Download Surgical treatment of severe epistaxis: an

Eur Arch Otorhinolaryngol
DOI 10.1007/s00405-011-1659-y
RHINOLOGY
Serious spontaneous epistaxis and hypertension
in hospitalized patients
Cyril Page • Aurélie Biet • Sophie Liabeuf
Vladimir Strunski • Albert Fournier
•
Received: 25 February 2011 / Accepted: 25 May 2011
Springer-Verlag 2011
Abstract The aim of the study was to evaluate the role of
hypertension in patients hospitalized for serious spontaneous epistaxis. This 6-year retrospective study was based on
219 patients hospitalized in a University Hospital ENT and
Head and Neck surgery department for serious spontaneous
epistaxis. The following parameters were recorded: length
of hospital stay, history of hypertension, blood pressure
(BP) recordings (on admission, during hospitalization and
on discharge), epistaxis severity criteria, including medical
and/or surgical management of epistaxis (blood transfusion
depending on blood count, embolization, surgery), medications affecting clotting. Epistaxis was classified into two
groups: serious and severe. No significant differences were
observed between the two groups in terms of age, sex ratio,
history of epistaxis and BP characteristics including history
of hypertension, mean BP on admission, mean arterial
pressure on discharge and number of patients in whom BP
was difficult to control. Patients with more severe epistaxis
had a similar exposure to anticoagulant and platelet antiaggregant medications as patients with less severe epistaxis. Overall, on univariate logistic regression analysis,
no factors were independently associated with severity
C. Page (&) A. Biet V. Strunski
ENT and Head and Neck Surgery Department,
C.H.U Amiens, Centre Hospitalier Nord,
Place Victor Pauchet, 80054 Amiens cedex, France
e-mail: [email protected]
S. Liabeuf
Clinical Pharmacology Department, CHU AMIENS - Hopital
Sud, Avenue Laënnec, Salouel, 80054 Amiens cedex, France
A. Fournier
Nephrology Department, CHU AMIENS - Hopital Sud,
Avenue Laënnec, Salouel, 80054 Amiens cedex, France
of epistaxis. The pathophysiology of serious spontaneous
epistaxis remains to be unclear. It concerns elderly patients
([60–70 years old) with a history of hypertension in about
50% of cases. Serious spontaneous epistaxis may also be
the presenting sign of underlying true hypertension in
about 43% of patients with no history of hypertension.
However, hypertension per se does not appear to be a
statistically significant causal factor and/or a factor of
severity of serious spontaneous epistaxis.
Keywords
Epistaxis Hypertension
Introduction
Epistaxis is one of the commonest ENT emergencies
requiring hospital admission (15% of cases according to
Timsit) [1]. Although predominantly a benign condition
regardless of its etiology, epistaxis can be severe, particularly in elderly and/or frail patients, requiring hospitalization and ‘‘aggressive’’ management including repeated
nasal packing, blood transfusion, arterial embolization or
surgery [2–6].
Epistaxis can be posttraumatic, iatrogenic (nose surgery, particularly endonasal procedures) or ‘‘spontaneous’’,
resulting from numerous possible causative factors including local nasal factors (inflammation, infection…),
medications, and systemic factors such as platelet and
coagulation abnormalities, alcoholism, hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu disease) and
hypertension [1–6]. Hypertension has been considered to be
a major cause of spontaneous epistaxis for a long time [7, 8].
However, particularly in the recent medical literature, the
relationship between hypertension and epistaxis appears to
be more controversial [9–16].
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Eur Arch Otorhinolaryngol
This retrospective study concerning 219 patients hospitalized for serious spontaneous epistaxis was designed to
elucidate the role of hypertension in these patients managed in a university hospital ENT and Head and Neck
Surgery department.
Materials and methods
This retrospective study was performed over a 6-year
period from January 2004 to December 2009 in the University Hospital of Amiens, France. This study was
approved by the Amiens University Medical Center’s
institutional review board.
Patient selection
A total of 219 patients were included in the study. The
study inclusion criteria were:
–
–
male and female patients of any age
patients admitted to the ENT and Head and Neck
surgery department with a diagnosis of serious spontaneous epistaxis requiring at least one nasal pack.
The exclusion criteria were: patients with minor
epistaxis easily managed by first aid measures and/or
immediately successful local treatment (cauterization),
posttraumatic epistaxis (including iatrogenic epistaxis after
nasal surgery) and patients usually followed for Hereditary
Hemorrhagic Telangiectasia.
Four patients hospitalized for epistaxis (two patients
followed for nasal cancer, one patient with leukemia and
chemotherapy-induced pancytopenia and one patient with
Child-Pugh C cirrhosis were also excluded from the study.
Management of epistaxis
Management of epistaxis ranged from unilateral nasal
packing to endoscopic surgery or embolization depending
on the severity of epistaxis. Patients with systolic blood
pressure (BP) higher than 160 mmHg also received nicardipine intravenous infusion (syringe pump) to control BP.
Anterior nasal packing was performed with Polyvinyl
Alcohol sponge (MEROCEL Standard nasal dressing);
anterior and posterior nasal packing was performed with a
double balloon nasal catheter (BIVONA).
Nasal packs were removed after 24–48 h if the patient
did not re-bleed.
In cases of re-bleeding after removal of nasal packs,
nasal packing was repeated. Embolization or surgery was
only indicated in the case of anemia or persistent bleeding
after 2 or 3 nasal packs.
123
Study protocol
A history of hypertension was defined as patients treated
with antihypertensive drugs. Patients with a self-reported
history of epistaxis or who had been already hospitalized
for at least one episode of epistaxis were considered to
have a history of epistaxis. The mean of all BP measurements during hospitalization was determined, and BP that
was difficult to control was defined as BP higher than
140/80 mmHg. International Normalized Ratio (INR) for
prothrombin time was evaluated for 72 patients treated
with vitamin K antagonists.
Epistaxis was classified as grade 1 (serious) or grade 2
(severe).
Serious epistaxis was defined by the need for medical
management requiring hospitalization of the patient for
epistaxis. Severe epistaxis (grade 2) was defined as
follows:
–
–
–
–
–
length of hospital stay [3 days
nasal packing using double balloon nasal catheter
two or more nasal packs
presence of hematologic consequences: anemia (hemoglobin \10 g/dl) and/or blood transfusion
patients treated by embolization or surgery
Statistical analysis
Data were expressed as mean ± S.D., and range or frequency, as appropriate. For descriptive and analytical
purposes, patients were stratified by severity of epistaxis,
defined as Grade 1 or Grade 2.
Between-group comparisons were performed with a v2
test for categorical variables and Student’s t test or
Mann–Whitney test for continuous variables. Univariate
logistic regression analysis was then performed to identify
the variables independently associated with severity of
epistaxis. A p B 0.05 was considered to be statistically
significant. All statistical analyses were performed using
SPSS (SPSS Inc, Chicago, IL), version 13.0 for Windows
(Microsoft Corp, Redmond, WA).
Results
A total of 219 patients admitted to the ENT and Head and
Neck Surgery Department were included. Table 1 shows
the clinical characteristics of the patients according to the
severity of epistaxis.
No significant differences were observed between the
two groups in terms of age, sex ratio, history of epistaxis
and BP characteristics including history of hypertension,
mean BP on admission, mean BP on discharge and number
Eur Arch Otorhinolaryngol
Table 1 Clinical and demographic characteristics of the study population
Severity of epistaxis
All
n = 219
Grade 1
n = 94
Grade 2
n = 125
p
0.6
Age (years)
70 ± 15
70 ± 15
69 ± 15
Male gender, n (%)
123 (57)
48 (53)
75 (60)
0.3
Systolic blood pressure on admission (mmHg)
Diastolic blood pressure on admission (mmHg)
147 ± 2.9
80 ± 16
147 ± 2.5
80 ± 15
146 ± 3.2
80 ± 16
0.7
0.9
Number of patients in whom blood pressure as difficult to control, n (%)
127 (59)
51 (57)
76 (60)
0.5
Systolic blood pressure on discharge (mmHg)
128 ± 16
129 ± 17
127 ± 16
0.3
Diastolic blood pressure on discharge (mmHg)
71 ± 11
72 ± 11
70 ± 11
0.2
History of hypertension, n (%)
118 (55)
48 (53)
70 (56)
0.7
History of epistaxis, n (%)
72 (34)
29 (32)
43 (34)
0.7
Vitamin K antagonist n (%)
72 (34)
29 (32)
43 (34)
0.7
INR (n = 72)
3±1
2.9 ± 1.1
3 ± 1.6
0.6
Aspirin, n (%)
59 (27)
27 (30)
32 (26)
0.5
Clopidogrel, n (%)
11 (5)
4 (4)
7 (6)
0.7
Length of hospital stay (days)
3.1 ± 1.9
2.1 ± 0.8
3.9 ± 2
NA
Hemoglobin (g/dl)
11.7 ± 2.4
13 ± 1.4
11 ± 2.7
NA
Treatment with sphenopalatine artery surgical ligation or embolization n (%)
13 (3)
0 (0)
13 (4)
NA
Treatment with double-cuffed nasal tamponade balloon n (%)
65 (30)
0 (0)
65 (52)
NA
Treatment with more than 2 nasal packs n (%)
44 (20)
0 (0)
44 (35)
NA
of patients in whom BP was difficult to control. Patients
with more severe epistaxis had a similar exposure to anticoagulant and platelet antiaggregant medications as
patients with less severe epistaxis. On univariate logistic
regressions, no factors were independently associated with
severity of epistaxis (data not shown).
(Osler-Weber-Rendu disease), the cause of epistaxis can be
identified in only about 15% of patients [4].
In the absence of documented evidence (a visible
bleeding vessel on the nasal septum for example), no
obvious cause-and-effect relationship can be confirmed,
especially concerning hypertension. Only statistical associations between hypertension and epistaxis have been
reported [7–16].
Discussion
Definition of serious spontaneous epistaxis
Serious spontaneous epistaxis is a challenging medical
problem in otorhinolaryngology, particularly concerning its
physiopathology and its relationship with hypertension.
Etiologies of epistaxis
Classical teaching and medical literature highlight many
possible etiologic factors for epistaxis; including environmental factors (humidity, temperature), local factors
(inflammation, deviated septum and/or perforation, tumors,
foreign bodies, aneurysm), systemic factors (hypertension,
platelet and coagulation abnormalities, renal failure, alcoholism, arteriosclerosis, hereditary hemorrhagic telangiectasia), and medications affecting clotting (anticoagulants,
nonsteroidal anti-inflammatory drugs) [3]. Although some
etiologies of epistaxis are obvious such as trauma (iatrogenic or non-iatrogenic), nasal inflammation and/or infection or tumors and hereditary hemorrhagic telangiectasia
Epistaxis is a benign condition in the majority of cases, but
can sometimes be sufficiently serious (6% of cases
according to Pollice) [6] to require emergency hospitalization for medical and/or surgical management and close
follow-up, especially in patients older than 65 years [2].
However, in the majority of cases, patients present themselves (often to the emergency department) with ‘‘spontaneous’’ epistaxis with no obvious cause and emergency
management must be performed before determining
the etiology of the nose-bleed. Classical textbooks and the
medical literature do not provide a precise definition for
the severity of epistaxis which is often based on subjective
impressions (subjective evaluation of the volume of
bleeding) or anatomic features, essentially posterior epistaxis [5]. Hoag et al. recently proposed an epistaxis
severity score but specifically for hereditary hemorrhagic
telangiectasia [16]. In our opinion, epistaxis should be
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considered to be serious when it requires specific medical
and/or surgical management including at least one nasal
pack and hospitalization for close follow-up. The complete
criteria used to classify the severity of epistaxis as serious
or severe in the present study are shown in Table 1.
Finally, most articles in the medical literature concerning
the association between epistaxis and hypertension do not
clearly define the severity of epistaxis, which, in our
opinion, constitutes a major problem: is hypertension
related to serious spontaneous epistaxis?
In another study concerning 372 patients, Herkner et al.
[14] concluded that active epistaxis in the emergency
department was associated with hypertension, suggesting
that hypertension was a predisposing factor for acute nosebleed.
Knopfholz et al. [15] in a series of 36 patients, concluded that the incidence of epistaxis in hypertensive
patients was not associated with the severity of hypertension. Moreover, BP readings in the setting of epistaxis were
similar to those obtained in routine settings.
Association between epistaxis and hypertension
Comparison of the present series with the medical
literature
Epistaxis has been considered to be related to hypertension
for a long time. In 1959, Mitchell [7] statistically compared
two groups of patients (one group of 374 patients with a
history of hypertension and another group of 162 patients
with acute epistaxis but with no history of hypertension)
and concluded that, in the absence of local nasal disease,
epistaxis was associated with high BP. In 1977, Charles
and Corrigan [8] confirmed this conclusion in a series of
194 patients and, more recently, Isezuo et al. [9] also
showed a statistically significant association between epistaxis and hypertension in a series of 62 patients.
However, Fuchs et al. [10] in a sample of 1,174 subjects
over the age of 18 years representative of Porto Allegre
general population, found no association between epistaxis
and hypertension. The same group, however, [11] in a study
based on 323 adults with hypertension, pointed out however
that duration of hypertension and left ventricular hypertrophy were associated with epistaxis, suggesting that epistaxis
might be a consequence of long-lasting hypertension.
In another study of 121 hypertensive patients, Lubianca
Neto et al. tried to evaluate the association between
severity of hypertension and history of epistaxis. They
concluded that the severity of hypertension was not associated with a history of epistaxis, but they found a statistically significant tendency towards an association between
history of epistaxis with duration of hypertension and left
ventricular hypertrophy, in addition they noticed that
among the abnormalities detected at rhinoscopy, only the
presence of enlarged septal vessels was associated with a
history of epistaxis. They concluded that long lasting
hypertension might contribute to epistaxis but the role of
septal vessel abnormalities needed further work to be
established [12].
Herkner et al. [13] in a series of 426 patients admitted at
the emergency room, demonstrated that patients with epistaxis had higher BP than control patients. 79% of patients
with elevated BP during epistaxis had sustained hypertension and 27% of these patients were unaware of their
hypertension, indicating that epistaxis may be the presenting sign of hypertension.
123
The present series is fairly similar to other series of patients
hospitalized for epistaxis published in the medical literature, but the patients of this series were slightly older with a
mean age of 70 years versus 64.3 years for Viducich [5]
and 60 years for Pollice (with 70% of patients [50 years)
[6]. 55% of the patients in the present series had a history
of hypertension versus 48% for Viducich [5] and 47% for
Pollice [6].
The main bias of this retrospective series was that this
study only concerned patients hospitalized for serious
spontaneous epistaxis requiring medical and/or surgical
management and close follow-up in hospital. The majority
of cases of benign epistaxis were not considered in this
study, and it would have possibly been interesting to
compare the clinical features and concomitant diseases of
patients with benign epistaxis versus patients with serious
epistaxis.
However, this study reveals interesting results, as no
significant differences were observed between the two
patient groups concerning the role of hypertension.
A history of hypertension was not associated with severe
epistaxis versus serious epistaxis. No statistically significant difference was observed between patients with a
history of epistaxis in the two patient groups (with or
without a history of hypertension). No statistically significant difference was observed between BP recordings on
admission between the two patient groups (with or without
a history of hypertension). The severity of hypertension
(BP [160/100 mmHg) was not associated with severe
epistaxis versus serious epistaxis. Blood pressure recordings were also not significantly different between the two
groups of hypertensive versus non-hypertensive patients,
which may indicate that, as suggested by Tan and Calhoun
[3], hypertension at the time of treatment of epistaxis may
be anxiety-related, and BP returns to normal after control
of epistaxis and reassurance. However, 43 of the 127
patients with abnormal BP recordings during hospitalization had no history of hypertension. True hypertension was
diagnosed in these patients, i.e 42.57% of patients with no
Eur Arch Otorhinolaryngol
previous history of hypertension. However, we have
recorded BP only during their hospitalization and not
weeks after discharge as appropriately did Herkner et al.
[13] for confirming or excluding sustained hypertension
with a 24-h ambulatory BP recording.
In contrast to Lubianca Neto, in the present series, we
found only a dozen patients who underwent septal cauterization 3 weeks after the episode of epistaxis and no local
nasal factor was found on rhinoscopy performed at the D21
follow-up visit in the other patients. Overall, the very local
nasal origin of epistaxis remains to be unclear in the
majority if not all cases.
We can conclude like Celik et al. [16] that: the debate on
BP and epistaxis will continue. The potential influence of
BP levels on acute episodes of epistaxis still requires
investigations. Our clinical data are not sufficient to support
or dismiss the idea that epistaxis is secondary to end-organ
damage caused by hypertension. This is corroborated by
nasal examinations after the episode of epistaxis, since they
were normal in almost all cases in our ENT experience.
3.
4.
5.
6.
7.
8.
9.
10.
Conclusion
The pathophysiology of serious spontaneous epistaxis
remains to be unclear.
It mainly occurs in elderly patients ([60–70 years old)
with a history of hypertension in about 50% of cases.
Serious spontaneous epistaxis may reveal underlying true
hypertension in about 43% of patients (in this series) with
no previous history of hypertension. Serious spontaneous
epistaxis probably results from a combination of several
local and systemic causal factors or diseases. Further prospective studies are required to elucidate the pathophysiology and the exact role played by hypertension.
Conflict of interest
2.
11.
12.
13.
14.
The authors declare no conflict of interest.
15.
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J (1996) Management of epistaxis: a national survey. Ann R Coll
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clinical features and acute complications. Ann Emerg Med
25:592–596
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hospitalized patients. Otolaryngol Head Neck Surg 117:49–53
Mitchell JR (1959) Nose-bleeding and high blood pressure.
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Isezuo SA, Segun-Busari S, Ezunu E, Yakubu A, Iseh K, Legbo J,
Alabi BS, Dunmade AE, Ologe FE (2008) Relationship between
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Moraes RS, Wiehe M, Fuchs SC, Lubianca Neto JF (2003)
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Mafessoni R, Gleissner AL (1999) Is epistaxis evidence of endorgan damage in patients with hypertension? Laryngoscope.
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Estrella E, Pletsch A, Gus M, Lu L, Fuchs FD (1998) A study of
the association between epistaxis and the severity of hypertension. Am J Rhinol 12:269–272
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Gamper G, Woisetschläger C, Hirschl MM (2000) Hypertension
in patients presenting with epistaxis. Ann Emerg Med 35:
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Laggner AN, Hirschl MM (2002) Active epistaxis at ED presentation is associated with arterial hypertension. Am J Emerg
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(2009) Association between epistaxis and hypertension: a one
year follow-up after an index episode of nose bleeding in
hypertensive patients. Int J Cardiol 134:e107–e109
Celik T, Iyisoy A, Yuksel UC, Karahatay S, Tan Y, Isik E. A new
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Turkish Journal of Medical Sciences
http://journals.tubitak.gov.tr/medical/
Research Article
Turk J Med Sci
(2014) 44: 133-136
© TÜBİTAK
doi:10.3906/sag-1301-58
Epistaxis in geriatric patients
Alper YÜKSEL*, Hanifi KURTARAN, Ekrem Said KANKILIÇ, Nebil ARK, Kadriye Şerife UĞUR, Mehmet GÜNDÜZ
Department of Otolaryngology - Head and Neck Surgery, Faculty of Medicine, Fatih University, Ankara, Turkey
Received: 14.01.2013
Accepted: 22.02.2013
Published Online: 02.01.2014
Printed: 24.01.2014
Aim: Epistaxis is a common emergency in otolaryngology. The aim of this study is to analyze the etiology, management, and
accompanying disorders of epistaxis in geriatric patients by reviewing the literature
Materials and methods: Data of 117 patients 65 years old and older who presented to the Department of Otorhinolaryngology with
active epistaxis between 2004 and 2010 were retrospectively reviewed. Records were evaluated for age, sex, accompanying disorders,
drug medication, detailed otorhinolaryngological findings, and management of epistaxis.
Results: There were 67 women (57.26%) and 50 men (42.74%) with a mean age of 73.51 years (range: 65–90). Ninety-four (80.34%)
patients had accompanying disorders such as hypertension, diabetes mellitus, cerebrovascular disease, sinusitis, chronic obstructive
lung disease, nasal polyp, and drug treatment. The bleeding site was anterior in 90 patients (76.92%) and posterior in 16 (13.67%). In 11
patients (9.4%), the bleeding site was not identified. Fifty-seven patients (48.71%) were treated with cauterization, 17 patients (14.52%)
with nasal packing, 12 patients (10.25%) with medical treatment, 1 patient (0.85%) with mass excision and nasal packing, and 19
patients (16.23%) with more than 1 treatment method. Six patients (5.12%) were untreated because of the unidentified bleeding point.
Bleeding control was performed under local anesthesia in 113 patients (96.58%) and under general anesthesia in 4 patients (3.41%).
Twenty-one patients (17.94%) were hospitalized and 3 patients (2.56%) required a blood transfusion.
Conclusion: Epistaxis is the most common otorhinolaryngological emergency. It must be evaluated carefully to avoid the potential
complications resulting from both epistaxis and its associated disorders, especially in geriatric patients.
Key words: Epistaxis, cauterization
1. Introduction
Epistaxis is one of the most common nasal emergencies,
with an incidence ranging from 30 to 100 per 100,000
each year (1). The lifetime occurrence rate of epistaxis
is approximately 60% (2). However, most bleeding
episodes are minor and require no medical treatment.
Minor bleeding episodes occur more frequently in
children and adolescents, whereas severe bleeds requiring
otolaryngological intervention often occur in patients
older than 50 years (3).
Anterior nosebleeds are observed in approximately 80%
patients with epistaxis (4). They arise from an anastomosis
called Kiesselbach’s plexus in the lower portion of
the anterior septum, called Little’s area. Conservative
treatment methods are often sufficient for most patients
with anterior epistaxis. These methods include local
pressure, chemical cautery, and anterior nasal packing (5).
Posterior bleeding originates primarily from the posterior
septal nasal artery, a branch of the sphenopalatine artery,
and tends to be more serious compared with anterior
*Correspondence: [email protected]
bleeding. Conservative methods are generally insufficient
for the treatment of patients with posterior epistaxis, who
often require further otolaryngological intervention (6).
Further treatment options include posterior packing,
arterial ligation, and embolization. Treatment modalities
differ because of factors such as site and severity of
bleeding, predisposing conditions, and experience of the
otolaryngologist.
Various local and systemic factors cause epistaxis.
Common local factors include digital trauma, nasal septal
deviation, neoplasia, inflammation, and chemical irritants,
whereas coagulopathies, renal failure, alcoholism, and
vascular abnormalities are common systemic factors (7,8).
Patients presenting with epistaxis in the geriatric
population must be evaluated carefully. The clinical status
of geriatric patients may deteriorate quickly; therefore,
rapid evaluation and treatment of these patients must be
performed (4).
In this study, the etiology, management, and
accompanying disorders of epistaxis were analyzed in
133
YÜKSEL et al. / Turk J Med Sci
geriatric patients. A review of the relevant literature is also
presented.
2. Material and methods
The data of 156 patients aged ≥65 years, who presented
to the Department of Otorhinolaryngology with active
epistaxis between 2004 and 2010, were retrospectively
reviewed. Patients were identified by a search of the
electronic data record system of the hospital. In total, 39
patients were excluded, 22 because they presented with
epistaxis caused by trauma and 17 because of insufficient
data. Therefore, 117 patients with a diagnosis of epistaxis
as confirmed by chart review were eligible for the study.
Epistaxis was defined as bleeding from the nasal cavity as
confirmed by nasal inspection on initial evaluation. The
condition of active or inactive epistaxis was determined on
the basis of the nasal inspection results. The localization of
epistaxis was classified as diffuse or limited and unilateral
or bilateral. The bleeding site was identified as anterior or
posterior after nasal endoscopic examination using 0° and
30° rigid endoscopes. Anterior epistaxis was identified in
cases in which the bleeding site was visible on anterior
rhinoscopy (9).
Patients were labeled positive for hypertension if
this condition was stated in their medical charts or if
they were on antihypertensive medication. Treatment
with anticoagulant medication such as Coumadin,
heparin, Fraxiparine, or aspirin was ascertained during
evaluation. Records were examined to obtain information
regarding age, sex, accompanying disorders, detailed
otorhinolaryngological findings, and management of
epistaxis. This study was approved by the local ethics
committee of the hospital.
3. Results
This study included 67 women (57.26%) and 50 men
(42.74%) with a mean age of 73.51 years (range: 65–90
years). Ninety-four (80.34%) patients had accompanying
disorders such as hypertension, diabetes mellitus,
cerebrovascular disease, sinusitis, coronary artery disease,
nasal polyp, or a history of drug medication (Table 1).
Table 1. Underlying disorders.
Hypertension
91 (77.7%)
Diabetes mellitus
69 (58.9%)
Coronary artery disease
17 (14.5%)
Anticoagulant medication
13 (11.1%)
Sinusitis
11 (9.4%)
Nasal polyp
9 (7.6%)
Cerebrovascular disease
3 (2.5%)
134
The bleeding site was anterior in 90 patients (76.92%)
and posterior in 16 (13.67%). In 11 patients (9.4%), the
bleeding site was not identified. Treatment modalities
used for the management of epistaxis in the patients
included in this study are shown in Table 2. No bleeding
points were identifiable in 6 patients (5.12%). Epistaxis
healed spontaneously in all patients, with no evidence of
recurrence on follow-up. Bleeding control was performed
under local anesthesia in 113 patients (96.58%) and under
general anesthesia in 4 (3.41%). Twenty-one patients
(17.94%) were hospitalized and 3 (2.56%) required a blood
transfusion.
4. Discussion
Bleeding from the nose is a common complaint, and it
occurs in approximately 10% of the population at any given
time (10). Epistaxis may lead to mortality and morbidity in
vulnerable groups such as children and the elderly and in
patients with additional systemic disorders.
The interaction of several local and systemic factors
results in nosebleeds. These factors damage the nasal
mucosa, affect the vascular structure, and/or disrupt blood
clotting. They include environmental conditions, trauma,
nasal septal deviation, tumors, inflammation, bleeding
disorders, anticoagulant medications, hypertension,
and age. In geriatric patients, systemic factors such as
hypertension, advanced age, and bleeding disorders
are the most common causes of serious epistaxis (7,8).
Vascular wall changes associated with ageing, such as
fibrosis of the arterial tunica media, have been implicated
in the development of epistaxis. Therefore, elderly patients
are at higher risk of epistaxis (11).
The prevalence of hypertension in patients with
epistaxis reportedly ranges from 24% to 64% (12).
Another controlled study provided a relationship between
epistaxis and high blood pressure (13). In contrast, a crosssectional study in patients with hypertension found no
independent association between the severity of epistaxis
and hypertension (14). Other studies have suggested that
hypertension in patients with epistaxis may be related
to anxiety (15). Ninety-one (77.7%) of the 117 patients
in our study group had a history of epistaxis. The role of
hypertension in epistaxis is controversial, and the evidence
available is insufficient to prove a significant association
between hypertension and epistaxis. However, the
control of epistaxis may be more difficult in patients with
hypertension (7).
In rare cases, epistaxis may be a life-threatening
emergency, especially in elderly patients with hypertension
and severe hemorrhage (10). In our study group, none of
the patients required resuscitation despite old age (>65
years old) and underlying disorders (80.34% patients).
Coagulation screening is not routinely used in our
institution. Studies have shown that routine coagulation
YÜKSEL et al. / Turk J Med Sci
Table 2. Treatment modalities.
Anterior
Posterior
SN
EC
AP
48
2
10
7
5
PP
2
MT
SN + AP
ME + AP
12
17
1
2
SN = silver nitrate, EC = electrocautery, AP = anterior packing, PP =
posterior packing, MT = medical treatment, ME = mass excision.
studies such as prothrombin time and activated partial
thromboplastin time are not necessary in patients with
epistaxis. Coagulation screening should be used in
patients with suspected clotting disorders or in patients
who receive anticoagulation treatment (16,17).
The first step in the treatment of acute epistaxis is
identification of the bleeding point. In our study, 90
(76.92%) of the patients had anterior epistaxis. This
incidence rate is compatible with the rates reported in
the literature (4). After localization of the bleeding point,
chemical cautery or electrocautery can be performed.
Silver nitrate can be used as a chemical cauterization
agent, especially for minor bleeding, with minimal
discomfort. Electric cauterization must be performed
for more aggressive bleeding from the anterior septum.
Cauterization should be one-sided in order to prevent
septal perforation (18). There is no evidence to prove that
electrocautery has any advantage over silver nitrate cautery
(10). In our study group, 90 (76.92%) patients had anterior
epistaxis, 48 (41.02%) of whom were successfully treated
with silver nitrate cautery. Only 2 patients were treated
with electrocautery because of severe epistaxis from the
anterior septum.
In the case of cauterization failure, nasal packing
must be considered as the next treatment option. Many
different types of packs are available, including absorbable,
nonabsorbable, anterior, and posterior packs. Common
absorbable materials used for anterior packing include
oxidized cellulose (e.g., Surgicel, Johnson & Johnson,
New Brunswick, NJ, USA) and gelatin foams (e.g.,
Gelfoam, Pfizer, New York, NY, USA). Another product
that combines thrombin with gelatin (e.g., Floseal, Baxter
Health Care Corp, Deerfield, IL, USA) is used as a highviscosity gel for hemostasis (19). All these absorbable
products are easily used and cause minimal pain and
discomfort.
Various kinds of nonabsorbable packing materials
are also available, including inflatable balloons, calcium
alginate, polyvinyl alcohol (e.g., Merocel, Medtronic
XOMED, Jacksonville, FL, USA), and petroleum jellyimpregnated gauze. The major disadvantage of anterior
packing with these materials is the need for removal
of the material and the pain associated with placement
and removal. Complications caused by anterior packs
include ulcerations, septal perforation, sinusitis, synechia,
hypoxemia, and arrhythmias (20). Contrarily, Kurtaran
et al. reported that nasal packing with airway tubes is
not a cause for postoperative respiratory dysfunction and
hypoxia (21). Merocel is most commonly used for anterior
packing in our institution. None of the complications
mentioned above were observed in this study, although
our study group comprised geriatric patients.
Approximately 10% of all nosebleeds arise from the
posterior part of the nose (22). Posterior epistaxis is often
encountered in elderly individuals (23). This condition
may be associated with diseases such as hypertension and
arterial degeneration (24). In our study group, 16 (13.67%)
patients had posterior epistaxis. Although no research on
epistaxis in geriatric patients is available, the incidence
of posterior epistaxis in this study was not significantly
higher than that in the normal population. In this study,
a formal posterior pack made of ribbon gauze was used in
2 patients, although balloon catheters are more commonly
used. However, posterior packing is associated with
increased risk of mortality and morbidity. Nasal packing
may cause significant hypoxia, especially in patients with
chronic systemic disorders (10).
In some cases, traditional nasal packing fails to control
the epistaxis. Angiographic embolization or endoscopic
techniques for sphenopalatine artery ligation can be used
for the control of intractable bleeding. Angiographic
embolization for posterior epistaxis was first described
in 1974 (25), with success rates ranging from 79% to 96%
(26). Complications of embolization include rebleeding,
stroke, blindness, facial numbness, skin sloughing, and
groin hematoma. A success rate of 98% was reported for
endonasal ligation of the sphenopalatine artery to control
bleeding in 127 patients; no significant treatment-related
complications were reported in that study (27). In our study,
all patients with epistaxis were treated using conventional
methods. No further interventions such as embolization
or sphenopalatine artery ligation were required.
Some authors recommend a formal nasal examination
under general anesthesia in patients with posterior
epistaxis (23). In our study group, only 4 (3.41%) of the
16 (13.6%) patients with posterior epistaxis were treated
under general anesthesia. In fact, treatment of epistaxis
under general anesthesia is easier than treatment under
135
YÜKSEL et al. / Turk J Med Sci
local anesthesia for both the surgeon and the patient;
however, general anesthesia can be dangerous for geriatric
patients with systemic disorders. Bleeding control was
performed under local anesthesia in 113 patients (96.58%).
Twenty-one patients (17.94%) were hospitalized and 3
(2.56%) required a blood transfusion.
In conclusion, epistaxis, which is the most common
otorhinolaryngological emergency, must be evaluated
carefully to avoid the potential complications resulting
from both epistaxis and its associated disorders, especially
in geriatric patients. Multiple methods for treating anterior
and posterior epistaxis are available, and occasionally
more than one treatment is used. Otolaryngologists must
be prepared to deal with severe bleeding through the use
of medications, packing materials, and radiological or
surgical interventions, especially in geriatric patients.
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Derkay CS, Friedman N, Gluckman J, Healy GB, Jackler RK,
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21. Kurtaran H, Ark N, Sadıkoğlu F, Uğur KŞ, Yılmaz T, Yıldırım Z,
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The Laryngoscope
C 2010 The American Laryngological,
V
Rhinological and Otological Society, Inc.
An Epistaxis Severity Score for Hereditary
Hemorrhagic Telangiectasia
Jeffrey B. Hoag, MD, MS; Peter Terry, MD, MA; Sally Mitchell, MD; Douglas Reh, MD;
Christian A. Merlo, MD, MPH
Objectives/Hypothesis: Hereditary hemorrhagic telangiectasia (HHT)-related epistaxis leads to
alterations in social functioning and quality of life.
Although more than 95% experience epistaxis, there
is considerable variability of severity. Because no
standardized method exists to measure epistaxis severity, the purpose of this study was to determine factors associated with patient-reported severity to develop a severity score.
Study Design: Prospective, survey-based study.
Methods: HHT care providers and a focus group
of patients were interviewed to determine epistaxisassociated factors. From this, an electronic survey
was developed and administered to patients with
HHT. Descriptive analyses were performed with calculations of means and medians for continuous and
proportions for categorical variables. Multiple ordinal
logistic and linear regression models were developed
to determine risk factors for epistaxis severity.
Results: Nine hundred respondents from 21
countries were included. Eight hundred fifty-five
(95%) subjects reported epistaxis. The mean (standard deviation) age was 52.1 (13.9) years, and 61.4%
were female. Independently associated risk factors for
self-reported epistaxis severity included epistaxis frequency (odds ratio [OR] 1.57), duration (OR 2.17), intensity (OR 2.45), need for transfusion (OR 2.74), anemia (OR 1.44), and aggressiveness of treatment
required (OR 1.53, P < .001 for all).
Conclusions: Risk factors for increasing epistaxis severity in patients with HHT include frequency, duration, and intensity of episodes; invasive-
From the Department of Medicine (J.B.H.), the Drexel University
College of Medicine, Philadelphia, Pennsylvania; and Department of
Medicine (P.T., C.A.M.), Department of Interventional Radiology (S.M.), and
Department of Otolaryngology (D.R.), The Johns Hopkins University
School of Medicine, Baltimore, Maryland, U.S.A.
Editor’s Note: This Manuscript was accepted for publication
December 2, 2009.
This project was provided by the HHT Foundation International,
Inc. The authors have no other funding, financial relationships, or conflicts of interest to disclose.
Send correspondence to Jeffrey B. Hoag, MD, Division of Pulmonary, Critical Care, and Sleep Medicine, Drexel University College of
Medicine, 245 N. 15th St., Mail Stop 107, NCB 12th Floor, Philadelphia,
PA 19102. E-mail: [email protected]
DOI: 10.1002/lary.20818
Laryngoscope 120: April 2010
838
ness of prior therapy required to stop epistaxis; anemia; and the need for blood transfusion. From these
factors, an epistaxis severity score will be presented.
Key Words: Epistaxis, hereditary hemorrhagic
telangiectasia, Osler-Rendu-Weber severity score.
Level of Evidence: 1b.
Laryngoscope, 120:838–843, 2010
INTRODUCTION
Hereditary hemorrhagic telangiectasia (HHT) is an
autosomal dominant disease characterized by epistaxis,
telangiectases, and visceral arteriovenous malformations
that has nearly 100% penetrance by age 40 years. As
this disease afflicts an estimated one in 10,000 to 15,000
individuals,1 it represents a significant health burden.
Epistaxis related to HHT is a major complaint in up to
90% of patients with HHT,2 and has a significantly negative impact on quality of life.3,4
Many studies5–7 have described methods of assessing epistaxis severity (Table I), although none have
directly addressed the validity of the scoring system
itself. These instruments share several factors, such as
epistaxis frequency measured as number of bleeds per
unit time as well as the need for blood transfusions
specifically related to epistaxis. Similarly, duration of
bleeding episodes, intensity, and changes in quality of
life have served as factors to calculate epistaxis severity.
Al-Deen and Bachmann-Harildstad7 published a study
in which experts in the field of HHT-related epistaxis
were polled as to their impressions of factors that best
correlated with epistaxis severity. They determined that
a need for blood transfusions, ease of comprehension by
both patients and care providers, and frequency of
bleeds were the most important factors to calculate severity of bleeding in this patient population.
Although HHT care providers have extensive experience treating epistaxis in these complex patients, and
individual HHT centers of excellence utilize their particular systems for grading epistaxis severity, there has
been resistance to adopt any particular severity scoring
system as a universal, standardized system. Some of
this resistance may be due to particular care providers’
comfort with their own systems. Another possible reason
Hoag et al.: Epistaxis Severity Score for HHT
TABLE I.
Summary of HHT-Related Epistaxis Factors Used to Assess
Overall Severity Published in the Literature.5–7
Frequency
Duration
Intensity
Need for blood transfusion
Anemia and/or iron replacement therapy
Quality of life
Patient satisfaction with therapy
Duration of therapeutic effect
Side effects of therapy
Subject Recruitment
The survey was compiled and distributed using an internet-based
tool
(SurveyMonkey,
www.surveymonkey.com).
Subjects were recruited from the membership registry of the
HHT Foundation International, Inc. through an email blast
advertisement of the project and through posting of the survey
on the HHT Foundation International, Inc.’s website
(www.HHT.org). The survey was anonymous and deidentified.
Imbedded in the survey were questions to confirm the diagnosis
of HHT by the Curaçao Criteria as described by Shovlin et al.9
Subjects were included in the analysis if they completed a series
of mandatory response questions that included those used to
confirm the diagnosis of HHT, information about epistaxisrelated clinical factors, and treatments received for epistaxis.
See also online supplemental references.
Statistical Analysis
for not adopting a single system of grading may stem
from a lack of statistical support for any given system.
Several lines of evidence support the need for a
standardized severity scoring system in HHT. First, in
an informal survey of 100 patients with HHT (Terry
2007, unpublished data), epistaxis was the primary issue
that the patients wanted improvement in therapy. Second, the Scientific Medical Advisory Board (SMAB) of
the HHT Foundation International, Inc. came to the conclusion that epistaxis treatment is the highest priority
for future research. Finally, the SMAB issued a consensus statement from the recent International HHT
Clinical Guidelines Conference8 that there is insufficient
evidence on how to measure the severity of HHT-related
epistaxis.
Therefore, the purpose of this investigation was to
determine factors associated with epistaxis severity, and
to utilize these factors to develop a standardized, validated epistaxis severity score (ESS).
Data are presented as absolute numbers, percentages, and
means (6 standard deviation) where appropriate. A descriptive
analysis was performed with calculation of mean and medians
for continuous variables and percentages for categorical variables. Multiple ordered logistic regression models and linear
regression models were constructed to evaluate the association
between covariates and epistaxis severity. Analysis of variance
and Fisher exact testing were used where appropriate. Values
were considered statistically significant for P < .05. All statistical calculations were performed using STATA SE version 10
statistical software (STATA Corp., College Station, TX).
Validation
Internal validation was performed through bootstrapping
methods.10 External validation was performed by comparing
ESS calculations with invasiveness of treatment received for
epistaxis. Treatments were divided into minimally invasive (topical or oral medications, nasal packing), moderately invasive
(endoscopic procedures including laser therapy, electrocautery,
argon plasma coagulation), and most invasive (Young’s Procedure, septal dermoplasty, arterial ligation, or embolization).
MATERIALS AND METHODS
This study was approved by the institutional review
boards of both Johns Hopkins University School of Medicine
and Drexel University College of Medicine.
Development of Survey
A comprehensive list of covariates including demographics
and clinical characteristics related to epistaxis severity was
obtained through discussions with care providers from HHT
centers of excellence, informal discussions with HHT patients,
and review of previously published studies utilizing measures of
epistaxis severity. From this comprehensive list, a cross-sectional survey was developed that utilized 120 questions to
gather demographic information, disease specific data, and
treatments received for epistaxis. The survey also contained 19
open-ended questions to allow for more detailed responses and
clarifications by the participants.
Only respondents with HHT were included in the analysis.
Diagnosis of HHT was determined using the Curaçao Criteria,9
in which subjects with three or four criteria have a definite diagnosis. In those patients with two criteria (possible HHT),
specific survey responses and open-ended questions were evaluated for potentially omitted diagnostic criteria. From these 253
respondents, more than 90% had other corroborating evidence
for the diagnosis of HHT and were thus included in the analysis
of factors correlating to epistaxis severity. Table II describes the
diagnostic criteria to support HHT in the subject cohort.
Laryngoscope 120: April 2010
RESULTS
Demographics and HHT Diagnostic Criteria
Nine hundred fifteen survey responses were collected for a 6-month period of time from March 2008
through August 2008. Fifteen subjects were excluded
due to age outside the range approved by the
TABLE II.
Distribution of Study Subject Curaçao Criteria for Diagnosis of
HHT and Specific Factors Leading to Diagnosis.
Description of HHT Criteria
No.
%
4
3
229
386
25.7
43.4
2
Curaçao Criteria
253
28.4
1
Epistaxis
21
855
2.4
98.5
Visceral AVMs (diagnosed)
505
58.1
Family history
Telangiectasia
763
382
87.9
44.0
HHT ¼ hereditary hemorrhagic telangiectasia; AVMS ¼ arteriovenous
malformations.
Hoag et al.: Epistaxis Severity Score for HHT
839
TABLE III.
Demographic Data of Respondents.
Descriptions of Respondents
TABLE IV.
Correlation of Factors With Self-Reported Severity of Epistaxis.
No. (%)
Variable
Coefficient
SE
P Value
Intensity
0.25
0.07
<.001
Frequency
0.14
0.02
<.001
353 (38.6)
Duration
Need for medical attention
0.25
0.30
0.02
0.07
<.001
<.001
Age, yr
Diagnosis
Transfusion related to epistaxis
0.31
0.07
<.001
32.0616
Anemia
0.20
0.06
.001
Current
52.6613.9
No.
894
Gender
Female
561 (61.4)
Male
Location of respondents
North America
813 (89)
Europe
46 (5)
Australia
Asia
37 (4)
9 (1)
South America
7 (0.8)
Africa
2 (0.2)
institutional review board protocol (age <18 or >89). Table III shows the demographic data of the cohort of
respondents. The average age of the cohort was 52.6
(613.9) years, and there were more female respondents
(61.4%) than male. Most of the respondents from this
cohort were from North America, with approximately
80% from the United States, reflecting the membership
of the HHT Foundation International, Inc.
Descriptive Distribution of Epistaxis-Related
Factors
Approximately 45% of the cohort self-reported epistaxis severity in the moderate range, with 29.9% selfclassifying above and 26.2% below (Fig. 1). Factors
leading to particular self-classification were similar to
factors previously described in the literature as being
important predictors of epistaxis. Epistaxis episode duration ranged from <1 minute to >30 minutes, with a
mean duration of about 6 to 15 minutes of bleeding per
epistaxis episode. There was considerable variability in
the frequency of epistaxis episodes ranging from several
per day to more than a month between episodes of bleeding. Of the patients, 13.7% described their epistaxis
SE ¼ standard error.
intensity as either gushing or pouring. Of notable interest,
17.5% of this cohort had never sought medical attention
related specifically to epistaxis. Furthermore, more than
30% of respondents had never seen an otolaryngologist,
suggesting that a significant percentage of these individuals are seeking epistaxis therapy from other types of care
providers. Of the study subjects, 59.8% reported a prior
history of anemia, whereas 35.9% reported anemia at the
time of the survey. Red cell transfusions were also common, with 26.6% receiving a blood transfusion related to
blood loss from epistaxis at some point in life; however,
only 22.6% of study subjects knew their current hemoglobin (9.9 6 2.1 mg/dL; range, 3.5–16.5).
Epistaxis Severity Score
Six factors were independent predictors of selfdescribed epistaxis severity (Table IV). Using these six
predictors of epistaxis severity, we developed an ESS
(Table V). The responses are weighted by respective
TABLE V.
Data Sheet for the Calculation of the Epistaxis Severity Score for
Hereditary Hemorrhagic Telangiectasia.
How often do you TYPICALLY have nose bleeding?
(coefficient 0.14)
0 — Less than monthly
1 — Once per month
3 — Several per week
4 — Once per day
2 — Once per week
5 — Several each day
How long do your TYPICAL nose bleeds last? (coefficient 0.25)
0 — <1 minute
3 — 16–30 minutes
1 — 1–5 minutes
4 — >30 minutes
2 — 6–15 minutes
How would you describe your TYPICAL nose bleeding intensity?
(coefficient 0.25)
0 — Not typically gushing
1 — Typically gushing or pouring
Have you every sought medical attention for nose bleeding?
(coefficient 0.30)
0 — No
1 — Yes
Are you anemic (low blood count) currently? (coefficient 0.20)
0 — No
1 — Yes
Have you ever received a red blood cell transfusion specifically
because of nose bleeding? (coefficient 0.31)
0 — No
1 — Yes
Fig. 1. Self-reported epistaxis severity and general factors leading
to severity characterization.
Laryngoscope 120: April 2010
840
Six questions are answered, the number of the response is multiplied
by the respective coefficient, and the sum of these gives the raw epistaxis
severity score.
Hoag et al.: Epistaxis Severity Score for HHT
Fig. 2. Calculation of the raw and normalized epistaxis severity score (ESS).
The responses to each of the six questions are assigned a weighted integer
that is multiplied by the question’s coefficient. These are added to yield the
raw score. The raw score is then normalized by dividing the raw score by
the maximum possible score (2.71),
then multiplied by 10 to give the normalized ESS. HHT ¼ hereditary hemorrhagic telangiectasia.
coefficients from the model, and these are added together yielding a raw ESS. This is then divided by the
range of the raw score (2.71) and multiplied by 10 to
give the normalized ESS within a range of 0 (no epistaxis) to 10 (most severe epistaxis) (Fig. 2).
Validation of the ESS
Bootstrapping resampling using 1,000 replications
was performed to obtain variance of the independent
predictor variables in the final ESS model to ensure internal model validation.10 The standard errors of the
predictor variables presented in the final ESS are those
obtained through bootstrapping resampling. Logistic
regression models were also fit to evaluate the association between ESS and prior invasiveness of treatment
for epistaxis as a means of external validation. The ESS
was found to be a significant predictor of invasiveness of
treatment (Fig. 3), as patients with higher ESS had a
much greater risk of requiring surgical procedures for
epistaxis (odds ratio, 1.61; 95% confidence interval, 1.461.78).
with HHT, we were able to identify six factors with the
highest correlation to epistaxis severity. The resulting
ESS questionnaire is easy to administer and comprehend, and it should provide an effective tool in assessing
epistaxis severity.
We sought to develop a scoring system that can be
administered by either care providers or self-administered by patients. The questions are easy to understand
by both medical and lay persons. Because of this it may
serve as an adjunct for therapeutic algorithms. Treating
physicians may utilize the questionnaire or individual
DISCUSSION
This is the first paper to propose a statistically validated ESS based on a comprehensive survey of a large
cohort of HHT patients. Through review of a comprehensive list of possible related factors derived from
information obtained from otolaryngologists with extensive experience with HHT, non-ear, nose, and throat
HHT center of excellence care providers, and patients
Laryngoscope 120: April 2010
Fig. 3. Correlation between invasiveness of therapy and normalized epistaxis severity score (ESS). Trends were statistically significant (P < .0001; Fisher exact test).
Hoag et al.: Epistaxis Severity Score for HHT
841
scores to gauge patient responses to various epistaxis
therapies. This scoring system is not meant to supplant
expert evaluation; however, as we demonstrated in this
survey, a significant number of HHT patients are not
seeing experienced otolaryngologists (40%). Many of
these patients are frequently visiting emergency rooms
and primary care providers. Such a score may help to
identify unrecognized epistaxis severity that should be
referred to more appropriate providers. Second, this
scoring system, through its ease of interpretation, may
help patients to monitor their own symptoms with an
objective measurement. Many patients with chronic disease have improved outcomes through utilization of
patient-centered treatment aids.11,12 This may serve as a
benchmark for epistaxis in this group of patients who
have a lifetime of experience caring for the nasal bleeding complications of the illness.
Finally, this ESS fills an unmet need as an accurate, reproducible, and validated objective measure of
epistaxis severity to be used to compare existing and
new therapeutics. Several reports5–7 have utilized epistaxis severity scoring systems to assess treatment
efficacy; however, they all suffer from an important limitation, a lack of systematic evaluation of validity of the
score itself. Nevertheless, it is important to point out
that our system was derived, in part, by the tremendous
experience compiled by these earlier investigators. Very
few randomized clinical trial have been performed in
HHT, and moreover, almost no multicenter trials have
been undertaken. Part of the inability to pool patients
from multiple centers and conduct these necessary trials
comes from the lack of standardized measurement tools
for standardization among centers.
Al-Deen and Bachmann-Harildstad determined that
ease of understanding for both care providers and
patients, inclusion of transfusion needs, and association
for a fixed time interval were important attributes of an
epistaxis severity survey.7 Their proposed scoring scale
shares measures of intensity, frequency, and transfusion
needs, although their scale was not been systematically
validated.
Despite the many strengths of this investigation,
there are several limitations that warrant mentioning.
First, data included in the project were derived from
survey responses to an anonymous, deidentified survey.
This adds potential misclassification of study subjects
without disease. We believe that we overcame this limitation by targeting membership of the disease-specific
foundation for inclusion and by using questions embedded into the questionnaire that accurately predict the
diagnosis of HHT.13
Another piece of information that is lacking from
this analysis stems from the cross-sectional nature of
the data used to calculate the ESS. Future studies could
collect data longitudinally from this patient group to
determine measures such as minimum clinically relevant changes.
A possible criticism to this scoring system may center on the ease of calculation. With the inclusion of
weighted factors, on-the-spot calculations may be difficult without a computer program or calculator. Although
Laryngoscope 120: April 2010
842
this is a valid argument, as the ease of calculation is
improved, the robust, statistically supported nature of
this score is weakened. This score is analogous to other
clinical scoring systems, like the lung allocation score,
used for lung transplantation listing.14 Although a computerized method of calculating the score may be
necessary, we believe the fear of using a labor-intensive
system can be overcome with only six questions requiring single selection responses.
Finally, this ESS has not yet been correlated with
existing grading of nasal telangiectases. Mahoney and
Shapshay15 developed objective grading of nasal involvement of telangiectases, which described a range from
small, punctuate telangiectases to confluent, large nasal
arteriovenous malformations. Although this grading
system did not correlate epistaxis severity with the particular lesions, there could be a linear correlation that
could be corroborated with further analysis using this
study’s proposed ESS.
CONCLUSION
Through the evaluation of a comprehensive list of
factors related to epistaxis severity in patients with hereditary hemorrhagic telangiectasia, we determined six
factors associated with self-reported severity, including:
frequency, duration, intensity, need for medical attention, anemia, and need for transfusion. By compiling
responses to six questions focused on these factors, an
ESS can be generated that is accurate and validated.
This ESS can serve as a clinical and therapeutic outcome measure for epistaxis in HHT.
Acknowledgments
This project was supported by a generous grant from
the Hereditary Hemorrhagic Telangiectasia Foundation
International, Inc. We would like to thank Dr. Douglas
Ross and Dr. Urban Geisthoff, who led the section for
epistaxis at the 2009 International HHT Conference
in Santander, Spain for their insights into the topic.
We would also like to thank the HHT center of excellence
care providers from around the world for their support and
assistance with this project.
BIBLIOGRAPHY
1. Westermann CJJ, Rosina AF, de Vries V, de Coteau PA. The
prevalence and manifestations of hereditary hemorrhagic
telangiectasia in the Afro-Caribbean population of the
Netherlands Antilles: a family screening. Am J Med
Genet A 2003;116:324–328.
2. Guttmacher AE, Marchuk DA, White RI Jr. Hereditary
hemorrhagic telangiectasia. N Engl J Med 1995;333:
918–924.
3. Pasculli G, Resta F, Guastamacchia E, Di Gennaro L, Suppressa P, Sabba C. Health-related quality of life in a rare
disease: hereditary hemorrhagic telangiectasia (HHT) or
Rendu-Osler-Weber disease. Qual Life Res 2004;13:
1715–1723.
4. Lennox PA, Hitchings AE, Lund VJ, Howard DJ. The SF-36
health status questionnaire in assessing patients with
epistaxis secondary to hereditary hemorrhagic telangiectasia. Am J Rhinol 2005;19:71–74.
5. Levine CG, Ross DA, Henderson KJ, Leder SB, White RI
Jr. Long-term complications of septal dermoplasty in
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Geisthoff UW, Heckmann K, D’Amelio R, et al. Healthrelated quality of life in hereditary hemorrhagic telangiectasia. Otolaryngol Head Neck Surg 2007;136:726–733.
Al-Deen S, Bachmann-Harildstad G. A grading scale for
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Faughnan ME, Palda VA, Garcia-Tsao G, et al. International Guidelines for the Diagnosis and Management of
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Shovlin CL, Guttmacher AE, Buscarini E, et al. Diagnostic
criteria for hereditary hemorrhagic telangiectasia
(Rendu-Osler-Weber Syndrome). Am J Med Genet 2000;
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Efron B. Bootstrap methods: another look at the jackknife.
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11. Lorig KR, Sobel DS, Stewart AL, et al. Evidence suggesting
that a chronic disease self-management program can
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Accessed October 1, 2008.
13. Van Gent MWF, Post MC, Mager JJ, et al. Diagnostic Curacao criteria for HHT; are they still valid? Haematol Meet
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frm_LAS_Calculator.asp. Accessed August 20, 2009.
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843
ACTA otorhinolaryngologica italica 2014;34:1-8
Review
Endoscopic management of posterior epistaxis:
a review
Il trattamento endoscopico delle epistassi posteriori: revisione della letteratura
S.W. McClurg, R. Carrau
Department of Otolaryngology-Head and Neck Surgery, The Ohio State University, Columbus, OH, USA
Summary
The paradigm for the management of epistaxis, specifically posterior epistaxis, has undergone significant changes in the recent past. Recent
prospective and retrospective data has shown that the endonasal surgical management of posterior epistaxis is superior to posterior nasal
packing and angiography/embolization with regards to various factors including pain, cost-effectiveness, risk and overall control of bleeding. Endonasal endoscopic surgical techniques for posterior epistaxis include direct cauterization and transnasal endoscopic sphenopalatine/posterior nasal artery ligation or cauterization with or without control of the anterior ethmoidal artery. Despite the evidence provided
by the current literature, a universal treatment protocol has not yet been established. This review article provides an up-to-date assessment
of the available literature, and presents a structured paradigm for the management of posterior epistaxis.
Key words: Epistaxis • Endoscopic sphenopalatine artery ligation • Posterior epistaxis • Sphenopalatine artery
Riassunto
Il trattamento delle epistassi posteriori ha subito significativi cambiamenti negli ultimi anni. I recenti dati prospettici e retrospettivi hanno
dimostrato che il trattamento chirurgico endoscopico delle epistassi posteriori presenta dei vantaggi rispetto al tamponamento nasale e/o
all’embolizzazione previa angiografia ed in particolare in termini di dolore, rapporto costo-beneficio, effetti collaterali, e infine in termini
di controllo di sanguinamento. Il trattamento endoscopico chirurgico delle epistassi posteriori include la cauterizzazione diretta e la legatura dell’arteria sfeno-palatina e/o cauterizzazione dell’arteria etmoidale anteriore. Nonostante le evidenze presenti in letteratura un protocollo universale non è stato ancora realizzato. Questa revisione della letteratura offre un aggiornamento sui dati attuali sull’argomento,
proponendo un algoritmo per il trattamento delle epistassi posteriori.
Parole chiave: Epistassi • Legatura endoscopica della arteria sfeno palatina • Epistassi posteriore • Arteria sfeno-palatina
Acta Otorhinolaryngol Ital 2014;34:1-8
Introduction
Epistaxis is a very common presenting complaint and
the most common emergency for the OtolaryngologistHead and Neck Surgeon. The distribution of epistaxis
is bimodal. It is most common before age 10, and then
peaks again between ages 45 and 65 years of age 1 2. Many
factors including seasonal variation, concomitant inhalational allergy, oestrogens (extraneous and endogenous),
environmental humidity and upper respiratory tract infections affect the incidence of epistaxis.
Epistaxis can be divided into anterior and posterior based
upon the arterial supply and location of the offending
vessel. Most cases of epistaxis are anteriorly located
(90-95%), and are usually treated effectively after visual
localization with local chemical or electrical cauterization via anterior rhinoscopy 3. Approximately 5-10% of
epistaxis arises posteriorly 3, and requires more aggressive
measures for control. It has been prospectively shown that
patients with posterior epistaxis are more likely to require
hospitalization, are twice as likely to require nasal packing and require a longer hospital stay 4.
The sphenopalatine (SPA) and posterior nasal (PNA) arteries, terminal branches of the internal maxillary artery
(IMA), provide blood supply to the lateral nasal wall below the middle turbinate, rostrum of the sphenoid sinus
and posterior nasal septum. Therefore, a majority of posterior epistaxes arise from these two vessels. Measures to
control posterior epistaxis include direct cauterization,
posterior nasal packing, embolization or surgery. Many
studies have shown surgical control to be superior to angiography/embolization 3 5 as well as posterior packing 3.
Intervention for posterior epistaxis is direct endonasal endoscopic cauterization of the offending site. However, in a
significant number of patients, if not most, with posterior
epistaxis, the site will remain undefined. Recent reports
suggest that ligation of the sphenopalatine and posterior
nasal arteries seems to be the best option for patients with
1
S.W. McClurg, R. Carrau
posterior epistaxis and without comorbidities that would of the palatine bone (Fig. 1), usually lies at the posterior
preclude a surgical intervention 3 5.
end of the middle turbinate, in the lower part of the supeThe surgical management of epistaxis has undergone rior meatus, and at the junction between the palatine and
significant transitions and changes. Carnochan 6 de- sphenoid bone on the lateral nasal wall. Simmen reported
scribed the first surgical technique to the pterygopala- that the mean vertical and horizontal diameters of the SPF
tine fossa (PTPF) in 1858, using a transfacial-transantral are 6.2 and 5.1 mm, respectively 7. From an endoscopic
approach to the pterygopalatine fossa (PTPF). In 1890, standpoint, the foramen can be found just posterior to the
Segond introduced a lateral transfacial approach to the superior one-third of the posterior wall of the antrum. Anpterygopalatine fossa 6. Subsequently, Hide introduced other reliable landmark is the crista ethmoidalis, which is
the ligation of the external carotid artery for the manage- a small spur of bone just anterior to the sphenopalatine
ment of epistaxis. In 1948, Silverblatt first described the foramen (Fig. 2).
ligation of the anterior ethmoid artery. These techniques The arterial configuration within the pterygopalatine
are still utilized around the world to manage patients fossa is also highly variable and complex. In a cadaveric
with refractory epistaxis. In 1929, Seiffert described the study of 128 tissue blocks by Chiu 8, it was found that
sublabial-transantral approach for ligation of the max- the internal maxillary artery bifurcates before reaching
illary artery, which was subsequently standardized and the sphenopalatine foramen in 89% of cases, splitting off
popularized by Chandler (1956); and, further improved into two (69%), three (19%) or four branches (2%). In a
upon by Simpson (1982) by focusing on its terminal similar anatomical study, Simmen documented that there
branches (i.e. sphenopalatine and posterior nasal arter- may even be up to 10 arterial branches 7. This study also
ies) 6. In 1976, Prades described an endonasal micro- demonstrated that in 58% of cases the SPF lies in both the
scopic ligation of the sphenopalatine artery, which was superior and middle meati.
emulated by Borgstein who introduced the endoscope as Variability of the vascular anatomy within the pterygopalaa visualization tool in 1987 6.
tine fossa is remarkable and ranges from a relatively simple
A thorough knowledge of the anatomy of the posterior or “classic” pattern to one that is highly complex 9. In turn,
nasal cavity and pterygopalatine fossa is essential for the the branching pattern of the sphenopalatine artery is also
proper surgical management of posterior epistaxis. Arte- striking. Schartzbauer showed that in fresh cadavers, aprial supply to the nasal cavity is both robust and variable, proximately 16% of the terminal branches split off from
with contributing arteries deriving from both the internal the maxillary artery distal to the sphenopalatine foramen,
and external carotid arteries. Contributions from the ex- 42% branch proximally and 42% branch through separate
ternal carotid artery include the sphenopalatine, posterior foramina 10. In 75 cadaveric specimens, Simmen showed
nasal, superior labial, greater palatine, angular and as- that in 97% of the samples the sphenopalatine artery had
cending pharyngeal arteries. The internal carotid artery 2 or more branches exiting the lateral nasal wall, 67% had
furnishes the anterior ethmoid and posterior ethmoid ar- 3 or more branches, 35% had 4 or more branches, 3% had
teries via the ophthalmic artery. Branches of the ethmoi- 1 single trunk and 1% had 10 branches 7. A representative
dal arteries supply the lateral nasal wall above the level example of the sphenopalatine artery is shown in Fig. 1.
of the middle turbinate. It
must be noted that there
is ample communication
between the two systems.
The vidian artery and the
artery that accompanies
V2 (artery of the foramen
rotundum) are robust examples of these communications that can lead to
collateral blood flow, thus
causing re-bleeding and
which must be considered
when embolizing the internal maxillary artery.
The sphenopalatine foramen (SPF), which is a
notch between the orbital
and sphenoidal processes Fig. 1. Right pterygopalatine fossa.
of the ascending aspect PF: pterygopalatine fossa; SPA: sphenopalatine artery; MAX: posterior wall of maxillary sinus.
2
Endoscopic management of posterior epistaxis
considered. If the airway
is deemed stable, nonsurgical approaches for
haemostasis should first
be attempted. Local vasoconstrictors (i.e. epinephrine), either topical and/or
injected, may assist with
haemostasis. If the site
of bleeding is visible, its
cauterization may be possible. Posterior epistaxis
is usually quite brisk, and
also due to its inherent
position in the posterior
nasal cavity, it is often difficult to pinpoint the location of bleeding. In the
surgical theatre, however,
Thornton et al. 13 were
able to identify the location of posterior epistaxis
in 36 of 43 cases. Of these,
20% were located on the
Fig. 2. Right ethmoid crest. Yellow arrow pointing to crista ethmoidalis. Red dashed arrow showing the path of the
posterior nasal septum,
internal maxillary before it divides in to the sphenopalatine and posterior nasal arteries.
and 80% of those were located on the lateral aspect
of the middle or inferior
Another common and useful landmark for the identi- turbinates or the lateral aspect of the middle or inferior
fication of the sphenopalatine foramen is the ethmoid meatus. It should be noted that all identified sites were locrest or crista ethmoidalis (CE), (Fig. 2). In a study by cated within the distribution of the sphenopalatine artery.
Rezende, the crista ethmoidalis was found in 96% of ca- Intraoperatively, anaesthesia-induced hypotension and/or
daveric specimens, and was located just anterior to the elevation of the head of the bed may decrease bleeding;
SPF in most cases 11. Similar to other aforementioned thus, potentially facilitating the identification and control
studies, they found that 43% of specimens had accessory of the bleeding site.
foramina. Similarly, Padua showed that the crista ethmoi- Any surgical intervention requires prior stabilization of
dalis was anterior to the sphenopalatine foramen in 98% the patient and control of bleeding. If the patient had preof specimens 12. In this latter study, the SPF was located viously been treated (commonly by a non-otolaryngolobetween the middle meatus and the superior meatus in gist), the patient may present with posterior packing al87% of specimens, and at the superior meatus in 13%. In ready in place. In the hands of a non-specialist, posterior
Padua’s study accessory foramina were present in 10% of packing is efficacious in approximately 70% of cases 14.
specimens. These studies suggest that, in fact, the most re- In the untreated patient, a posterior nasal pack using traliable localizer for the SPF is the crista ethmoidalis; how- ditional tonsil packs with ribbon-gauze coated with antiever, the frequency of multiple foramina and branches is biotic ointment, expandable sponges such as the Merocel
significant; thus, the surgeon should anticipate their pres- Pope nasal packing (Medtronic ENT, Jacksonville, FL,
USA), Rapid Rhino (Applied Therapeutics, Tampa, FL,
ence 12.
USA) Epistat, Postpac (Medtronic ENT, Jacksonville, FL,
USA) or any of the multiple available balloon-packing deInitial management
vices may be effective. Topical haemostatic compounds
The initial evaluation of the patient presenting with such as a mixture of gelatin and thrombin (e.g. Floseal,
epistaxis should focus on evaluating the stability of the Baxter Healthcare Corp., Deerfield, IL, USA) has been
airway, initial control of the bleeding and stabilization of shown to be effective in anterior epistaxis 15, but it has not
vital signs with fluid replacement or blood transfusions. In been properly assessed for posterior bleeds; thus, it is not
a patient with severe uncontrolled epistaxis, the need for advocated in the setting of posterior epistaxis where a speintubation or even a surgical airway, albeit rare, must be cific site of bleeding cannot be identified.
3
S.W. McClurg, R. Carrau
There have been multiple studies comparing the various
types of nasal packing for anterior bleeds, but unfortunately, there are relatively few studies looking at comparisons between various posterior nasal packings. In a
comparison study by Callejo 16, classic tetracaine-coated
gauze packing was compared to a bi-chambered pneumatic packing device. They found that the classic packing was
less expedient, and less comfortable, but was associated
with fewer episodes of re-bleeding (17% against 28%, respectively) and less expensive (€ 1327 vs. € 1648).
Posterior packing is associated with its own set of specific
complications, such as the naso-vagal reflex that can trigger cardiac dysfunction or respiratory arrest 17. In addition,
packing may be inadvertently swallowed or aspirated if
not adequately secured 18. Conversely, if the packing is secured too tightly, it may lead to alar, columellar or septal
necrosis 19. Due to the possible compressive ischaemia of
nasal structures, we advocate to avoid bilateral posterior
packing whenever possible, and to routinely deflate the
cuff of balloon occlusive devices to allow septal blood
flow.
If a Foley balloon-type device (i.e. any inflatable balloon)
is used for posterior packing, air is not suitable for inflating the balloon. Rashid showed that Foley catheters
inflated with air deflated within approximately 48 hr 20;
therefore, saline or sterile water should be utilized for balloon inflation.
We recommend utilizing antibiotics while the posterior
packing is in place, even though prophylactic antibiotics have not been shown to decrease infectious complications 21. However, rare complications such as infective
endocarditis and spondylodiscitis have been reported in
patients with posterior nasal packing who were not covered with systemic antibiotic prophylaxis 22.
Once the bleeding is controlled, all contributing factors that may be exacerbating the epistaxis should be
addressed. These may include co-morbidities such as
coagulopathies (congenital or acquired), hypertension,
maxillofacial trauma, recent endonasal or orthognathic
surgery and history of hereditary hemorrhagic telangiectasia (HHT). Basic laboratory studies (including complete
blood count, chemistry panel, platelet count, prothrombin
time and partial thromboblastin time) should be obtained
during initial workup. Consider blood transfusion if haemoglobin is noted to be significantly low (this varies according to patient’s cardiovascular reserve, comorbidities,
symptoms and regional practices). These contributing factors should be addressed prior to any operative intervention whenever feasible.
There are specific clinical scenarios that deserve special
consideration. In patients with hereditary hemorrhagic
telangiectasia (HHT), an autosomal dominant disorder resulting in localized vascular malformations, these malformations may extend posteriorly, and their acute management includes surgical cauterization or angiography and
4
embolization. Ligation of the arteries is rarely performed
as this precludes the possibility of angiography and embolization and due to the nature of the disease, and the
benefits of the surgery are short-lived. The possibility of
a primary or metastatic tumour causing the epistaxis may
also need to be addressed with thorough history and physical examination and possibly further imaging studies. In
any adolescent male patient, the possibility of a juvenile
nasopharyngeal angiofibroma should also be considered.
A history of recent maxillofacial trauma, or recent endonasal or orthognathic surgery, poses the possibility of
an arterial injury or a pseudoaneurysm. This latter lesion
results from an incomplete tear a major artery, causing
bleeding from the artery into the arterial adventitia, resulting in a localized haematoma with a continued connection to the offending artery. Pseudoaneurysms are usually
unresponsive to nasal packing (immediate re-bleeding
upon packing removal). They may arise from any sinonasal artery, but the arteries most commonly involved after
orthognathic surgery are the internal maxillary artery and
the sphenopalatine artery 2. The treatment for a pseudoaneurysm is arterial selective embolization 2.
Surgery
After haemodynamic stabilization, the patient is taken to
the operative suite. As previously discussed, anaesthesiacontrolled hypotension and/or elevation of the head of
the bed decreases the bleeding, and potentially facilitates
localization of the offending bleeding site. Any previous
nasal packing is removed and a thorough nasal endoscopy is performed to identify the specific site of bleeding. Some common locations for bleeding include the
spheno-ethmoid recess, turbinates, middle meatus and the
septum. If a bleeding site is identified, it may be directly
cauterized. Local cauterization has the advantage of requiring no packing, and is associated with shorter hospital stay and greater patient comfort 23. Direct cauterization
may also be conducted under topical or local anaesthesia.
A potential disadvantage of this technique include a lower
success rate than formal sphenopalatine artery ligation
(mostly due to inadequate identification of the bleeding
site).
Some propose attempting a local cauterization of bleeding sites in cases of posterior epistaxis 23 under general
or local anaesthesia, by first visualizing the various sites
of possible bleeding including the posterior aspect of the
lateral wall of inferior meatus; posterior part of lateral nasal wall near the sphenopalatine foramen; posterior end of
inferior turbinate; the middle turbinate and its medial surface; middle and posterior part of septum and floor of nose
beneath the inferior turbinate 23. However, the preferred
approach for surgical management of posterior epistaxis,
in which a specific site is indisputably identified, is endonasal endoscopic ligation of the sphenopalatine and pos-
Endoscopic management of posterior epistaxis
terior nasal arteries. The efficacy of this technique is de- tine fossa. It is important to dissect the sphenopalatine and
pendent on controlling the multiple, robust branches that posterior nasal arteries free from the posterior aspect of
the sphenopalatine and posterior nasal arteries give rise the SPF, as this will allow a complete clipping or cauterito. Indications for surgical ligation include the inability to zation of the arteries.
place packing effectively due to an anatomical deformity, A concurrent anterior ethmoid artery (AEA) ligation
failure of non-surgical therapy, recurrent epistaxis, con- along with the endonasal endoscopic ligation of the sphetraindications for embolization and patient preference. nopalatine and posterior nasal arteries should be considContraindications for embolization include severe carotid ered, if the site of bleeding is not known pre-operatively,
atherosclerosis, prior external carotid or internal maxil- if the patient’s history is unreliable, if packing was placed
lary artery ligation or bleeding from the anterior ethmoid at an outside institution, or if there is no evidence of
artery (which arises from the ophthalmic artery, a branch bleeding at the time of surgery (unidentified site of bleeding). AEA ligation has a low morbidity, and should be
of the ICA).
A cost analysis study by Dedhia 24, showed that first-line strongly considered if the patient has been referred for
endonasal endoscopic sphenopalatine/posterior nasal definitive treatment from a region distant from the hosarteries ligation results in a significant overall cost sav- pital. Approaches for AEA ligation include an external
ings if ≥ 3 days of posterior nasal packing were required incision and dissection between the lamina papyracea and
($ 6,450 vs. $ 8,246, respectively). Therefore, it is rec- the periorbita with endoscopic assistance, and endonasal
ommended that endonasal endoscopic sphenopalatine approach with bipolar cauterization of the AEA (Fig. 3).
and posterior nasal artery ligation should be offered as an Identification of the anterior ethmoidal artery on coronal
initial treatment option for medically stable patients diag- computed tomography is assisted with its location at the
retro-bulbar level, or by utilizing the “nipple or pyramidal
nosed with posterior epistaxis 24.
Our preferred technique for endonasal endoscopic sphe- sign” (a triangular evagination of the lamina papyracea
nopalatine and posterior nasal artery ligation 25 26 involves between the superior oblique and medial rectus muscles)
performing a standard uncinectomy, with identification of (Fig. 4). It has been shown that 36% of anterior ethmoidal
the natural maxillary sinus ostium and its enlargement in- arteries were located in a mesentery, and 20% could be
feriorly (to the level of the inferior turbinate), superiorly clipped endoscopically 27. However, an external approach
(to the level of the orbit) and posteriorly (to be flush with is safer to access the AEA. A small naso-orbital incision
the back wall of the antrum). Next, the sphenopalatine provides access to the periorbita, which is incised and
foramen is identified using all the previously discussed elevated under endoscopic visualization. Following the
anatomical landmarks (posterior wall of the antrum, mid- frontoethmoidal suture leads to the ethmoidal foramina,
dle turbinate root, and crista ethmoidalis). Using a Freer located an average of 24 mm from the lacrimal crest. In
or Cottle periosteal elevator, the mucoperiosteum over the turn, the posterior ethmoid artery (PEA) is located 12 mm
ascending process of the palatine bone is widely elevated to
expose the sphenopalatine foramen and the sphenopalatine
and posterior nasal arteries.
Wide elevation is important to
identify anatomical variants
such as multiple foramina
and/or multiple vessels traversing the lateral nasal wall
from the pterygopalatine fossa. The vessels can frequently
be controlled at this point either with haemostatic clips
or bipolar electrocautery. If
necessary a longer segment of
the arteries can be exposed by
removing the anterior aspect
of the sphenopalatine foramen (i.e. posterior nasal wall)
using a Kerrison or Citelli Fig. 3. Endoscopic view of left nasal cavity. Orbital decompression with lamina papyracea bone (LP) removed.
rongeur; thus, following the This specimen shows a middle ethmoidal artery.
arteries into the pterygopala- AE: anterior ethmoid artery; ME: middle ethmoid artery; PE: posterior ethmoid artery/
5
S.W. McClurg, R. Carrau
Fig. 4. Coronal cut of CT image showing “nipple sign” at the level of entry
(white arrow) of the anterior ethmoid artery into the nasal cavity.
posterior to the anterior ethmoidal artery, and the optic
canal is located 6 mm posterior to the posterior ethmoid
artery. After surgical control is achieved, silicone septal
splints are placed if there was excessive trauma to the
mucosa or if there is a possibility of post-operative nasal
synechiae.
In a retrospective review, Kumar showed that the overall
mean success rate of sphenopalatine artery ligation in 11
case series including 127 patients was 98% (range 92100%) 28. In a retrospective study of 678 patients, Soyka 5 showed that the successful treatment in patients with
posterior epistaxis could be achieved in 62% by packing
(Foley + fat-gauze), and in 97% by surgery. Despite the
high success rate of arterial ligation, there is still the possibility of failure. Possible reasons for recurrent bleeding
include failure to ligate all terminal branches of the sphenopalatine artery, dislodged clips, bleeding diatheses, the
development of collateral blood vessels or unrecognized
AEA bleeding sites.
In a recent prospective study by Nikolaou 29, it was shown
that surgery was the most cost effective and least painful treatment regimen for posterior epistaxis. Their treatment regimen consisted of placement of either a Rapid
Rhino 7.5 cm packing or balloon packing for posterior
epistaxis, followed by endonasal endoscopic sphenopalatine and posterior nasal artery ligation for patients that
had further bleeding upon removal of the packing. In this
study of 61 patients (45 with anterior epistaxis, 16 with
posterior epistaxis), they showed that the median visual
analogue scale for the evaluation of pain (VAS score) for
Rapid Rhino packing, surgery and balloon packing was
6.0, 3.0 and 7.5, respectively. The median costs of treat6
ment for 96 patients were calculated, and were found to
be approximately the same for patients with Rapid Rhino
packing and surgery (10,192 Swiss Francs), balloon packing and surgery (10,192 Swiss Francs) and surgery alone
(10,269 Swiss Francs). Overall, their findings suggested
that surgery is less troublesome to the patient, and does
not increase the costs of treatment. This technique has also been shown to be efficacious and safe in the paediatric
population 30.
After control of the posterior epistaxis is achieved, appropriate postoperative care is needed. Elevate the head
of the bed, avoid hypertension, provide appropriate analgesia and promote aggressive nasal hygiene. Nasal
hygiene includes saline nasal sprays, saline irrigations,
use of oxymetazoline and/or a nasal sling. The patient
should follow-up in clinic 5-7 days after surgical intervention for removal of silicone splints, if they were
placed.
If endonasal endoscopic sphenopalatine and posterior nasal arteries ligation is not successful, a transantral internal
maxillary artery (IMAX) ligation or angiography with
embolization may be considered. Further, if IMAX ligation is not successful or angiography with embolization
is not available, an external carotid artery ligation may be
considered. It should be noted that this is a last resort, as
a retrospective review conducted by Spafford 31 showed a
high rate of re-bleeding with external carotid artery ligation (45%), but showed that IMAX ligation was successful in 90% of patients.
Embolization is an alternative option for posterior
epistaxis, and is our preferred intervention for recurrent
epistaxis after a seemingly adequate endonasal endoscopic sphenopalatine and posterior nasal artery ligation. Angiographic embolization was first described for
posterior epistaxis in 1974 by Sokolof 32. Possible candidates for embolization include patients with HHT (Osler-Weber-Rendu) syndrome, bleeding tumours, poor
surgical candidates or if the patient chooses it. Bleeding
during transphenoidal or maxillofacial surgery should
be considered for endovascular management due to possible internal carotid artery injury or pseudoaneurysm
formation 33. Possible minor complications of angiography include trismus, facial pain, facial paresthesia
or haematoma. Possible major complications include
cerebrovascular accident, internal carotid artery dissection, blindness, necrosis or facial paralysis. In a retrospective review of 70 patients, Christensen found that
86% of their cases had minor or no complications after
embolization, and were discharged within 24 hours 34.
A major re-bleed, requiring surgical intervention, occurred within 6 weeks of embolization in 13% of these
patients, and one patient had a significant cerebrovascular accident. Also of note, this study showed that the average cost of hospitalization in the respective institution
was $ 18,000 per patient with epistaxis, and the cost
Endoscopic management of posterior epistaxis
of embolization was an average
of $ 11,000 34. In a retrospective study by Cohen, 19 patients
underwent endovascular embolization with no minor or major
complications, and an average
hospital stay of 11.1 days 35. As
previously mentioned, in any
adolescent male patient, the possibility of a juvenile nasopharyngeal angiofibroma should also
be assessed. In these patients,
embolization via angiography is
usually utilized prior to surgical
resection 33.
Given the various presentations
and possible sources of bleeding
in a patient with posterior epistaxis, we propose the following diagnostic workup and treatment
(Fig. 5) to optimize the management of posterior epistaxis.
Conclusion
Fig. 5. Flow diagram for management of posterior epistaxis. Note that this diagram should be used for
patients that have failed conservative management and local cauterization in the non-operative setting.
AE: anterior ethmoid artery; A&E: angiography and embolization; SPA: sphenopalatine artery; PNA: posterior
nasal artery.
Ligation of the sphenopalatine and posterior nasal arteries
is a very effective treatment for severe posterior epistaxis.
Concomitant anterior ethmoidal artery ligation may be
more effective than sphenopalatine artery/posterior nasal artery ligation alone. Surgical intervention of posterior epistaxis provides a low-morbidity and cost-effective
treatment. We present a flow diagram for management of
posterior epistaxis.
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Schartzbauer HR, Shete M, Tami TA. Endoscopic Anatomy
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Rezende GL, Soares VY, Moraes WC, et al. The sphenopalatine artery: a surgical challenge in epistaxis. Braz J Otorhinolaryngol 2012;78:42-7.
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Padua FG; Voegels RL. Severe posterior epistaxis - endoscopic surgical anatomy. Laryngoscope 2008;118:156-61.
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Thornton MA, Mahesh BN, Lang J. Posterior epistaxis:
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Schlosser RJ. Clinical practice. Epistaxis. N Engl J Med
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Mathiasen RA, Cruz RM. Prospective, randomized, controlled clinical trial of a novel matrix hemostaticsealant
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Nikoyan L, Matthews S. Epistaxis and hemostatic devices.
Oral Maxillofac Surg Clin North Am 2012;24:219-28.
3
Douglas R, Wormald PJ. Update on epistaxis. Curr Opin
Otolaryngol Head Neck Surg 2007;15:180-3.
4
Supriya M, Shakeel M, Veitch D, et al. Epistaxis: prospective evaluation of bleeding site and its impact on patient outcome. J Laryngol Otol 2010;124:744-9.
5
Soyka MB, Nikolaou G, Rufibach K, et al. On the effectiveness of treatment options in epistaxis: an analysis of 678 interventions. Rhinology 2011;49:474-8.
16
García Callejo FJ, Muñoz Fernández N, Achiques Martínez
MT, et al. Nasal packing in posterior epistaxis. Comparison
of two methods. Acta Otorrinolaringol Esp 2010;61:196-201.
6
Wentges RT. Surgical anatomy of the pterygopalatine fossa.
J Laryngol Otol 1975;89:35-45.
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Fairbanks DN. Complications of nasal packing. Otolaryngol
Head Neck Surg 1986;94:412-5.
7
Simmen DB, Raghavan U, Briner HR, et al The anatomy of
the sphenopalatine artery for the endoscopic sinus surgeon.
Am J Rhinol 2006;20:502-5.
18
Hashmi SM, Gopaul SR, Prinsley PR, et al. Swallowed nasal
pack: a rare but serious complication of the management of
epistaxis. J Laryngol Otol 2004;118:372-3.
8
Chiu T. A study of the maxillary and sphenopalatine arteries
in the pterygopalatine fossa and at the sphenopalatine foramen. Rhinology 2009;47:264-70.
19
Civelek B, Kargi AE, Sensöz O, et al. Rare complication of
nasal packing: alar region necrosis. Otolaryngol Head Neck
Surg 2000;123:656-7.
7
S.W. McClurg, R. Carrau
20
Rashid M, Karagama Y. Inflation of Foley catheters for postnasal packing. J Laryngol Otol 2010;124:997-8.
21
Pepper C, Lo S, Toma A. Prospective study of the risk of not
using prophylactic antibiotics in nasal packing for epistaxis.
J Laryngol Otol 2012;126:257-9.
22
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24
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28
Kumar S, Shetty A, Rocker J, et al. Contemporary surgical
treatment of epistaxis. What is the evidence for SPA ligation?
Clin Otolaryngol Allied Sci 2003;28:360-3.
29
Nikolaou G, Holzmann D, Soyka MB. Discomfort and
costs in epistaxis treatment. Eur Arch Otorhinolaryngol
2013;270:2239-44.
30
Eladl HM, Khafagy YW, Abu-Samra M. Endoscopic cauterization of the sphenopalatine artery in pediatric intractable posterior epistaxis. Int J Pediatr Otorhinolaryngol
2011;75:1545-8.
31
Spafford P, Durham JS. Epistaxis: efficacy of arterial ligation and long-term outcome. J Otolaryngol 1992;21:252-6.
32
Sokoloff J, Wickbom I, McDonald D, et al. Therapeutic percutaneous embolization in intractable epistaxis. Radiology
1974;111:285-7.
33
Snyderman C, Carrau R. Endoscopic ligation of the sphenopalatine artery for epistaxis. Operative Techniques in Otolaryngology - Head and Neck Surgery 1997;8:85-9.
Abruzzo TA, Heran MK. Neuroendovascular therapies in
pediatric interventional radiology. Tech Vasc Interv Radiol
2011;14:50-6.
34
Snyderman C, Goldman S, Carrau R, et al. Endoscopic sphenopalatine artery ligation is an effective method of treatment
for posterior epistaxis. Am J of Rhinol 1999;13:137-40.
Christensen NP, Smith DS, Barnwell SL, et al. Arterial embolization in the management of posterior epistaxis. Otolaryngol Head Neck Surg 2005;133:748-53.
35
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 2012;19:687-90.
Gungor H, Ayik MF, Gul I, et al. Infective endocarditis
and spondylodiscitis due to posterior nasal packing in a
patient with a bioprosthetic aortic valve. Cardiovasc J Afr
2012;23:e5-7.
Paul J, Kanotra SP, Kanotra S. Endoscopic management of
posterior epistaxis. Indian J Otolaryngol Head Neck Surg
2011;63:141-4.
Dedhia RC, Desai SS, Smith KJ, et al. Cost-effectiveness of
endoscopic sphenopalatine artery ligation vs. nasal packing
as first-line treatment for posterior epistaxis. Int Forum Allergy Rhinol 2013;3:563-6.
Floreani SR, Nair SB, Switajewski MC, et al. Endoscopic
anterior ethmoidal artery ligation: a cadaver study. Laryngoscope 2006;116:1263-7.
Received: June 21, 2013 - Accepted: June 27, 2013
Address for correspondence: Ricardo L. Carrau, Department of
Otolaryngology-Head & Neck Surgery, The Ohio State University
Medical Center, Starling Loving Hall – Room B221, 320 West 10th
Avenue, Columbus, OH 43210, USA. E-mail: Ricardo.Carrau@
osumc.edu
8
World J Gastroenterol 2014 October 14; 20(38): 13993-13998
ISSN 1007-9327 (print) ISSN 2219-2840 (online)
Submit a Manuscript: http://www.wjgnet.com/esps/
Help Desk: http://www.wjgnet.com/esps/helpdesk.aspx
DOI: 10.3748/wjg.v20.i38.13993
© 2014 Baishideng Publishing Group Inc. All rights reserved.
OBSERVATIONAL STUDY
Epistaxis in end stage liver disease masquerading as severe
upper gastrointestinal hemorrhage
Marine Camus, Dennis M Jensen, Jason D Matthews, Gordon V Ohning, Thomas O Kovacs, Rome Jutabha,
Kevin A Ghassemi, Gustavo A Machicado, Gareth S Dulai
Marine Camus, Dennis M Jensen, Gordon V Ohning, Thomas O Kovacs, Rome Jutabha, Kevin A Ghassemi, Gustavo
A Machicado, Gareth S Dulai, CURE Hemostasis Research
Group, CURE Digestive Diseases Research Center, David Geffen School of Medicine at University of California, Los Angeles,
Los Angeles, CA 90095, United States
Marine Camus, Dennis M Jensen, Thomas O Kovacs, Rome
Jutabha, Kevin A Ghassemi, Gustavo A Machicado, Gareth
S Dulai, Division of Digestive Diseases at University of California, Los Angeles, Ronald Reagan Medical Center, Los Angeles,
CA 90095, United States
Marine Camus, University Paris 7, Department of Gastroenterology, Lariboisiere Hospital, APHP, Paris 75010, France
Dennis M Jensen, Gordon V Ohning, Thomas O Kovacs,
Gustavo A Machicado, Gareth S Dulai, Gastroenterology Division at VA Greater Los Angeles Healthcare System, Los Angeles,
CA 90095, United States
Jason D Matthews, Hunterdon Gastrointestinal Associates,
Flemington, NJ 08822, United States
Author contributions: Jensen DM and Matthews JD designed
research; Ohning GV, Kovacs TO, Jutabha R, Ghassemi KA,
Machicado GA and Dulai GS performed research; Camus M
contributed new reagents/analytic tools; Camus M and Jensen
DM analyzed data; Camus M, Matthews JD and Jensen DM
wrote the paper.
Supported by National Institutes of Health, No. 41301; Veteran Administration Clinical Merit Review Grant, to Dr Dennis
M Jensen; and Philippe Foundation Grant, to Dr. Marine Camus
Correspondence to: Marine Camus, MD, Assistant Professor, Department of Gastroenterology, Lariboisiere Hospital,
APHP, 2 rue Ambroise Pare, 75010 Paris,
France. [email protected]
Telephone: +33-6-81933140 Fax: +33-1-49952577
Received: April 9, 2014
Revised: June 8, 2014
Accepted: July 11, 2014
Published online: October 14, 2014
Abstract
AIM: To describe the prevalence, diagnosis, treatment, and outcomes of end stage liver disease (ESLD)
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patients with severe epistaxis thought to be severe upper gastrointestinal hemorrhage (UGIH).
METHODS: This observational single center study included all consecutive patients with ESLD and epistaxis
identified from consecutive subjects hospitalized with
suspected UGIH and prospectively enrolled in our databases of severe UGIH between 1998 and 2011.
RESULTS: A total of 1249 patients were registered for
severe UGIH in the data basis, 461 (36.9%) were cirrhotics. Epistaxis rather than UGIH was the bleeding
source in 20 patients. All patients had severe coagulopathy. Epistaxis was initially controlled in all cases.
Fifteen (75%) subjects required posterior nasal packing and 2 (10%) embolization in addition to correction
of coagulopathy. Five (25%) patients died in the hospital, 12 (60%) received orthotopic liver transplantation
(OLT), and 3 (15%) were discharged without OLT. The
mortality rate was 63% in patients without OLT.
CONCLUSION: Severe epistaxis in patients with ESLD
is (1) a diagnosis of exclusion that requires upper endoscopy to exclude severe UGIH; and (2) associated
with a high mortality rate in patients not receiving OLT.
© 2014 Baishideng Publishing Group Inc. All rights reserved.
Key words: Epistaxis; Upper gastrointestinal bleeding;
End stage liver disease; Cirrhosis; Nasogastric tube;
Liver transplantation; Digestive bleeding; Nasal packing; Coagulopathy
Core tip: Severe posterior nasopharyngeal epistaxis
in hospitalized patients with end stage liver disease
(ESLD): (1) is a diagnosis of exclusion that requires
upper endoscopy to rule out common causes of upper
gastrointestinal hemorrhage (UGIH); (2) can usually
be effectively treated with nasal packing and correction
of coagulopathy; (3) was the diagnosis of the bleeding
13993
October 14, 2014|Volume 20|Issue 38|
Camus M et al . Epistaxis in end stage liver disease
source in 4.3 % of cirrhotic patients with a suspected
UGIH; and (4) is associated with a high rate of mortality
(63%) in those not receiving liver transplantation. Physicians managing patients with ESLD should be aware
that epistaxis can masquerade as massive UGIH, particularly in those with severe coagulopathy.
Camus M, Jensen DM, Matthews JD, Ohning GV, Kovacs
TO, Jutabha R, Ghassemi KA, Machicado GA, Dulai GS.
Epistaxis in end stage liver disease masquerading as severe
upper gastrointestinal hemorrhage. World J Gastroenterol 2014;
20(38): 13993-13998 Available from: URL: http://www.wjgnet.
com/1007-9327/full/v20/i38/13993.htm DOI: http://dx.doi.
org/10.3748/wjg.v20.i38.13993
INTRODUCTION
Massive upper gastrointestinal hemorrhage (UGIH) in
patients with end stage liver disease (ESLD) is often
fatal[1,2]. Concomitant coagulopathy is a common comorbidity in cirrhotics and it frequently worsens the outcome. Expedient diagnosis and intervention are therefore imperative when encountering such cases.
Although rare, severe epistaxis is a diagnosis that must
be considered in patients presenting with signs and symptoms of severe UGIH, in order to avoid delays in the
provision of potentially life-saving therapy[3]. About 5%
of epistaxis originates from a posterior nasal source[4].
Bleeding in these cases can be especially severe. Local
therapy such as nasal packing or cauterization is usually
sufficient, but continued or intractable hemorrhage may
require arterial ligation, embolization or more recently
endoscopic ligation[4]. Delayed treatment may lead to excessive blood loss and increased morbidity and mortality.
Literature about epistaxis and cirrhosis is limited as
few case reports[5].
Our aims were (1) to describe the diagnosis, treatment,
and outcomes of ESLD patients with severe epistaxis
whose initial clinical diagnosis prior to endoscopy was
severe UGIH probably secondary to esophageal varices;
and (2) to estimate the prevalence of epistaxis as the final
diagnosis in cirrhotics who present with signs of severe
UGIH.
MATERIALS AND METHODS
University of California, Los Angeles Center for Health
Sciences (UCLA-CHS) is an urban, academic, tertiary
care referral medical center. Nearly 30000 patients are discharged from this facility yearly. Attending gastroenterologists from the Center for Ulcer Research and Education
(CURE) Hemostasis Research Group are available 24 h a
day for the evaluation and treatment of patients hospitalized with severe gastrointestinal (GI) hemorrhage.
The UCLA Ronald Reagan Medical Center (RRMC)
also has a liver transplant program that is one of the
largest in the world by volume. As the most experienced
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liver transplantation program in the western United
States, UCLA serves the area from California, Oregon,
Washington, and throughout the Southwest.
Cases in this report were retrospectively identified
from consecutive hospitalized subjects with severe UGIH
who were enrolled in our studies of severe UGIH in
ESLD between September 26, 1998 and June 1, 2011.
This observational study was approved by the UCLA Office for the Protection of Research Subjects. Informed
consent for endoscopy was obtained before each clinically indicated procedure. ESLD disease was diagnosed
based upon clinical parameters, radiologic imaging, and/
or liver biopsy results. Suspected severe UGIH was defined as (1) signs or symptoms of UGI hemorrhage (hematemesis and/or melena); (2) decrease in hemoglobin
from baseline of ≥ 2 g/dL; and (3) and/or transfusions
of ≥ 2 units of packed red blood cell (PRBC).
All upper endoscopies were performed by experienced endoscopists using therapeutic sized video endoscopes. Patients underwent emergency endoscopy after
resuscitation. Careful examination of the esophagus,
stomach (including retroflex views), and duodenum was
performed in each case.
Members of the CURE Hemostasis Group and a skilled
research coordinator collected prospective data from the
time of presentation using standardized data forms. All
patients underwent clinical evaluation about bleeding
symptoms: hematemesis, melena, hematochezia; bleeding severity: hypotension, shock, need for pressors;
and cirrhosis data: etiology of cirrhosis, severity of cirrhosis (Child-Pugh class and Model of End Stage Liver
Disease - MELD score) from the time of presentation.
Laboratory data (creatinine, hematocrit, hemoglobin and
coagulation tests) and endoscopic findings were also recorded from the time of presentation. The patients were
prospectively followed-up from the date of diagnosis to
hospital discharge, death, or liver transplantation.
Coagulopathy was defined as values of prothrombin
time (PT), international normalized ratio (INR), or platelet count outside the institutional normal ranges. ChildPugh class and MELD score were calculated according to
a well-accepted classification[6-8]. Hypotension was defined
as a systolic blood pressure persistently less than 100
mmHg despite adequate volume resuscitation. Rebleeding was defined as recurrent severe epistaxis (or signs
of UGI bleeding) at least 24 h after observed complete
cessation of pharyngeal bleeding following appropriate
treatment, with decrease in hemoglobin of ≥ 2 g/dL after resuscitation and initial diagnosis and/or ≥ 2 units of
PRBC. Follow-up time was calculated from the time of
presentation to the GI Hemostasis Team until death, liver
transplantation, or discharge from the hospital.
Statistical analysis
All data were de-identified and entered onto data files. SAS
software, version 9.1 (SAS Institute, Cary, NC) was used
for data management. Missing or inconsistent data were resolved by a joint review of the medical record and discussion with program instructor (DMJ) and co-investigators
13994
October 14, 2014|Volume 20|Issue 38|
Camus M et al . Epistaxis in end stage liver disease
Table 1 Characteristics of patients n (%)
Characteristic
Data
Age (yr, mean ± SD, range)
54.4 ± 9.7 (40-75)
Sex (Male/Female)
12/8 (60/40)
Child Pugh class
A: 0; B: 1 (5); C: 19 (95)
MELD score, (mean ± SD, range)
29.6 ± 7.5
Etiology
HCV + Alcoholic
5 (25)
Alcoholic
5 (25)
Cryptogenetic
5 (25)
HCV
4 (20)
PBC + AIH
1 (5)
Inpatient start of bleeding
18 (90)
Nasogastric tube placed prior to bleeding
16 (80)
Hematemesis
15 (75)
Melena and/or Hematochezia
9 (45)
PT (s, mean ± SD, range)
20.7 ± 6.8 (13.4-42.6)
INR (mean ± SD, range)
2.3 ± 1.4 (1.4-7.8)
Platelet count (/mm3, mean ± SD, range) 51000 ± 32082 (11000-120000)
Hematocrit (mean ± SD, range)
23.5% ± 2.9% (18.5%-29.9%)
AIH: Autoimmune hepatitis; HCV: Hepatitis C virus; INR: International
normalized ratio; MELD: Model for end stage liver disease; PBC: Primary
biliary cirrhosis; PT: Prothrombin time; SD: Standard deviation.
(JM or MC).
RESULTS
A total of 1249 patients were registered for severe UGIH
in the data basis, 461 (36.9%) were cirrhotic patients. Epistaxis was determined to be the source of severe hemorrhage in 20 patients with ESLD hospitalized for severe
UGIH. Based on the number of cirrhotic patients evaluated for severe UGIB during the same period of time, we
estimated that the epistaxis diagnosis represented 4.3%
(20/461) of all cirrhotic patients hospitalized for suspected severe UGIH. Most patients (18/20 = 90%) developed what was clinically diagnosed as inpatient UGIH
after hospitalization for worsening liver disease and did
not have signs of UGIH on admission. In this particular
subgroup of inpatients with cirrhosis and severe UGI
hemorrhage, the prevalence of epistaxis was higher and
was estimated to be 15.3% (18/117) (Table 1).
The age (mean ± SD) of the subjects with epistaxis
was 54.4 ± 9.7 year with men comprising 12/20 (60%).
Etiologies of ESLD were hepatitis C and alcohol in 5
(25%), cryptogenic cirrhosis in 5 (25%), alcohol alone in
5 (25%), hepatitis C alone in 4 (20%), and primary biliary cirrhosis plus autoimmune hepatitis in 1 (5%). Most
patients (19/20 = 95%) were Child-Pugh class C.
The majority (16/20 = 80%) had a nasogastric (NG)
tube placed prior to the onset of bleeding. The reasons
of NG tube placement were intubation, decompression
or suctioning the stomach, checking for bright red bleeding (BRB) in stomach to establish the acuity of bleeding,
and assisting of esophagogastroduodenoscopy (EGD)
by clearing of blood, clots, or gastric contents. Seventeen (85%) patients required endotracheal intubation for
airway protection.
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All patients had clinically severe bleeding presenting
as hematemesis (15/20; 75%) or hematochezia/melena
(9/20; 45%). In 9 (45%) patients, bleeding was accompanied by shock or persistent hypotension requiring administration of intravenous pressor agents.
All patients had concurrent severe coagulopathy with
a mean PT ± SD of 20.7 ± 6.8 s (range: 13.4-42.6), INR
(mean ± SD) of 2.3 ± 1.4 (range: 1.4-7.8), and platelet
count (mean ± SD) of 51000 ± 32082/mm 3 (range:
11000-120000). The hematocrit (mean ± SD) before resuscitation was 23.5% ± 2.9% (range: 18.5-29.9).
Most (14/20; 70%) patients had esophageal varices
but none had active bleeding, platelet plugs, or other
stigmata of recent hemorrhage[9]. No other upper GI
lesions with active bleeding, visible vessels, or adherent
clots were found. Upon withdrawal of the endoscope,
fresh red blood (indicating active bleeding) was found in
the proximal esophagus coming down from the posterior nasopharynx in each case.
Once diagnosed by endoscopy, epistaxis was initially
controlled in all cases. Fifteen (75%) patients required
posterior nasal packing by an otolaryngologist in addition to correction of coagulopathy. Two (10%) patients
had angiographic embolization of branches of the splenopalatine artery after failure of nasal packing.
Five (25%) patients rebled during follow-up. During
follow-up, the number of RBC units transfused (mean ±
SD) was 9.8 ± 11.7, the number of FFP units transfused
(mean ± SD) was 14.7 ± 21.8, and the number of platelets units transfused (mean ± SD) was 8 ± 9.9.
Patients’ outcomes were summarized in Table 2. Five
(25%) patients died in the hospital, 12 (60%) received
orthotopic liver transplantation (OLT) during the hospitalization, and 3 (15%) were discharged without OLT.
The mortality rate was 63% (5/8) in patients who did
not undergo OLT. The mean ± SD length of time until
death, liver transplantation, or discharge from the hospital was 13.6± 18.3 d.
Among the 5 deaths in the hospital, one was due to
uncontrolled recurrent epistaxis and very severe hemorrhage and all others were from ESLD or severe co-morbiditis. The patient who died of uncontrolled epistaxis
was a 75-year-old male with hepatitis C and alcoholic
cirrhosis who was maintained on oral anticoagulation
with warfarin for a St. Judes mitral valve replacement.
He developed epistaxis after an increase in his outpatient warfarin dose and was admitted with an INR of
7.7. The epistaxis was controlled after correction of his
coagulopathy and posterior nasal packing but recurred 8
d later days after the packing was removed. At the time
of the rebleed, the INR was 1.5 and platelet count was
above 100000/mm. Bleeding continued despite repeat
posterior nasal packing and transfusion with fresh frozen
plasma and platelets, and the patient subsequently developed a myocardial infarction and cardiogenic shock.
The patient’s family chose to withdraw care given his
very poor prognosis and he expired soon after. Among
the four other deaths, one patient died during OLT pro-
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October 14, 2014|Volume 20|Issue 38|
Camus M et al . Epistaxis in end stage liver disease
Table 2 Outcomes of patients n (%)
OLT
Death in
hospital
Discharge
without OLT
No. of
patients
Age (yr)
PT (s)
INR
Platelet count
3
(/mm )
MELD score
Time between diagnosis and
death, OLT or discharge (d)
Rebleeding before death,
OLT or discharge
12 (60)
5 (25)
51.5 ± 8.7
57.6 ± 10.1
22.6 ± 7.9
17.7 ± 5.5
2.7 ± 1.7
1.8 ± 0.5
43333 ± 27955
54400 ± 41578
31.8 ± 6.4
30.8 ± 9.5
8.4 ± 8.2
10.8 ± 6.0
3 (25)
1 (20)
3 (15)
60.3 ± 11.7
18.6 ± 0.7
1.8 ± 0.1
76000 ± 26514
20.5 ± 2.1
39.0 ± 39.9
1 (33)
MELD: Model for end stage liver disease; OLT: Orthotopic liver transplantation; PT: Prothrombin time; INR: International normalized ratio; SD: Standard
deviation.
cedure and the tree other patients died in intensive care
unit (ICU) because of multiorgan failure due ESLD.
DISCUSSION
Patients with ESLD presenting with massive hematemesis, hematochezia, and/or melena require rapid diagnosis
and intervention to reduce the high mortality associated
with cirrhosis[2]. Many of these patients have coexisting coagulopathies that can worsen their outcomes. In
patients, with ESLD, epistaxis can be a cause of severe
hemorrhage which may be overlooked and usually masquerades as UGIH, because of the clinical presentation[5].
We estimated that in cirrhotic patients hospitalized for
severe UGIH symptoms, epistaxis was the diagnosis in
4.3% of cases. This prevalence increased more than three
times when cirrhotic patients were already hospitalized
before they started bleeding (15.3%). Few data have been
reported about the prevalence of epistaxis in patients
presenting with signs of severe UGIH. Hutchison et al[3]
reported 10 cases with apparent upper gastrointestinal
bleeding, comprising a 0.55% incidence of hematemesis and melena in the population studied of patients
referred for UGIH without information on their liver
function.
In ambulatory patients without cirrhosis, epistaxis
most commonly arises from the vessels located in the
anterior nasopharynx (Kiesselbach’s plexus), especially in
children and young adults. The source of bleeding is usually obvious, often related to local trauma, and rarely is
clinically severe[10]. In contrast, posterior nasopharyngeal
epistaxis may be occult, large volume, and associated
with high mortality[11]. It is reported to be more common in older patients, less likely trauma-related given its
anatomic location, and more likely the result of spontaneous bleeding from a sclerotic vessel. In contrast to
published figures that only 5% of all epistaxis is from a
posterior nasopharyngeal source, all of our patients with
epistaxis had posterior hemorrhage and most 15 (75%)
required posterior nasal packing. Although ESLD is now
more often considered as a procoagulant state, in our
cirrhotic patients with epistaxis, portal hypertension and
coagulopathy were risk factors in all patients. These risk
factors predisposed them to severe posterior nasopharyngeal hemorrhage.
One of the most common causes of epistaxis is trau-
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ma. Most patients (80%) in this study had epistaxis after a
recently placed nasogastric tube. Nasogastric tube placement may initiate or exacerbate pharyngeal bleeding, especially in patients with ESLD. Altered mental status from
hepatic encephalopathy, shock, or mechanical ventilation
related sedation might increase the risk of pharyngeal
trauma during nasogastric tube placement by blunting a
patient’s natural response to pain or discomfort. Abnormal coagulation may also increase the risk of epistaxis
arising from minimal pharyngeal trauma. Therefore, NG
tube placement should be avoided as often as possible
especially forceful or traumatic insertion in the patients
with ESLD. However by clearing the stomach of blood,
clots, or gastric contents and helping establish the acuity of bleeding, these devices may help localize a bleeding source, decrease the risk of massive aspiration, and
increase the amount of gastric mucosa seen during endoscopy[12-14]. NG or orogastric tubes are also useful for
enteral delivery of medications and nutrition in ESLD
patients with severe encephalopathy. If there is concern
about inducing epistaxis in patients with ESLD and coagulopathy and a gastric tube is required, an orogastric
tube can be considered instead of a nasogastric tube.
Most patients with ESLD without epistaxis tolerate such
tubes well and do not have complications in current practice. However it would be interesting to know the prevalence of epistaxis in population of patients with ESLD
who underwent ng tube placement and further studies
are warranted.
Mortality rates approaching 5% have been reported
for all patients with posterior epistaxis[3]. Given associated
coagulopathy and other factors, it is expected that patients
with ESLD who develop a severe posterior nasopharyngeal bleed would have significantly higher mortality. Our
overall mortality rate of 25% (5/20) supports this idea,
and the rate in those not receiving liver transplantation
was even higher (5/8, 63%).
Epistaxis as a source of severe bleeding must be included in the differential diagnosis of inpatient hemorrhage for patients with ESLD and nasogastric tubes or
nasotracheal intubation. However, this is still a diagnosis
of exclusion. Especially in cirrhotic patients who often
have variceal hemorrhage, upper endoscopy should always be performed to rule out more common causes of
UGIH, and in the absence of an actively bleeding lesion
on esophagogastroduodenoscopy, careful examination
13996
October 14, 2014|Volume 20|Issue 38|
Camus M et al . Epistaxis in end stage liver disease
of the mouth and nasopharynx should be performed.
Delayed diagnosis of severe epistaxis from posterior
pharyngeal sources can lead to significant blood loss and
resulting hypovolemia, shock, and death[5].
Once the diagnosis of posterior nasopharyngeal epistaxis is established, an otolaryngologist should be consulted about treatment options, which include posterior
nasal packing, possible embolization of arteries supplying that region, and/or endoscopic ligation[10,15]. Posterior nasal packing is not without potential complications,
including aspiration, hypoxia, and toxic shock as the
most serious. Supplemental oxygen should be provided
and, whenever necessary, intubation and mechanical
ventilation should be considered to help prevent aspiration and hypoxia. Nonetheless, despite rapid diagnosis
and treatment, the outcome for these patients is poor,
most likely influenced by their significant comorbidities,
particularly ESLD and coagulopathy.
In the absence of an early otolarygoscopic exam, turning the patient onto the side and looking for nasal blood
loss may help suggest an occult posterior pharyngeal hemorrhage as well as facilitate drainage. Other measures that
might influence diagnosis, treatment, and outcome include
oral passage of a gastric lavage tube and early referral for
liver transplantation.
In conclusion, severe posterior nasopharyngeal epistaxis in hospitalized patients with ESLD: (1) is a diagnosis of exclusion that requires upper endoscopy to rule
out common causes of UGIH; (2) can usually be effectively treated with nasal packing and correction of coagulopathy; (3) was the diagnosis of the bleeding source in
4.3% of cirrhotic patients with a suspected UGIH and
this prevalence increased to 15.3% in the subgroup of
cirrhotic patients in whom the hemorrhage started after
hospitalization for worsening liver disease and did not
have signs of UGIH on admission; and (4) is associated
with a high rate of mortality (63%) in those not receiving
liver transplantation. Physicians managing patients with
ESLD should be aware that posterior nasopharyngeal
epistaxis can masquerade as massive UGIH, particularly
in those with severe coagulopathy.
ACKNOWLEDGMENTS
The authors are grateful to Nan Sun, MS and Mary Ellen
Jensen, MLS for data management, and Martha Carrico,
RN, as the research coordinator.
COMMENTS
COMMENTS
Background
Severe epistaxis is a rare cause of massive bleeding which can masquerade
as upper gastrointestinal hemorrhage (UGIH) in patients with end stage liver
disease (ESLD).
Research frontiers
Little is known about prevalence, treatment and outcomes of patients suffering
from epistaxis in case of ESLD. Only few cases series are available in literature.
Innovations and breakthroughs
The authors described that epistaxis was the diagnosis of the bleeding source
in 4.3% of cirrhotic patients with a suspected UGIH and this prevalence in-
WJG|www.wjgnet.com
creased to 15.3% in the population of cirrhotic patients in whom the hemorrhage
occurred after hospitalization for worsening liver disease and did not have signs
of UGIH on admission. The authors found that epistaxis in such cases could
usually be effectively treated with nasal packing and correction of coagulopathy.
This treatment should not be delayed. In fact, epistaxis in ESLD was associated
with a high rate of mortality (63%) in those not receiving liver transplantation.
Applications
Physicians managing patients with ESLD should be aware that posterior nasopharyngeal epistaxis can masquerade as massive UGIH, particularly in those
with severe coagulopathy.
Peer review
Well written and discussed study. The authors described the prevalence, diagnosis, treatment, and outcomes of ESLD patients with severe epistaxis masqueraded as upper gastrointestinal hemorrhage. We have limited knowledge in
this subject and the authors made an important observation.
REFERENCES
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Cholongitas E, Senzolo M, Patch D, Kwong K, Nikolopoulou V, Leandro G, Shaw S, Burroughs AK. Risk factors, sequential organ failure assessment and model for end-stage
liver disease scores for predicting short term mortality in
cirrhotic patients admitted to intensive care unit. Aliment
Pharmacol Ther 2006; 23: 883-893 [PMID: 16573791 DOI:
10.1111/j.1365-2036.2006.02842.x]
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intensive care unit: early prognosis and long-term survival.
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10.1097/CCM.0b013e3181f3dea9]
Hutchison SM, Finlayson ND. Epistaxis as a cause of he3
matemesis and melena. J Clin Gastroenterol 1987; 9: 283-285
[PMID: 3497188]
Gifford TO, Orlandi RR. Epistaxis. Otolaryngol Clin North
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Am 2008; 41: 525-536, viii [PMID: 18435996 DOI: 10.1016/
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Johal SS, Austin AS, Ryder SD. Epistaxis: an overlooked
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cause of massive haematemesis in cirrhosis. BMJ 2003; 326:
440-441 [PMID: 12595387 DOI: 10.1136/bmj.326.7386.440]
D'Amico G, Garcia-Tsao G, Pagliaro L. Natural history and
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prognostic indicators of survival in cirrhosis: a systematic
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Kamath PS, Wiesner RH, Malinchoc M, Kremers W, Ther7
neau TM, Kosberg CL, D’Amico G, Dickson ER, Kim WR.
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10.1053/jhep.2001.22172]
Kremers WK, van IJperen M, Kim WR, Freeman RB, Harper
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AM, Kamath PS, Wiesner RH. MELD score as a predictor of
pretransplant and posttransplant survival in OPTN/UNOS
status 1 patients. Hepatology 2004; 39: 764-769 [PMID: 14999695
DOI: 10.1002/hep.20083]
Jensen DM. Endoscopic screening for varices in cirrhosis:
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122: 1620-1630 [PMID: 12016427]
10 Douglas R, Wormald PJ. Update on epistaxis. Curr Opin Otolaryngol Head Neck Surg 2007; 15: 180-183 [PMID: 17483687
DOI: 10.1097/MOO.0b013e32814b06ed]
11 Tan LK, Calhoun KH. Epistaxis. Med Clin North Am 1999;
83: 43-56 [PMID: 9927959]
12 Pallin DJ, Saltzman JR. Is nasogastric tube lavage in patients with acute upper GI bleeding indicated or antiquated?
Gastrointest Endosc 2011; 74: 981-984 [PMID: 22032314 DOI:
10.1016/j.gie.2011.07.007]
13 Perng CL, Lin HJ, Chen CJ, Lee FY, Lee SD, Lee CH. Characteristics of patients with bleeding peptic ulcer requiring
emergency endoscopy and aggressive treatment. Am J Gastroenterol 1994; 89: 1811-1814 [PMID: 7942673]
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Stollman NH, Putcha RV, Neustater BR, Tagle M, Raskin
JB, Rogers AI. The uncleared fundal pool in acute upper
gastrointestinal bleeding: implications and outcomes. Gastrointest Endosc 1997; 46: 324-327 [PMID: 9351035]
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Tateshima S, Froehler M, Cramer R, Rastogi S, Viñuela F.
Trans-radial embolization of epistaxis in patients with endstage liver disease. Neuroradiology 2012; 54: 1241-1244 [PMID:
22205340 DOI: 10.1007/s00234-011-0999-z]
P- Reviewer: Celikbilek M, Ding SG, Malnick SDH
S- Editor: Nan J L- Editor: A E- Editor: Liu XM
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B-ENT, 2005, 1, Suppl. 1, 27-43
Guidelines to the management of epistaxis
B. Bertrand*, Ph. Eloy*, Ph. Rombaux*, C. Lamarque**, J. B. Watelet***, S. Collet*.
* ENT and HNS Department, Catholic University of Louvain, Cliniques Universitaires UCL de Mont-Godinne, Yvoir,
Cliniques Universitaires Saint-Luc, Brussels; ** ORL Department, Cliniques Saint-Luc, Bouge; *** ENT and HNS
Department, University of Ghent, UZ Gent, Ghent
Key-Words. Epistaxis; nose bleeding; management; conservative treatment; surgery; endoscopic surgery; medical treatment; cost analysis
Abstract. This article is a review of the literature on epistaxis and its treatment. Data were collected from MedLine until
mid September 2005, and from others readings and books. Its first goal was to present to the Belgian ENT practitioners
an overview, as complete as possible, of the modern concepts in etiologies, medical, conservative, surgical (including
embolization), and adjunctive therapies of epistaxis. All these topics are discussed and commented, from a medico-surgical point of view, and also from a cost effectiveness one.
Foreword
First of all, it has to be stressed on
that this topic on epistaxis – or
nose bleed – is presented to you as
a guideline only and no more.
The elements of history, discussion of pathophysiology, and
details of manoeuvres are presented to help the physician best
assess which patients are likely to
benefit from this guideline, and
which are most likely to need surgical therapy.
The suggested studies, physical
examination – of the nasal cavities
and of the total body –, medical
material including rigid endoscope and fiberscope, plain X-ray,
CT, MRI, lab exams, and others,
are intended to maximize the
adherence process to these guideline, they will not ensure successful treatments in every patient nor
in every situation.
The present guideline should
not be considered inclusive of all
accepted methods of caring nose
bleeds or exclusive of other cares
that can be assumed as reasonably
aimed toward gaining the same
results. The ultimate decision
regarding the appropriateness of
any specific procedure, therapy, or
referral must be made by the
physician him or herself in lights
of – and depending on – all the
circumstances presented by the
patient as an individual and all
surroundings.
Furthermore, medicine is a permanently changing science and
not all therapies are clearly and
definitely established. Obviously,
new researches and discoveries
are modifying medical and surgical treatments daily. That is why
the reader should confirm the
information in this guideline from
other sources prior to use. In particular, all drug doses, indications,
and contraindications should be
confirmed in the package insert.
Background
Bleeding from the nose, or epistaxis – Greek for nosebleed that
means “which is leaking on, drop
by drop” –, is a problem that has
been a part of the human experience from earliest times. It was the
subject for folklore and myth, and
has been treated by physicians –
and others – from the earliest
times.
Centuries ago, Hippocrates
reported that pinching the nose
may help to stop bleeding. His
technique is still in use today.
Writing magical words on the
forehead with the patient’s own
blood, having the patient sniff
his/her own fried blood into their
nose, wearing amulets preferably
tinted in red, have also been tried
with more or less success obviously.
Carl Michel (1871), James
Little (1879), and Wilhelm
Kiesselbach were the first to identify the nasal septum’s anterior
plexus as a source of nasal bleeding.
Pilz was the first to treat epistaxis with ligature of the common
carotid artery (1869). This was
28
followed by Seiffert who was
doing the same with the internal
maxillary artery via the maxillary
sinus in 1928. Henry Goodyear
performed the first anterior ethmoid artery ligature in the treatment of epistaxis.
The medical community’s understanding of epistaxis has
increased dramatically. Our treatment, though somewhat modified
over the years, has continued to
include techniques first noted several thousand years ago.
Epistaxis is very common in its
frequency and varied in its presentation. The true incidence of epistaxis is not known in the literature
because most episodes are selftreated and thus are not reported.
Most nose bleeds are mere nuisances, but some are quite frightening, and a few are even life
threatening. The site of a patient
covered in blood surrounded by a
hoard of anxious family members
can make even the most experienced emergency physician feel a
sense of dread. When medical
cares are needed, it is usually
because of the problem is either
recurrent or severe. Treatment
depends on the clinical picture,
the experience of the physician,
the availability of ancillary services and for some cases, the hospital medical equipment and the
expertise and skill of members of
the staff.1
In children, nosebleeds occurs
also very commonly, especially in
those between the ages of 2 and 10
years old. In most cases, they are
secondary to local trauma and can
be cared for by primary care
physicians. In rare instances, however, a nosebleed may be difficult
to control or may be a manifestation of a serious systemic illness.
Referral to an otorhinolaryngologist or hematologist/oncologist is
B. Bertrand et al.
usually not required except in
these situations, and hospitalization is generally unnecessary.
Pathophysiology
The blood supply of the nose is
complex and particularly rich with
contribution from both internal
and external carotid arteries.
The external carotid system
supplies blood to the nose via the
facial and internal maxillary arteries. The superior labial artery one of the terminal branches of the
facial artery - contributes to the
blood supply of the anterior part
of the nasal floor and of the septum through a septal branch. The
internal maxillary artery enters the
pterygomaxillary fossa and divides into 6 branches: posterior superior alveolar, descending palatine,
infraorbital, sphenopalatine, pterygoid canal, and pharyngeal. The
descending palatine arteries are
running down through the greater
palatine canals and supply the lateral walls of the nasal cavities.
They go back to the nose via a
branch in the incisive foramen to
irrigate the anterior septum. The
sphenopalatine arteries enter the
nose through the sphenopalatine
foramen which is situated approximately 10 mm dorsally to a theoretical line drawn between both
the posterior attachments of the
middle and lower turbinates to
supply the lateral nasal walls. It
also gives a branch to the septum.
The internal carotid artery irrigates the nose through the ophthalmic artery that enters the bony
orbit via the superior orbital fissure and divides into several
branches.
One of which – the posterior
ethmoid artery – exits the orbit for
the nose through the posterior ethmoid foramen, located 2 mm to 9
mm anterior to the optic canal.
The anterior ethmoid artery exits
the orbit through the anterior ethmoid foramen. Both of the vessels
cross the ethmoid roof to enter the
anterior cranial fossa and then
descend into the nasal cavity
wherein they divide into lateral
and septal branches to supply the
lateral wall of the nose and the
nasal septum. The Kiesselbach
plexus, or Little area, is located on
the lower third of the septal cartilage and is a very common spring
for most anterior epistaxis. Many
of the arteries supplying the septum have anastomotic connections
in this plexus. The mucosa covering the area is thin and friable and
the small vessels supplying the
nasal mucous membrane have little structural support. Congestion
of the vessels caused by conditions such as a URI or drying of
the mucosa from low environmental humidity makes this area susceptible to bleeding. Sensory
nerves follow the anatomical general pattern of the vessels.
Trigeminal cranial nerves V1 and
V2 supply the interior nose (anterior ethmoidal nerve and nasopalatine nerve respectively).
Clinical presentation
Nosebleeds may be either anterior
or posterior in origin. Of the two
categories of epistaxis, mundane
and severe, the mundane, usually
anterior epistaxis is the more common.
All individuals suffer occasional nose bleeds, of which the great
majority are minor and occur on
the anterior septum where they are
easily managed.
Occasionally patients present
with severe, life-threatening epistaxis arising from the larger vessels in the posterior and superior
Guidelines to the management of epistaxis
nasal cavity. Such bleeds occur
primarily in older patients, often
with significant comorbidities.
Then the bleeding compromises
the patient’s airway and results in
hemodynamic instability. Management can be complex and severely tax the health care provider
especially if he is not an otolaryngologist.
With anterior nosebleeds blood
exits almost entirely from the
anterior portion of the nose. With
posterior nosebleeds, most of the
bleeding occurs in the nasopharynx and mouth, although some
blood exits through the anterior
nose as well. Posterior epistaxis
are often more severe and more
difficult to control, and patients
may present in a hemodynamically unstable condition as written
before.
Patients with bleeding disorders
may have recurrent nosebleeds
and a history of prolonged bleeding, easy bruisability, or multiple
bruises in unlikely locations.
Alternatively, some patients who
present with hematemesis have
vomited swallowed nasal blood.
In children, most have a history
of bleeding at home and minimal
or no bleeding at all at the time of
presentation. Parents and children,
who are often frightened by nosebleeds, frequently overestimate
the amount of blood lost.
Understanding and reassurance
are important in dealing with
patient anxiety.2
Epidemiology
Epistaxis is the second most common cause of spontaneous bleedings. Sixty per cent of patients
may experience at least one
episode of epistaxis during their
lifetime. Eighty per cent of epis-
taxis occurs in Kiesselbach’s plexus.3
In children, one can estimate
that thirty percent have one nosebleed by the time they are 5 years
of age. In children between 6 and
10 years old, frequency increases
to 56%. Nosebleeds are rare in
early infancy and infrequent after
puberty. They occur much more
frequently in the late fall and winter months, when URIs are common, environmental humidity is
relatively low, and the use of heating systems results in dryness.
Nosebleeds are also more common in children who live in dry
climates, especially if they have a
URI or allergic rhinitis.
Frequency
The true frequency of epistaxis is
quite impossible to determine
because most episodes resolve
either spontaneously or with selftreatment, and therefore, are not
reported.
Age
The general distribution is bimodal, with peaks in young children and elderly individuals.
Sex ratio
Incidence of epistaxis is a little bit
higher in males than in females.
Mortality/Morbidity
For most people, epistaxis is a
kind of a nuisance only. However,
the problem can be life threatening, especially in elderly patients
and among those with underlying
additional medical problems.
Etiology
A sum up of etiologies can be displayed as follows below; they
have been divided in local and
systemic causes for more clarity.
29
Most etiologies are evident and
commonly accepted. Some are not
and/or are matter of discussions in
the literature. That is why immediately after this synthetic paragraph
a special discussion is done of
some particular etiologies on
which there is no definite consensus or clues. Some others are simply requesting further explanation
and comments.
1. Local causes
1. Trauma (most common)
• Fracture(s): facial and nasal,
of bone(s) and / or cartilage(s)
• Self-induced digital trauma,
foreign body
• Iatrogenic: nasal / sinus /
orbital / skull base surgery
2. Barometric changes
3. Nasal dryness - combination of
dry air, septal deformities
4. Septal perforation
5. Chemical
• Cocaine abuse
• Nasal sprays (both steroids
and decongestants)
• Ammonia
• Others: gasoline, phosphorus,
chromium salts, sulfuric acid,
etc.
6. Tumours
• Benign: polyps, inverting
papilloma, juvenile nasal
angiofibroma, septal angioma
• Malignant: squamous cell carcinoma, esthesioneuroblastoma
7. Inflammation
• Rhinitis: allergic, non allergic
• Sinusitis
• Infections: bacterial, viral,
fungal
2. Systemic causes
1. Coagulopathies
• Anticoagulant use: coumadin,
30
heparin
• NSAIDS, aspirin
• Hemophilia
• Von Willebrandt disease
• Platelet defects
• Catamenial and pregnancy
• Hepatic insufficiency and
alcohol4
• Scurvy
• Hemorragic fever (Dengue,
Ebola, …)5,6
2. Granulomatous disorders
• Wegener’s disease
• Mid face granuloma
• Sarcoidosis
• Syphilis
• Tuberculosis
• Rhinoscleroma
• Systemic lupus erythematosis
• Periarteritis nodosa
3. Intoxications: cobalt, phosphorus, arsenic, lead
4. Vascular
• Hypertension
• Circadian onset
• Atherosclerosis
• Osler-Weber-Rendu disease or
hereditary hemorrhagic telangiectasia (HHT)
3. Idiopathic causes
4. Discussion of some etiologies
1. Trauma
Self-induced trauma from
repeated nasal picking can
cause anterior septal mucosal
ulceration and bleeding. This
scenario frequently is observed
in young children. Acute facial
and nasal trauma commonly
leads to epistaxis. If the bleeding is from minor mucosal laceration, it is usually limited.
However, extensive facial trauma can result in severe bleeding
requiring nasal packing. In
these patients, delayed epistaxis
may signal the presence of a
traumatic aneurysm.
B. Bertrand et al.
Patients undergoing nasal
surgery should be warned of the
potential for epistaxis. As with
nasal trauma, bleeding can
range from minor (due to mucosal laceration) to severe (due
to transection of a major vessel).
3. Inflammatory diseases
Bacterial, viral, fungal and
allergic rhinosinusitis cause
mucosal inflammation and may
lead to epistaxis. Bleeding in
these cases is usually minor and
frequently manifests as bloodstreaked nasal discharge.
Granulomatosis diseases such
as sarcoidosis, Wegener granulomatosis,
tuberculosis,
syphilis, and rhinoscleroma
often lead to crusting and friable mucosa and may be a
cause of recurrent epistaxis.
trauma or surgery. Acquired
coagulopathies can be primary
or secondary. Among the more
common acquired coagulopathies are thrombocytopenia
and liver disease with its consequential reduction in coagulation factors. Even in the absence of liver disease, alcoholism also has been associated
with coagulopathy and epistaxis.
For those patients on anticoagulants, the altered coagulation
should be carefully checked
and monitored. For those on
aspirin as a general prophylaxis
80 mg/d of aspirin is sufficient.
Most use 300 mg daily or even
more, as the adult aspirin
tablets are easier to find and
cheaper to purchase; 80 mg
P.O. daily are enough to protect
the heart and free the nose from
an increased epistaxis risk.
In the pediatric age group,
about one third of children with
recurrent epistaxis have a diagnosable coagulopathy. In those
cases, together with a positive
family history, a prothrombin
time (PT) and a partial thromboplastin time (PTT) are giving
the most useful and cost-effective data.7
4. Blood dyscrasias
There is a caveat for epistaxis.
While most are simple,
straightforward problems, they
also can be the heralding sign
of underlying coagulopathy.
Hemophilia, von Willebrandt
disease, thrombocytopenia, all
may have epistaxis as their initial symptom.
Congenital
coagulopathies
should be suspected in individuals with a positive family history, easy bruising, or prolonged bleeding from minor
5. Scurvy
In western countries the incidence of scurvy appears to be
on the rise. Populations at risk
include the elderly, chronic
alcoholics, diet faddists, the
mentally ill, and patients with
cancer, malabsorption, or who
are on renal dialysis. The symptoms of scurvy are weakness,
lassitude, depression, arthralgias, petechiae, perifollicular
hemorrhage, follicular hyperkeratosis, corkscrew hairs, purpura, ecchymoses, gingival
2. Septal deformities and perforations
Septal deviations and spurs
may disrupt the normal nasal
airflow, leading to dryness and
epistaxis. The bleeding sites
usually are located anterior to
the spurs in most patients. The
edges of septal perforations frequently harbor crusting and are
common sources of epistaxis.
Guidelines to the management of epistaxis
swelling, hemorrhage, halitosis,
poor wound healing, and loss of
teeth.
Adults should receive 100 mg
of vitamin C 3-5 x a day up to 4
gr followed by 100 mg/day.
Infants and children should
receive 10-25 mg 3 times a day.
Symptoms disappear within 3-5
days.
6. Hypertension
Beran et al.8 reported that the
distribution of blood pressure of
habitual nose bleeders did not
differ from that of the control
group. This is in concordance
with the data of Lubianca Neto
et al.9, who also could not
establish a definite association
between blood pressure and
history of adult epistaxis in
hypertensive patients, although
they found a link to left ventricular hypertrophy. The evidence
for an association of duration of
hypertension and left ventricular hypertrophy with epistaxis
suggests that epistaxis might be
a consequence of long term
hypertension. They observed
also the presence of enlarged
vessels at rhinoscopy in hypertensive patients with a history
of epistaxis.
Herkner et al.10 found higher
blood pressure values in bleeding patients compared with controls. Padgham et al.11 found a
positive correlation between
hypertension and bleeding from
the middle meatus, but not with
the severity of bleeding. The
discussion on blood pressure
and epistaxis will continue.12
7. Circadian variation of onset
Several
physiopathological
phenomena show two peaks
during the day. In epistaxis, the
time between the two peaks is
about 12 hours.
Globally, all circadian rhythms
in the cardiovascular system
and the blood parameters
enhance blood coagulation and
formation of thrombus in the
morning, whereas blood coagulation decreases in the afternoon. In a clinical study,
Manfredini et al.13 suggest that
blood pressure might trigger or
be conductive to epistaxis and
that might show circadian variation. A circadian rhythm of
epistaxis was significantly
found with a primary peak in
the morning (8:00) and a smaller secondary peak in the
evening (20:00). This is quite
similar with hypertension, subarachnoid hemorrhage and rupture of aortic aneurysms. This
deserves further investigation.
8. Arteriosclerosis
Atherosclerotic vascular disease is considered a reason for
the higher prevalence of epistaxis in elderly individuals.
9. Hereditary hemorrhagic telangiectasia (HHT)
Hereditary hemorrhagic telangiectasia (Osler-Rendu-Weber
disease) is an autosomal dominant disease associated with
recurrent bleeding from vascular anomalies. The condition
can affect vessels ranging from
capillaries to arteries, leading to
the formation of telangiectasias
and arteriovenous malformations.
Histopathologic examination of
these lesions reveals a lack of
elastic or muscular tissue in the
vessel wall. As a result, epistaxis can occur from minor
trauma and tends not to stop
spontaneously. Various organ
systems such as the respiratory,
gastrointestinal, brain and genitourinary systems may be in-
31
volved. The epistaxis in these
individuals is variable in severity but is almost universally
recurrent.
10. Idiopathic causes
Approximately 10% of patients
with epistaxis have no identifiable causes even after a thorough evaluation.
Management and work up
1. History
• Specific questions about the
severity, frequency, duration,
and laterality of the epistaxis
have to be asked.
• Inquiries about precipitating
and aggravating factors and
methods previously used to
stop the bleeding must be
made.
• A head and neck history with
an emphasis on nasal symptoms has to be obtained.
• In addition, a general medical
history concerning relevant
medical conditions (e.g.,
hypertension, arteriosclerosis,
coagulopathies, liver disease),
current medications (e.g.,
coumadin, nonsteroidal antiinflammatory drugs), smoking and drinking habits must
be elicited.
2. General Assessment
• Airway patency has to be controlled and restored when necessary.
• Vital signs, pulse, respiration
have to be checked.
• Pressure on nose has to be
maintained (patient pinches
anterior nose and leans forward). A swimmer’s nose
clip14 can be a very useful adjunct when treating patients
with spontaneous, anterior
epistaxis. This clip is efficient
at providing constant, local-
32
ized pressure over the bleeding vessel, and alleviates the
need to pinch the nose.
• Assessment of blood loss and
side of bleeding (ask patient
to quantify blood loss).
• Important and relevant medical problems: cardiac, cancer,
previous epistaxis, allergies to
medications
(i.e.:
local
anaestetics).
See details on drug safety in
Table 1.
• Intravenous access has to be
set up in place if indicated.
• Communication with patient
can obtain consent and cooperation by explaining what is
going to be done.
3. Examination
• Preparation
The patient has to blow his or
her nose and all packing have
to be removed even if bleeding
is not active.
• Hardware
Before evaluating a patient
with epistaxis, all the necessary topical medications, cauterization and packing materials should be ready. A good
light is mandatory as well as
an appropriate suction device,
in order to clean up the nasal
fossa from any cloths.
• Head and neck examination
A thorough head and neck
examination must be performed if the patient’s condition permits as well as anterior
rhinoscopy before and after
topical administration of medication.
• Anaestesia +/- vasoconstrictors
See Table 1 for details on use,
doses, safety in both adult and
pediatric groups.
A good local anaestesia allows
further examination and pot-
B. Bertrand et al.
ential treatments to be done in
cozy conditions both for
patient and physician. A topical anaestetic, such as 4%
aqueous lidocaine, and a vasoconstrictor, such as 0.05%
oxymetazoline or 0.0002%
epinephrine or another decongestant if not contraindicated,
may be used. They can be
applied via aerosolizing spray
or cotton pledgets inside the
nose for 7-10 minutes. With
sprays topical medication may
not stay in place long enough
to be effective due to the blood
flow.
Some epistaxis will stop at
this early step.
• Endoscopy
Finally, endoscopy has to be
performed using a flexible or
preferably a rigid endoscope
to inspect the entire nasal cavity, including the nasopharynx. The rigid endoscope is
generally preferred because of
its superior optic resolution
and its ability to allow endoscopic suction and cauterization.
4. Conservative Treatment
1. Anterior Epistaxis
1. With patient in a sitting up
position to squeeze anterior
(compressible cartilaginous
part) nose for 10 minutes.
2. Nasal cream
In children an antiseptic
nasal cream can be very
effective and avoids further
manipulations in most
cases.15
3. Cautery
Bleeding from the Kiesselbach plexus often is treated
with silver nitrate cauterization. Other cauterizing
agents are also used: chromic
acid, acetic acid, etc. Silver
nitrate should be preferred
because of the absence of
any demonstrated carcinogenesis. The vessels leading
to the site have to be treated
first before treating the actual bleeding site. Random and
aggressive cautery and
cautery on opposing surfaces
of the septum which is potential for septum perforation
must be avoided. Silver
nitrate doesn’t work very
well in active bleeding.
Thirty seconds of exposure
allowed silver nitrate to penetrate to a depth of approximately 1 mm penetration in a
study by Lloyd et al.16
Longer exposure resulted in
no significant additional.
There was also no direct evidence that silver nitrate damaged directly the septal cartilage. Sseptal perforations in
patients treated by means of
topical silver nitrate may be
attributable to necrosis of the
septal cartilage due to damage to the perichondrium,
from which it receive its
blood supply.
4. Electrocautery using an insulated suction cautery unit
also can be used. This
method usually is reserved
for more severe bleedings
and for bleedings which are
more posteriorly located. It
requires local anaesthesia.17
The effectiveness of both
cauterization methods can be
enhanced by using rigid
endoscopes, especially in the
case of more posteriorly
located bleeding sites.18
After the bleeding has been
controlled, the patient is
Guidelines to the management of epistaxis
33
Table 1
Drugs and material of epistaxis managment
Drug
category
Vasoconstrictor ;
Act on alphaadrenergic receptors in the nasal
mucosa
Anesthetics ;
see under (c)
Proof Name
Adult Dose
Level
Ia
Oxymetazoline 2-3 sprays in
0.05%
each nostril
q12h
Pediatric Contraindications Pregnancy
Dose
6-12 years : Hypersensitivity ; Safety not
1-2 sprays MAOIs
established
each nostril
q12h
III
Not
Hypersensitivity ; Usually
established Adams-Stokes
safe
syndrome ;
Wolf-ParkinsonWhite syndrome
Antibiotic
ointments ;
prevent local
infection ; local
moisturization
Ib
Cauterizing
Ia
agents ;
coagulate cel
lular proteins ;
antibacterial
effects
Packing ;
III
mechanical effect
Thrombin ; as
local hemostatic
Ib
Adrenochromazo III
ne; enhance capillary resistance
Terlipressin
Ib
Interactions
Precautions
Guanethidine ; Do not use
Phenothiazine ; topical
see under (a)
decongestants
for >3-5 d ;
see under (b)
None reported Mucous membrane use
only
Lidocaine 2 or
4%;
Xylocaine 2 or
4%;
Pantocaine 2 or
4%;
Cocaine 2 or
4% : see under
(d) (use not
permitted in
some countries)
Mupirocin
ointment 2%
(Bactroban®);
Bacitracin
ointment
Spray or
cotton
pledgets
0.5 g in each Not
Hypersensitivity
nostril bid
formally
for 5 d
established
Usually
safe
None reported
Prolonged use
may result in
growth of
resistant
organisms
Silver nitrate ;
cautery sticks
and
pearls
Not formally Not
Hypersensitivity
established formally
established,
but
commonly
used
NA
NA
NA
Not
Decreases
established effects of
sulfacetamide
preparations
Not for oral
use ;
Cauterize vessels one side
at a time
Safe
None reported
Mouth breathing, hypoventilation
FloSeal®
Not forNot formally
mally
established
established
Unknown None reported
None reported
Potential
abortion
effect
before the
4th month
Monitoring of
blood pressure and electrocardiogram
Gauze;
Surgicel® ;
Meroce®l ;
Oxycel®
Thrombase® ;
Cotton
pledgets
Gel
adrenochrome Per Os: 10 Per Os : 5
semicarbazone ; to 30 mgr
to 10 mgr
AC-17® ;
Also IM and Also IM
Adona® ;
IV – check and IV –
Adrenosem® ; package
check
Adrenoxyl® ;
insert
package
Emex® ;
insert
Ibioxyl® ;
carbazochrome
salicylate ;
carbazochrome
sodium
sulfonate ;
adrenochrome
semicarbazone
sodium
sulfonate
Glypressine® ; Gel;
Not
Glypressin®
IV: 20 to 30 formally
microgr/kg; established
check package insert
Not formally
established
Hypersensitivity
Hypersensitivity,
asthma, hypertension, renal insufficiency, epilepsy
34
B. Bertrand et al.
Table 1 (continuation)
Drug
Proof Name
category
Level
Tranexamic acid III
Exacyl®
Vitamin K,
III
Phytonadione
(Vitamin K1) ;
Treat vitamin K
deficiency
Etamsylate ;
II
Benzenesulfonate
derivative used as
a systemic hemostatic.
EstrogenII
progesterone ;
Ethynil-estradiol ;
Hormonotherapy
of HTT
Snake venoms
II
Synkavit® ;
Konakion® ;
Vitamon K®
Adult Dose Pediatric
Dose
PO : 1 to
20
1.5 gr/3/d ; mgr/kg/d ;
check packIV : 0.5 to
age insert
1 gr/2 to
4/d ;
Nose gel
PO, IM, IV PO, IM, IV
ContraPregnancy
indications
Hypersensitivit ; To be
history of
avoided
thrombosis ;
renal insufficiency
Interactions
Precautions
Hormonal
contraception
Chronic renal
insufficiency :
check
creatinin level
Hypersensitivity Unknown
Warfarin
(Coumadin) ;
Cholestyramin ;
Aspirin ;
NSAID
Cyclonamine ; 2-3 amp(of Half of the Acute porphyria. Unknown
No interaction As a precauEtamsylate ;
250mgr)/day adult dose
is known up to tion should
Altodor® ;
IM or IV
now
not be adminthen 6 co/d
istered during
Dicynone®
for 10 days
the first
trimester of
pregnancy,
whereas during the second
and third
trimesters, it
should be
administered
only if the
expected
therapeutic
benefit is
judged as
superior to the
potential risk
for the foetus.
Prémarin®
IM or IV
Not
Check package Check pack- Check package Check pack20 mgr ; as established insert
age insert
insert
age insert
for hormonal contraception
Reptilase® 1 U 1 amp IM
1 amp IM Check package Check pack- Check package Check packKlobusitzky /
insert
age insert
insert
age insert
amp IM ;
Reptilase® -R,
20 BU®,
1 ml/amp
Table 1 comments.
a) Hypotensive action of may be reversed; concurrent administration with methyldopa may increase vasopressor response; concurrent use of MAOIs and ephedrine may result in hypertensive crisis. Pressor sensitivity to mixed-acting agents such as ephedrine
may be increased. Guanethidine potentiates epinephrine and inhibits ephedrine. may reverse action of nasal decongestants such
as oxymetazoline. TCAs potentiate vasopressor response and may result in dysrhythmias.
b) Caution in: hyperthyroidism, coronary artery and ischemic heart disease, diabetes mellitus, glaucoma and in patients with an
increased intraocular pressure, and prostatic hypertrophy. Hypertensive patients may experience change in blood pressure.
c) Together with vasoconstrictors and b-adrenergics, their effect is prolonged and the pain threshold is increased (Oxymetazoline
0.05%; Ephedrine, Epinephrine, Adrenaline 1/50.000 or 1/100.000).
d) Pantocaine and cocaine have additional vasoconstrictive effects on the blood vessels, and a particularly high affinity for fat tissues.
Guidelines to the management of epistaxis
instructed to use saline spray
and antibiotic ointment in
his/her nose and to avoid
strenuous activities for 7-10
days. NSAIDs are not to be
used if at all possible. Digital
manipulation of the nose is to
be avoided. A topical vasoconstrictor may be used if
minor bleeding recurs when
eschars dislodge.
5. Gelfoam or Surgicel
Local resorbable hemostatic
agents can be placed against
the bleeding site. Absorbable
materials may be used in
patients with coagulopathy
to avoid trauma upon packing removal.
6. Thrombin locally applied
On pledgets in the nose or
more recently under the form
of a gel.
Floseal, a hemostatic sealant
composed of collagenderived particles and topical
bovine-derived thrombin, has
been used as a high-viscosity
gel for hemostasis in anterior
epistaxis and as an easy alternative to nasal packing in
patients suffering from acute
anterior epistaxis in a study
by Mathiasen and Cruz.19 A
former work was done with
this compound in ESS by
Chandra et al.20
7. Conventional packing
Nasal packing can be used
to treat epistaxis that is
not responsive to cautery.
Two types of packing,
anterior and posterior, can
be placed. In both cases,
adequate anaesthesia and
vasoconstriction are necessary.
For anterior packing, various
packing materials are avail-
able. They could be coated
with an antibiotic and can be
moisturized with a topical
vasoconstrictor.
Anterior packs stay in 2-5
days, and patients may
require analgesics. They also
should be given an antibiotic
to prevent rhinosinusitis and
possible toxic shock syndrome.
Here are going some examples of material:
1. Nasal catheter – Epistat®
(Xomed)
• Anaesthetize nose then
before inserting
• Place ports horizontally
so patient can eat/talk
• Inflate balloons with
saline
2. Nasal tampon/sponge
Merocel® sponges can be
placed relatively easily
and quickly but may not
provide adequate pressure.
• The nose has to be anaesthetized and sponge
lubricated before inserting.
• Once inserted, sterile
saline is injected into the
sponge.
• Rewet prior to removal,
check that none has broken off after removal.
3. Vaseline gauze
Petroleum jelly gauze with
or without an antibiotic
ointment traditionally is
used. Layer it tightly and
far enough backwards to
provide adequate pressure.
Blind packing with loose
gauze is to be avoided.
• Leave ends protruding
from anterior nose and
don’t let them dangle
down pharynx.
35
• Packing has to be made
in layers from nasal
floor up.
2. Pediatric group
Most pediatric epistaxis can be
effectively managed with a single out-patient consultation
(91%) using a topical chlorhexidine and neomycin cream in
addition in some case with a
chemical nasal cautery with silver nitrate.15,21
3. Posterior Epistaxis
Epistaxis that cannot be controlled by anterior packing can
be treated with a posterior pack.
Classically, rolled gauzes are
used, but medium tonsil
sponges can be substituted.
Inflatable balloon devices, such
as 12F or 14F Foley catheters,
or specially designed (eg, Storz
Epistaxis Catheter®, Xomed
Treace Nasal Post Pac®) have
become popular because they
are easier to place.
Avoiding overinflation of the
balloon is important because it
can cause pain and displacement of the soft palate inferiorly, interfering with swallowing.
Regardless of the type of posterior pack, an anterior pack also
should be placed.
Patients with posterior packing
should be admitted for close
monitoring of oxygenation,
fluid status, and adequate pain
control. Need of adequate pain
control has to be balanced with
the concern over hypoventilation in the patient with posterior pack. They also should be
given an antibiotic to prevent
rhinosinusitis and possible
toxic shock syndrome.
In a double blind placebo controlled study about antibiotherapy and nasal packing, Derkay
et al. demonstrated that the
36
B. Bertrand et al.
packing in the placebo group
were foul smelling and heavily
colonized with gram – while
those from the antibiotic group
were odor-free and lightly colonized by gram +. But no infectious complications were noted
in both groups.22
5. Surgical cares
Among most patients, the
bleeding responds to cautery
and/or packing. For those who
have recurrent or severe bleeding for which medical therapy
has failed, various surgical
options are available.
Packing failure can be caused
by inadequate placement from
either lack of cooperation by
the patient (especially those in
the pediatric age group) or from
anatomic factors such as a deviated septum. In these patients, a
careful endoscopic examination
under general anaesthesia may
be considered.
1. Examination under general
anaesthesia and septoplasty
Bleeding sites can be cauterized under endoscopic guidance, a deviated septum can
be straightened, spurs can be
removed, and meticulous
packing can be placed. In
addition, arterial ligation
may be performed during
the same setting if these
steps fail to control the
bleeding.
2. Fibrin glue
Topical use of fibrin glue
especially in coagulopathies
has been advocated.23
3. Arterial ligation
The specific vessel(s) to be
ligated depend on the location of the epistaxis. In general, the closer the ligation is
to the bleeding site, the more
effective the procedure tends
to be.
1. External carotid artery ligation
Ligation of the external
carotid artery can be performed with the patient
under local or general
anaesthesia. A horizontal
skin incision is made
between the hyoid bone
and the superior border of
the thyroid cartilage.
Subplatysmal skin flaps
are then raised, and the
sternocleidomastoid muscle is retracted posteriorly.
Next, the carotid sheath is
opened, and its contents
exposed. The external
carotid artery is identified
by following the internal
carotid for a few centimeters and dissecting the
external carotid beyond its
first few branches. After
the external carotid has
been positively identified,
it usually is ligated just
distal to the superior thyroid artery. Continued
bleeding after ligation
may be from anastomoses
with the opposite carotid
system or the ipsilateral
internal carotid artery.
2. Internal maxillary artery
ligation
This procedure has a higher success rate than external carotid artery ligation
because of the more distal
site of intervention.
Traditionally, the internal
maxillary artery was
accessed
transantrally
through a Caldwell-Luc
approach.24
The posterior sinus wall is
removed, and the posterior
periosteum opened. The
internal maxillary artery
and 3 of its terminal
branches (i.e., sphenopalatine, descending palatine,
pharyngeal) are elevated
and clipped. The posterior
sinus wall is then packed
with gelfoam, and the
Caldwell-Luc incision is
closed.
Transoral and transnasal
endoscopic approaches
have been described.
The transoral approach is
useful in patients with
midface trauma, hypoplastic antra, or maxillary
tumours.25
The buccinator space
entered through a gingivobuccal incision. The
buccal fat pad is removed,
and the attachment of the
temporalis muscle to the
coronoid process is identified next. This process
facilitates the identification of the internal maxillary artery which is
clipped. This procedure
has a higher failure rate
because the site of ligation
is more proximal than in
the transantral approach.
The endoscopic method
requires high skills with
endoscopes and endoscopic instruments. A large
middle meatal antrostomy
is made to expose the posterior sinus wall. The middle turbinate can be resected partially to ensure adequate exposure. The
remaining steps are similar to the traditional
transantral approach.
3. Endoscopic sphenopalatine artery ligation (ESAL)
Guidelines to the management of epistaxis
or transnasal endoscopic
sphenopalatine artery ligation (TESPAL)
Endoscopic technique also
can be used to ligate the
sphenopalatine artery at
its exit from the sphenopalatine foramen, results
are good and abundantly
reported in the literature.26-30
An incision is made just
dorsally to the posterior
attachment of the middle
turbinate. The mucosal
flap is elevated to reveal
the sphenopalatine artery,
which is clipped and ligated.
A recurrent bleed rate of
3/10 was found, which is
higher than previously
published results, in a
study
published
by
Rockey and Anand.31
4. Ethmoid artery ligation
If bleedings occur high in
the nasal vault, consider
ligation of the anterior
and/or posterior ethmoid
arteries. These arteries are
approached through an
external ethmoidectomy
incision. The anterior ethmoid artery usually is
found 22 mm (range, 1629 mm) from the anterior
lacrimal crest. If clipping
the artery does not stop the
bleeding, then the posterior ethmoid artery may be
ligated. This artery is
found approximately 12
mm posterior to its anterior counterpart. It should
be clipped, not cauterized,
because it is only 4-7 mm
anterior to the optic nerve.
A description of an endoscopic, intranasal tech-
37
nique for ligation of the
anterior ethmoid artery in
a single case report was
made by Woolford and
Jones.32
4. Embolization / Interventional
radiology
Bleeding from the external
carotid system may be treated with embolization, either
as a primary modality in poor
surgical candidates or as a
second-line treatment in
those for whom surgery has
failed.33-35
Preembolization angiography is performed to check for
the presence of any unsafe
communications between the
internal and external carotid
systems. Selective embolization of the internal maxillary
artery and sometimes the
facial artery may be performed. Ligature of the internal maxillary artery and
selective
percutaneous
embolization gave similar
results in a study performed
by Romagnoli et al. among
203 patients.36
Superselective embolization
with gelatin sponge for
intractable epistaxis report
no complication in 37
patients with a success rate
of 94.6% after 7 days ,
remaining stables after 21
months.37
Postprocedure angiography
can be used to evaluate the
degree of occlusion. The
most common reason for
failure is continued bleeding
from the ethmoid arteries. As
the anterior ethmoid arteries
arise from the ophthalmic
which itself comes from the
internal carotid, they must
not be embolized.
The disadvantages of arteriography and embolization
are the expense and the small - risk of a stroke (CVA
is quoted as 1 in 100) even
among skilled and long
trained radiology teams. For
the most part angiography
and
embolization
are
reserved for very sick individuals and for whom
surgery is an unsafe option.
Embolization works best in
active bleeding as one can
see which artery is involved.
5. Treatment of hereditary
hemorrhagic telangiectasia
(HHT)38
Treatment of this disease is
palliative because the underlying defect is not curable.
Options include coagulation
with potassium-titanyl-phosphate (KTP) or neodymium:yttrium-aluminum-garnet (Nd:YAG) lasers39,40
septodermoplasty, embolization, nasal closure, and/or
estrogen-progesterone therapy. Topical estrogens combined with argon plasma
coagulation in the management of epistaxis in HHT
significantly prolong the
hemorrhage-free interval.41
We find also a single case
report of an intractable epistaxis secondary to HHT successfully controlled by the
application of fibrin glue.
Further studies are needed.42
In some very difficult cases,
nasal obliteration (Young’s
procedure)43
has been proposed, with
more recently a variant
through a nasal obturator.44
Systemic estrogen-progesterone at doses used for oral
contraception may eliminate
38
B. Bertrand et al.
bleeding in symptomatic
HHT. Tamoxifen has been
successfully used in two
cases.45
6. Sequential management
The therapeutic escalation
has been discussed by
Simmen and Heinz in a
review of 335 hospitalized
patients. Their conclusions
can be summarized as follows: i) first, localization of
bleeding and bipolar cautery
have to be performed, ii) if
they not succeed, Merocel®
pack, iii) if rebleeding, there
is the time for operating theater and general anaestesia
for an endoscopic control
and/or balloon and, iv) if failure again, embolization, ligation, endonasal obliteration
can take place.46
6. Compared cost-effectiveness
A retrospective review of
Nationwide Inpatient Sample in
the USA (1998-2000) was published recently by Goddard and
Reiter.47
A total of 9778 admissions with
admitting diagnosis “epistaxis”
were identified. Among admissions involving 1 treatment,
454 (9.6%) received arterial ligation, 94 (2.0%) embolization,
and 4188 (88.4%) nasal packing. There were no differences
in length of stay, transfusions,
complications,
or
deaths
between groups. Mean total
hospital charges were USD
6282 for the packing group,
USD 12805 for the ligation
group, and USD 17517 for the
embolization group; differences
between ligation and packing
groups, and embolization and
packing groups are statistically
significant. They concluded
that nasal packing is associated
with lower hospital charges and
similar complication rates as
arterial ligation or embolization. And they conclude also
that further studies are needed
to quantify other outcome
measures, such as recurrence
rates and patient quality of
life.
In the treatment of recurrent
posterior epistaxis ESAL was
compared to conventional packing by Moshaver et al.48
The overall calculated cost of
patients undergoing ESAL was
CAD 5133 compared with
CAD 12213 in the conservative
group, resulting in an average
saving of CAD 7080 per
patient. There was overwhelming patient satisfaction with
ESAL compared with nasal
packings.
At comparing endoscopic ligation to embolization Miller et
al.49 demonstrated that the mean
total charge was USD 14088 for
embolization and USD 7561 for
transnasal endoscopic sphenopalatine artery ligation (TESPAL).
7. Patient self cares
Nose picking is a contributing
factor in epistaxis. Adults can
usually be instructed to be more
careful. Children pick their
nose at night and this is best
controlled by placing a glove or
sock over their hands so that
they can not pick their nose any
longer.
Patients should avoid hot and
spicy foods and drink plenty of
fluids and strenuous activities,
hot showers, and digital trauma.
Nasal saline spray can be liberally used. Digital pressure and
ice packs are to be used as
needed for minor recurrences.
Dry climates predispose to
recurrent nose bleeds. Daily or
twice daily application of
vasolinated ointment provides
substantial benefit.
8. Medications
Pharmacotherapy plays only a
supportive role in treating the
patient with epistaxis.
See Table 1 for details on use,
doses, safety and level of proof.
Let us cite:
Adrenochromazone
(Adrenoxyl‚)50-52
Etamsylate (Dycinone‚)53
Terlipressin (Glypressine‚)
Vinayak et al found a statistically significant benefit compared to placebo with intravenous glypressin in acute epistaxis where no localized point
was found and in place of a
form of nasal packing.54
In an other study, although 50%
of epistaxis with not clearly
localized lesions did stop bleeding, there was no significant
difference in effect with placebo.55
Tranexamic acid (Exacyl‚)
Oral tranexamic acid is of no
proven value as an adjunct in
the treatment of epistaxis in
patients requiring hospital
admission concerning severe
rebleeds. But the gel seemed to
have a beneficial effect.56,57
9. Complications of treaments
1. Cautery
Synechia, septal perforation
2. Anterior packing
Synechia,
rhinosinusitis,
toxic shock syndrome,
eustachian tube dysfunction
3. Posterior packing
Synechia,
rhinosinusitis,
toxic shock syndrome, eustachian tube dysfunction, dysphagia, scarring of nasal ala
and columella, hypoventilation, sudden death
Guidelines to the management of epistaxis
4. Transantral internal maxillary artery ligation
Anaestetic risks, rhinosinusitis, oroantral fistula, infraorbital numbness, dental injury
5. Transoral internal maxillary
artery ligation
Anaestetic risks, cheek
numbness, trismus, tongue
paresthesia
6. Anterior/posterior ethmoid
artery ligation
Anaestetic risks, rhinosinusitis, lacrimal duct injury, telecanthus
7. Embolization
Facial pain, trismus, facial
paralysis, skin necrosis,
stroke, hematoma
10. Prognosis
The prognosis is good but
variable. With adequate supportive care and control of
underlying medical problems,
most patients may not experience any rebleeding. Others
may have minor recurrences
that resolve spontaneously or
with minimal self-treatment.
A small percentage of patients
may require repacking or
more aggressive treatments.
Patient with Osler-WeberRendu disease tends to have
multiple recurrences regardless of the treatment modality.
Factors predicting rebleeding
are age, prior hypertension,
anticoagulant use, vital signs,
type of posterior packing
(gauze or balloon), prior
severe posterior epistaxis and
pack removal within 48 hours
after admission.58
At a first sight rebleeding is
not driven by whether the
treatment was surgical or not.
The rebleeding rate was 33%
after embolization, 33% after
endoscopic cautery and 20%
39
Table 2
Short guide to interrpret PT and PTT results
PT
PTT
Long
Normal Liver disease or vitamin K deficiency
Long
Lupus anticoagulant
Acquired factor VIII inhibitor
Long
DIC, liver disease
Normal
Long
Normal
Acquired Disorder
Congenital Disorder
Normal Thrombocytopenia, qualitative
platelet disorder
after ligation in a study by
Barlow et al.59
11. Patient education
Use nasal saline spray
Avoid hard nose blowing or
sneezing
Sneeze with the mouth open
Do not use nasal digital
manipulation
Avoid hot and spicy foods
Avoid taking hot showers
Avoid aspirin and other
NSAIDs, avoid local nasal
sprays of corticosteroids for a
while when possible
Self treatment for minor epistaxis: firm digital pressure on
the nasal pyramid for 5-10
minutes, use of an ice pack
12. Lab studies
Lab tests to evaluate the
patient’s condition and underlying medical problems may
be ordered depending on the
clinical picture at the time of
presentation.
If the bleeding is minor and
not recurrent, then a lab evaluation may not be needed.
If bleeding is recurrent or
severe, studies to evaluate the
fluid status, coagulation profiles, and relevant systemic
diseases are needed. These
may include a complete blood
count (including platelet
Factor VII deficiency
Factor VIII (hemophilia A), IX
(hemophilia B), or XI deficiency
Fibrinogen, prothrombin, factor
V or X deficiency
Mild factor deficiency, mild von
Willebrandt disease, factor XIII
deficiency
count), prothrombin time,
activated partial thromboplastin time, and a chemistry panel
(including liver function
tests).Other more specialized
studies, such as bleeding time
and various assays for coagulation factors and platelet
function, may be considered if
warranted.
These tests are to be performed in the absence of anticoagulant therapy but when
bleeding suggests a coagulopathy. When results are out
of range it could be suggested
to address to a hematologist
for further advices, investigations and treatments (See
Table 2).
a) Prothrombin time (PT)
When increased, deficiencies of the “extrinsic” and
“common” factors prothrombin, fibrinogen, V,
VII, or X are suspected.
b) Partial thromboplastin
time (PTT)
When increased, deficiencies of the “intrinsic” and
“common” factors prothrombin, fibrinogen, V,
VIII, IX, X, or XI are suspected. Deficiencies of the
“contact” factors XII,
Fletcher, or Fitzgerald fac-
40
B. Bertrand et al.
tors also prolong the PTT
but are not associated with
bleedings.
13. Imaging studies
CT scanning and/or MRI may
be indicated to evaluate the
surgical anatomy and to determine the presence and extent
of rhinosinusitis, foreign bodies, benign tumours and neoplasms.
Medico-legal pitfalls
1. Failure to recognize the severity
of the bleeding, especially in
patients with posterior epistaxis
in whom most of the blood may
be swallowed.
2. Failure to diagnose serious etiologies (e.g., neoplasm, aneurysm, systemic coagulopathies).
3. Failure to prescribe antibiotic
therapy to prevent rhinosinusitis and possibly toxic shock
syndrome in patients with nasal
packing either anterior or posterior or both.
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Further readings
Anand VK. Practical Endoscopic Sinus
Surgery. McGraw-Hill, Inc., New
York; 1993.
Bailey BJ. Head & Neck Surgery – Otolaryngology. Lippincott, Philadelphia;
2001.
King HC. A Practical Guide to the
Management of Nasal and Sinus
Disorders. Thieme Medical Publishers Inc., New York; 1993.
Marks SC. Nasal and Sinus Surgery.
Saunders, Philadelphia; 2000.
Navarro JAC. The Nasal Cavity and
Paranasal Sinuses. Springer-Verlag,
Berlin; 2001.
Abelson TI: Epistaxis. In: Schaefer SD,
ed. Rhinology and Sinus Disease.
1st ed. Mosby, New York; 1998:4350.
Emanuel JM: Epistaxis. In: Cummings
CW, ed. Otolaryngology-Head and
Neck Surgery. 3rd ed. Mosby, St.
Louis; 1998:852-865.
McQueen CT, DiRuggiero DC, Campbell
JP, Shockley WW. Orbital osteology:
a study of the surgical landmarks.
Laryngoscope. 1995;105:783-788.
Prof. Bernard BERTRAND
ENT and HNS Dept.
Cliniques universitaires UCL de MontGodinne
avenue Thérasse, 1, B-5530 Yvoir,
Belgium.
E-mail: [email protected]
42
B. Bertrand et al.
CME questions
1. The sphenopalatine artery enters the nose through the sphenopalatine foramen which is situated :
A - 10 mm dorsally to a theoretical line drawn between both the posterior attachments of the superior and
middle turbinates
B - 10 mm dorsally to a theoretical line drawn between both the posterior attachments of the inferior and
middle turbinates
C - 30 mm dorsally to a theoretical line drawn between both the posterior attachments of the inferior and
middle turbinates
D - 2 mm – 9 mm anterior to the optic canal
E - on the lower third of the septal cartilage
2. Hereditary hemorrhagic telangiectasia is characterized by … except one
A
B
C
D
E
- autosomal dominant disease
- formation of telangiectasia and arteriovenous malformation
- high incidence of angiofibroma
- a lack of elastic or muscular tissue in the vessel
- multisystemic involvment
3. Endoscopic sphenopalatin artery ligation can be performed … except one
A
B
C
D
- for posterior epistaxis
- to ligate sphenopalatine artery
- to ligate ethmoid anterior artery
- after a mucosal incision on a line just posterior to the posterior attachments of the middle and lower
turbinates
E - under general anaestesia
4. Nasal packings require
A
B
C
D
E
- antihypertensive agents
- thrombine
- tranexamic acid
- mupirocin
- oral antibiotherapy
5. A 12 year old boy complaints of nasal obstruction and epistaxis. The demographics and symptoms are
most typical of :
A - Choanal polyp
B - Cystic fibrosis
C - Juvenile nasal angiofibroma
D - Nasopharyngeal sarcoma
E - Osler-Weber-Rendu disease
6. To determine which patients will have coagulopathy associated with epistaxis, the most complete and
cost-effective method is :
A - CBC, platelet count, and bleeding time
B - platelet count
C - bleeding time
Guidelines to the management of epistaxis
43
D - history, prothrombin time and partial thromboplastin time
E - careful history
7. Which one of the following arteries must not be embolized when treating epistaxis ?
A
B
C
D
E
- Anterior ethmoid artery
- Sphenopalatine artery
- Internal maxillary artery
- Facial artery
- Descending palatine artery
8. Which one of the followings signals the presence of a traumatic aneurysm ?
A
B
C
D
E
- Severe anterior epistaxis
- Facial trauma
- Fever and vomiting
- Delayed epistaxis
- Out of range results for PTT
9. In case of recurrent epistaxis PT normal and PTT long do not suggest one of the following coagulopathies
A
B
C
D
E
- Acquired factor VIII inhibitor
- Factor VIII deficiency (hemophilia A)
- Factor IX deficiency (hemophilia B)
- Factor XI deficiency
- Factor VII deficiency
10. Which one of these medical adjuntive therapies is granted of a Ia level of proof ?
A
B
C
D
E
- Adrenochromazone
- Etamsylate
- Terlipressin
- Tranexamic acid
- None of the above
.
Answers: 1B; 2C; 3C; 4E; 5C; 6D; 7A; 8D; 9E; 10E
Cardiovasc Intervent Radiol (2014) 37:26–36
DOI 10.1007/s00270-013-0776-y
REVIEW
Radiological Diagnosis and Management of Epistaxis
Antonı́n Krajina • Viktor Chrobok
Received: 24 October 2012 / Accepted: 4 October 2013 / Published online: 15 November 2013
Ó The Author(s) 2013. This article is published with open access at Springerlink.com
Abstract The majority of episodes of spontaneous posterior epistaxis treated with embolisation are idiopathic in
nature. The angiographic findings are typically normal.
Specific angiographic signs are rare and may include the
following: a tumour blush, telangiectasia, aneurysm, and/or
extravasation. Selective internal carotid artery (ICA)
angiography may show rare causes of epistaxis, such as
traumatic or mycotic aneurysms, which require different
treatment approaches. Complete bilateral selective external
and internal carotid angiograms are essential to evaluation.
The images should be analysed for detection of central
retinal blush in the external carotid artery (ECA) and
anastomoses between the branches of the ECA and ICA.
Monocular blindness and stroke are two of the most severe
complications. Embolisation aims to decrease flow to the
bleeding nasal mucosa while avoiding necrosis of the nasal
skin and palate mucosa. Embolisation is routinely performed with a microcatheter positioned in the internal
maxillary artery distal to the origin of the meningeal
arteries. A guiding catheter should be placed in the proximal portion of the ECA to avoid vasospasm. Embolisation
with microparticles is halted when the peripheral branches
of the sphenopalatine artery are occluded. The use of coils
A. Krajina (&)
Department of Radiology, University Hospital Hradec Kralove
and Medical Faculty of Charles University,
500 05 Hradec Kralove, Czech Republic
e-mail: [email protected]
V. Chrobok
Department of Otorhinolaryngology and Head and Neck
Surgery, University Hospital Hradec Kralove and Medical
Faculty of Charles University, 500 05 Hradec Kralove,
Czech Republic
e-mail: [email protected]
123
is not recommended because recurrent epistaxis may occur
due to proximal embolization; moreover, the option of
repeat distal embolisation is lost. The success rate of embolisation therapy (accounting for late recurrence of
bleeding) varies between 71 and 94 %. Results from
endoscopic surgery are quite comparable. When epistaxis
is refractory to nasal packing or endoscopic surgery, embolisation is the treatment of choice in some centres.
Keywords Posterior epistaxis Selective
percutaneous embolisation Endovascular
intervention
Introduction
Haemorrhage from the nose is formally referred to as
‘‘epistaxis.’’ Haemostasis within the nose can be compromised by mucosal abnormalities, vessel pathology, or
coagulation disorders. The aetiology of epistaxis is divided
into groups: local and systemic factors. Local factors
include the following: trauma, local inflammatory reactions, foreign bodies, postsurgical anatomical deformities,
intranasal tumours, chemical inhalants, nasal-prong oxygen
administration, and continuous positive airway pressure
therapy for obstructive sleep apnoea. Systemic causes of
epistaxis include the following: vascular disorders, especially hereditary haemorrhagic telangiectasia (HHT); blood
dyscrasias; hematologic malignancies; and drugs affecting
the normal clotting mechanism. Epistaxis arising from the
anterior septal area (anterior epistaxis) is more common in
children and young adults; it is the most common type of
epistaxis and is more often venous in origin. This condition
is usually responsive to treatment because it is readily
accessible for nasal packing if bleeding does not resolve
A. Krajina, V. Chrobok: Radiological Diagnosis and Management of Epistaxis
spontaneously [1, 2]. Therefore, endovascular therapy is
usually not indicated for anterior epistaxis.
Approximately 5 % of epistaxis episodes arise from the
posterior and superior portions of the nasal cavity, and the
majority of posterior epistaxis episodes arise from the
arteries of the septum. Posterior epistaxis is more common
in older patients than in children [3] The most common
factors associated with posterior epistaxis are hypertension
[4, 5], acetylsalicylic acid or nonsteroidal anti-inflammatory drug use [6], previous episodes of epistaxis, alcohol
use, and anticoagulant use. However, the majority of these
cases are idiopathic [7]. Refractory epistaxis is defined as
recurrent or persistent bleeding after appropriate packing or
multiple episodes of epistaxis during a short period of time,
each requiring medical attention. Embolisation for intractable epistaxis was first reported as an alternative to surgery
and other methods by Sokoloff [8].
Nonendovascular Therapy for Epistaxis
The management of epistaxis should begin with general
measures, including calming the patient (with sedatives if
necessary), application of a cold compress to the nape of the
neck, decreasing the blood pressure if the patient is hypertensive, fluid resuscitation, and correction of any underlying
coagulopathy. Local measures include the following: various methods of bleeding control, such as local application
of haemostatic agents, infiltration of the bleeding area with
vasoconstrictive agents, and cautery. Anterior nasal packing
is performed by positioning strips of ointment-saturated
gauze so as to produce satisfactory pressure on the bleeding
mucosa. Posterior nasal packing is an option if anterior
packing is insufficient to stop the haemorrhage or if the
bleeding originates posteriorly. Posterior nasal packing
requires general anaesthesia. A balloon catheter is inflated
in the nasopharynx to stop the flow of blood posteriorly, and
the anterior part of the nasal cavity is packed. The catheter
coming out of the nose is fixed in place [3, 9].The patient
should be monitored because posterior nasal packing can
lead to nasal trauma, vasovagal reaction, and infection.
Traditional gauze packing or balloon devices may be left in
the nasal cavity for B48 h to prevent such complications.
The success rate of posterior packing is reported to be
between 48 and 83 %. Subsequent therapy can include
either surgical endonasal coagulation or ligation [10]. An
endoscopic approach has been used for direct electrocauterisation of the active bleeding site and endoscopic ligation
of the sphenopalatine and ethmoidal arteries [11]. Surgical
intervention is clearly indicated in anterior ethmoid bleeding because the ethmoidal arteries arise from the ophthalmic artery, the embolisation of which is generally
considered to be dangerous.
27
Endovascular Therapy of Epistaxis
Relevant Anatomy
Detailed knowledge of the arterial anatomy of this region is
important for safe and successful treatment. Stroke and
blindness are two of the most severe complications. When
retinal opacification from branches of the external carotid
artery (ECA) is identified, embolisation must not be performed, and the patient should be referred for surgical
treatment [12–15].
The arterial branches involved in epistaxis include the
following: the internal maxillary artery (IMA), the facial
artery, and the ophthalmic artery (Fig. 1). The other
branches of the ECA are rarely involved.
The IMA is divided into three parts based on its relationship to the external pterygoid muscle [16, 17]
(Table 1). The proximal portion is referred to as the
‘‘mandibular portion’’ and originates behind the neck of the
mandible. The second, or pterygoid, portion is in contact
with the external pterygoid muscle and varies in its location
in relationship to this muscle. It is most commonly located
superficial to the external pterygoid muscle, although in
one third of cases, it is deep to this muscle. The middle
meningeal artery arises in front of the inferior alveolar
artery in the superficial variant and behind the inferior
alveolar artery in the deep variant. The third, or pterygopalatine, portion is the terminal portion of the IMA, creating a loop within the pterygopalatine fossa. This vessel is
the target for endovascular therapy in the treatment of
posterior epistaxis (Table 2) (Fig. 2).
The sphenopalatine artery, which is the branch of the
third part of the IMA, leaves the pterygopalatine fossa by
way of the sphenopalatine foramen [18] (Fig. 3). This
artery is the major arterial supply to the nasal fossa and
enters this fossa posteriorly to the superior meatus. Its
lateral nasal branches supply the nasal turbinates, and the
medial branches supply the nasal septum [19].
The descending palatine artery, another branch of the
pterygopalatine portion of the IMA, supplies the nasal
fossa. This artery courses through the pterygopalatine canal
and emerges from the palatine foramen. It outlines the
posterior wall and floor of the maxillary antrum. The terminal branch enters the incisive foramen and supplies the
inferior nasal septum. Here, the branch anastomoses with
the medial nasal branches of the sphenopalatine artery. The
infraorbital artery enters the orbit through the infraorbital
fissure and runs through the infraorbital foramen. Its
branches supply the cheek, lower eyelid, and upper lip, and
nose. This artery does not supply the nasal mucosa.
The ophthalmic artery gives rise to a collateral network
with the sphenopalatine artery by way of the anterior and
posterior ethmoidal branches. These arteries pass through
123
28
A. Krajina, V. Chrobok: Radiological Diagnosis and Management of Epistaxis
Fig. 1 Schematic arterial
supply of the sinonasal cavity.
The majority of the posterior
epistaxis episodes arise from the
septum. The arterial branches
involved in epistaxis include the
internal maxillary artery, the
facial artery, and the ophthalmic
artery (Courtesy of V.
Machova)
Table 1 Branches of the maxillary artery (modified according Allen
et al. [16])
Table 2 Distribution of the third (pterygopalatine) portion of the
maxillary artery (modified according Allen et al. [16])
I. First (mandibular) portion
Direction
a. Anterior tympanic
b. Deep auricular
c. Middle meningeala
d. Accessory meningeala
e. Inferior alveolar
II. Second (pterygoid) portion
a. Deep temporal
Branch
Route of exit
Lateral
Posterior superior alveolar
Pterygomaxillary fissure
Anterior
Infraorbital
Inferior orbital fissure
Inferior
Greater palatine
Pterygopalatine canal
Medial
Sphenopalatine
Sphenopalatine foramen
Posterior
Artery of foramen rotundum
Foramen rotundum
Artery of pterygoid canal
Pterygoid canal
Pharyngeal
Palatinovaginal canal
b. Pterygoid
c. Masseteric
d. Buccal
III. Third (pterygopalatine) portion
a. Posterior superior alveolar
b. Infraorbital
c. Greater (descending) palatineb
d. Artery to foramen rotunduma
e. Artery of pterygoid canal (vidian artery)a
f. Pharyngeal
g. Sphenopalatineb
a
Dangerous arteries for embolisation. The pterygoid artery and
Vidian artery are considered to be two different branches by Lasjaunias et al. [20]
b
These arteries are targets for embolisation
123
the cribriform plate of the ethmoid. The superior labial
artery, a small branch of the facial artery, contributes to the
arterial supply of the nasal septum. This branch is not
regularly visible on angiographic studies.
The facial artery is in hemodynamic balance with the
other branches of the ECA. The preferred arterial supply is
established in accordance with local hemodynamic needs
[20]. This situation means that the direction of blood flow
through anastomoses among the facial, internal maxillary,
and ophthalmic arteries depends on the force and rate of
injection, proximal vasospasm, and pre-existing occlusion
due to ligation or embolisation [15] (Fig. 4).
A. Krajina, V. Chrobok: Radiological Diagnosis and Management of Epistaxis
Fig. 2 A External carotid angiogram of a patient with HHT and
multiple episodes of severe epistaxis. The target artery for embolisation is the sphenopalatine artery (double black arrows) and the
terminal portion of the facial artery (double white arrows). A
microcatheter for embolisation should be placed distal to the middle
meningeal artery (small black arrowhead) and accessory meningeal
artery (small white arrowhead). B Selective internal maxillary
angiogram showing the position of a microcatheter (large white
arrow). There are separate mucosal hypervascular areas caused by
telangiectasias (small black arrows). C Selective facial angiogram
that shows the supply to the nasal cavity
29
Fig. 3 A Angiographic anatomy of the distal internal maxillary
artery. The descending palatine artery (black arrows) outlines the
posterior wall and floor of the maxillary antrum. The infraorbital
artery (double white arrows) enters the orbit through the infraorbital
fissure. B Selective distal internal maxillary artery angiogram in a
lateral view. C Completion angiogram after embolisation with
microparticles (Courtesy of J. J. Vitek)
123
30
A. Krajina, V. Chrobok: Radiological Diagnosis and Management of Epistaxis
whether general anaesthesia is required for the procedure.
General anaesthesia is routinely used only in children,
noncompliant patients, and patients having uncontrolled
epistaxis with possible compromise of the airway. The
majority of embolisation procedures can be performed with
intravenous sedation and analgesia with standard monitoring of blood pressure, electrocardiogram, and pulse
oxymetry. Nasal packing, which is radiopaque, should
be avoided in patients who might be candidates for
embolotherapy.
Underlying Coagulopathy
The presence of any underlying coagulopathy should be
evaluated because embolisation with polyvinylalcohol
(PVA) microparticles is more effective in patients with
normal platelet and plasma protein functions [22].
A proposed protocol for anticoagulants and epistaxis is
as follows [1, 23]:
1.
2.
3.
Fig. 4 A Internal carotid angiogram in a patient with recurrent
epistaxis. There is a rich collateral supply to the nasal cavity from the
ophthalmic artery (arrows). B The cause of such a collateral pathway
is previous proximal embolisation of the internal maxillary artery
using coils (arrow) (Courtesy of Dr. M. Vavrova)
Some investigators state that a venous plexus, called
Woodruff’s plexus, is a common source of bleeding in
cases of posterior epistaxis. This plexus is located in the
posterior part of the inferior meatus and around the choanae [21].
Endovascular Therapy for Idiopathic Posterior
Epistaxis
Preprocedure Preparation
Computed tomography (CT) or magnetic resonance imaging is not typically indicated for the investigation of epistaxis unless tumour or other local diseases are suspected
as an underlying cause. Idiopathic epistaxis is classified
after exclusion of local or systemic causes. The interventional radiologist should be aware of the laterality of the
nose bleed, the current severity of bleeding, and the
patient’s history. These factors are crucial in deciding
123
Obtain full blood count, platelet count, and
international normalised ratio (INR)
Patients with metallic heart valves on warfarin should
be kept only on a therapeutic level of INR. A
cardiologist should be contacted if life-threatening
bleeding occurs
Patients with coronary stents treated with
acetylsalicylic acid or other antiplatelet therapy
should be discussed with a cardiologist for possible
platelet transfusion in cases of life-threatening epistaxis
Angiography and Embolisation
Complete selective external and internal carotid angiograms are essential to evaluation. Angiograms should be
analysed for the detection for arterial variants and anastomoses between branches originating from the external
carotid and internal carotid arteries [14, 15]. Standard
catheterisation of the common carotid artery (CCA) is
performed. Depending on the type of the aortic arch, various diagnostic and guiding catheters are selected. The
most frequently used are vertebral, Berenstein, Davis,
Simmons, or Vitek catheters. A 5F or 6F guide catheter
permits angiography while a microcatheter is in the target
artery. A standard continual pressure flush with heparinised
normal saline must be used to prevent the backflow of
blood into the guiding catheter.
The first injection of 7–10 ml of iodinated contrast
medium into the CCA is performed using the posterioanterior and lateral views. The angiogram should show any
potential arterial pathology at the common carotid artery
bifurcation, including atherosclerotic plaque or occlusion
of the internal carotid artery (ICA) (Table 3). Because the
A. Krajina, V. Chrobok: Radiological Diagnosis and Management of Epistaxis
31
Table 3 Angiographic and embolisation protocol in epistaxis
A. The ICA angiogram
1. Start on the side of epistaxis (if identified)
2. Check the carotid bifurcation for stenosis or occlusion
3. Look for central retinae blush, ophthalmic retina feeders to the
nasal mucosa
4. Exclude source of epistaxis from the ICA
B. The ECA angiogram
1. Position the guide catheter with its tip just within the ECA to
avoid vasospasm
2. Exclude filling of the ophthalmic artery (retinae blush on
lateral view)
3. Exclude collaterals to the ICA
4. Show any arterial pathology as a source of bleeding
C. Embolisation of the IMA
1. Place microcatheter into the pterygopalatine portion of the
IMA sufficiently distal to the accessory or middle meningeal
arteries, preferably distal to the infraorbital artery
Fig. 5 External carotid angiogram showing the supply of the retina
(arrows)
2. Perform flow-directed embolisation with PVA particles
(250–500 lm) in nondiluted contrast agent using a 1-ml syringe
the lateral view (Figs. 4B, 5). Most commonly, supply of
the ophthalmic artery from the ECA branches occurs due to
collateralisation observed in chronic ICA stenosis or
occlusion. The terminal branches of the pterygopalatine
segment are best seen in frontal views.
Microparticle embolisation is performed using a standard
free-flow technique. A wedged position of the microcatheter
should be avoided (Fig. 3B). Ideally, the capillary bed of the
nasal cavity is slowly saturated with embolic microparticles.
This goal is accomplished using fluoroscopic guidance in the
lateral view to assess blood flow velocity in the artery,
potential backflow, and reflux of the embolic agent
(Fig. 3C). During embolisation, the operator should perform
selective angiograms, the quality of which enables not only
assessment of occlusion progress but also the potential filling
of collaterals. The tip of a microcatheter is placed into the
IMA distal to the origin of the middle meningeal and
accessory meningeal artery due to the anastomoses with the
ICA (Fig. 2A) In addition to the medial and lateral branches
of the sphenopalatine artery, it is also desirable to embolise
the descending palatine artery (Fig. 3A). This artery originates distal to the infraorbital artery (Fig. 3A). Reflux of
embolic particles into the infraorbital artery is generally
considered to be safe. The penetration of microparticles into
the middle deep temporal artery may cause pain and trismus
after embolisation. The embolic microparticles are mixed
with nondiluted contrast medium to achieve the best visibility during injection using a 1-ml syringe. The mixture
should not be too concentrated and must be continually
mixed because the PVA microparticles have a tendency to
sediment and occlude the microcatheter. Spherical microparticles make a more stable mixture. Spherical microparticles can penetrate deeper into arteries than PVA
microparticles of the same size. Particles should lodge distal
enough to control haemorrhage and yet proximal enough to
3. Avoid reflux and coil embolisation
D. Perform contralateral ICA and ECA angiograms as well as
IMA embolisation
E. Remove the nasal packing and check the nasal pathway for
bleeding; if no bleeding appears for 15 min, remove the
microcatheter and perform a completion ECA angiogram
F. Perform embolisation of the ipsilateral facial artery with the
microcatheter placed as distally as possible (at least distal to the
submandibular part of the facial artery) using 250- to 350-lm
PVA particles if significant contribution to the nasal mucosa is
angiographically visible
majority of posterior epistaxis episodes treated by embolisation are idiopathic, angiographic findings in these cases
may be normal. Specific angiographic signs are rare and
may include the following: tumour blush, telangiectasia,
traumatic pseudoaneurysm, and even contrast extravasation. Selective ICA angiography may show other sources of
epistaxis, such as mycotic or traumatic aneurysm [12, 13].
Arterial vasospasm is an undesired but common consequence of forceful manipulation, particularly manipulation
with the tip of the guiding catheter in the proximal part of the
ECA or microwire manipulation in the branches of the ECA.
The presence of proximal vasospasm impairing the arterial
flow in the access artery can alter the hemodynamic pattern
of the arterial feeders in the target area, thus rendering embolisation impossible. Vasodilators may be administered
intra-arterially to treat or prevent vasospasm [24, 25].
A microcatheter that will allow the use of microparticles
B500 lm in diameter is placed coaxially in the pterygopalatine segment of the IMA, and angiography is performed to determine if there are any large anastomoses
involving the ICA or ophthalmic artery. The most useful
projection to evaluate the ECA, IMA, and retinal blush is
123
32
A. Krajina, V. Chrobok: Radiological Diagnosis and Management of Epistaxis
preserve the distal supply of the terminal alar artery, which
supplies the skin of the nose. The PVA microparticles
200–500 lm in size are usually selected. It is useful to talk to
the patient if he or she is awake to show any ischaemic
neurological deficit as soon as possible. In the sleeping
patient, we must rely on anatomical angiographic studies and
a thorough knowledge of the anatomy [26].
Embolisation is halted when the peripheral branches of
the sphenopalatine segment are not opacified and the
arterial tree seems to be debranched (Fig. 3C). The amount
of microparticles required varies. Special care must be
taken as soon as the flow begins to slow because even small
additional amounts of microparticles may result in unexpected arterial stasis or even reflux.
The strategy for embolisation in patients with idiopathic
epistaxis relies on the identification of the side of bleeding
and the collateral pathways involving the contralateral IMA
and the ipsilateral facial artery (Fig. 2C). The distribution of
embolised arteries varies significantly in published series.
The bilateral IMAs together with the ipsilateral facial artery
were embolised in 27–48 %, the bilateral IMAs in 15–35 %,
and the unilateral IMA in 13–70 % of cases. The bilateral
IMAs are embolised if the side of haemorrhage is unknown
or bilateral IMAs and ipsilateral facial artery if the side of
haemorrhage is known. There also exist published case
reports describing embolisation of the ascending pharyngeal
and accessory meningeal supply to the nasal fossa for the
management of epistaxis [27–29].
Nasal Packing Removal
Two different strategies regarding nasal packing removal
have been reported in the literature. Some operators
remove the packs while the catheters are still in the arteries,
check the nasal pathway for bleeding, and finish the procedure if the nasal pathway remains dry for 15 min. Persistent bleeding influences the decision to embolise the
contralateral IMA or the ipsilateral facial artery [30]. Other
practitioners leave the packs in place to facilitate the synergistic effects of external compression and devascularisation. Nasal packing removal is influenced by the duration
of its placement, the severity and intractability of the epistaxis, and occasionally by the time of day the procedure is
performed. Care must be taken to prevent the aspiration of
pooled blood into the respiratory tract.
Clinical Success
The primary success rates of epistaxis embolization therapy range from 71 to 95 % in the literature (Table 4). The
success rate is influenced by the embolisation protocol
used. Embolisation of the bilateral distal IMAs and ipsilateral distal facial artery with 200-lm PVA microparticles
123
significantly decreases short-term failure rates and carries a
very low risk for ischemic complications. The rate of early
recurrence decreases with embolisation of more arteries
[22]. Patients taking oral anticoagulants or antiplatelet
medication are noted to have greater rate of early rebleeding than patients not taking these medications [22].
Failures of embolisation therapy to control epistaxis are
due to dominant ICA supply by way of the anterior and/or
posterior ethmoid arteries. This arterial supply requires
external surgical ligation. Late rebleeds are dependent on
the underlying pathology and are more frequent with HHT.
Often these patients are included in studies involving idiopathic epistaxis [30].
Surgical Versus Endovascular Therapy
The decision between surgery and embolisation should be
based on the individual patient’s comorbidities, the anatomical setting, and the availability of adequate interventional radiology [11]. There are retrospective studies
available comparing IMA ligation (with or without ethmoid artery ligation) [11] with PVA embolisation of the
bilateral IMAs and ipsilateral facial artery [31] for the
treatment of refractory epistaxis. The embolised arteries
were not specified in one of those studies [11]. The success
rates for IMA ligation and embolisation were 89 and 94 %,
respectively [31]. The other study reported success rates of
73 and 79 %, respectively [11]. The investigators in both
studies concluded that complication and failure rates of
IMA ligation and embolisation were comparable. However,
although the major complication rates were not significantly different between the two therapies, the complications associated with embolisation were more serious than
those associated with IMA ligation.
The advantages of PVA embolisation include the use of
local anaesthesia; pretreatment angiogram, which may
show less common causes of epistaxis; distal embolisation;
and shorter hospitalisation times. Embolisation is indicated
in patients with cardiovascular instability. However, embolisation is available only in specialised centres. Furthermore, if bleeding originates from the ethmoid arteries,
embolisation by way of the ophthalmic artery is considered
to be hazardous. Ophthalmic artery embolisation should be
avoided, even in cases of long-standing blindness in the
ipsilateral eye, because retinal necrosis may lead to autoimmune retinal inflammation and loss of vision in the
contralateral eye [15]. In the presence of dangerous collaterals, the embolisation material must be exchanged for
microcoils, which results in a more proximal and less
effective embolisation or referral for surgical treatment.
Surgical ligation of the IMA with or without anterior ethmoid artery ligation seems to be the more common technique and requires general anaesthesia in all cases.
A. Krajina, V. Chrobok: Radiological Diagnosis and Management of Epistaxis
33
Table 4 Review of studies on posterior epistaxis treated with embolisation
First author
(reference)
Yeara
Vı́tek [30]
1991
30
62
34
Elden [32]
1994
97
53
Elahi [57]
1995
57
53.1
Tseng [7]
1998
112
Moreau [58]
1998
45
48.8
Leppanen [59]
1999
37
Oguni [60]
Andersen [33]
2000
2005
Christensen [61]
Sadri [34]
No. of
patients
Mean age
(year)
Embolic material
for ECA branches
Immediate clinical
success (%)b
Severe
complications (%)c
GS
87
3.3 hemiparesis
108
PVA
88
2 stroke, skin slough
54
PVA
91
6 stroke
PVA, GS
91
0.9 stroke
46
PVA
95
4
53
38
PVA, coils
89
0
37
22
57.3
59
40
30
GS
PVA, spheres
95
87
0
5 nose necrosis
2005
70
59.1
70
PVA, GS, coils
87
1 stroke
2006
14
57
15
PVA
71
7 nose necrosis, palate necrosis
Fukutsuji [62]
2008
22
56.8
23
GS, coils
77.3
0
Strach [35]
2011
48
58.7
53
PVA, coils
93.5
4 nose necrosis, hemiparesis
Gottumukkala [56]
2013
84
63.8
85
PVA
89
1
55
No. of
procedures
114
GS = gelatin sponge
a
The table includes studies with selective embolisation using microcatheters
b
The overall clinical success also depended on the proportions of patients with HHT
c
Definitions of severe stroke were variable
Complications
Embolisation should decrease flow to the bleeding nasal
mucosa while avoiding necrosis of the nasal skin or palate
mucosa. Skin necrosis requires plastic surgical repair [32–
35]. Smaller particles (45–150 lm) carry a greater risk of
collateral tissue ischemia, including ischemia of the vasa
nervorum [36].
The most frequent causes of neurologic deficit and
blindness [37] after embolisation in the ECA territory are
reflux of emboli due to vasospasm, nonselective injection,
injection of excessive particles at an excessive rate, and
failure to recognise dangerous anastomoses due to incomplete angiograms and inadequate analysis [27, 38].
Minor complications include postembolisation ischemic
syndrome, which typically lasts for a short time and
requires only symptomatic therapy. Acute ischemic sialadenitis has been reported after reflux of microparticles
into the proximal branches of the facial artery [39].
Management of Angiographically Proven Causes
of Epistaxis
Traumatic Epistaxis
The clinical presentation of traumatic epistaxis is lifethreatening haemorrhage at the time of trauma [40]. CT
imaging is indicated in all cases of suspected arterial epistaxis. Angiogram may show focal active extravasation,
pseudoaneurysm [41], or arterial pseudo-occlusion. The
embolisation technique for these cases differs from that for
idiopathic epistaxis. The tip of the microcatheter must be as
close as possible to the arterial pathology. In the case of
possibly dangerous collaterals, microcoils are preferred.
The most common sources of bleeding are the sphenopalatine and facial arteries. In a significant number of cases,
bilateral extravasation is present [42].
When trauma or infection [43] of the ICA arterial wall
results in pseudoaneurysm formation, the patient can present
with delayed epistaxis. This pseudoaneurysm should be
expected in the cervical, petrous, or cavernous portions of the
ICA [44]. Arterial injuries during craniofacial surgery are
uncommon but have been well described [45–48].
Juvenile Nasopharyngeal Angiofibroma and Other
Tumours
Juvenile nasopharyngeal angiofibroma (JNA) is a benign
hypervascular tumour that occurs in young males between
8 and 23 years of age. Symptoms are related to the size and
direction of spread. These symptoms may include recurrent
epistaxis (observed in 59 % of cases), which may be lifethreatening. The lesion originates from the posterolateral
wall of the nasal cavity in close proximity to the superior
aspect of the middle sphenopalatine foramen, the attachment site of the posterior part of the middle turbinate.
The systematic angiographic protocol for JNA begins
with injection in the contralateral CCA followed by
injections in the ICA ipsilateral common and internal
123
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A. Krajina, V. Chrobok: Radiological Diagnosis and Management of Epistaxis
carotid arteries. Next, ipsilateral external carotid angiography for evaluation of the maxillary and ascending pharyngeal arteries is performed. The maxillary, accessory
meningeal, ascending pharyngeal, and ascending palatine
arteries are most commonly embolised vessels. If the
tumour crosses the midline, additional embolisation of the
appropriate contralateral feeders is performed.
In cases with extensive tumour spread, the supply from
the ICA branches may be embolised if possible, especially if
the ICA must be sacrificed before surgery. Neurologic deficit is the most feared complication of preoperative embolisation. Blindness, in particular, is of major concern as a
result of involvement of the ethmoidal blood supply [38].
Since the introduction of embolisation of JNA by Roberson [49], several studies have been published proving the
benefit of preoperative embolisation by decreasing blood
loss and operative times. Other sinonasal neoplasms that
can cause life-threatening epistaxis include nasopharyngeal
carcinoma and hemangiopericytoma [13].
Epistaxis in HHT
HHT, a hereditary disease, is associated with skin and
mucosal telangiectasias and arteriovenous shunts most
commonly involving the lung, brain, and liver. It is easily
recognised in individuals displaying the classic triad of
epistaxis, telangiectasia, and a relevant family history [50].
Epistaxis is caused by spontaneous bleeding from telangiectasias of the nasal mucosa (Fig. 2B). Recurrent
epistaxis begins by the age of 10–21 years and the severity
of the episodes increases with age [51].
Among numerous local and surgical treatments, transcatheter embolotherapy has been used with the intent of
decreasing the number and severity of epistaxis episodes.
Microparticle embolisation should decrease flow to the
nasal mucosa, but care must be taken to leave the proximal
arteries patent. Embolisation with coils should be avoided
because the artery cannot be made again accessible distal
to the proximal occlusion in recurrent epistaxis. Preventive
embolisation is considered to have a questionable longterm effect [32, 52].
Conclusion
Ninety five per cent of all epistaxis episodes have their origin
in the anterior septum and are easily controlled with local
endonasal therapy using anterior packing if bleeding does
not resolve spontaneously. Posterior epistaxis represents
5 % of cases and is more difficult to treat. The placement of
posterior nasal packs may predispose patients toward vasovagal reaction, infection, and significant discomfort [53–56].
123
Endoscopic ligation or electrocauterisation of the sphenopalatine and anterior ethmoidal arteries is a routine technique
for local control of active bleeding. Embolisation of the
distal branches of the bilateral IMAs and ipsilateral distal
branches of the facial artery is the preferred therapy in
patients with poor cardiovascular status because this procedure can be performed with the patient under local anaesthesia in a majority of cases [22]. Embolisation is also used in
the treatment of epistaxis refractory to previous endonasal or
surgical therapy, including IMA ligation. Rare but major
complications of embolisation therapy are mainly due to the
penetration of embolic material into the intracranial and
ophthalmic arteries. Embolisation therapy is relatively contraindicated when the bleeding originates mainly from the
ethmoid branches of the ophthalmic artery or in the presence
of anastomoses between the ECA and the ICA. In our
experience, close collaboration between the otorhinolaryngologist and the interventional radiologist provides the best
chance of controlling posterior epistaxis.
Conflict of interest Antonı́n Krajina and Viktor Chrobok have no
conflicts of interest.
Open Access This article is distributed under the terms of the
Creative Commons Attribution License which permits any use, distribution, and reproduction in any medium, provided the original
author(s) and the source are credited.
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37. Ashwin PT, Mirza S, Ajithkumar N, Tsaloumas MD (2007) Iatrogenic central retinal artery occlusion during treatment for epistaxis. Br J Ophthalmol 91(1):122–123
38. Lasjaunias P (1980) Nasopharyngeal angiofibromas: hazards of
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39. Duncan IC, Spiro FI, van Staden D (2004) Acute ischemic sialadenitis following facial artery embolization. Cardiovasc Interv
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41. Kurata A, Kitahara T, Miyasaka Y, Ohwada T, Yada, Kan S
(1993) Superselective embolisation for severe traumatic epistaxis
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Braz J Otorhinolaryngol.
2013;79(1):59-64.
DOI: 10.5935/1808-8694.20130011
original article
BJORL
.org
Surgical treatment of severe epistaxis: an eleven-year experience
Paulo Saraceni Neto1, Leonardo Mendes Acatauassu Nunes2, Luis Carlos Gregório3, Rodrigo de Paula Santos4,
Eduardo Macoto Kosugi5
Keywords:
epistaxis;
natural orifice
endoscopic surgery;
otorhinolaryngologic
surgical procedures.
Abstract
E
pistaxis is one of the most prevalent emergencies in ENT practice, and its surgical treatment is
part of the routine at services for emergency care, especially in cases refractory to clinical procedures.
Objective: To analyze the profile of patients and the results this service has had in the surgical
treatment of epistaxis for the last 11 years.
Method: Data from 98 patients submitted to surgery for epistaxis between 2000 and 2011 were
analyzed retrospectively.
Results: Most in the sample were males, and mean age was around 46 years. Hypertension was
identified in 58% of patients, and most events occurred during fall and winter. The re-bleeding rate
was 13.27%.
Conclusion: This study concluded that the surgical treatment for epistaxis, when indicated, had
good success rates and low incidence of complications. In our service, it remains as the gold-standard
procedure for nosebleeds refractory to initial management measures.
1
ENT at UNIFESP-EPM (Fellow in Rhinology at UNIFESP-EPM).
ENT at UNIFESP-EPM (Assistant Physician in the Rhinology Sector at UNIFESP-EPM).
3
PhD in Medicine from UNIFESP-EPM (Head of the Department of ENT & HNS at UNIFESP-EPM).
4
PhD in Sciences from UNIFESP-EPM (Head of the Rhinology Sector at UNIFESP-EPM).
5
PhD in Sciences from UNIFESP-EPM (Coordinator of the Rhinology Fellowship and Lead Preceptor in the ENT Medical Residency at UNIFESP-EPM).
Division of Rhinology, Department of Otorhinolaryngology and Head and Neck Surgery UNIFESP.
Send correspondence to: Eduardo Macoto Kosugi. Rua Prof. João de Oliveira Torres, nº 416. Jd. Anália Franco. São Paulo - SP. Brazil. CEP: 03337-010.
Tel: (11) 2671-5883. E-mail: [email protected]
Paper submitted to the BJORL-SGP (Publishing Management System - Brazilian Journal of Otorhinolaryngology) on August 18, 2012;
and accepted on November 4, 2012. cod. 10394.
2
Brazilian Journal of Otorhinolaryngology 79 (1) January/February 2013
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59
INTRODUCTION
Epistaxis is one of the most frequent emergencies
in ENT care. The prevalence rate of this potentially risky
occurrence in the general population is of approximately
12%1. However, only 10% of the patients with epistaxis
seek medical care, and the initial measures taken to treat
these subjects usually suffice in handling nosebleeds.
Among such measures are: keeping the airways patent,
attaining hemodynamic stability, and packing the nose - an
effective procedure in most cases, but unlike many think,
a method that introduces considerable risk of morbidity2.
Yet, approximately 1% of the patients require surgical
intervention to manage epistaxis3,4.
Several procedures to treat epistaxis refractory to
clinical management have been described in the literature,
such as irrigation with warm water, chemical and electrical
cauterization of the nasal mucosa, arterial embolization,
open and endoscopic artery ligation surgery5-7. The ligation
of the distal arterial branches has been performed more
recently to prevent direct and antegrade circulation of the
carotid system that irrigates the nasal cavity and known
to have plenty anastomoses. Consequence, the ligation
of the maxillary or external carotid artery have been less
used due to reduced efficacy and increased morbidity6,8.
The vessels most frequently ligated to that end are the
sphenopalatine and anterior ethmoidal arteries.
The sphenopalatine artery ligation procedure was
first described by Prades in 1970 through microsurgery.
Only in 1992, with the development and refinement of
nasal endoscopic surgery, did Budrovich & Saetti report
the use of an endoscope to perform the procedure8. The
anterior ethmoidal artery ligation technique is older. It was
described in 1946 by Weddell, and was performed through
external access via Lynch incision3. Potential consequences
of the external access approach such as scars, edema, and
facial ecchymosis led to the study and development of
endoscopic techniques to approach this artery4.
This study aimed to present data from the ENT
Residency Program regarding the surgical management
of severe epistaxis performed between June 2000 and
June 2011.
were no exclusion criteria. This study was approved by
the institution’s Research Ethics Committee and given
permit 87081.
The patients seen for epistaxis at our service were
submitted to the initial emergency protocol, which included airway and respiratory care, along with hemodynamic stabilization procedures. Then, they were offered
specific care for epistaxis such as suction of clots and
administration of topical vasoconstrictors to identify the
sites of bleeding and elect the best course of therapy
among the options of chemical cauterization with 70%
trichloroacetic acid and anterior or anteroposterior nose
packing. The patients submitted to surgery were the
ones who still bled in spite of the nose packing, who
bled soon after nose packing removal, and those submitted to anteroposterior nose packing without clinical
contraindication for surgery.
Surgery was carried out with the patients under
general anesthesia by third-year medical residents supervised by medical doctors from the Rhinology Sector or
attending physicians from the ENT emergency care unit.
Ligation and/or cauterization of the sphenopalatine artery branches was carried out by transnasal endoscopy.
Cauterization of the anterior ethmoidal artery was preferentially performed through the external approach
(Lynch incision) with the aid of an endoscope, and
occasionally by transnasal endoscopy. In our service
we approach the sphenopalatine artery or the sphenopalatine and anterior ethmoidal arteries, depending on
the site of bleeding.
The following data were considered in the definition of the profile of our patients: age, gender, and
present comorbidities. Bleeding-related characteristics
were also considered, such as side, possible etiology, admission blood tests (hemoglobin, hematocrit,
and platelet count), and need for blood transfusion.
The following were considered in regards to surgery:
date of the procedure, approached artery, number of
approached branches of the sphenopalatine artery,
time of surgery, complications, surgery effectiveness,
and failure. The seasonality of cases of severe epistaxis
was also analyzed.
METHOD
RESULTS
This retrospective longitudinal study included the
review of the medical charts of patients seen at the ENT
emergency care unit for severe epistaxis and treated
surgically between June 2000 and June 2011. Severe
epistaxis was defined as a life-threatening episode of
nasal bleeding, usually of posterior origin, requiring
immediate anteroposterior nose packing to attain hemodynamic stability9,10. All patients treated endoscopically
for severe epistaxis through sphenopalatine and/or
anterior ethmoidal artery ligation were included. There
The charts of 109 patients submitted to surgery
for severe epistaxis between June 2000 and June 2011
were included. Seven charts were excluded for lack of
information and another four subjects submitted to nose
packing under general anesthesia were not included. The
characteristics of the patients enrolled in the study are
shown on Table 1.
The characteristics related to bleeding can be seen
on Table 2.
Brazilian Journal of Otorhinolaryngology 79 (1) January/February 2013
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60
Table 1. Characteristics of enrolled patients.
Data
Unit
Age
Years
Gender
Comorbidities
Table 3. Blood transfusion characteristics.
Value
Data
Unit
Hemoglobin
g/dL
Mean
46.68
Mean
11.42
SD
15.28
SD
2.75
Minimum
13
Minimum
5.6
Median
48
Median
11.1
Female
28 (28.57)
SD
8.2
SHT
57 (58.16)
Minimum
12.2
Chronic alcohol abuse
10 (10.2)
Median
33.05
DM
7 (7.14)
Maximum
49.5
Chronic use of ASA
5 (5.1)
Mean
241.779,41
120.787,32
Hematocrit
%
Platelet count
N/mL
Liver disease
4 (4.08)
SD
CKD
3 (3.06)
Minimum
42.000
NHL
2 (2.04)
Median
228.500
Arrhythmia
2 (2.04)
Hypothyroidism
2 (2.04)
Heart disease
1 (1.02)
1 (1.02)
Maximum
972.000
Blood transfusion
N (%)
Yes
21 (21.43)
No
77 (78.57)
Transfusion patients
PRBC units
Mean
2.81
N: number; %: percentage; SD: standard deviation; SHT: systemic
hypertension; DM: diabetes mellitus; ASA: acetylsalicylic acid; CKD:
chronic kidney disease; NHL: non-Hodgkin’s lymphoma.
Table 2. Features of epistaxis.
N (%)
Location
Etiology
N (%)
N (%)
33.82
70 (71.43)
Thrombocytosis
Side
16.3
Mean
81
Male
N (%)
Unit
Maximum
Maximum
N (%)
Data
Value
SD
1.12
Minimum
2
Median
2
Maximum
6
N: number; %: percentage; SD: standard deviation; PRBC: packed
red blood cells.
Value
Right
48 (48.98)
Left
35 (35.71)
Bilateral
15 (15.31)
Data
Anterior
14 (14.29)
Approached arteries
Table 4. Characteristics of initial surgical approach.
Values N (%)
Posterior
35 (35.71)
Sphenopalatine 1 branch
93 (86.11)
Not identified
49 (50)
Sphenopalatine 2 branches
7 (6.47)
Undefined
64 (65.31)
Sphenopalatine 3 branches
1 (0.95)
Hypertensive peak
19 (19.39)
Anterior Ethmoidal
7 (6.47)
Nose surgery FU
5 (5.1)
Total
108 (100)
Trauma
5 (5.1)
Operated patients
Coagulopathy
4 (4.08)
Success
85 (86.73)
Nasal tumor
2 (2.04)
Failure
13 (13.27)
Rendu-Osler-Weber
1 (1.02)
Total
98 (100)
N: number; %: percentage; FU: follow-up.
N: number; %: percentage.
Blood test and transfusion data can be verified on
Table 3.
The 98 patients enrolled in the study underwent surgery under general anesthesia, and had solely their sphenopalatine arteries or their sphenopalatine and anterior ethmoidal
arteries approached, on one or both sides. Some patients
had more than one artery approached. The data on the first
procedure the patients underwent can be seen on Table 4.
Epistaxis was successfully managed in 85 cases
(86.73%). Six (46.15%) of the 13 patients with failed surgery
bled within 24 hours of surgery. Table 5 shows what was
done for the 13 patients whose first procedures failed.
In the 13 patients with failed first surgery, only one
branch of the sphenopalatine artery was found. More anterior ethmoidal artery ligations were indicated after the
failure of the first procedure (eight of the nine re-operated
Brazilian Journal of Otorhinolaryngology 79 (1) January/February 2013
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61
Table 5. Conduct in failed surgery.
Conduct
N (%)
Nose packing
4 (30.77)
Sphenopalatine Revision
1 (7.69)
Anterior ethmoidal + Sphenopalatine Revision
8 (61.54)
Total
13 (100)
N: number; %: percentage.
patients) than as a first procedure (seven of 98 operated
patients). Indication of anterior ethmoidal artery surgery
was significantly higher in reoperations, as seen on Table 6.
Graph 2. Distribution of surgical procedures per season.
Table 6. Anterior ethmoidal artery.
Time of surgery
N (%)
Initial approach
7 (46.67)
Approach after failure
8 (53.33)
Total
15 (100)
Four complications (4.08%) were recorded. Two
(2.04%) related to surgery (septum perforation and amaurosis), one (1.02%) to anesthesia (death by acute myocardial
infarction during anesthesia recovery), and one (1.02%) to
hospitalization (hospital-acquired pneumonia).
N: number; %: percentage.
DISCUSSION
Hospitalization and surgery times are shown on
Table 7.
The ninety-eight surgical patients enrolled in this
study represent a significant series when compared to
other papers in the literature2,3,6,11,12. Patients with severe
epistaxis are usually between the third and eighth decade
of life, and the most numerous age group comprehends
subjects in their seventies and eighties2,3,6,8. The mean age
of the subjects in our study was lower (46 years), probably a reflection of the fact that endoscopic surgery was
offered to all patients with anteroposterior nose packing,
and not only to cases in which surgery failed. There is a
slight predominance of males in studies on epistaxis1-3,5.
In our study, males prevailed by a ratio of 2.5:1.
The side of bleeding has been recently discussed,
and a predilection for right epistaxis - albeit without
statistical significance - was observed in a group of 326
patients11. Our study presented similar results, as 48.98%
of the patients had right nasal fossa involvement (n = 48),
35.71% had left nosebleeds (n = 35), and 15,.31% had
bilateral epistaxis (n = 15). In terms of the site of bleeding - anterior, posterior, or diffuse - the charts revealed
that posterior bleeds were more frequent, with 35.71%
(n = 35), against 14.29% (n = 14) of anterior nosebleeds.
The remaining 50% did not have defined bleed sites or
were described as ‘diffuse’. Most nosebleeds are known
to occur in anterior sites associated with Kiesselbach’s
plexus and account for approximately 85% of all cases1,11,
but our study indicated a preponderant role of posterior
bleeds in severe epistaxis.
The etiology of severe epistaxis cannot be defined
for all cases. There is confusion between predisposing and
aggravating factors, and they do not necessarily establish
a causal link to bleeding, which adds to the difficulty
of comparing this study to others8,11. Clear nosebleed
Table 7. Length of hospitalization and surgery.
Duration
Hospitalization (days)
Surgery (minutes)
Value
Mean
3.38
SD
4.53
Minimum
1
Median
2
Maximum
41
Mode
2
Mean
113.48
SD
44.31
Minimum
20
Median
110
Maximum
250
SD: standard deviation.
The distribution of procedures and months in which
they were performed can be seen on Graphs 1 and 2.
Graph 1. Distribution of surgical procedures per month.
Brazilian Journal of Otorhinolaryngology 79 (1) January/February 2013
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62
etiology is established for only 15% of the subjects, and
idiopathic cases are more prevalent8. In our study, etiology
was defined in 34.69% (n = 34) of the cases of epistaxis.
The diagnoses included: hypertensive peaks (19.39%),
bleeds following recent nose and paranasal sinus surgery
(5.1%), trauma (5.1%), coagulopathy (4.08%), nasal tumors
(2.04%), and hereditary hemorrhagic telangiectasia (1.02%).
The treatment for severe epistaxis of known etiology must
include, whenever possible, solutions for the cause of the
problem; for example, the management of hypertensive
peaks and reversal of coagulopathy13. Coagulopathy has
been traditionally seen as a contraindication to surgery,
but the ligation or cauterization of the branches of the
sphenopalatine artery have provided for satisfactory results
in these cases9. In epistaxis caused by nasal tumors, the
role of arterial ligation alone is more limited. Treatment of
such cases usually involves the resection of the tumor that
originated the nosebleed, in addition to artery ligation13.
Artery ligation is not the main option to treat hereditary
hemorrhagic telangiectasia, and was used in one of our
patients solely because of severe epistaxis, and not for the
underlying condition.
The most prevalent comorbidity found in the
studied population was systemic hypertension, seen in
58.16% of the patients (n = 57), as similarly reported by
other authors3,8. Despite the difficulties establishing a causal
correlation between systemic hypertension and epistaxis and even more so severe epistaxis - it is important to stress
that the prevalence rate seen in the studied population
was considerably higher than the rates observed in the
Brazilian population, which range around an estimated
20%14. Other aggravating factors and conditions related
to nosebleeds include diabetes mellitus, chronic alcohol
abuse accompanied or not by alcoholic liver disease,
smoking, heart arrhythmias, tumors, use of antiplatelet
drugs, anticoagulants, and illicit drugs such as cocaine.
These factors have also been cited by other authors in
varying degrees of relevance, although never at the same
level of importance as systemic hypertension1,2,11.
This study also assessed the hemodynamic impact of
surgical cases of epistaxis. In some cases, this information
was essential for surgical indication. It should be noted
that the top platelet count seen in our study due to a case
of thrombocytosis without clinical repercussions pulled
up the mean value of this variable. The variation of blood
test results observed in this study was similar to previous
reports in the literature6,12. Low platelet count has been
considered an isolated risk factor for early rebleed in patients submitted to epistaxis surgery1, but our study failed
to reproduce such finding. The literature also indicates
that 50% of the patients with epistaxis submitted to surgery
require blood transfusion1,6,12, whereas in our study only
21.4% of the patients (n = 21) needed transfusion. A mean
2.8 units of packed red blood cells were administered to
patients requiring transfusion.
The number of arterial branches in the sphenopalatine foramen has also been a topic of controversy. A
study done on cadavers submitted to nasal endoscopy
showed that 67.21% of the nasal fossae had one arterial
trunk leaving the sphenopalatine foramen, 21.31% had
two branches, and 11.47% had three15. In our study, one
branch in the sphenopalatine foramen was seen in 86.11%
of the nasal fossae. The difference against the literature
may be explained by the greater difficulty dissecting the
sphenopalatine foramen during surgery in live patients
than in fresh cadavers.
Success rates were quite good, and rebleeds were
seen in 13.27% (n = 13) of the patients. Most patients in this
situation (n = 8) were reoperated and had the hemostasis
of the sphenopalatine artery territory revised and the anterior ethmoidal artery (AEA) ligated. All rebleeds had one
branch of the sphenopalatine artery identified. A study by
Holzmann showed similar results, as higher rebleed rates
were seen in cases in which only the lateral branches of
the sphenopalatine artery were occluded2. This data supports the need to thoroughly explore the sphenopalatine
foramen, in an active search for all branches arising from
it. Holzmann also reported increased success rates when
dissection and occlusion of the septal branches of this
vessel were performed. Rebleeds occurring in those cases
can be accounted for by the antegrade flow that occurs
mainly in the septal territory, an area with many anastomoses between different arterial systems2.
AEA ligation to manage epistaxis is still controversial. Although many authors believe that this vessel
should be approached in the first procedure along with the
sphenopalatine artery and its branches, most papers show
this technique being used to manage rebleed cases2,16. The
improvement of the techniques used to endoscopically
approach the AEA may facilitate the indication of AEA
ligation as the procedure of choice. The approach in use
today includes external access using the Lynch incision
which, aside from a scar, may leave other complications
such as facial edema and epiphora - possibly the reasons
why surgeons are no longer opting to indicate this procedure initially4.
Time of hospitalization in the revision cases shows
that, in addition to being effective, surgery does not lead
to prolonged hospital stays. The mean hospital stay length
was three days, as also reported in the literature8,16. The
mean time of hospitalization was overestimated in our
study, as one patient with complications had to stay in for
41 days. The mode, however, was two days of hospitalization. Surgery mean length was one hour and 53 minutes.
The influence of weather conditions in the incidence of epistaxis has been analyzed by a number of
authors17,18. However, controversy and contradicting results
still abound. In our sample, more cases were seen in the
fall and winter months. However, one cannot state that
Brazilian Journal of Otorhinolaryngology 79 (1) January/February 2013
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63
such finding is truly related to the weather. An inventory of
meteorological data for each year of the study would have
to be analyzed along with the variations in temperature
and humidity before statements of this sort could be made.
The observed complication rate of 4.08% shows
how safe the employed procedures were, mainly if one
takes into account that only half of these complications
were related to surgery. The main of them, a case of
amaurosis, may be explained by the lack of experience
of the surgeon while performing electrocoagulation in an
area too close to the nerve bundles of the orbit.
5.Novoa E, Schlegel-Wagner C. Hot water irrigation as treatment for
intractable posterior epistaxes in an out-patient setting. J Laryngol
Otol. 2012;126(1):58-60.
6. Santos RP, Leonhardt FD, Ferri RG, Gregório LC. Ligadura endoscópica
endonasal da artéria esfenopalatina para epistaxe severa. Rev Bras
Otorrinolaringol. 2002;68(4):511-4.
7.Kamani T, Shaw S, Ali A, Manjaly G, Jeffree M. Sphenopalatine-sphenopalatine anastomosis: A unique case of intractable epistaxis,
safely treated with microcatheter embolization: a case report. J Med
Case Rep. 2007;1:125.
8.Page C, Biet A, Liabeuf S, Strunski V, Fournier A. Serious spontaneous epistaxis and hypertension in hospitalized patients. Eur Arch
Otorhinolaryngol. 2011;268(12):1749-53.
9. Shah AG, Stachler RJ, Krouse JH. Endoscopic ligation of the sphenopalatine artery as a primary management of severe posterior epistaxes in
patients with coagulopathy. Ear Nose Throat J. 2005;84(5):296-7,306.
10.Barlow DW, Deleyiannis WB, Pinczower EF. Effectiveness of surgical
management of epistaxis at a tertiary care center. Laryngoscope.
1997;107(1):21-4.
11.Reiss M, Reiss G. Epistaxis: some aspects of laterality in 326 patients.
Eur Arch Otorhinolaryngol. 2012;269(3):905-9.
12.Rabelo FA, Prado VB, Valera FC, Demarco RC, Tamashiro E, Lima
WT. Surgical treatment of nasal packing refractory epistaxis. Bras J
Otorhinolaryngol. 2009;75(3):335-9.
13.Gifford TO, Orlandi RR. Epistaxis. Otolaryngol Clin North Am.
2008;41(3):525-36.
14.Passos VMA, Assis TD, Barreto SM. Hipertensão arterial no Brasil:
estimativa de prevalência a partir de estudos de base populacional.
Epidemiol Serv Saúde. 2006;(15):35-45.
15.Pádua FG, Voegels RL. Severe posterior epistaxis - endoscopic surgical
anatomy. Laryngoscope. 2008;118(1):156-61.
16.Rockey JG, Anand R. A critical audit of the surgical management of
intractable epistaxis using sphenopalatine artery ligation/diathermy.
Rhinology. 2002;40(3):147-9.
17.Rezende GL, Granjeiro RC, Furtado PL, Pinheiro GB, Nakanishi M. Is
dry climate related with hospitals admissions for epistaxis? Int Arch
Otorhinolaryngol. 2009;13(2):172-7.
18.Danielides V, Kontogiannis N, Bartzokas A, Lolis CJ, Skevas A. The
influence of meteorological factors on the frequency of epistaxis.
Clin Otolaryngol Allied Sci. 2002;27(2):84-8.
CONCLUSION
This study presented the 11 years of experience of
our service in surgically managing severe epistaxis with a
success rate of 86.73%. In our series, careful identification
of all arterial branches in the sphenopalatine foramen and
early anterior ethmoidal artery ligation were identified as
contributing factors to higher success rates.
REFERENCES
1.Nouraei SA, Maani T, Hajioff D, Saleh HA, Mackay IS. Outcome of
endoscopic sphenopalatine artery occlusion for intractable epistaxis:
a 10-year experience. Laryngoscope. 2007;117(8):1452-6.
2. Holzmann D, Kaufmann T, Pedrini P, Valavanis A. Posterior epistaxis:
endonasal exposure and occlusion of the branches of the sphenopalatine artery. Eur Arch Otorhinolaryngol. 2003;260(8):425-8.
3.Agreda B, Urpegui A, Alfonso J, Valles H. Ligadura de la artéria
esfenopalatina em la epistaxis posterior. Estudio retrospectivo de 50
pacientes. Acta Otorrinolaringol Esp. 2011;62(3):194-8.
4. Araújo Filho BC, Pinheiro-Neto CD, Ramos HF, Voegels RL, Sennes LU.
Endoscopic ligation of the anterior ethmoidal artery: a cadaver dissection study. Braz J Otorhinolaryngol. 2011;77(1):33-8.
Brazilian Journal of Otorhinolaryngology 79 (1) January/February 2013
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