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Sudden Deafness, Acute Tinnitus and Acute Acoustic
Trauma treated with Hyperbaric Oxygen ( HBO2 )

Presentation at the
Congress on Cerebral Ischemia, Vascular Dementia, Epilepsy and CNS Injury
Washington, DC May 9-13, 1998
by

Ch. Heiden, E. Biesinger, R. Hoeing
ENT Department Traunstein, Germany

Summary:

The pathophysiological reasons for sudden deafness and acute tinnitus, if not result of acoustic trauma, are not identifiable in the individual patient. Various hypotheses suggest that their development may be the result of an acute oxygen deficit. Experimental results show a significant decrease in partial pressure of oxygen in the lymph of the corti organ following exposure to noise.

The report deals with the statistical evaluation of treatment success of own studies and is displaying those from literature. The principles behind the use of hyperbaric oxygen therapy for inner ear disorders are explained.

Introduction:

Sudden deafness – one of the most impressive and easiest to evaluate inner ear dysfunctions – is one of the most common reasons to apply hyperbaric oxygenation in many countries around the world. We learned this at the joint meeting of a UHMS delegation to Chinese hyperbaric Centres 1996. Also in Japan and Europe a large number of these patients has been evaluated ( 1 ).

In Germany there are approximately 80 multiplace chambers. 80% of their patients are treated because of inner ear dysfunctions. The German Society for ENT Diseases, Head and Neck Surgery developed guidelines in accordance with the German Association of Scientific Medical Societies ( AWMF ). These guidelines ( 3 ) refer to hyperbaric oxygen as one among other treatment options for those symptoms listed in Table 1

This table is very surprising compared to the situation in the United States of America. Why do the German Society for ENT as well as the German national and the European scientific societies for hyperbaric medicine recommend HBO2 for inner ear dysfunctions?

Table 1 : Indications for HBO2 in the field of ENT

Indications for HBO2 in the field of ENT
From Guidelines of the
German Soc. ENT-Diseases, Head and Neck Surgery

Tinnitus

Related to acoustic trauma, head injury, sudden deafness, M. Ménière

Hearing Loss:

Related to sudden deafness, M. Ménière, ototoxic damage, acoustic trauma, trauma, infection

Deafness:

Related to sudden deafness, M. Ménière, ototoxic damage, acoustic trauma, contusio labyrinthii, barotrauma, zoster oticus, postoperative

Vertigo:

Related to acute functional loss of peripher vestibular organ, irritation of labyrinth, contusio labyrinthii, M. Ménière, sudden deafness

Otitis externa maligna

Pathophysiologic Aspects of Inner Ear Dysfunctions

The inner ear, with its anatomical and functional unit of cochlear and vestibular organs falls ill as a whole or in its parts. Any sensory organ is only able to show reactions according to its function. For instance a patient receiving a blow on an eye will tell you of optical phenomenons like seeing stars and darkness. So, in our case, we will find varying combinations of the three symptoms referring to inner ear function: vertigo, hearing loss and tinnitus.

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

Reactions of inner ear structures
to noxious agents

swelling of dendrites
structural damage of dendrites
alterations of mitochondria
alteration of cell-structure
separation of hair-cells from tectorial membrane
swelling of endothelium
oedematous closure of endarteries

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

Therapy of inner ear disturbances

Haemodilution ( NaCl, Haes, Dextrane )
”vasodilative” ( Naftidrofuryl, Pentoxifylline, Flunarizine, Ginkgo biloba, Cinnarizine, Nicotinamide, Piracetam etc.)
Prednisolone
Vitamines
Stellate Ganglion block
Hyperbaric Oxygen ( HBO2 )

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

Noxious Factors for inner Ear

Perfusion disturbance Oedema
Vasomotoric disturb. Prolif. of endothelia
Hypotonia Ototoxic substances
Endolymphhydrops Bact. Toxines
Allergy Angiopathy
Viral infection Diabetes
Thrombocyte aggreg. Immunologic disease
Noise Trauma etc.

Experimental results

Usually the model for experimental work is the guinea pig exposed to noise, gun shots or explosions to produce acoustic trauma. The groups Lamm, Fisch and Japanese authors have published a profound decrease in the O2 partial-pressure in the lymph of the cochlea in animal and man during and after acoustic stress and in acute hearing loss. During exposure to HBO2 the pO2 increases up to 460 % in the cochlea and is still 60% above normal 1 hour after the termination of HBO2 ( 11 ).

Table 3 : Models for inner ear disturbances

Models for examination of inner ear dysfunction

Sudden deafness:
subjective / objective audiometry

Guinea pig / acoustic trauma
in situ measurements of pO²

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

Some controlled trials concerning around 1100 patients in 8 publications ( 12, - 19 ) confirm the results of retrospective case evaluations of around 7280 patients in 19 publications with sudden deafness. After ineffective conservative treatment including plasmaexpander such as Hydroxyaethylstarch or others, normovolaemic haemodilution, cortisone and oral haemo-rheological substances HBO2 is effective in 50% of the cases to reduce hearing loss by 20 dB or more. Approximately 11% have a complete recovery. Late application of HBO2 with a delay of more than 3 month reduce a beneficial outcome to 30 %. All authors confirm better results with earlier onset of HBO2 ( 1 ).

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:

Since August 1995 in our multiplace chamber 70% of the patients have been treated for inner ear dysfunction. In 2200 sessions 1600 patients were treated for acute tinnitus, sudden deafness and acoustic trauma. The retrospectively evaluated results compared favourably to those in the literature.

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

Results of Haemodilution for Tinnitus

69 cases
36,2 % healed completely
63,8% unchanged (25% decompensation)

Results of HBO2 for Tinnitus

142 cases
64,1 % healed completely
35,9% unchanged (18% decompensation)

Results of secondary HBO2 for Tinnitus

72 cases
51,4% healed completely
37,5 % improved
11,1% unchanged
0% worsened

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

  1. University Düsseldorf:
    Ineffective conservative treated patients continued with HBO2-therapy
  2. techn. University Munich
    Ineffective conservative treated patients continued with HBO2-therapy
  3. University Hannover
    Randomised primary treatment conservative vs. HBO2
  4. University Homburg and University Freiburg
    Randomised: Haemorheologic and antiinflammatory treatment tested against this treatment in combination with HBO2
  5. University Lübeck and German Navy
    Randomised sudden deafness, acoustic trauma, tinnitus controlled against conservative treatment and controlled against hyperbaric air
  6. University Hannover
    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:

  1. Lamm H: Der Einfluß der hyperbaren Sauerstofftherapie auf den Tinnitus und den Hörverlust bei akuten und chronischen Innenohrschäden. Otolaryngol Nova 5 (1995) 161-9
  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
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