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CASE REPORT 13-1E. History A 56-year-old drama lecturer was on holiday m Europe, having travelled by rail, when he noticed a sudden deterioration in hearing in his left ear. There was no tinnitus or disequilibrium but he did complain of extreme discomfort when exposed to loud sounds. There was no relevant past otological history. He visited a doctor in France who confirmed, by pure-tone audiometry, a profound left-sided sensorineural hearing impairment and prescribed a course of oral steroids. There had been no improvement in his symptoms by the time of his return to Scotland 2 weeks later. Otoscopic examination at that time was normal. Clinical voice tests of hearing were normal in the right ear, but he could only hear a conversational voice 6 inches (15cm) from the left ear. Tuning fork tests suggested the left-sided hearing impairment to be sensorineural in origin. Further pure-tone audiometry showed normal thresholds in his right ear, with a 60 dB HL flat sensorineural hearing loss in the left ear. Serial audiometry performed over the next 2 weeks failed to show any improvement in the hearing thresholds. Questions 1. Discuss the evaluation of the above patient. 2. What are the management options for a patient with a sudden onset sensorineural hearing impairment? PF: Conductive and sensorineural hearing loss PA atherosclerosis Discussion 1 Evaluation of a patient with a sudden onset hearing impairment is aimed at determining the severity of the impairment and attempting to identify the site of the defect and any possible etiological agent. A detailed history and examination should detect any obvious relevant factors such as recent head injury, ototoxic drugs and aural surgery. Routine blood investigations, including serological tests for syphilis, are commonly ordered. These are unlikely to be helpful, but it is probably reasonable to measure the ESR and serum immunoglobulins as investigation for autoimmune ear disease. Audiometric investigations are essential. A pure-tone audiogram should be the first test performed; others such as speech audiometry, otoadmittance studies and electronystagmography with caloric testing may be carried out later but often fail to add further worthwhile information. It is reported that sudden sensorineural hearing loss will be the initial presentation in up to 13% of acoustic neuromas and, as in other cases of asymmetric sensorineural hearing impairments, it is worthwhile performing brain-stem evoked response audiometry, a reasonably sensitive method of screening for such a tumor. It should be remembered, however, that acoustic neuromas probably account for less than 1% of cases of sudden deafness. If the evoked response audiometry fails satisfactorily to exclude a posterior fossa lesion (by analysis of the interval between waves I and V and the mteraural latency difference for wave V), then scanning of the •cerebellopontine angle by CT or MRI should be performed. Despite such investigation, it is likely that the cause of the hearing impairment will remain unknown in the majority of cases. It should also be borne in mind that a small percentage of patients will have a nonorganic hearing impairment. 2 Sudden onsets sensorineural hearing loss is an uncommon condition, the etiology is often obscure and, therefore, treatment directed at the cause cannot often be prescribed. The management options that are often advocated are by no means proven as Most centers do not see a sufficient number of cases to permit randomized controlled trials to be performed, and in assessing the potential benefit of treatment, the situation is further complicated by the high spontaneous improvement rate. Unless there is an obvious reason for surgical intervention (i.e. trauma), initial management will be medical. Daily pure-tone audiograms are an important means of documenting the patient's progress, as is clinical evaluation of the vestibular system. Systemic steroid therapy, commenced early, is popular and often recommended if it is considered that the cause is inflammatory. However, reports suggest that steroids may only be of benefit in patients with a mild to moderate hearing loss, and that patients with a severe loss are unlikely to respond. Should an underlying vascular etiology be considered, anticoagulant/vasodilator therapy is often commenced. Low molecular weight dextrans, intravenous histamine, oral nicotinic acid, grosgrain and inhalation of carbon dioxide have all been administered. There is as yet no substantial evidence that any of these agents will alter the natural history of the condition. Autoimmune ear disease has attracted some attention in the literature since first being described in 1979, The presenting symptoms can be auditory, vestibular or a combination and, although it can present as a sudden hearing loss, the majority of patients will typically have bilateral disease progressing over a period of weeks or even months. Management with a combination of steroids and immunosuppressive (cyclophosphamide) is advocated but there are no controlled trials to support the use of these drugs. Surgery (exploratory tympanotomy) should be considered if, despite conservative measures, the patient's cochlear and/or vestibular function continues to deteriorate, the purpose of the tympanotomy is to exclude a perilymph fistula, but both the indications for such a procedure and the time at which it should be performed are matters for debate. It would appear that surgical closure of the fistula is more likely to resolve vestibular symptoms than have any significant effect on hearing. Finally, management of residual hearing impairment should be considered. The patient may obtain the greatest benefit from provision of an appropriate hearing aid system if there is significant overall hearing disability. This was not the case in the patient described, as he had a unilateral loss. Further investigations of this man failed to reveal any underlying cause and no further management was offered.