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Reversible sensorineural hearing loss after non-otological surgery under general anaesthetic
  1. H Pau,
  2. D Selvadurai,
  3. G E Murty
  1. Department of Otolaryngology, Leicester Royal Infirmary, Leicester, UK
  1. Mr H Pau, Countess of Chester Hospital, Health Park, Liverpool Road, Chester CH2 1UL, UK (e-mail: hpau{at}globalnet.co.uk)

Abstract

Acute sensorineural hearing loss can occur after both otolaryngological and non-otolaryngological procedures. The mechanism of such hearing loss remains unproved; but nitrous oxide has been implicated and where used, attendants should be aware of its potential damage to hearing. It is essential that patients with sudden hearing loss are identified as soon as possible as the recovery rate had been shown to be higher in those who presented early; and as our case demonstrates, complete recovery is possible. Anaesthetists, non-otolaryngological surgeons, and ward nurses must be aware of this early postoperative complication if appropriate treatment is to be instituted.

  • surgery
  • sensorineural hearing loss

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Cases of sudden sensorineural hearing loss after non-otological surgical procedures are rare. Most of these were surgical complications after cardiopulmonary bypass, and to date there have been only 29 cases (table 1) of sensorineural hearing loss after non-otological and non-cardiopulmonary surgery. We present a patient who suffered unilateral sensorineural hearing loss after varicose vein surgery under general anaesthetic.

Table 1

Twenty nine cases of sensorineural hearing loss after general anaesthetic after distant site surgery and non-cardiopulmonary surgery

Case report

A 29 year old male smoker presented to the ear, nose and throat department two days after undergoing long saphenous vein stripping and avulsions under general anaesthetic. The general anaesthetic involved induction with intravenous propofol, droperidol, fentanyl, and atropine. Ventilation was via a laryngeal mask airway size 4. Maintenance was achieved by spontaneous ventilation with a gas mixture of 40% oxygen in nitrous oxide and isoflurane vapour. Postoperative pain was controlled by a diclofenac suppository and by infiltrating a solution of 0.5% bupivacaine with adrenaline (epinephrine) to the wounds.

On awakening, he complained of sudden deafness in the right ear and described right sided tinnitus. He was otherwise healthy with no significant past medical history and on no medications. On physical examination he was apyrexial; the cardiovascular system was normal with no carotid bruits and examination of the remaining cranial nerves and peripheral nervous system revealed no abnormalities. The appearance of the pinna, the external acoustic meati, and the tympanic membrane was unremarkable. Rinne's test produced a false negative in the right ear and Weber's test lateralised to the left. A pure tone audiogram showed profound sensorineural hearing deficit in the right ear (fig 1). A full blood count, plasma viscosity, clinical chemistry, and autoantibody screen were normal. Magnetic resonance imaging of the posterior cranial fossa showed no evidence of an acoustic neuroma.

Figure 1

Pure tone audiogram showing profound sensorineural hearing deficit in the right ear.

He was admitted for regular carbogen (a mixture of 95% oxygen and 5% carbon dioxide) inhalation hourly for the first 24 hours, intravenous infusion of Dextran 70 solution at a rate of one litre every 12 hours for the first four days, oral flucloxacillin 250 mg four times daily for five days, and oral prednisolone treatment, starting with 60 mg once daily which was later reduced gradually and eventually stopped on the 11th day. Pure tone audiograms were repeated at daily intervals and gradually returned to normal by day 5. He was then discharged from the ward and his follow up pure tone audiogram at six weeks was normal.

Discussion

Box 1 shows a list of some common causes of acute sensorineural hearing loss. However in some cases, the aetiology remains unknown.1 Idiopathic acute sensorineural hearing loss has been reported to have an incidence of between five to 20 new cases per 100 000 population per year.2 Several theories including viral, autoimmune, vascular, embolism, and inner ear membrane rupture have been postulated.

Box 1: Common causes of acute sensorineural hearing loss

  • Trauma (direct, surgical, barotrauma, or noise)

  • Ototoxic drugs

  • Acoustic neuromas

  • Meniere's disease

  • Multiple sclerosis

Sensorineural hearing loss has been reported in several specialties after surgery: (1) local surgery including neuro-otological and dental; (2) cardiopulmonary; and (3) distant site surgery including ophthalmic, gastrointestinal, gynaecological, urological, orthopaedic, and endocrine (table 1).

In neuro-otological surgery, local trauma in acoustic neuroma resection can lead to sudden sensorineural hearing loss.3 In dental procedures, local factors including opening the jaw widely, and the noise intensity and duration of drilling were thought to be responsible.2 There have also been a number of cases of sudden hearing loss after cardiopulmonary bypass surgery.4-8

Twenty nine cases of sudden sensorineural hearing loss after distant site surgery including our case are listed in table 1. There were five orthopaedic, one ophthalmic, one cardiac pacemaker implantation, 13 general surgical, one nasal, one urological, three endocrine, and three gynaecological operations. The type of operation in one case was not recorded. Nitrous oxide was administered in 17 of the cases but information regarding the length of the operations were not available. Hearing improvements were noted in 10 patients, but whether complete reversibility was achieved in these patients was not clearly demonstrated.

The type of anaesthetic has been postulated to have a causative role in these patients. It is well known that nitrous oxide can affect middle ear pressures9 and sensorineural hearing loss can be caused by a formation of a perilymph fistula secondary to a ruptured round window. Goodhill10 and Goodhillet al 11 postulated an “implosive” and an “explosive” route for rupture of the round window membrane. The former creates rupture by increased pressure in the middle ear and the latter by an increase in the cerebrospinal fluid. Segal et al stated that a rupture of the round window by the “implosive” route can take place during induction of anaesthesia with nitrous oxide by outward movement of the tympanic membrane and thus the stapes.12 However, four of the cases shown in table 1 certainly did not receive nitrous oxide during their operations. The other anaesthetic agents used may act indirectly on the auditory system by altering the general haemodynamics—for example, isoflurane will increase intracranial pressure, propofol at therapeutic dose increases cerebral vascular resistance by 50% and decreases systolic blood pressure by 20%–30%, and fentanyl causes bradycardia and hypotension.13 Direct neurotoxic effect on the auditory nerve of any anaesthetic agent has not been reported.

Byl reported on prognostic indicators for sudden hearing loss including age, time from onset to initial presentation, severity of initial hearing loss, the hearing in the opposite ear, tinnitus, and erythrocyte sedimentation rate (ESR).1 He found that patients under the age of 15 years and over the age of 60 years did not recover as well as the other age groups. He hypothesised that the body's immune defence mechanisms were not yet developed in the young and, in the aged, were deteriorating. His study confirmed that the sooner a patient is seen, the better the recovery; and a direct relationship between the severity of the initial hearing loss and potential recovery was demonstrated. Patients with below normal pure tone audiogram in the opposite ear proved to have only partial or no recovery. Tinnitus and ESR were regarded to have little prognostic value.

The treatment of acute sensorineural hearing loss is largely empirical due to the number of potential causes. The use of systemic steroids, for example, prednisolone, to combat the inflammatory effect of any viral infection and inhaled carbogen to improve the oxygen tension in the perilymph has been advocated by Fisch,14 and the management of our case was a modification of this. Dextran 70 has been used as a plasma expander to improve the cochlear circulation.15 In our case, flucloxacillin was given prophylactically against possible secondary bacterial labyrinthitis. However it is difficult to judge whether a suggested treatment would result in a higher recovery rate than a spontaneous recovery. Wilkinset al showed that there was no statistically significant difference between the patients who received treatment and those who did not.16 Further evaluation of our current methods of treatment is important.

Learning points

  • Acute sensorineural hearing loss can occur after both otolaryngological and non-otolaryngological procedures.

  • Patients with sudden hearing loss postoperatively should be identified as soon as possible as the recovery rate had been shown to be higher in those who presented early.

References

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