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Therapeutic Approaches in Acute Heart Failure
Published in Andreas P. Kalogeropoulos, Hal A. Skopicki, Javed Butler, Heart Failure, 2023
Getu Teressa, Rachel A. Bright, Andreas P. Kalogeropoulos
Ototoxicity is a rare but serious toxicity that occurs with high dose of diuretic therapy at a dose above 250 mg IV bolus infusion of furosemide or equivalent doses of bumetanide and torsemide. Ototoxicity can occur at lower doses in patients with renal failure, hypoproteinemia, or concurrent therapy with aminoglycoside or other ototoxic drugs. Compared with other loop diuretics, ethacrynic acid may be more toxic at higher doses. Ototoxicity may manifest as tinnitus, temporary hearing loss, or in rare cases, permanent deafness. The mechanism of ototoxicity development is discussed further in Chapter 5.
Critical Appraisal of Animal Models for Antibiotic Toxicity
Published in Adorjan Aszalos, Modern Analysis of Antibiotics, 2020
Patricia D. Williams, Girard H. Hottendorf
A number of antibiotics have been implicated as causing impairment of hearing and/or equilibrium associated with inner ear damage [41]. Of the commonly administered antibiotics, the aminoglycosides are most frequently associated with ototoxic reactions [21], The prevalence of ototoxicity in humans has been reported to range from 2 to 20% [42]. The aminoglycosides vary in their propensity to cause vestibular (equilibrium) or cochlear (hearing) damage to the ear. Gentamicin, along with streptomycin and tobramycin, predominantly affects the vestibular apparatus; neomycin, kanamycin, and amikacin chiefly cause hearing loss [43]. If detected early, ototoxicity may be reversible, but with continued drug administration damage is often permanent. Other antibiotics less frequently associated with human ototoxicity include the tetracyclines, polymixin B, vancomycin, and erythromycin [43].
Testicular Cancer
Published in Manit Arya, Taimur T. Shah, Jas S. Kalsi, Herman S. Fernando, Iqbal S. Shergill, Asif Muneer, Hashim U. Ahmed, MCQs for the FRCS(Urol) and Postgraduate Urology Examinations, 2020
Nkwam Nkwam, Chitranjan J. Shukla, David A. Manson-Bahr, Taimur T. Shah, Farooq Khan
Cisplatin can cause a range of side effects. It is nephrotoxic and is contraindicated in patients with an eGFR of <60 mL/min/1.73 m2. Ototoxicity is another common side effect where patients present with tinnitus and hearing loss. An increased risk of acute myeloid leukaemia has also been observed along with increased risk of hypogonadism and cardiovascular disease.
Cancer survivors treated with platinum-based chemotherapy affected by ototoxicity and the impact on quality of life: a narrative synthesis systematic review
Published in International Journal of Audiology, 2019
Stephanie E. Pearson, John Taylor, Poulam Patel, David M. Baguley
Platinum-based chemotherapy is typically used to treat most solid tumours, including breast, testicular and ovarian cancers (Oun, Moussa, and Wheate 2018; Theile 2017; Kelland 2007). Due to its cost-effective systematic and cytotoxic effects, it has been one of the most efficient and widely available chemotherapies (Paken et al. 2016). However, it is widely known that platinum-based chemotherapy can cause ototoxicity (Campbell and Le Prell 2018; Saladin et al. 2015). Ototoxicity refers to any hearing deficit or tinnitus resulting from a temporary or permanent inner ear dysfunction, following treatment with an ototoxic drug (Paken et al. 2016). Ototoxic drugs include aminoglycoside antibiotics such as gentamicin, loop diuretics such as torasemide and neurologic drugs, such as sodium valproate (Bisht and Bist 2011). Ototoxic effects commonly manifest as tinnitus and/or high-frequency hearing loss that can later progress to lower frequencies (Waissbluth, Peleva, and Daniel 2017). Both tinnitus and hearing loss are associated with a higher risk of depression, social isolation, anxiety (Nordvik et al. 2018) and dementia (Gurgel et al. 2014; Deal et al. 2016).
Current practice of ototoxicity management across the United Kingdom (UK)
Published in International Journal of Audiology, 2018
Drug ototoxicity is defined as a temporary or permanent drug-induced ear dysfunction resulting in sensorineural hearing loss, tinnitus and/or disequilibrium. One of the basic tenants of medicine is to ‘do no harm’ (Ruhl et al. 2014); however, clinicians are faced with the challenge of weighing the benefits of combating a life-threatening disease and the risks of developing the ototoxic consequences of the drug. The discovery and use in the 1940s of aminoglycosides, coupled with the clinical findings of drug-induced damage to hearing and vestibular end organs of the inner ear, led to a vast amount of clinical and scientific research into the aetiology and mechanisms of ototoxicity. However, currently there is very limited evidence of actual current practice across the UK for ototoxicity monitoring and the management of patients when diagnosed with this condition.
Protection for medication-induced hearing loss: the state of the science
Published in International Journal of Audiology, 2018
Tanisha L. Hammill, Kathleen C. Campbell
The term “ototoxic” can be used to refer to any source of non-mechanical damage to the ear, including several medications, many solvents, some heavy metals, and possibly select asphyxiants (Johnson and Morata 2010) yet ototoxicity is most often used in the context of clinical, medication-induced hearing loss or vestibular dysfunction. The field of pharmaceutical interventions for noise-induced hearing loss (NIHL), a condition which is also largely a result of toxic metabolic cochlear changes, is worthy of its own review. As such, and coupled with the paucity of research into any treatment modalities for other ototoxic injuries, this review focuses on the current state of the science for preventing or treating ototoxicity as most often seen in the clinical setting: induced by medications. While physicians are ultimately responsible for pharmaceutical treatment decisions, this review aims to inform the audiologist as an interdisciplinary partner and trusted provider in patient care.