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Pathophysiologic
Aspects of Inner Ear Dysfunctions In the literature it is well documented, that irrespective of the source of damage the stria vascularis and the cells of the organ of corti in the inner ear react uniformly (4). In the cochlea histological findings are swelling and structural damage of the dendrites (5), alterations of mitochondria and the cell-structure, separation of hair-cells from tectorial membrane (6), oedema of the endothelium, oedematous closure of functional endarteries with blocking of the microcirculation. These alterations due to damage or vascular reactions limit the function. Improved oxygen supply and enhanced healing processes are seen as the solving keys for dysfunction of the inner ear. (7, 8, 9, 10). Table 2 Reactions of inner ear to noxious agents
Because of the uniform pathophysiological response of the cochlea, the therapy of inner ear dysfunctions is also uniform for sudden deafness, hearing losses, acute tinnitus and vertigo whether you prefer haemodilution, cortisone or HBO2 (see table 3). Exeptions are few diseases for which we have causal approach, for instance Ménière´s disease and autoimmunologic failures. Table 3 Therapy of inner ear disturbances
Until today it is not possible to state the reasons for the failure of inner ear malfunction in an individual. Therefore I will not discuss the large scale of pathogenetic factors. Table 4 Noxius factors causing inner ear disturbance
Experimental
results Table 5 Models for inner ear disturbances
With an increase of the partial-pressure of oxygen in the cochlea, which means in the perilymph and endolymph, it is possible to influence the sensory cells of the inner ear. These cells have no direct vascular supply and depend entirely on oxygen supply by diffusion. Only an increase in oxygen partial-pressure can compensate oxygen deficiency. With transcutaneous pO2 monitoring hyperoxygenation of the organism can be controlled. Evidence for the effect of hyperbaric oxygen is obtained by measuring microphonepotentials and summationpotentials of the auditory nerve after acoustic trauma with a significant increase in the speed of recovery. The efficiency of HBO2 against oedema, infection, reperfusion-injury etc. and to supply oxygen even to areas of poor perfusion is well established and applies also for inner ear disorders. Evaluation of a hearing loss by subjective or objective audiometry is comparatively easy to perform and the results are reproducible. That is the main reason why these parameters are used to evaluate treatment of inner ear dysfunction in the model of sudden deafness. But we have to stress the point, that for the patient vertigo and tinnitus are much more disabling than the hearing loss. These basic considerations provide our argument for the use of HBO2 in otoneurologic disorders. Literature
Survey A randomised prospective trial of primary HBO2 versus primary conservative treatment in Germany is 50% completed and shows a better outcome in the HBO2-group with substantial recovery in 80% of the patients. Another controlled prospective trial including patients after ineffective conservative treatment including cortisone shows substantial improvement in more than 30% of the cases even if the delay was more than 3 month. Another identical trial of a university department showed the same results. The evidence for HBO2 therapy for acute isolated tinnitus based on controlled trials is poor. But retrospective studies show encouraging results equal to those tinnitus-symptoms arising in combination with sudden deafness and acoustic trauma. Tinnitus as a accompanying symptom is the predominant reason for patients to search relief. Often the hearing loss is not even realised. Evaluations of 7766 patients in 13 publications show reduction of the molestation and intensity of tinnitus by 50% in around 70% of the cases (30% - 88%) if treated within 3 month of onset. Around 30% loose their tinnitus completely. Chronic tinnitus with a duration of more than 3 month or bilateral manifestation shows improvement rates of 50% in around 30% of the cases after ineffective conservative treatment. Follow ups show no change in 12 month (1). Based on 1200 cases of acoustic trauma – partially evaluated in prospective studies - Pilgramm (20) states the best results by HBO2 in combination with Haes. Because of 50% spontaneous remission within the first 48 hours, HBO2 should start immediately the third day after trauma. If hyperbaric oxygenation is begun later, the effectiveness decreases rapidly. So far we learned, that the outcome of HBO2 treatment of inner ear dysfunctin depends on the underlying disease. We have the impression that results are unsatisfying after viral otitis and head trauma. But at present our data are not sufficient to exclude some of the listed maladies from HBO2 treatment because of poor response. Own
Results A prospective controlled study was performed 1996 (2): Out of 625 patients treated for tinnitus in our clinic from Okt. 1996 to Dec 1996 211 cases with acute tinnitus were included in the study. 69 Patients were treated with haemodilution and cortisone alone and had no HBO2 142 patients had HBO2, 72 of these after unsuccessful haemodilution
These results show a better outcome for patients with acute tinnitus ( duration less than 3 month ) if they get HBO2. Especially the high rate of decompensated tinnitus from 63% chronifications ( duration more than 3 month ) after conservative therapy with the consequence of long lasting and expensive treatment with tinnitus masker, psychological based retraining procedures and often intensive behaviour therapy as in-patient treatment shows HBO2 not only as effective but also cost saving. In Germany refunding by health insurances for HBO2 treatment of sudden deafness and tinnitus is accepted by the majority of these institutions. To support this therapy from the scientific and economic aspect 5 major prospective trials are carried out in Germany at the moment – with a sixth in planning. Controlled
prospective studies randomised primary treatment HBO2, conservative treatment, no treatment The results of established, conservative but unproven medical treatment regimes for the mentioned inner ear dysfunctions are unsatisfying. Therefore it is necessary to search for new treatment options based on pathological considerations. Hyperbaric oxygen has beneficial effect for these patients. This has been demonstrated in various retrospective studies and in controlled prospective trials. A final evidence based recommendation will be possible after conclusion of the randomised trials which are now in progress. Literature: 2. Biesinger E, Ch. Heiden, V. Greimel, T. Lendle, R. Höing, K. Albegger: Strategien in der ambulanten Behandlung des Tinnitus. HNO 46 (1998) 157-169 3. Ganzer, E., Arnold, W.: Leitlinien / Algorithmen der Deutschen Gesellschaft für Hals- Nasen- Ohrenheilkunde, Kopf- und Halschirurgie. Laryngo. Rhino. Otol. 75 (1996): 499-512 Internet : http://www.hno.org/leitl.htm 4. Beck C: Pathologie der Innenohrschwerhörigkeiten. Arch Otorhinolaryngol Suppl I (1984) 1-57 5. Robertson: Functional significance of dendritic swelling after loud sounds in the guinea pig cochlea. Hear Res. 9 (1983) 263-78 6. Tonndorf: Acute cochlear disorder: The combination of hearing loss, recruitment, poor speech discrimination and tinnitus. Ann Otol 89 (1980) 353-8 7. Yamane et al.: Strial circulation impairment due to acoustic trauma. Acta Otolaryngol. 111 (1991) 85-93 8. Hawkins: Comparative otopathology: aging, noise and ototoxic drugs. Adv.Oto-Rhino-Laryng 20 (1973) 124-41 9. Beck et al.: Morphologische Veränderungen an der Schnecke des Meerschweinchens bei Sauerstoffmangel und Lärmbelastung. Arch. Otolaryngol. 172 (1957) 238-45 10. Axelsson et al.: The effect of noise on histological measures of cochlear vasculature and red cell: A review. Hear Res. 31, (1987) 183-92 11. Lamm K.: Simultane Sauerstoffpartialdruckbestimmung in der Skala Tympani, Elektrokochleographie und Blutdruckmessungen nach Knalltraumata bei Meerschweinchen. HNO 37 (1989) 48-55 12. Takahashi H, Sakakibara K, Murahashi K, Yanagita N: HBO for sudden deafness - a statistical survey over 907 ears. In: Bakker DJ, Schmutz J (eds) Hyperbaric Medicine. Proceedings of the Joint Meeting 2nd Swiss Symposium and 2nd European Conference on Hyperbaric Medicine. Basel, Switzerland, Sep 1988. Foundation for Hyperbaric Medicine, Basel, 1990 (ISBN : 3-908229-01-4) : 249-258 13. Pilgramm M, Lamm H, Schumann K: Zur hyperbaren Sauerstofftherapie beim Hörsturz. (Hyperbaric oxygentherapy in sudden deafness). Laryngol Rhinol Otol (Stuttg) 64 (1985) 351-354 14. Schmidt R.: Hyperbare Sauerstofftherapie bei therapieresistentem Hörsturz. Dissertation Uni Frankfurt 1995 15. Dauman R, Poisot D, Cros AM, Mehsen M: Hemodilution, oxygenotherapie hyperbare et vasodilatateurs dans les surdites brusques. J Fr Otorhinolaryng (Lyon) 34 (1985) 93-96 16. Daumann R., AM. Cros, D. Poisot: Traitements des surdites brusques: premiers resultats d'une etude comparative. (Treatment of sudden deafness: first results of a comparative Study.). J. Otolaryngol (Toronto)14 (1985) 49-56 17. Desloovere C., Knecht R., B.Rosemann, R.Schmidt, D.Böhmer, G.Hoffmann, B.Böckler: Hyperbare Sauerstofftherapie bei therapieresistenten Hörstürzen. Eur Arch Otolaryngol Suppl II, (1992) 195-7 18. Goto F, Fujita T, Kitani Y, Kanno M, Kamei T, Ishii H.: Hyperbaric oxygen and stellate ganglion blocks for idiopathic sudden hearing loss. Acta Otolaryngol (Stockh) 88 (1979) 335-342 19. Hoffmann G., D Böhmer, Chr Desloovere: Hyperbaric oxygenation as a treatment for sudden deafness and acute Tinnitus. Proc. 11. Int. Kongr. Hyperb. Med. Best Publ. Comp. 1995, 146 – 152 und 24 – 25 20. Pilgramm: Zur Anwendung der HBO-Therapie beim akuten Knalltrauma. in Tirpitz (Hrsg): Therapie mit hyperbarem Sauerstoff (HBO) in Traumatologie und Notfallmedizin. Symposium Duisburg 1993. Springer (1994) 51 – 62
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