Loss of hearing after spinal anaesthesia gets little mention in the standard anaesthesia textbooks, although there has been some research into it . Most patients do not notice the hearing loss , which is probably caused by a leak of cerebrospinal fluid. Walsted claimed that the leak causes a relative endolymphatic hydrops secondary to perilymphatic hypotension. Until now, the only factor investigated that may cause hearing loss has been the diameter of the spinal needle . Wang believed that the irrigating solution used during transurethral resection is also a factor, passing into the bloodstream and reducing the osmolarity relative to cerebrospinal fluid . We think this is unlikely, because hearing loss occurs even when irrigation fluids are not used. Sundberg thought that the shape of the needle was important for the size of leak . Lee and Peachman reported a case of unilateral hearing loss after spinal anaesthesia treated with an epidural blood patch . No other factor is known to explain the hearing loss, which occurs after myelography and diagnostic lumbar puncture [8,9,10,11] as well as after spinal anaesthesia.
In the present study, we investigated the effect of two different local anaesthetic drugs on hearing loss after spinal anaesthesia.
With the permission of the hospital ethics committee, 44 patients, all ASA I and about to undergo inguinal hernia repair, were allocated randomly by systematic sampling to two groups. Patients were excluded from the study if they had conductive hearing loss. Patients in one group were given 6mL prilocaine 2%, while the other group received 3 mL bupivacaine 0.5%.
Atropine 0.5 mg and pethidine 50 mg were injected intramuscularly 30-45 min before surgery was due to begin. Intravenous access was established and 400 mL saline 0.9% infused at 6 mL kg−1 h−1. Spinal anaesthesia was performed by the same anaesthetist, using a 22-gauge Quincke needle, at the L3-L4 vertebral interspace, with the patient in a sitting position. The local anaesthetic drug was injected at 0.2 mL s−1. Infusion of saline was continued at 4 mL kg−1 h−1.
The anaesthetist knew which drug was injected, but neither the patients nor the audiologist who later did the hearing tests, which were carried out 1 day before and 1-2 days after the surgery, were aware of this detail. For the evaluation of hearing losses, average losses at 125 and 250 Hz were taken for low frequencies; average losses at 500, 1000 and 2000 Hz for speech frequencies; and average losses at 2000, 4000 and 6000 Hz for high frequencies. We considered a hearing loss of 5 dB to be a clinically important loss for an individual patient.
Hearing levels before and after surgery were compared by χ2 test, and a probability of P ≤ 0.05 was accepted as significant.
The two groups of patients were comparable (see Table 1).
Every patient received 3L of saline. No patient developed a headache, vertigo or any sign of paralysis of a cranial nerve.
Post-operative hearing losses are shown inTable 2. Ten out of the 22 patients who received prilocaine developed hearing losses, but not necessarily the same in the two ears. Fewer (4 out of 22) of the patients who received bupivacaine developed hearing loss (P<0.05).
We were unable to follow-up patients to check for recovery of hearing.
Hearing loss as a result of spinal anaesthesia is not often considered in daily practice, although there are case reports of cranial nerve palsies. The most important cause of hearing loss is probably the diameter of the spinal needle because of its effect on the leak of cerebrospinal fluid. Panning and Laubert suggested replacing the lost cerebrospinal fluid with an equal volume of isotonic saline to prevent the hearing loss .
We observed that hearing loss was different with two different local anaesthetics used for spinal anaesthesia in otherwise similar conditions. In patients in whom prilocaine was injected, the incidence of hearing loss was greater. We suggest that this difference may be caused by differences in the osmotic or other physical properties of the two local anaesthetic preparations, which affect the cerebrospinal pressures differently.
The direct factor connecting a cerebrospinal fluid leak and hearing loss is the consequent leak of perilymph into the subarachnoid space via the cochlear aqueduct. As a result, perilymph pressure decreases. The endolymphatic and perilymphatic pressures also change, resulting in a relative increase in endolymphatic pressure. The hearing loss in our patients was greater at the low frequencies, which is similar to the hearing loss in patients with Meniere's disease, who also have increased endolymphatic pressure. Dreyer has stated that the hearing loss after spinal anaesthesia is most frequent at 125-200 Hz and that it recovers spontaneously within 3 days. Other studies also indicate that loss is most common at the low frequencies [4,12-15].
Hearing losses after spinal anaesthesia recover within a period of between 3 days and 7 months [1,14,16]. Although Dreyer  reported that 16% of patients complain of hearing loss, none of our patients did so. We are unable to report long-term follow-up.
This study emphasizes that factors affecting the pressure and flow of cerebrospinal fluid must be considered in the development of sudden hearing loss, especially at low frequencies. We believe that there is still much to learn about sudden hearing loss. Further studies on hearing loss caused by spinal anaesthesia may prove instructive.
We are most grateful to Dr Ahmet Ömer Ikiz for his kind help in revising this manuscript.
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