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Systemic Hypotension and the Development of Acute Sensorineural Hearing Loss in Young Healthy Subjects
Antonio Pirodda, MD;
Gian Gaetano Ferri, MD;
Giovanni Carlo Modugno, MD;
Claudio Borghi, MD
Arch Otolaryngol Head Neck Surg. 2001;127:1049-1052.
ABSTRACT
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Background Sudden sensorineural hearing loss (SSHL) is an acute disorder whose
origin is often unclear. A vascular disorder may be a causative factor.
Objective To determine whether hypotension influences the genesis of SSHL in healthy
subjects.
Design To investigate the role of a 24-hour blood pressure (BP) profile in
a population of young subjects with SSHL from January 1, 1996, to December
31, 1999, by a nonrandomized controlled trial.
Setting The Ear, Nose and Throat Section of the Department of Surgical and Anaesthesiological
Sciences and the Department of Internal Medicine, S. Orsola Hospital, University
of Bologna, Bologna, Italy.
Patients The study population consisted of 23 untreated healthy patients diagnosed
as having SSHL compared with 20 age- and sex-matched normotensive control
subjects. Both groups underwent 24-hour BP monitoring, and their BP profiles
were analyzed and compared with routine BP values. The data were analyzed
with the Statistical Package for the Social Sciences, version 7.1, and the
results are expressed as mean ± SD.
Main Outcome Measures The mean BP values were expected to be lower in the study population.
Results The average clinic and ambulatory BP values were significantly lower
in patients with SSHL, for systolic (clinic, P =
.004; ambulatory BP, P = .02) and diastolic (clinic, P = .03; ambulatory BP, P = .03)
values. The occurrence of persistent hypotension
(the presence of >2 consecutive recordings of systolic BP of  105 mm Hg
and/or diastolic BP of 60 mm Hg) was increased in the population with
SSHL.
Conclusion Systemic hypotension must be considered as the possible cause responsible
for the development of SSHL in young healthy subjects.
INTRODUCTION
SUDDEN sensorineural hearing loss (SSHL) is an acute disorder that affects
a considerable proportion of the adult population of both sexes.1
Its etiology is still uncertain, and many different possibilities have been
suggested, ranging from viral infections to systemic or local circulatory
defects.2-7
As for the latter, a causative role is generally accepted for a sudden increase
in systemic blood pressure (BP) values either in normotensive patients or
in subjects with arterial hypertension in whom the sustained BP increase could
be responsible for the local development of thrombotic and/or hemorrhagic
complications at the site of an end organ. From an opposite viewpoint, to
further investigate the mechanism(s) responsible for the onset of SSHL, the
role of systemic hypotension has been considered.8-11
A preliminary report11 suggested that SSHL
is common in young subjects who frequently experience a complete recovery
of hearing function.7 In these patients, who
are usually completely free from the more common vascular risk factors, a
possible functional origin of SSHL11 related
to the negative hemodynamic effects of arterial hypotension over the terminal-type
cochlear vascularization has been hypothesized. Indeed, the routine BP values
recorded in our young adult patients complaining of SSHL were significantly
(P = .005) lower when compared with those of an age-matched
control group, thus suggesting the need for further and more complete investigations
in this field. In particular, these observations, if confirmed, could have
some important implications for the therapeutic approach to SSHL, with a strong
limitation in the use of vasodilatory and antihypertensive drugs that could
further decrease the local cochlear perfusion pressure and enhance the sensorial
loss, thus reducing the probability of a complete functional recovery.
This study investigates the characteristics of the 24-hour BP profile
of young subjects with SSHL.
PATIENTS AND METHODS
Forty-seven patients (30 women and 17 men) younger than 50 years (mean
± SD age, 37.10 ± 7.94 years; range, 22-49 years), admitted,
from January 1, 1996, to December 31, 1999, to the Ear, Nose and Throat Section
of the S. Orsola Hospital of the University of Bologna, Bologna, Italy, with
the diagnosis of SSHL, were subsequently studied. The diagnosis of SSHL was
based on the widely accepted definition of a sensorineural hearing loss of
30 dB or more over at least 3 contiguous audiometric frequencies occurring
within 3 days or less1 and without any other
otologic cause for hearing impairment. Our diagnostic protocol included a
complete clinical examination, including anamnesis, otoscopy, and an audiometric
test battery. Evoked-response audiometry was always used; when the ipsilateral
pattern was absent or evocative for retrocochlear involvement, a cerebral
magnetic resonance image with gadolinium was obtained. In 12 patients, the
type of audiometric curve suggested performing a glycerol perfusion, which
proved effective in 7 (partial [5 patients] or complete [2 patients] immediate
recovery). However, as in previous studies,10-11
we considered these patients to be included in our series based on the possibility
of an involvement of the same hypotensive mechanisms as in menieric hearing
loss.8, 12 In any case, no vestibular
symptoms were observed at follow-up in these patients.
Patients affected by arterial hypertension, diabetes (insulin dependent
and non–insulin dependent), and peripheral vascular disease and those
with a history of coronary or cerebrovascular accidents were excluded from
the study. We also excluded the patients unable to cooperate with the study
protocol, those who refused to give informed consent, and those showing a
poor capacity to comply with the procedures for 24-hour BP monitoring. Patients
were also excluded if they were taking any kind of cardiovascular, vasoactive,
and/or antiplatelet drug.
The final population examined included 23 untreated normotensive patients
(17 women and 6 men) whose age ranged between 22 and 49 years (mean ±
SD age, 36.4 ± 8.0 years). The study group was compared with a group
of 20 age- and sex-matched untreated normotensive control subjects (12 females
and 8 males), comparable for age (mean ± SD age, 34.3 ± 7.0
years; age range, 16-44 years), admitted to the Department of Internal Medicine
of the S. Orsola Hospital of the University of Bologna for reasons other than
cardiovascular diseases. Both groups of patients were examined according to
the same study protocol, which was approved by the Ethical Committee of the
University of Bologna, and informed consent was obtained from each subject
before inclusion in the trial.
Clinic BP measurements were obtained with a conventional mercury sphygmomanometer
using standardized criteria13 after patients
had been in the seated position for 5 minutes and again 2 minutes after patients
had assumed the standing position. The fifth Korotkoff sound was used to define
the diastolic BP (DBP).
Ambulatory BP monitoring was performed with an automated portable commercial
instrument (model 90207; SpaceLabs Inc, Bellevue, Wash). The principles of
this technique have been described elsewhere in more detail,14-15
and the device was programmed to automatically record systolic BP (SBP) and
DBP values with the cuff placed on the nondominant arm. The monitor was programmed
to measure the BP at 20-minute intervals between 6 AM and 11 PM and at 30-minute
intervals between 11 PM and 6 AM. This schedule was chosen to reduce the number
of measurements during sleep but to ensure adequate observations during the
day when the hearing loss occurs more commonly.
The data were analyzed with the Statistical Package for the Social Sciences,
version 7.1 (SPSS Inc, Chicago, Ill), and the results are expressed as mean
± SD. Hourly BP values were obtained from each patient, and the results
were averaged to achieve a final BP profile. Separated average values were
computed for daytime (6 AM-11 PM) and nighttime (11 PM-6 AM). The main statistical
analysis was the comparison between clinical and 24-hour SBP and DBP values
between the 2 groups of patients. Two-way analysis of variance was used to
compare the results of 24-hour BP monitoring in the 2 groups of patients.
The t test was used to compare the baseline clinical
characteristics of the populations.
RESULTS
The baseline characteristics of the 2 populations of patients are reported
in Table 1. Average clinic and
ambulatory BP values were significantly lower in the population with SSHL
when compared with controls for SBP and DBP values. Conversely, no significant
differences were observed between the 2 groups of patients for the other demographic
variables or risk factors for cardiovascular disease.
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Table 1. Baseline Characteristics of the Study Populations*
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Within the population of patients with SSHL, the average 24-hour daytime
and nighttime SBP and DBP values were slightly reduced in the female subgroup
(Table 2), and the difference
reached formal statistical significance for SBP values. Conversely, the extent
of the absolute decrease in SBP and DBP values between daytime and nighttime
is comparable in both sexes for SBP (-10.6 ± 4.0 mm Hg in females
vs -10.3 ± 4.0 mm Hg in males) and DBP (-11.1 ±
5.0 mm Hg in females vs -11.2 ± 4.0 mm Hg in males) values and
largely comparable with that observed in the control population for SBP and
DBP (SBP of -11.2 ± 4.0 and DBP of -11.5 ± 5.0 mm
Hg in females vs SBP of -11.6 ± 4.0 and DBP of -11.4 ±
5.0 in males [P = .44]), despite a significant difference
in baseline absolute BP values (SBP, P = .004; DBP, P = .03). This suggests the possibility that patients with
SSHL are at great risk of developing an impairment of the perfusion of the
ear vascular bed that could contribute to the development of abnormalities
of the cochlear function. To investigate the hypothesis that a relatively
short period of reduced perfusion of the inner ear could have been responsible
for transient or permanent cochlear damage, we analyzed the individual 24-hour
BP profiles with the aim of identifying those subjects with persistent hypotension, defined by the presence of more than 2 consecutive
recordings of SBP of 105 mm Hg or less and/or of DBP of 60 mm Hg or less.
This cutoff value for hypotension has been calculated by subtracting 1 SD
from the average value of nighttime BP recordings in the entire study population.
The proportion of patients who complied with such criteria was 70% (16/23)
during the daytime and 87% (20/23) during the nighttime, and was significantly
higher than that observed in the control population during the corresponding
periods (daytime, 25% [5/20] [P = .03] and nighttime,
35% [7/20] [P = .04]) (Figure 1). No differences were observed between groups for any of
the other variables known to influence the BP profile in the adult population,
such as sodium and potassium intake, smoking habits, physical activity, use
of oral contraceptives, occupational stress, and number of pregnancies.
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Table 2. Average 24-Hour, Daytime, and Nighttime BP Values in Male
and Female Patients With SSHL*
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Proportion of subjects with systemic hypotension in the patients
with sudden sensorineural hearing loss (SSHL) and in control subjects. The
differences between those with SSHL and controls were significant during the
daytime (P = .03) and the nighttime (P = .04).
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COMMENT
The results of the present study suggest that systemic hypotension must
be considered as the possible cause responsible for the development of SSHL
in young healthy subjects. Indeed, the average 24-hour BP values recorded
in our population of patients complaining of such disease were significantly
lower when compared with those recorded in a control population of age- and
sex-matched normotensive subjects. Moreover, patients with SSHL have also
shown a greater prevalence of persistent hypotension,
as defined by the presence of multiple BP readings below the cutoff value
for normotension, thus suggesting that SSHL could result from a condition
of regional hypoperfusion of the cochlear circulation in a setting of local
hemodynamic derangement. The differences in BP profile that we observed between
the 2 populations of patients, although within the normal range, could bear
some clinical relevance. Many well-documented studies16
in the literature support the existence of a so-called J-shaped curve relating
the rate of cardiovascular complications to systemic BP levels. In particular,
a BP decrease below the range of normotension (DBP, 70-75 mm Hg) has been
reported to be associated with an excessive rate of cardiovascular complications,
and the same mechanism could apply to the cochlear circulation, whose threshold
level for functional damage in response to BP changes is still largely unknown.
These findings could have some implications in general practice, particularly
for the clinical and pharmacological approaches to the problem of SSHL. In
particular, patients complaining of SSHL should be better examined in terms
of BP profile because any condition leading to a further BP decrease (even
if mostly transitory) could jeopardize the possibility of even a partial recovery
of the cochlear function. Furthermore, the involvement of systemic hypotension
in the pathophysiological features of SSHL should influence the use of drugs
during the early phases of the disease, suggesting, for instance, a limited
use of drugs with vasodilatory activity that could further impair the inner
ear perfusion.
Among the possible pathophysiological mechanisms that could be responsible
for the development of SSHL, most of the available studies2-7
have emphasized the possible causative role of abnormalities in the inner
ear circulation, while this topic has been poorly investigated in the setting
of the systemic hemodynamic profile. To our knowledge, the only study available
in the literature and carried out in this field with ambulatory BP monitoring
was published by Ross et al,9 who examined
a population of patients with SSHL of "idiopathic" origin, but they did not
consider the age of the patients and the presence of concomitant risk factors
for cardiovascular diseases. In this study, in which only 24-hour SBP values
were considered, the occurrence of hypotension was
arbitrarily defined by the presence of a single value of SBP lower than 90
mm Hg and/or by the detection of a value of SBP lower than 100 mm Hg in at
least 10% of the recordings. According to these criteria, hypotension was
observed in 25 (31%) of the 81 patients with SSHL, and this proportion was
significantly lower that that observed in the present study (>75%). The differences
observed between the 2 studies can be reasonably explained by the less conservative
criteria used in our study to define hypotension. The decision to select a
higher cutoff level of BP to define hypotension was based on the assumption
that this could enable us to definitely understand the role of even mild systemic
hypotension in the development of SSHL.
Lehnhardt and Hesch17 suggested that
the effects of hypotension on cochlear function might not uniformly apply
to the whole range of hearing frequencies. They reported a stronger relationship
between systemic hypotension and sensorineural hearing loss affecting lower
frequencies. This observation was recently confirmed,18
showing a selective loss of lower hearing frequencies in 20 young (aged <50
years) asymptomatic hypotensive subjects, free of cardiovascular complications
and enrolled among the population of a large epidemiological survey, the Brisighella
Heart Study. In this study, the presence of hypotension (casual SBP of <105
mm Hg and/or DBP of <60 mm Hg) was associated with a 35% prevalence of
sensorineural hearing loss involving low frequencies, and this proportion
was significantly higher than that observed in a control, age-matched, normotensive
population (3%) (P<.001). These data seem to confirm
the relationship between systemic hypotension and sensorineural hearing loss,
and suggest that the phenomenon can be more evident for low frequencies, thereby
providing more support for the clinical approach to the disease.
As far as the mechanistic hypothesis linking hypotension to the loss
of cochlear function is concerned, the present data are sufficiently in agreement
with those published by Maass8 in an animal
model of hemorrhagic hypotension. In this experimental setting, Maass showed
a decrease in intracochlear PO2 proportional to the extent of hypotension
and associated with a marked precapillary vasoconstriction caused by an increase
in sympathetic tone. These observations, together with those published by
Hultcrantz et al19 in the same field, clearly
suggest a dependence of the inner ear circulation on the modifications in
sympathetic tone that can be associated with a decrease in systemic BP. The
effects of hypotension can also be enhanced by the reduced ability for autoregulation
of the inner ear circulation compared with cerebral blood flow.20
As reported before, a similar pathophysiological mechanism has been hypothesized8, 12 in most patients with Meniere disease
who have a combination of systemic hypotension and a history of stress: this
could elicit a situation of exaggerated sympathetic activation involving the
inner ear circulation. This is why responders to glycerol infusion were included
in this series; on the other hand, an osmotic mechanism could feasibly be
responsible for peripheral vasodilation.
Taken together, all this evidence could have some important practical
clinical implications. First, patients presenting with SSHL should be examined
for a history of hypotension and undergo a careful BP evaluation during the
early phase of the disease. Second, in patients who prove to be hypotensive,
the use of vasoactive drugs could have some negative effects and promote relapses
that have been shown to be rather common,21
and could probably be related to a condition of hemodynamic imbalance at the
level of the inner ear circulation. Finally, patients who have had SSHL should
adopt any available preventive measure to avoid further potential damage.
In particular, we suggest that 24-hour ambulatory BP monitoring be carried
out to identify the presence of significant hypotensive episodes that could
contribute to provide a reliable explanation for the occurrence of the disease.
AUTHOR INFORMATION
Accepted for publication March 19, 2001.
Corresponding author and reprints: Antonio Pirodda, MD, Ear, Nose
and Throat Section, Department of Surgical and Anaesthesiological Sciences,
S. Orsola Hospital, Via Massarenti 9, 40138 Bologna, Italy (e-mail:
corlboml{at}bo.nettuno.it).
From the Ear, Nose and Throat Section, the Department of Surgical and
Anaesthesiological Sciences (Drs Pirodda, Ferri, and Modugno), and the Department
of Internal Medicine (Dr Borghi), S. Orsola Hospital, University of Bologna,
Bologna, Italy.
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