Year : 2022 | Volume
: 8 | Issue : 2 | Page : 74--79
Perioperative hearing loss after nonotological surgeries – What is the role of anesthesia?
Shibu Sasidharan1, Vijay Singh2, Abdul Nasser3, Harpreet Dhillon4, M Babitha5,
1 Department of Anaesthesia and Critical Care, Level III IFH MONUSCO, Goma, DR Congo
2 Department of Anaesthesia & Critical Care, Command Hospital, Chandimandir, Haryana, India
3 Department of Psychiatry, Level III IFH MONUSCO, Goma, DR Congo
4 Indian Naval Hospital, Vasco da Gama, Goa
5 Department of Radio-Diagnosis and Imaging, Alchemist - Ojas Hospital, Panchkula, Haryana, India
Dr. Shibu Sasidharan
Department of Anaesthesia & Critical Care, Command Hospital, Chandimandir, Haryana - 134 117
Transient, low-frequency hearing loss after anesthesia, especially due to neuraxial block, usually goes unnoticed by patients, and thus they do not report to a physician. However, the chances of anesthesia-induced perioperative hearing loss (POHL) to occur are generally underestimated. The true incidence of POHL regardless of anesthetic technique is unknown due to lack of reporting and subclinical presentation, which often goes unnoticed unless pure-tone audiometry is performed. However, the anesthesiologist should be aware of hearing loss as a potential perioperative complication and should be discussed with the patients in the perioperative period and should preferably be included in the informed consent for medicolegal and ethical reasons. The cognizance of POHL should be disseminated to the treating team by educating anesthesiologists, surgeons, and healthcare personnel about its possible occurrence. A better understanding of the incidence, etiology, prognosis, and management for POHL is essential for the anesthesiologist to prevent or to minimize the risk of hearing loss. In this review article, we emphasize the abovementioned aspects.
The following core competencies are addressed in this article: Patient care and procedural skills, Medical knowledge.
|How to cite this article:|
Sasidharan S, Singh V, Nasser A, Dhillon H, Babitha M. Perioperative hearing loss after nonotological surgeries – What is the role of anesthesia?.Int J Acad Med 2022;8:74-79
|How to cite this URL:|
Sasidharan S, Singh V, Nasser A, Dhillon H, Babitha M. Perioperative hearing loss after nonotological surgeries – What is the role of anesthesia?. Int J Acad Med [serial online] 2022 [cited 2022 Jul 5 ];8:74-79
Available from: https://www.ijam-web.org/text.asp?2022/8/2/74/347823
Perioperative hearing loss (POHL) after anesthesia is a rare complication and may be more common for some operative procedures than others, but the incidence is more frequent than what we suspect. Sprung et al. mentioned that POHLs can be conductive or sensorineural, unilateral or bilateral, transient or permanent and typically affect the low-frequency range. An overwhelming majority of patients' hearing deficits are transient, resolving without treatment within several days. However, perioperative hearing impairment is a poorly reported, uncommon, and distressing morbidity related to anesthesia. Singh et al. found 52 reported cases of hearing losses following general anesthesia. They also reported that hearing loss after spinal anesthesia is more common, with an incidence as high as 50%. However, the true incidence is unknown, owing both to lack of reporting and its subclinical presentation, which often goes unnoticed unless audiometry is performed.
We evaluated existing systematic reviews from our search in MEDLINE, EMBASE, Cochrane Registry of Controlled Trials, Database of Abstracts of Reviews of Effects (OvidSP), CINAHL (EBSCOHost), and Web of Science (Thomson Reuters) from the date of the last systematic review to December 2020, without language restrictions. Panel members were also asked to highlight any additional studies not identified by the search. Recommendations are either “strong” or “conditional” according to the GRADE approach. We used the GRADE phrases “we recommend” for strong recommendations and “we suggest” for conditional recommendations. This manuscript was prepared by the authors in the writing committee (SS, VS), who drafted the guideline document, and was subsequently electronically reviewed by the entire panel.
The etiology of POHL mostly includes mechanical, traumatic, noise-induced changes in cerebrospinal fluid (CSF) pressure, nitrous oxide, embolism, pharmacologic, and other miscellaneous causes. POHL from anesthesia can be because of the following reasons.
Hearing loss from neuraxial anesthesia
The first case of hearing loss associated with spinal anesthesia was reported back in 1914. Clinical or subclinical hearing loss following spinal anesthesia or lumbar puncture has been reported frequently.,,,, Despite many reports, very few anesthesiologists are aware of the possibility of this complication. Since there has been no large-scale audiometric study of hearing loss associated with spinal anesthesia, the precise incidence of clinical or subclinical hearing loss is unknown but may occur more frequently than what is appreciated. Further, the specific presentation and onset of the hearing deficit after spinal anesthesia can vary widely.
Mechanisms of hearing loss
The mechanism of hearing loss is thought to be similar to that of post-dural puncture headache (PDPH). The hearing loss may result from CSF leakage even when the CSF loss is insufficient to cause a PDPH. The CSF dynamics are essential for the auditory function of the inner ear. The structures of the inner ear are embedded in the labyrinth of the temporal bone and consist of separate receptor mechanisms: the vestibule and semi-circular canals (vestibular end organ) and cochlea. Both the round and the oval windows open to the inner ear from the middle ear. The membranous labyrinth encloses endolymph that fills a hollow system within the inner ear. Perilymph, a filtrate of blood and CSF, is the substrate for the inner ear cells and is present in the cochlea. There is a passive diffusion as well as active transport of ions between endolymph and perilymph. The mechanism of hearing loss after spinal anesthesia is attributed to the disruption of this endolymph/perilymph balance caused by the decreased CSF pressure due to leakage of CSF through the dural puncture site. CSF leakage can cause a decrease in the CSF pressure that may be transmitted to the inner ear. Disruption of this pressure balance can cause hearing impairment as well as impairment of semi-circular canal function. In most individuals, fluid movement between the endolymph and the perilymph is small and well-compensated. Hearing loss confined to the low frequencies is unlikely due to CSF pressure-mediated stretch or pressure injury to cranial nerve VII. Interestingly, the low-frequency hearing loss observed in Ménière's syndrome involves a similar mechanism. The increased flow in the cochlear aqueduct decreases the perilymphatic pressure when CSF pressure decreases after a dural puncture. This decrease in perilymphatic pressure leads to an increase in the endolymphatic pressure resulting in the formation of endolymphatic hydrops, which displaces the hair cells on the basement membrane and results in low-frequency hearing loss.
Needle design and size may also play a role in hearing impairment following lumbar puncture. In patients with hearing deficits, the mean hearing level was significantly worsened when the Quincke needle was used. Spinal anesthesia performed with a 22-gauge needle had a 10-dB or greater hearing loss than performed with a 26-gauge needle. Oncel et al. used pure-tone audiometry preoperatively and postoperatively to assess hearing loss and found that patients who were given an epidural block had no hearing impairments, and there was a significant hearing loss when a 22-gauge needle was used compared to a 25-gauge needle.
Pressure changes in the CSF associated with injection of an epidural bolus may also contribute to hearing loss.
Hearing loss from other types of regional anesthesia
Apart from the neuraxial block, various studies show that hearing loss is also seen after other types of regional anesthesia, namely interscalene brachial plexus block, anesthesia for dental surgery, and inferior nerve block.
Dental surgeries are reported to cause unilateral POHL. This is postulated by the presence of several channels of communication between the teeth and the ear. Nociceptive 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 antidromic fibres – duplicating inappropriately in the branches of the internal auditory artery. The vascular system provides another channel. Dental extraction is known to release microemboli into the circulation, and these can include potentially pathogenic bacteria. The tendency to unilaterality seen in many cases could be explained by proximity and local communicating vessels.
Hearing loss from general anesthesia
Hearing impairment after general anesthesia for noncardiopulmonary bypass (CPB) surgery and nonotologic surgery are rare but prevalent.,,, The most common anesthetic agent causing the hearing loss is nitrous oxide. Other anesthetic agents such as isoflurane and fentanyl may indirectly affect the auditory pathway by altering the general hemodynamics (e.g., hypotension), thus leading to POHL. Direct neurotoxic effect on the auditory nerve by any anesthetic agent has not been reported.
Mechanisms of hearing loss
The exact etiology of hearing loss associated with general anesthesia often cannot be ascertained. There are, however, several potential etiologies such as changes in middle ear pressure, vascular pathology, embolism (most likely in cardiopulmonary bypass), ototoxic drugs, CSF leaks secondary to otolaryngologic or neurosurgical procedures, and other rare causes.
Middle ear pressure changes
Excessive or sudden changes in middle ear pressure due to nitrous oxide can disrupt the tympanic membrane, round window, and conducting structures. Excessive middle ear pressure can also cause the round window to rupture, resulting in significant hearing loss.
Two theories have thus far been suggested “implosive” and “explosive” routes. The implosive route theory states that there is a sudden increase in middle ear pressure which is caused after a forceful Valsalva that is strong enough in opening the Eustachian tube. With the sudden increase in the size of the middle ear, the TM expands rapidly outward, pulling the bones of the ear with it, and with the bones, so too the oval window through the attachment of the annular ligament creating low pressure in the cochlea. This can cause a tear of the oval or round window due to the velocity of changes. In the explosive route, the nitrous oxide-induced increases in the venous and CSF pressure are transmitted to the perilymphatic space via the cochlear duct, causing displacement or rupture of the membrane. The patency of the Eustachian tube may play a major role in potential injury during nitrous oxide anesthesia. Eustachian tube obstruction can result in significant negative middle ear pressure and tympanic perforation during nitrous oxide elimination.
Another possible mechanism of POHL from general anesthesia is vascular pathology. The injury to the inner ear's microcirculation, either in the stria vascularis or the vessels of the spiral ligament due to the photochemical method, leads to ischemic damage of the hair cells and POHL.
Although POHL incidence is reported up to 10%–15%, the incidence of permanent hearing impairment following CPB has been estimated to be <0.1%. Hearing loss after general anesthesia is more frequently associated with CPB than other types of surgery., Various etiologies have been proposed to investigate the pathophysiology of this phenomenon. Microembolic phenomena (fat, air, or particulate thrombi), perioperative hypotension or perfusion failure, hypercoagulable states, and ototoxic drug usage are some of the recognized causes of this hearing loss. The particulate emboli generated during CPB have been considered the likely cause of most sensory neural hearing losses (SNHLs) after cardiovascular surgery. The number of arterial microemboli is significantly increased during extracorporeal perfusion and aortic cross-clamping, and microemboli to the basilar artery and the branches to the inner ear are the most likely cause of hearing loss following the use of pump-oxygenator systems.,
Various drugs have been documented to cause ototoxicity. The following drugs are not used in isolation in anesthesia for surgical procedures but, in many cases, are given alongside either as an ongoing medication or for an antibiotic cover. Commonly used ototoxic drugs are as follows:
Diuretics (furosemide, ethacrynic acid, and bumetanide)Salicylates (aspirin)Nonsteroidal anti-inflammatory drugs (ketorolac, naproxen, and piroxicam)AminoglycosidesQuinineVancomycinAntineoplastic agents (cisplatin, vinblastine, and vincristine)Chronic use of amphetamineAntiepileptic drugs (sodium valproate and vigabatrin).
High-dose therapy with either diuretics or anti-inflammatory agents is primarily associated with acute and transient impairment of hearing or tinnitus. However, long-term treatment with antineoplastic agents or aminoglycosides is typically associated with delayed and irreversible loss of hearing due to the destruction of auditory sensory cells. Ototoxic drugs can also compromise vestibular function. The simultaneous administration of multiple agents, which are potentially ototoxic, can lead to synergistic loss of hearing. Exposure to loud noise may also potentiate hearing loss due to ototoxic drugs.
Other rare causes of hearing loss
Apart from the abovementioned causes, many other factors can cause transient/prolonged/permanent hearing loss after a surgical procedure. The other rare causes of hearing loss are as under:
Noise-induced hearing loss – Excessive noise from surgical equipment's or other sources may result in SNHLPatients taken to the operating theatre after prolonged intubation in an intensive care unit may develop hearing loss due to middle ear effusion or infectionFat embolism – Sudden-onset sensorineural hearing loss after knee replacement can occur due to fat embolismBlockage of the external ear – Blockage of the auditory canal by protective wax or cotton balls, clotted blood, and other foreign bodies such as syringe caps can cause hearing lossHead trauma – Sustained intraoperatively while positioning can result in either a unilateral or bilateral hearing loss that is conductive, sensorineural, or mixedVarious phenomena associated with anesthesia and emergence from anesthesia may mimic a hearing loss.
The central anticholinergic syndrome occasionally observed after general anesthesia, which resolves after physostigmine administration, may give the impression of hearing lossResidual muscle relaxant may permit adequate ventilation but prevent the patient from responding to verbal instructions, simulating a hearing lossNeurolept anesthesia with droperidol leads to unpleasant anxiety, nightmarish, or panicky experiences. It may lead the anesthesiologist to suspect a hearing loss.
Medicolegal aspects with perioperative hearing loss
The medical literature has not mentioned the incidence of litigations or medicolegal problems from POHL due to anesthesia. However, it is essential to realize that POHL due to anesthesia can occur even in healthy patients, and it may involve litigation or medicolegal problems for anesthesiologists. Hence, POHL risk discussed with patients in the perioperative period may be a reasonable medicolegal advice. Sprung et al. stated that true incidence of perioperative hearing impairments regardless of anesthetic technique will remain unknown unless studied explicitly on a large scale using audiometry. However, the anesthesiologists should be increasingly aware of hearing impairment as a potential perioperative complication, especially concerning neuraxial anesthesia, where the incidence may be as high as 50%. AO Lasisi et al. described that hearing loss due to neuraxial block is significant and associated with the duration of the procedure. Thus, it should be included in informed consent for medicolegal and ethical reasons.
Prognosis of perioperative hearing loss
The majority of perioperative hearing deficits due to neuraxial blocks are transient and are in the low-frequency range. They usually resolve without treatment within days to weeks. If necessary, an epidural blood patch can be effective in hastening recovery. However, when these POHLs do not reverse spontaneously, it becomes a sudden hearing loss. Unilateral hearing loss following CPB almost uniformly results in some permanent hearing deficits, probably due to embolism and subsequent ischemic injury to areas of the organ of Corti, and hearing loss following general anesthesia for non bypass surgery does not appear to have a uniform prognosis. The outcome is more a function of the specific etiology.
Treatment of perioperative hearing loss
POHL, in most cases, has high spontaneous recovery. However, the persistence of POHL warrants treatment. Most treatment protocols do not yet have the required level of evidence. However, the protocols enumerated below have some promising results:
Sensorineural hearing loss
Treatment options are as under: 
Systemic and intratympanic steroidsHyperbaric oxygenVasodilators (calcium channel blockers)Plasma expandersCarbogen (5% carbon dioxide and 95% oxygen)Inhalation steroids.
The mainstay of treatment is usually based on corticosteroid administration regardless of the initiating cause of SNHL. Steroids are used to reduce the inflammatory effect and endolymphatic pressure. The recommended treatment doses of prednisolone are 1 mg/kg/day with the maximum dose of 60 mg daily and a treatment duration of 7–14 days. It should then be tapered down. Hyperbaric oxygen, vasodilators, and plasma expanders are used to improve blood circulation, and inhaled carbogen is used to improve the blood supply in the perilymph.,, A hearing aid and other supportive measures are indicated if the patient has partial or no hearing recovery.
A more recent method of corticosteroid delivery is the intratympanic route. Intratympanic dexamethasone injection can be administered into the middle ear space every 3–7 days for a total of 3–4 sessions. Intratympanic steroids can be a valuable solution for patients with sudden SNHL who either cannot tolerate systemic steroid therapy or are refractory to it
Conductive hearing loss
Many of the causes of conductive hearing loss, such as wax, cotton balls, clotted blood, foreign bodies (syringe caps), or otitis externa, can usually be managed in the general practice setting, with only complicated cases requiring referral to an ENT surgeon for consideration of repair of the tympanic membrane. Tympanic membrane perforations (from infection or trauma) usually heal spontaneously within a few days to weeks. Topical antibiotics are not routinely required unless there is an associated infection.
Transient, low-frequency hearing loss after anesthesia, especially due to neuraxial block, usually goes unnoticed by the patients and thus unreported to the treating physician. However, POHL occurs more frequently than it is generally assumed. The true incidence of POHL regardless of anesthetic technique is unknown due to lack of reporting and subclinical presentation and goes unnoticed unless pure-tone audiometry is performed. However, the anesthesiologists should be aware of hearing loss as a perioperative complication and should be discussed with the patients in the perioperative period, and it is to be included in informed consent for medicolegal and ethical reasons. When medicolegal aspects are addressed to hearing loss after surgery, it is prudent to consider all the contributing and preexisting causes before relating it purely to anesthesia. The awareness of POHL should be made by educating anesthesiologists, surgeons, and healthcare personnel about its incidence and management. A better understanding of the incidence, etiology, prognosis, and management for POHL is essential for the anesthesiologist to prevent or to minimize the risk of hearing loss.
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Conflicts of interest
There are no conflicts of interest.
Ethical conduct of research
The authors of this manuscript declare that this scientific work complies with reporting quality, formatting, and reproducibility guidelines set forth by the EQUATOR network. The authors also attest that this clinical investigation was determined not to require institutional review board/ethics committee review.
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