Sudden deafness after dental surgery.

Comment The firstfactor that can be assessed from the medical histories of these patients is the side of the dental procedure. This may be important as three out of the four cases had an ipsilateral hearing loss, though the site (upper or lower) is evidently not important. Both age and sex are irrelevant, and the form of anaesthesia cannot play a prime role as three patients had local anaesthesia and one had general anaesthesia. Thus the only common factors were opening the jaw widely and undergoing a dental procedure. This could have led to deafness in several ways. If physical trauma were to account for inner ear damage it could take several forms. Direct trauma on the part of the dentist is possible but unlikely. Those patients who required drilling would have been exposed to a small degree of noise, which is well transmitted from teeth to the ear, but the product of noise intensity and the duration of drilling seems slight in comparison to that leading to industrial noise-induced deafness or to the amount that dentists are exposed to.3 There are several channels of communication between the teeth and the ear. Nocioceptive afferents of the trigeminal nerve might be involved in a reflex effect on the inner ear; or there might be an autonomic reflex-possibly through antidroniic fibres-duplicating inappropriately in the branches of the internal auditory artery. Another channel is provided by the vascular system. Dental extraction is known to release microemboli into the circulation, and these can include potentially pathogenic bacteria. The tendency to unilaterality seen in our series could be explained by proximity and local communicating vessels. The venous system could also provide channels of direct communication. These channels could offer toxic agents access to the ear. Three patients had local anaesthesia, and it is usual to use a vasoconstrictor in all dental surgery; this could induce localised vasospasm of the cochlear division of the internal auditory artery. Experimental studies of microembolism of this vessel have produced varying degrees of endolymphatic hydrops.4 Ototoxicity is a second possibility as localised concentrations of these agents in tissue would be high. However, local anaesthetics (especially lignocaine) have been used to treat Menieres disease with no reported deleterious side effects.5 Although none of these hypotheses can explain the cause of deafness in all the patients in our series, if any of them were the cause of even one case it would be expected that for every case of severe hearing loss there would be many less severe cases and that the association would have been recognised. We believe that the association between dental surgery and a sensorineural hearing deficit has not previously been described. Perhaps the recognition of this loss is obscured by a gradual onset and by the lapse of time between dental treatment and the detection of asymmetrical hearing loss.