Afgewerkte en gepubliceerde studieprojecten

• Sudden deafness of unknown origin: successful treatment with hyperbaric oxygen after a > 7 day treatment delay
• Sudden sensorineural deafness: treatment with hyperbaric oxygen therapy after failure of a ten day course of “classical” drug therapy

Lopende studieprojecten

• Hyperbaric Oxygen Therapy for Idiopathic Sudden Sensorineural Hearing Loss: a prospective, randomised double-blind clinical trial

SUDDEN SENSORINEURAL DEAFNESS:
TREATMENT WITH HYPERBARIC OXYGEN THERAPY AFTER FAILURE OF A TEN DAY COURSE OF “CLASSICAL” DRUG THERAPY

C. Desloovere MD, P. Germonpré MD
ENT Dept., University of Leuven, Belgium; Centre for Hyperbaric Oxygen Therapy, Military Hospital, Brussels, Belgium

Introduction

Sudden Sensorineural Hearing Loss (SSHL) has an incidence of between 5 and 20 / 100.000 per year. It can occur at any age but seems to strike more at middle age. Tinnitus and a feeling of increased pressure are often present, vertigo is less commonly associated with the syndrome. Only in approximately 20% of cases, a causal factor can be identified. This can be a viral infection, such as mumps, trauma, Ménière’s disease, acoustic neurinoma, ototoxic medication, multiple sclerosis. In the remaining 80%, no clear cause can be found.

Four possible etiologies can be hypothesised:

• vascular: since the a. labyrinthi is a terminal artery, any thrombosis or embolus of this artery would lead to a profound deafness with a poor prognosis. A less pessimistic view considers a mainly rheological disturbance, with sludge and a reduction of the partial pressures of oxygen in the inner ear (Corti’s organ). This reduction would cause the sensory cells to stop functioning, however, cell death would not occur until a critically low oxygen partial pressure is attained.
• viral: many viral infections could lead to sensorineural hearing loss. Serologic studies are difficult to obtain in a systematic way, are expensive and have a poor chance of positive outcome. Moreover, some known viral infections, such as mumps, lead to an always irreversible acoustic damage. Finally, few cases of SSHL are accompanied by signs of viral infection.
• round window rupture: in some cases, the clinical history can give arguments for a rupture of the round window (trauma to the inner ear, heavy weight lifting, intracranial pressure rise).
• auto-immune disease: some authors propose an auto-immune cause for ISSD; however, most known auto-immune syndromes leading to deafness have a slow progressive course of disease.

Spontaneous recovery occurs in approximately 65% of all patients (Weinaug, 1984). Most recoveries happen during the first 10 days. No reliable pre-therapeutic outcome predictors are available, imposing an urgent need for maximal treatment for all patients.
Prognostically negative factors have been identified:

• vertigo
• profound deafness (all frequencies)
• therapeutic delay of more than 10-14 days
• increased blood viscosity
• hypertension

There is probably no other disease for which such a variety of treatments have been proposed, and still today, many different treatment regimens, some more invasive than others, are propagated. Their therapeutic efficacy is very difficult to establish. It seems however, that the therapeutic outcome of several proposed drug treatment regimes is in the same range as the spontaneous recovery rate. This is well illustrated in several double-blind prospective studies, where no advantage over NaCl infusion could be established (Weinaug, 1984; Probst, 1992). A significant improvement vs. placebo therapy could however be observed with haemodiluton therapy in patients with an increased haematocrit (above 44%) (Desloovere et al., 1988).

Hyperbaric Oxygen Therapy (HBOT) is a minimally invasive method of rising arterial pO2 to levels of approx. 1800 mmHg. It has been shown in animals that HBOT, but not normobaric 100% oxygen breathing, could induce a rise in the perilymphatic pO2 by 500-900% (Lamm et al., 1988).

The efficacy of HBOT has not been conclusively established. A French study (Dauman et al., 1985) compared HBOT/vasodilator/corticotherapy to vasodilator/corticotherapy alone and to haemodilution therapy. Although the HBOT group scored better, the results were not significant. Another study (Pilgramm et al., 1985), comparing 37 patients, treated with haemodilution with or without HBOT, showed a similar, not significant advantage of adjutant HBOT. A disadvantage of these studies is that they initiated therapy as soon as possible after the onset of deafness, thereby including the large number of patients who would recover spontaneously, no matter how or even if treated.

Methods

During the last two years, 26 patients have been treated with Hyperbaric Oxygen Therapy (HBOT) following a strict stepwise therapeutic protocol. All patients were treated initially with high-dose intravenous steroids, associated with hypervolemic haemodilution if indicated (see below). Only upon failure of this treatment after 10 treatment days, patients were additionally treated with HBOT.

Upon admission, all patients were initially evaluated by physical examination, including blood pressure measurement, ENT examination, tonal and speech audiometry, stapedius reflex decay, and the following laboratory tests: blood cell count, haematocrit, erythrocyte sedimentation rate, creatinin, plasma viscosity, immunological tests (auto-antibodies, T4-T8 lymphocyte ratio), total cholesterol, triglycerides, glucose, lues serology. A complete vestibular evaluation, BERA, and ocular fundoscopy were obtained in the first days of hospitalisation. Cerebral NMR was obtained upon guidance of an abnormal BERA only.

Hearing loss was calculated as Mean Hearing Loss (MHL), i.e. the mean of the hearing loss over frequencies 500-1000-2000-4000 Hz.

In patients with a total haemoglobin (Hb) level of less that 14g/100ml and a haematocrit (Hct) of less than 44%, initial treatment consisted of NaCl 0.9% IV infusion, 125ml/hour, and oral intake of at least 2l of water per day. If Hb was > 14g/100ml or Hct > 44%, IV infusion was performed with hydroxy-ethyl starch (HAES-steril) 125ml/hour. If Hct was higher than 48%, an isovolemic haemodilution was performed.

This haemodilution was complemented by high-dose corticosteroid therapy (dexamethasone) if after 5 days no or insufficient amelioration was observed (hearing recovery of at least 10dB on at least 3 frequencies), according to the following protocol:

• days 1 & 2: 24 mg IV
• day 3: 16mg IV
• days 4 & 5: 8 mg IV
• day 6: 3 mg orally
• days 7 & 8: 1.5 mg orally
• days 9 & 10: 0.75 mg orally

If after 10 days of treatment, insufficient results were obtained (see criteria above), HBOT was added. Patients were then treated daily on an outpatient basis, in a multiplace chamber. Prior to initiation of HBOT, a chest X-ray, ECG and a new tonal audiometric test were obtained. HBOT was administered at a pressure of 2.5 ATA, for 90 minutes (3 periods of 25 minutes of 100% oxygen, with 5 minutes “air breaks”), for 10 days. Patients who refused HBOT, who presented a contra-indication for HBOT, or who were unable to equalise their middle ear pressure, were excluded.

Hearing recovery was calculated as “percentage hearing gain”, according to the following formula:

% (gain) = [{MHL(dB)initial - MHL(dB)final} / MHL(dB)initial ] *100

Results

26 patients completed this pilot study. The mean delay before initial treatment was 5 (± 4) days. After a mean of 11 HBOT sessions (9-30), we found a mean 43% (±23%) hearing gain, that persisted up to a 3-month follow-up. No significant side effects were noted.

Conclusions

In this group of negatively selected patients, the addition of HBOT seems to be able to obtain an important hearing gain. Because of the lack of randomised prospective studies, this preliminary uncontrolled study will now be extended and randomised versus placebo, to include a valid control group. Only after this, we feel large randomised studies with HBOT at an earlier point in the therapeutic process, with inclusion of large numbers of patients, will be possible.

References

• Dauman, R., A. Cros, and D. Poisot (1985). Traitement des surdités brusques: premiers résultats d’une étude comparative. J. Otolaryngol. 14: 49-56.
• Desloovere, C. and E. Böhmer (1992). Hyperbare Sauerstofftherapie bei therapieresistenten Hörsturzen. Eur. Arch. Oto-Rhino-Laryngol. Suppl II: 451
• Desloovere, C., E. Meyer-Breiting, and C. Von Ilberg (1988). Randomisierte Doppelblindstudie zur Hörsturztherapie: Erste Ergebnisse. HNO 36: 417-422.
• Lamm, Ch., U. Walliser, K. Schumann, and H. Lamm (1988). Sauerstoffpartialdruckmessungen in der Perilymphe der Scala tympani unter normo- und hyperbare Bedingungen. HNO 36: 363-366.
• Nagahara, K., K. Fisch, and M. Yagi (1983). Perilymph oxygenation in sudden and progressive sensorineural hearing loss. Acta Otolaryngol. 96: 57-69.
• Pilgramm, M., H. Lamm, and K. Schumann (1985). Zur hyperbaren Sauerstofftherapie beim Hörsturz. Laryng. Rhinol. Otol. 64: 351-354.
• Probst, R., K. Tschop, and E. Luden (1992). A randomised, double-blind, placebo-controlled study of dextran/pentoxyphilline medication in acute acoiustic trauma and sudden hearing loss. Acta Otolaryngol (Stockh) 112: 435
• Weinaug, P. (1984). Die Spontanremission beim Hörsturz. HNO 32: 346-351.