ORIGINAL ARTICLE

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

Background: Sudden sensorineural hearing loss (SSHL)
is an acute disorder whose origin is often unclear. A vas-
cular disorder may be a causative factor.
Objective: To determine whether hypotension influ-
ences the genesis of SSHL in healthy subjects.
Design: To investigate the role of a 24-hour blood pres-
sure (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 De-
partment of Surgical and Anaesthesiological Sciences and
the Department of Internal Medicine, S. Orsola Hospi-
tal, University of Bologna, Bologna, Italy.
Patients: The study population consisted of 23 un-
treated healthy patients diagnosed as having SSHL com-
pared with 20 age- and sex-matched normotensive con-
trol subjects. Both groups underwent 24-hour BP
monitoring, and their BP profiles were analyzed and com-
pared 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 persis-
tent hypotension (the presence of .2 consecutive record-
ings 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.
Arch Otolaryngol Head Neck Surg. 2001;127:1049-1052

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.
S
UDDEN sensorineural hearing
loss (SSHL) is an acute disor-
der that affects a considerable
proportion of the adult popu-
lation of both sexes.1 Its eti-
ology is still uncertain, and many differ-
ent possibilities have been suggested,
ranging from viral infections to systemic
or local circulatory defects.2-7 As for the lat-
ter, a causative role is generally accepted
for a sudden increase in systemic blood
pressure (BP) values either in normoten-
sive patients or in subjects with arterial
hypertension in whom the sustained BP
increase could be responsible for the lo-
cal development of thrombotic and/or hem-
orrhagic complications at the site of an end
organ. From an opposite viewpoint, to fur-
ther investigate the mechanism(s) respon-
sible for the onset of SSHL, the role of sys-
temic hypotension has been considered.8-11
A preliminary report11 suggested that SSHL
is common in young subjects who fre-
quently 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 co-
chlear vascularization has been hypoth-
esized. Indeed, the routine BP values
recorded in our young adult patients com-
plaining of SSHL were significantly
(P=.005) lower when compared with those
of an age-matched control group, thus sug-
gesting the need for further and more com-
plete investigations in this field. In par-
ticular, these observations, if confirmed,
could have some important implications
for the therapeutic approach to SSHL, with
a strong limitation in the use of vasodila-
tory and antihypertensive drugs that could
further decrease the local cochlear perfu-
sion pressure and enhance the sensorial
loss, thus reducing the probability of a com-
plete functional recovery.
This study investigates the charac-
teristics of the 24-hour BP profile of young
subjects with SSHL.

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 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 Hospi-
tal of the University of Bologna, Bologna, Italy, with the di-
agnosis of SSHL, were subsequently studied. The diagnosis
of SSHL was based on the widely accepted definition of a sen-
sorineural hearing loss of 30 dB or more over at least 3 con-
tiguous audiometric frequencies occurring within 3 days or
less1 and without any other otologic cause for hearing im-
pairment. Our diagnostic protocol included a complete clini-
cal examination, including anamnesis, otoscopy, and an au-
diometric test battery. Evoked-response audiometry was
always used; when the ipsilateral pattern was absent or evoca-
tive for retrocochlear involvement, a cerebral magnetic reso-
nance image with gadolinium was obtained. In 12 patients,
the type of audiometric curve suggested performing a glyc-
erol perfusion, which proved effective in 7 (partial [5 pa-
tients] or complete [2 patients] immediate recovery). How-
ever, 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 me-
nieric hearing loss.8,12 In any case, no vestibular symptoms
were observed at follow-up in these patients.
Patients affected by arterial hypertension, diabetes (in-
sulin dependent and non–insulin dependent), and periph-
eral 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 con-
sent, 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 cardiovascu-
lar, vasoactive, and/or antiplatelet drug.
The final population examined included 23 un-
treated 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
RESULTS
The baseline characteristics of the 2 populations of pa-
tients are reported in Table 1. Average clinic and am-
bulatory BP values were significantly lower in the popu-
lation 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 cardio-
vascular disease.
Within the population of patients with SSHL, the av-
erage 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 de-
crease in SBP and DBP values between daytime and night-
time 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
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group of 20 age- and sex-matched untreated normoten-
sive control subjects (12 females and 8 males), compa-
rable for age (mean ± SD age, 34.3 ± 7.0 years; age range,
16-44 years), admitted to the Department of Internal Medi-
cine 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 pro-
tocol, which was approved by the Ethical Committee of the
University of Bologna, and informed consent was ob-
tained from each subject before inclusion in the trial.
Clinic BP measurements were obtained with a con-
ventional mercury sphygmomanometer using standard-
ized criteria13 after patients had been in the seated posi-
tion 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 au-
tomated portable commercial instrument (model 90207;
SpaceLabs Inc, Bellevue, Wash). The principles of this tech-
nique have been described elsewhere in more detail,14,15 and
the device was programmed to automatically record sys-
tolic BP (SBP) and DBP values with the cuff placed on the
nondominant arm. The monitor was programmed to mea-
sure 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 measure-
ments during sleep but to ensure adequate observations dur-
ing 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 val-
ues were obtained from each patient, and the results were
averaged to achieve a final BP profile. Separated average val-
ues were computed for daytime (6 AM-11 PM) and night-
time (11 PM-6 AM). The main statistical analysis was the
comparison between clinical and 24-hour SBP and DBP val-
ues 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.
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]), de-
spite a significant difference in baseline absolute BP val-
ues (SBP, P=.004; DBP, P=.03). This suggests the possi-
bility 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 co-
chlear damage, we analyzed the individual 24-hour BP pro-
files with the aim of identifying those subjects with persis-
tent 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 hypo-
tension 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%
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 Table 1. Baseline Characteristics of the Study Populations* Table 2. Average 24-Hour, Daytime, and Nighttime
BP Values in Male and Female Patients With SSHL*
Patients Control
With SSHL Subjects P Average BP, Women Men
Variable (n = 23) (n = 20) Value mm Hg (n = 17) (n = 6)
Age, y 36.4 ± 8.0 34.3 ± 7.0 .23 24 h
Male-female ratio 6:17 8:12 .65 SBP† 113.0 ± 10.0 122.6 ± 7.4
Clinic BP, mm Hg DBP 70.4 ± 7.7 74.8 ± 3.3
Systolic 111.9 ± 17.0 128.3 ± 8.0 .004 Daytime
Diastolic 69.1 ± 12.0 79.5 ± 5.0 .03 SBP† 116.2 ± 11.5 125.6 ± 6.4
Mean 83.3 ± 7.0 96.1 ± 6.0 .004 DBP 74.0 ± 8.0 78.0 ± 4.5
Heart rate, beats/min 77.0 ± 8.0 74.3 ± 11.0 .53 Nighttime
24-h BP, mm Hg SBP† 105.6 ± 9.1 115.3 ± 9.7
Systolic 115.5 ± 10.0 124.0 ± 6.0 .02 DBP 62.9 ± 6.9 66.8 ± 4.1
Diastolic 72.4 ± 7.0 76.9 ± 4.0 .03
Mean 86.7 ± 5.0 92.6 ± 6.0 .03 *Data are given as mean ± SD. BP indicates blood pressure; SSHL, sudden
Plasma level, mg/dL sensorineural hearing loss; SBP, systolic BP; and DBP, diastolic BP.
Total cholesterol 187.8 ± 15.0 187.0 ± 31.0 .81 †The difference between women and men was significant (P = .05).
HDL cholesterol 42.0 ± 7.0 41.5 ± 13.0 .72
Triglycerides 180.5 ± 37.0 179.0 ± 33.0 .89
Patients With SSHL (n=23)
*Data are given as mean ± SD unless otherwise indicated. SSHL indicates Control Subjects (n=20)
sudden sensorineural hearing loss; BP, blood pressure; and HDL, high-density
lipoprotein. 100
†To convert total cholesterol and HDL cholesterol from milligrams per

% of Patients With Systemic Hypotension

deciliter to millimoles per liter, multiply milligrams per deciliter by 0.02586; 90
and to convert triglycerides from milligrams per deciliter to millimoles per 80
liter, multiply milligrams per deciliter by 0.01129.
70
60

(20/23) during the nighttime, and was significantly higher 50

than that observed in the control population during the cor- 40

responding periods (daytime, 25% [5/20] [P=.03] and 30

nighttime, 35% [7/20] [P=.04]) (Figure). No differences 20
were observed between groups for any of the other vari- 10
ables known to influence the BP profile in the adult popu- 0
lation, such as sodium and potassium intake, smoking hab- Daytime Nighttime

its, physical activity, use of oral contraceptives, occupational Proportion of subjects with systemic hypotension in the patients with sudden
stress, and number of pregnancies. 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).
COMMENT

The results of the present study suggest that systemic hy-
potension must be considered as the possible cause re-
sponsible 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 re-
corded in a control population of age- and sex-matched nor-
motensive subjects. Moreover, patients with SSHL have also
shown a greater prevalence of persistent hypotension, as de-
fined 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 ob-
served between the 2 populations of patients, although
within the normal range, could bear some clinical rel-
evance. Many well-documented studies16 in the literature
support the existence of a so-called J-shaped curve relat-
ing the rate of cardiovascular complications to systemic BP
levels. In particular, a BP decrease below the range of nor-
motension (DBP, 70-75 mm Hg) has been reported to be
associated with an excessive rate of cardiovascular com-
plications, and the same mechanism could apply to the co-
chlear circulation, whose threshold level for functional dam-
age in response to BP changes is still largely unknown.
These findings could have some implications in gen-
eral practice, particularly for the clinical and pharmaco-
logical 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 jeop-
ardize the possibility of even a partial recovery of the co-
chlear function. Furthermore, the involvement of sys-
temic 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 mecha-
nisms 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

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 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 consid-
ered, the occurrence of hypotension was arbitrarily de-
fined 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. Ac-
cording 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 conserva-
tive criteria used in our study to define hypotension. The
decision to select a higher cutoff level of BP to define hy-
potension was based on the assumption that this could en-
able us to definitely understand the role of even mild sys-
temic hypotension in the development of SSHL.
Lehnhardt and Hesch17 suggested that the effects of
hypotension on cochlear function might not uniformly ap-
ply to the whole range of hearing frequencies. They re-
ported a stronger relationship between systemic hypoten-
sion 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 sub-
jects, 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 sen-
sorineural 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 be-
tween 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 hypo-
tension to the loss of cochlear function is concerned, the
present data are sufficiently in agreement with those pub-
lished by Maass8 in an animal model of hemorrhagic hy-
potension. In this experimental setting, Maass showed a
decrease in intracochlear PO2 proportional to the extent of
hypotension and associated with a marked precapillary va-
soconstriction caused by an increase in sympathetic tone.
These observations, together with those published by Hult-
crantz et al19 in the same field, clearly suggest a depen-
dence 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 en-
hanced by the reduced ability for autoregulation of the in-
ner ear circulation compared with cerebral blood flow.20
As reported before, a similar pathophysiological mecha-
nism has been hypothesized8,12 in most patients with Me-
niere disease who have a combination of systemic hypo-
tension 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 infu-
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sion were included in this series; on the other hand, an os-
motic mechanism could feasibly be responsible for periph-
eral 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 dur-
ing 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 mea-
sure to avoid further potential damage. In particular, we
suggest that 24-hour ambulatory BP monitoring be car-
ried out to identify the presence of significant hypoten-
sive episodes that could contribute to provide a reliable
explanation for the occurrence of the disease.
Accepted for publication March 19, 2001.
Corresponding author and reprints: Antonio Pirodda,
MD, Ear, Nose and Throat Section, Department of Surgi-
cal and Anaesthesiological Sciences, S. Orsola Hospital, Via
Massarenti 9, 40138 Bologna, Italy (e-mail: corlboml
@bo.nettuno.it).
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