Download Serious spontaneous epistaxis and hypertension

Survey
yes no Was this document useful for you?
   Thank you for your participation!

* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project

Document related concepts

Hemolytic-uremic syndrome wikipedia , lookup

Transcript
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].
123
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
123
Eur Arch Otorhinolaryngol
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.
References
16.
1. Timsit CA, Bouchène K, Olfatpour B, Tsigaridis P, Herman P,
Tran Ba Huy P (2001) Etude épidémiologique et clinique portant
sur 20 563 patients accueillis à la grande garde d’urgence ORL
adulte de Paris Ile de France (Epidemiology and clinical findings
in 20, 563 patients attending the Lariboisière Hospital ENT Adult
Emergency Clinic, French). Ann Otolaryngol Chir Cervicofac
118:215–224
Klossek JM, Dufour X, de Montreuil CB, Fontanel JP, Peynègre
R, Reyt E, Rugina M, Samardzic M, Serrano E, Stoll D,
Chevillard C (2006) Epistaxis and its management: an observational pilot study carried out in 23 hospital centres in France.
Rhinology 44:151–155
Tan LK, Calhoun KH (1999) Epistaxis. Med Clin North Am
83:43–56
Kotecha B, Fowler S, Harkness P, Walmsley J, Brown P, Topham
J (1996) Management of epistaxis: a national survey. Ann R Coll
Surg Engl 78(5):444–446
Viducich RA, Blanda MP, Gerson LW (1995) Posterior epistaxis:
clinical features and acute complications. Ann Emerg Med
25:592–596
Pollice PA, Yoder MG (1997) Epistaxis: a retrospective review of
hospitalized patients. Otolaryngol Head Neck Surg 117:49–53
Mitchell JR (1959) Nose-bleeding and high blood pressure.
Br Med J 1:25–27
Charles R, Corrigan E (1977) Epistaxis and hypertension. Postgrad Med J 53:260–261
Isezuo SA, Segun-Busari S, Ezunu E, Yakubu A, Iseh K, Legbo J,
Alabi BS, Dunmade AE, Ologe FE (2008) Relationship between
epistaxis and hypertension: a study of patients seen in the
emergency units of two tertiary health institutions in Nigeria.
Niger J Clin Pract 11:379–382
Fuchs FD, Moreira LB, Pires CP, Torres FS, Furtado MV,
Moraes RS, Wiehe M, Fuchs SC, Lubianca Neto JF (2003)
Absence of association between hypertension and epistaxis: a
population-based study. Blood Press 12(3):145–148
Lubianca Neto JF, Fuchs FD, Facco SR, Gus M, Fasolo L,
Mafessoni R, Gleissner AL (1999) Is epistaxis evidence of endorgan damage in patients with hypertension? Laryngoscope.
109:1111–1115
Lubianca-Neto JF, Bredemeier M, Carvalhal EF, Arruda CA,
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
Herkner H, Laggner AN, Müllner M, Formanek M, Bur A,
Gamper G, Woisetschläger C, Hirschl MM (2000) Hypertension
in patients presenting with epistaxis. Ann Emerg Med 35:
126–130
Herkner H, Havel C, Müllner M, Gamper G, Bur A, Temmel AF,
Laggner AN, Hirschl MM (2002) Active epistaxis at ED presentation is associated with arterial hypertension. Am J Emerg
Med 20:92–95
Knopfholz J, Lima-Junior E, Précoma-Neto D, Faria-Neto JR
(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
evidence of end-organ damage in the patients with arterial
hypertension: epistaxis? Int J Cardiol 2009; doi:10.1016/j.ijcard.
2008.11.090
123