Perioperative hearing loss (POHL) after anesthesia is a relatively uncommon complication, occurring in about 10-15% of cases; however, when it occurs, it is usually transient and therefore often goes unnoticed by patients and unreported in medical records [1]. Interestingly, POHL after spinal anesthesia yields a much higher incidence rate, as high as 50% according to some reports [2]. POHL is thought to be caused by cerebrospinal fluid (CSF) leakage from the inner ear – specifically, by an imbalance of fluid movement from the perilymph to the endolymph. Perilymph refers to fluid surrounding the bones of the inner ear, while endolymph is the fluid inside the membranous system, which contains the receptors responsible for hearing and balance [1]. Sound waves are converted to nerve impulses through movement between the perilymph and endolymph. Spinal anesthesia may involve dural puncture, which could cause CSF leakage. The subsequent increased flow in the cochlear aqueduct reduces perilymphatic pressure, which in turn increases endolymphatic pressure, causing displacement of certain hair cells and ultimately hearing loss related to anesthesia [1,3,4].
Another mechanism for hearing loss is middle ear pressure changes resulting from general anesthesia, especially nitrous oxide. Anesthetics such as nitrous oxide affects the tympanic membrane, round window, and other sound conducting structures in the ear. An excessive amount of pressure on the round window can cause it to distort and even rupture. Two theories have been suggested to explain middle ear pressure changes. The “implosive” theory proposes that an increase in middle ear pressure causes the tympanic membrane to stretch outward and pull at the oval window, creating low pressure in the cochlea, which can cause the fine ligaments of either the oval or round window to tear [1,5]. On the other hand, the “explosive” theory proposes that anesthesia-induced increases in CSF pressure are transmitted to the perilymphatic space, causing a tear or rupture of the tympanic membrane in the process [1,6].
Hearing loss after general anesthesia is frequently associated with cardiopulmonary bypass surgery [7]. Some of the recognized causes of this particular hearing loss are hypercoagulable states, perioperative hypotension and microembolic phenomena (for example, air or particulate thrombi, i.e. clots) [7-9]. Recently, particulate emboli have been perceived as the cause of most cases of sensorineural hearing loss (SNHL) following cardiovascular surgery. Cardiopulmonary bypass surgery requires aortic cross-clamping and the use of pump-oxygenator systems, which often generate microemboli in the basilar artery and branches to the inner ear, resulting in hearing loss [9,10].
Several drugs have also been documented to be harmful to cells needed for hearing. While these drugs are not used in isolation during surgical procedures, they may be used at the same time as anesthetics [1]. Commonly used ototoxic drugs in anesthesia are aminoglycosides, chemotherapeutic agents, and loop diuretics [11,12]. The effects of loop diuretics such as furosemide, torsemide and bumetanide are reversible and usually disappear once the drug is discontinued; however, ototoxicity caused by aminoglycosides (neomycin, gentamycin, kanamycin, amikacin, among others) and platinum-based chemotherapeutic agents (cisplatin, carboplatin, etc.) are usually irreversible [12]. Among the anti-cancer drugs, cisplatin is most frequently used in clinical settings; its ototoxicity correlates directly to the amount of platinum bound to DNA (cisplatin preferentially binds to the nucleoside guanine). Platination of mitochondrial DNA inhibits transcription and translation of proteins, which decreases mitochondrial metabolism and increases the formation of reactive oxygen species [12,13].
Despite the limited amount of extant literature surrounding POHL, anesthesiologists should be aware of hearing loss as a potential anesthesia-related complication. In general, a more informed understanding of the etiology, incidence, and management of POHL is needed for physicians to better assess and treat their patients.
References
- Sasidharan, S., Singh, V., Nasser, A., Dhillon, H., & Babitha, M. (2022). Perioperative Hearing Loss After Nonotological Surgeries – What is the Role of Anesthesia? International Journal of Academic Medicine, 8(2), 74. https://doi.org/10.4103/IJAM.IJAM_29_21
- Singh, V., Sinha, A., & Madan, R. (2012). Peri-operative Hearing Impairment. Open Journal of Anesthesiology, 2(4). https://doi.org/10.4236/ojanes.2012.24039
- Walter, B., Naumann, H. H., Pfaltz, C. R. Ear, Nose and Throat Disease, a Pocket Reference. New York: Thieme Medical Publishers; 1989.
- Ahmed, M., Chowdhury, M. R. A., Islam, M. S., & Ahmmed, S. (2009). Bilateral Hearing Loss After Spinal Anaesthesia. Journal of Armed Forces Medical College, Bangladesh, 5(1), 53–55. https://doi.org/10.3329/jafmc.v5i1.2854
- Goodhill, V., Harris, I., Brockman, S. J., & Hantz, O. (1973). Sudden Deafness and Labyrinthine Window Ruptures: Audio-vestibular Observations. Annals of Otology, Rhinology & Laryngology, 82(1), 2–12. https://doi.org/10.1177/000348947308200103
- Thomsen, K. A., Terkildsen, K., & Arnfred, I. (1965). Middle Ear Pressure Variations During Anesthesia. Archives of Otolaryngology, 82(6), 609–611. https://doi.org/10.1001/archotol.1965.00760010611009
- Arenberg, I. K., Allen, G. W., & DeBoer, A. (1972). Sudden Deafness Immediately Following Cardiopulmonary Bypass. The Journal of Laryngology & Otology, 86(1), 73–77. https://doi.org/10.1017/S0022215100074946
- Shapiro, M. J., Purn, J. M., & Raskin, C. (1981). A Study of the Effects of Cardiopulmonary Bypass Surgery on Auditory Function: The Laryngoscope, 91(12), 2046-2052. https://doi.org/10.1288/00005537-198112000-00007
- Wright, J. L. W., & Saunders, S. H. (1975). Sudden Deafness Following Cardio-pulmonary Bypass Surgery. The Journal of Laryngology & Otology, 89(7), 757–759. https://doi.org/10.1017/S0022215100080956
- Dutton, R. C., & Edmunds, L. H. (1973). Measurement of Emboli in Extracorporeal Perfusion Systems. The Journal of Thoracic and Cardiovascular Surgery, 65(4), 523–530. https://doi.org/10.1016/S0022-5223(19)40729-0
- Palomar García, F. A. M., E. Bodet Agustí, L. Andreu Mencía, V. Palomar Asenjo, V. (2001). Drug-induced Otoxicity: Current Status. Acta Oto-Laryngologica, 121(5), 569–572. https://doi.org/10.1080/00016480121545
- Lanvers-Kaminsky, C., Zehnhoff-Dinnesen, A. am, Parfitt, R., & Ciarimboli, G. (2017). Drug-induced Ototoxicity: Mechanisms, Pharmacogenetics, and Protective Strategies. Clinical Pharmacology & Therapeutics, 101(4), 491–500. https://doi.org/10.1002/cpt.603
- Yang, Z., Schumaker, L. M., Egorin, M. J., Zuhowski, E. G., Guo, Z., & Cullen, K. J. (2006). Cisplatin Preferentially Binds Mitochondrial DNA and Voltage-dependent Anion Channel Protein in the Mitochondrial Membrane of Head and Neck Squamous Cell Carcinoma: Possible Role in Apoptosis. Clinical Cancer Research, 12(19), 5817–5825. https://doi.org/10.1158/1078-0432.CCR-06-1037