. 114. Geisthoff UW, Heckmann K, D’Amelio R, et al: Health-related quality of life in hereditary hemorrhagic telangiectasia, Otolaryngol Head Neck Surg 136:726–733, discussion 34–35, 2007. 115. Lennox PA, Hitchings AE, Lund VJ, et al: The SF-36 health status questionnaire in assessing patients with epistaxis secondary to hereditary hemorrhagic telangiectasia, Am J Rhinol 19:71–74, 2005. 116. Merlo CA, Yin LX, Hoag JB, et al: The effects of epistaxis on health-related quality of life in patients with hereditary hemorrhagic telangiectasia, Int Forum Allergy Rhinol 4:921–925, 2014. 117. Thompson CF, Suh JD, McWilliams J, et al: Initial experience of a hereditary hemorrhagic telangiectasia center of excellence, Ear Nose Throat J 96:E33–E36, 2017. 118. Silva BM, Hosman AE, Devlin HL, et al: Lifestyle and dietary influ- ences on nosebleed severity in hereditary hemorrhagic telangiectasia, Laryngoscope 123:1092–1099, 2013. 119. Jameson JJ, Cave DR: Hormonal and antihormonal therapy for epistaxis in hereditary hemorrhagic telangiectasia, Laryngoscope 114:705–709, 2004. 120. Yaniv E, Preis M, Hadar T, et al: Antiestrogen therapy for hereditary hemorrhagic telangiectasia: a double-blind placebo-controlled clinical trial, Laryngoscope 119:284–288, 2009. 121. Yaniv E, Preis M, Shevro J, et al: Anti-estrogen therapy for hereditary hemorrhagic telangiectasia—a long-term clinical trial, Rhinology 49:214–216, 2011. 122. Chin CJ: Is bevacizumab effective for reducing epistaxis in hereditary hemorrhagic telangiectasia?, Laryngoscope 127:289–290, 2017. 123. Dheyauldeen S, Ostertun Geirdal A, Osnes T, et al: Bevacizumab in hereditary hemorrhagic telangiectasia-associated epistaxis: effectiveness of an injection protocol based on the vascular anatomy of the nose, Laryngoscope 122:1210–1214, 2012. 124. Steineger J, Osnes T, Heimdal K, et al: Long-term experience with intranasal bevacizumab therapy, Laryngoscope 2018. 125. Stokes P, Rimmer J: Intranasal bevacizumab in the treatment of HHT—related epistaxis: a systematic review, Rhinology 2017. Descargado para ALEX LARA (ua.alexlara@uniandes.edu.ec) en Regional Autonomous University of the Andes de ClinicalKey.es por Elsevier en diciembre 04, 2022. Para uso personal exclusivamente. No se permiten otros usos sin autorización. Copyright ©2022. Elsevier Inc. Todos los derechos reservados.