SUDDEN
SENSORINEURAL DEAFNESS: C. Desloovere MD, P. Germonpré MD 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, Méničre’s disease, acoustic neurinoma, ototoxic medication, multiple sclerosis. In the remaining 80%, no clear cause can be found. Four possible etiologies can be hypothesised:
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.
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:
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
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