Drug-Induced Hearing Loss Prevention
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Certain medications like aminoglycoside antibiotics and chemotherapy drugs can damage hearing and balance by harming delicate inner ear cells. Regular audiometric monitoring above 8 kHz, where hearing is lost first, is the most effective way to detect this potentially preventable ototoxicity early. Protective strategies are being studied to allow safer use of these important drugs.
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Drug-Induced Hearing Loss Prevention
- 1. OTOTOXICITY Dr. Ghulam Saqulain Head Of Department of ENT Capital Hospital
- 2. Close to 200 prescription and OTC medications have ototoxic potential. “Drug-induced hearing loss accounts for most cases of preventable hearing loss worldwide”
- 3. Two categories of medications that have the greatest potential for permanent changes in hearing and or balance are: aminoglycosides and anti-neoplastic agents. Others Are: Diuretic- furosemide, ethacrynic acid Salicylate-aspirin antimalarial drug- quinine
- 4. X
- 5. X
- 6. Clinical characteristics of ototoxic deafness Bilateral hearing loss Hearing loss happens at high frequency Reversible or progressive With tinnitus, vertigo
- 7. Audiometric Monitoring for Ototoxicity The only way to detect ototoxicity is by audiometric monitoring of extended high frequencies, above 8 KHz.
- 8. Pathophysiology of Ototoxicity Hair cells in the inner ear are primarily affected. In the vestibular system type I hair cells of the crista of the semi-circular canals are targeted X
- 10. X
- 11. X
- 12. Incidence of aminoglycoside Ototoxicity Incidence ranges 20-33% for commonly used aminoglycosides while balance is affected in 18% of cases.
- 13. Risk Factors Long term treatment i.e. TB patients Impaired renal function – increases drug half-life Concomitant use of loop diuretics Genetic – mitochondrial mutations (1555 mutation)
- 14. Aminoglycoside Ototoxicity Streptomycin was the first aminoglycosides antibiotic and the first drug effective against TB. Discovered by Selman Waksman et al in 1944. Adverse side effects on the kidney and inner ear (vestibular toxicity) were reported in 1945
- 15. Aminoglycoside Ototoxicity In the last 20 years the use of aminoglycosides has declined in industrial societies In developing countries, their effectiveness and low cost make them popular. They are often sold OTC and are the most commonly used antibiotics worldwide. X
- 16. Aminoglycoside Ototoxicity With the resurgence of drug resistant TB, there is renewed interest in aminoglycosides specifically streptomycin and amikacin/ kanamycin as part of the World Health Organization recommended multi drug regimen. X
- 17. Effect of Aminoglycosides on Auditory/Vestibular Functions Studies of human temporal bones and experimental animals show inner ear hair cells are the first to be affected followed by outer hair cells.. Outer hair cells are targeted in the cochlea extending from base to apex. Results in high frequency hearing loss which can extend to frequencies important to understanding speech.
- 18. In the vestibular system, its primary effect is loss of vestibular hair cells in the semi circular canals and Utricular macula. This leads to oscillopsia resulting in postural instability and risk of fall. It was once believed that maintaining peak and trough serum levels of a drug would mitigate ototoxic effects. Current evidence shows this not to be the case at least for vestibular toxicity.
- 19. Gentamycin and streptomycin are considered more vestibulotoxic. Amikacin and Neomycin are considered more cochleo-toxic.
- 20. Pharmokinetics Presence of the drug does not necessarily cause toxicity Concentration of the drug in the inner ear does not exceed the serum level Half life in cochlear tissue has been measured to exceed one month Traces can be detected up to 6 months following the end of treatment.
- 21. Mechanisms of Aminoglycoside Ototoxicity Reactive Oxygen Species (ROS) formation appears to be key. Reactive oxygen species (ROS) are chemically reactive molecules containing oxygen. Examples include oxygen ions and peroxides. ROS are formed as a natural byproduct of the normal metabolism of oxygen Depletion of anti oxidant Glutathione (GSH) enhances ototoxicity while dietary supplementation inhibits toxicity.
- 22. Is Aminoglycoside ototoxicity preventable? Medications showing promise are d- methiomine and salicylate. Two issues need to be solved before protective treatment can be considered. Effective drug levels must be maintained. Drug must not interfere with the anti- bacterial activity of the aminoglycosides. X
- 23. One clinical study found aspirin was protective reducing incidence of hearing loss by 75%. Sha, S. H. , Qui, J. H. & Schacht, J. (2006) Aspirin to prevent gentamicin- induced hearing loss. New England Journal of Medicine, 354, 1856-7. X
- 24. Chemotheraputic Agents & Ototoxicity - Cisplatin Introduced in the 1970s and is effective against germ cell, ovarian, endometrial, cervical, urothelial, head and neck, brain and lung cancers. Highest ototoxic potential and is the most ototoxic drug in clinical use. Symptoms of ototoxicity begin with tinnitus and high frequency hearing loss.
- 25. Incidence of hearing loss has been reported at 11-91% with an overall incidence of 69%. In patients with head and neck cancer treated with Cisplatin, about 50% develop hearing loss.
- 26. Risk Factors for Cisplatin Ototoxicity Intravenous bolus administration or high cumulative dose Young children, under 5 years, or older > 46 years Renal insufficiency Prior cranial irradiation Co-administration of vincristin X
- 27. The best predictor of cisplatin ototoxicity is cumulative dose. The critical dose is 3-4 mg/Kg body weight. Ototoxicity increased dramatically when the total cumulative dose exceeds 400 mg/m2 X
- 28. Characteristics of Cisplatin Ototoxicity Bilateral and permanent. High frequencies affected first. It can occur suddenly. Speech discrimination may be markedly affected.
- 29. Mechanisms of Cisplatin Ototoxicity Hearing loss affected by free radical formation and anti-oxidant inhibition. Formation of reactive oxygen radicals produces glutathione depletion in the cochlea and lipid peroxidation. Induced apoptosis in hair cells causing permanent hearing loss.
- 30. Carboplatin Introduced due to its lower nephrotoxicity than cisplatin. It is used to treat small cell lung cancer, ovarian and head and neck cancers. carboplatin is less toxic than cisplatin but higher doses of carboplatin are used increasing ototoxicity
- 31. OTOTOXIC MONITORING Ototoxicity is determined by establishing baseline hearing test data ideally prior to treatment including testing at high frequencies. Results are compared to serial audiograms allowing the patient to serve as their own control.
- 32. The highest frequencies measuring 100 dB or less are monitored with testing ideally occurring just prior to each chemotherapeutic dose Monitoring 1-2 times per week for patients receiving ototoxic antibiotics. Post treatment evaluations are conducted as soon as possible after dispensing the drug and repeated at 1, 3 and 6 month post treatment.
- 33. The customized test protocol is called the Sensitive Range for Ototoxicity, or SRO and differs for each patient. It consists of the highest frequencies with thresholds 100 dB or better followed by the next six lower frequencies. The SRO is established during baseline testing prior to ototoxic drug administration.
- 34. Summary Audiometric monitoring using the patient’s own extended high frequency thresholds as a control, is the most sensitive method to detect ototoxicity. The test is easily tolerated High frequency hearing is affected first Speech perception can degrade if hearing loss extends below 8KHz.
Editor's Notes
- The changes can be temporary or permanent. (p.231)
- Ototoxic incidence is dependent on drug dosage, patient factors and concomitant ototoxic medication administration.
- p. 231
- For this presentation, we will concentrate on drugs that are primarily cochleotoxic although as you can see from the slide , some drugs also produce permanent changes in vestibular function leading to debilitating conditions affecting stability and risk of falling. (p.
- Without monitoring, ototoxic hearing loss may go unnoticed until hearing loss affects the ability to understand speech.
- Outer hair cells are important because they amplify soft sounds and help with frequency (pitch) sensitivity. Without them, sounds must be much louder to be perceived.
- Most standard audio tests are done at frequencies up to 8K. This leaves the early ototoxic effect undetected above this frequency. (p. 167)
- Patients with the 1555 mutation have increased toxicity to the cochlea from aminoglycocide. Profound deafness can occur after one injection of an aminoclycoside. (p.169)
- (p.164)
- (p.164)
- (p.164)
- (p.165)
- There are however no hard and fast rules and all aminoglycosides may affect either the vestibular system, cochlear or both. (p.166)
- This may explain the enhanced sensitivity of patients getting a second round of treatment. (p. 168)
- (p.169)
- In the case of salicylate there was no negative influence on efficacy of the aminoglycocide. (p.170)
- (p.171)
- (p.141)
- (p.142)
- (p.143)
- 71% of cisplatin hearing loss was detected first in frequency of 8000 Hz or above. (p.144). High frequency testing is the hallmark of the ototoxic monitoring program which will be discussed later.
- (p.144)
- These results are tabulated in graphical form to track changes from baseline
- Questions???