Cocaine-associated Eustachian tube stenosis causing chronic 'glue ear': a rare cocaine-induced destructive lesion.

BACKGROUND: Cocaine is one of the most used recreational drugs. Whilst medical uses exist, chronic recreational nasal use of cocaine is associated with progressive destruction of the osseocartilaginous structures of the nose, sinuses and palate - termed cocaine-induced midline destructive lesions. CASE REPORT: A 43-year-old male with a history of chronic cocaine use, presented with conductive hearing loss and unilateral middle-ear effusion. Examination under anaesthesia revealed a completely stenosed left Eustachian tube orifice with intra-nasal adhesions. The adhesions were divided and the hearing loss was treated conservatively with hearing aids. Whilst intra-nasal cocaine-induced midline destructive lesions are a well-described condition, this is the first known report of Eustachian tube stenosis associated with cocaine use. CONCLUSION: This unique report highlights the importance of thorough history-taking, rhinological and otological examination, and audiometric testing when assessing patients with a history of chronic cocaine use. This paper demonstrates the complexity of managing hearing loss in such cases, with multiple conservative and surgical options available.

Comprehensive Audiometric Analysis of Hearing Impairment and Tinnitus After Cisplatin-Based Chemotherapy in Survivors of Adult-Onset Cancer.

PURPOSE: Cisplatin is widely used but highly ototoxic. Effects of cumulative cisplatin dose on hearing loss have not been comprehensively evaluated in survivors of adult-onset cancer. PATIENTS AND METHODS: Comprehensive audiological measures were conducted on 488 North American male germ cell tumor (GCT) survivors in relation to cumulative cisplatin dose, including audiograms (0.25 to 12 kHz), tests of middle ear function, and tinnitus. American Speech-Language-Hearing Association criteria defined hearing loss severity. The geometric mean of hearing thresholds (0.25 to 12 kHz) summarized overall hearing status consistent with audiometric guidelines. Patients were sorted into quartiles of hearing thresholds of age- and sex-matched controls. RESULTS: Increasing cumulative cisplatin dose (median, 400 mg/m(2); range, 200 to 800 mg/m(2)) was significantly related to hearing loss at 4, 6, 8, 10, and 12 kHz (P trends, .021 to < .001): every 100 mg/m(2) increase resulted in a 3.2-dB impairment in age-adjusted overall hearing threshold (4 to 12 kHz; P < .001). Cumulative cisplatin doses > 300 mg/m(2) were associated with greater American Speech-Language-Hearing Association-defined hearing loss severity (odds ratio, 1.59; P = .0066) and worse normative-matched quartiles (odds ratio, 1.33; P = .093) compared with smaller doses. Almost one in five (18%) patients had severe to profound hearing loss. Tinnitus (40% patients) was significantly correlated with reduced hearing at each frequency (P < .001). Noise-induced damage (10% patients) was unaffected by cisplatin dose (P = .59). Hypertension was significantly related (P = .0066) to overall hearing threshold (4 to 12 kHz) in age- and cisplatin dose-adjusted analyses. Middle ear deficits occurred in 22.3% of patients but, as expected, were not related to cytotoxic drug dosage. CONCLUSION: Follow-up of adult-onset cancer survivors given cisplatin should include routine inquiry for hearing status and tinnitus, referral to audiologists as clinically indicated, and hypertension control. Patients should be urged to avoid noise exposure, ototoxic drugs, and other factors that further damage hearing.

Iatrogenic Phenol Injury Causing Facial Paralysis With Tympanic Membrane and Ossicular Necrosis.

OBJECTIVE: To describe a serious iatrogenic injury and propose means of reducing the risk of its reoccurrence. PATIENTS: A 21-year-old man who suffered facial paralysis, complete necrosis of the tympanic membrane, and ossicular discontinuity because of chemical burn from accidental application of copious amounts of topical anesthetic phenol into the ear. INTERVENTIONS: Conservative management of facial paralysis and delayed reconstruction of the tympanic membrane and ossicular chain. MAIN OUTCOME MEASURES: Gradual recovery to grade 1/6 facial function, successful repair of the tympanic membrane, but persistent 30-dB conductive hearing loss after partial ossicular replacement prosthesis presumably because of scarring. CONCLUSION: Phenol is a highly toxic chemical, topically to both skin and eyes. Absorbed through the skin it can have lethal cardiotoxicity. It is also potent neurotoxin at concentrations much lower (4-7%) than used for tympanic membrane anesthesia (89%) and has long been used therapeutically to destroy nerves in patients of contractions or intractable pain. Otologists need to have a healthy respect for the dangers of using phenol. As only a minute quantity is needed for tympanic anesthesia, commercially available prepackaged applicators are preferred. Storage of stock bottles of 89% phenol solutions in clinical settings risks injury to both patients and practitioners.

Middle and inner ear malformations in two siblings exposed to valproic acid during pregnancy: a case report.

Valproic acid (VPA) is a known teratogenic drug. Exposure to VPA during the pregnancy can lead to a distinct facial appearance, a cluster of major and minor anomalies and developmental delay. In this case report, two siblings with fetal valproate syndrome and a mild conductive hearing loss were investigated. Radiologic evaluation showed middle and inner ear malformations in both children. Audiologic, vestibular and motor examination was performed. This is the first case report to describe middle and inner ear malformations in children exposed to VPA.

External auditory canal stenosis due to the use of powdered boric acid.

Acquired stenosis of the external auditory canal (EAC) may occur because of chronic external otitis, recurrent chronic catarrhal otitis media associated with tympanic membrane perforation, chronic dermatitis, tumors, and trauma. Stenosis occurs generally at the one-third bone part of the external auditory canal. In this article, we present 3 cases of acquired EAC stenosis due to the previous powdered boric acid application. Besides the presentation of surgical intervetions in these cases, we want to notify the physicians not to use or carefully use powdered boric acid because of the complication of EAC stenosis.

Heptanol application to the mouse round window: a model for studying cochlear lateral wall regeneration.

OBJECTIVE: Identify cells supporting cochlear lateral wall regeneration. STUDY DESIGN: Prospective controlled trial. SETTING: Laboratory. Human presbyacusis occurs, in part, secondary to age-related degeneration of cochlear lateral wall structures such as the stria vascularis and spiral ligament fibrocytes. This degeneration is likely linked to the diminished regenerative capacity of lateral wall cells with age. While lateral wall regeneration is known to occur after an acute insult, this process remains poorly understood and the cells capable of self-replication unidentified. We hypothesized that spiral ligament fibrocytes constitute these proliferative cells. SUBJECTS AND METHODS: To test the hypothesis, an acute ototoxic insult was created in 65 normal-hearing, young adult mice via cochlear exposure to heptanol. Sacrifice occurred at 1 to 60 days posttreatment. Auditory brainstem responses, 5-ethynyl-2'-deoxyuridine assay, and immunostaining were used to assess regeneration. RESULTS: Posttreatment hearing thresholds were elevated in nearly all treated mice. Selective fibrocyte apoptosis and strial injury were observed at the time of peak hearing loss around 1 to 7 days posttreatment. Cellular proliferation was detected in the region of type II fibrocytes during this time. Hearing thresholds plateaued at 7 days posttreatment followed by a significant recovery of both hearing and morphologic appearance. Permanent outer hair cell degeneration was observed. CONCLUSIONS: Heptanol application to the round window of young adult mice is a rapid, selective, and reliable technique for investigating proliferation in the cochlear lateral wall. The data indirectly showed that spiral ligament fibrocytes may be the proliferative cells of the cochlear lateral wall. Further studies of this process are needed.

Accuracy of velocity distortion product otoacoustic emissions for estimating mechanically based hearing loss.

Distortion product otoacoustic emissions (DPOAEs) measured as vibration of the human eardrum have been successfully used to estimate hearing threshold. The estimates have proved more accurate than similar methods using sound-pressure DPOAEs. Nevertheless, the estimation accuracy of the new technique might have been influenced by endogenous noise, such as heart beat, breathing and swallowing. Here, we investigate in an animal model to what extent the accuracy of the threshold estimation technique using velocity-DPOAEs might be improved by reducing noise sources. Velocity-DPOAE I/O functions were measured in normal and hearing-impaired anaesthetized guinea pigs. Hearing loss was either conductive or induced by furosemide injection. The estimated distortion product threshold (EDPT) obtained by extrapolation of the I/O function to the abscissa was found to linearly correlate with the compound action potential threshold at the f(2) frequency, provided that furosemide data were excluded. The standard deviation of the linear regression fit was 6 dB as opposed to 8 dB in humans, suggesting that this accuracy should be achievable in humans with appropriate improvement of signal-to-noise ratio. For the furosemide animals, the CAP threshold relative to the regression line provided an estimate of the functional loss of the inner hair cell system. For mechanical losses in the middle ear and/or cochlear amplifier, DPOAEs measured as velocity of the umbo promise an accuracy of hearing threshold estimation comparable to classical audiometry.

Otologic effects of topical mitomycin C: phase I-evaluation of ototoxicity.

HYPOTHESIS: To determine ototoxicity of topical mitomycin C when placed in the middle ear at varying concentrations. BACKGROUND: Despite meticulous surgical technique and diligent postoperative care, some patients develop excessive scar and granulation tissue in the middle ear or mastoid cavity. Poor wound healing may result in infection, tympanic membrane perforation, or conductive hearing loss, which may necessitate further surgery. Use of topical mitomycin C in the ear may be beneficial in reducing scar and granulation tissue formation. This phase of the study was developed to determine the safety of topical mitomycin C in the rat model relative to ototoxicity. METHODS: Twelve Sprague-Dawley rats were evaluated with auditory brainstem response testing before and after treatments. Topical mitomycin C was injected in the middle ear of the right ear of eight animals. Varying concentrations of 0.125 to 0.5 mg/ml were used. Saline was injected in the left ear of each animal to serve as a control. Four separate animals were evaluated with placement of topical mitomycin C on Gelfoam into the middle ear. In two animals, Gelfoam was placed in the middle ear for 1 minute and then removed. In two animals, Gelfoam was placed in the middle ear and left in place. Auditory brainstem response testing was performed at 4 weeks and at 8 weeks. RESULTS: Using a high concentration of mitomycin C (>0.25 mg/ml) resulted in ototoxicity, with an increase in the auditory brainstem response threshold at 4 weeks and at 8 weeks. At low concentrations (<0.20 mg/ml), no change in auditory brainstem response threshold was noted. Animals treated with Gelfoam soaked in mitomycin C showed no change in auditory brainstem response threshold. CONCLUSION: The results of this study indicate that topical mitomycin C on Gelfoam applied in the middle ear appears safe when low concentrations are used, even in the rat, which has a higher susceptibility to gentamycin toxicity than humans. Higher concentrations may lead to ototoxicity based on changes in Wave V on auditory brainstem response. This treatment may prove to be an important option for patients suffering from chronic granulation tissue or scar tissue in the external or middle ear.

[Types of hearing disorders in drug addicts and individuals drinking non-consumable alcohols]. / Charakter uposledzen sluchu u narkomanów i osób spozywajacych alkohole niekonsumpcyjne.

All over the world an increase in the number of subjects addicted to various chemical substances has been observed. The studies of their toxic effect on the hearing have been so far most frequently limited to acute intoxication or direct effect: there are no data concerning distant and persistent effects. The aim of the study was to determine the type of hearing loss in drug addicts and individuals drinking non-consumable alcohols, examined during the period of abstinence. A group of 210 subjects addicted to various substances was examined using acumetry test and tuning forks, as well as threshold, suprathreshold and speech audiometry. Taking into consideration the threshold results for particular subjects, the percentage of hearing loss for both ears was calculated using CPT index. Most frequent complaints connected with the organ of hearing, such as tinnitus and hearing impairment were reported by alcoholics and opioid addicts. In the age adjusted threshold audiometry, perceptive hearing loss was diagnosed in nearly 50% of the subjects. The percentage of hearing loss calculated for both ears, using CPT index, demonstrated the highest values in the group of subjects drinking non-consumable alcohols and addicted to volatile organic substances.

[Hearing loss caused by high dose carboplatin therapy]. / Hörverlust durch Hochdosis-Carboplatintherapie.

BACKGROUND: Carboplatin is regarded as a non-ototoxic or low-grade ototoxic chemotherapeutic agent. METHOD: We report on three patients with a recurrence of testicular cancer after cisplatin chemotherapy who suffered hearing loss after subsequent high-dose carboplatin therapy. RESULTS: Audiometry demonstrated carboplatin-induced hearing loss primarily in the mid-range and high frequencies up to 45 dB at 3 kHz and up to 55 dB at 8 kHz. In two of three patients, transitory-evoked otoacoustic emissions were absent after carboplatin therapy. CONCLUSION: Following first-line cisplatin chemotherapy, salvage treatment with high-dose carboplatin can generate hearing loss in the middle and high frequencies.

The effects of four, commercial ceruminolytic agents on the middle ear.

Four, commercially available ceruminolytic agents and physiological saline were screened for ototoxic and inflammatory reactions on the middle ear mucosae of guinea pigs (n = 38) and dogs (n = 24). Each solution was injected transtympanically in anesthetized animals. The effects were assessed by brain stem auditory evoked response (BAER) tests to evaluate hearing function and by histological examination of the middle ear structures. Varying degrees of hearing loss and inflammation were observed in some guinea pigs and dogs treated with solutions A, C, and D, whereas no abnormal finding was associated with solution B or saline.

Neonatal cochlear hearing loss results in developmental abnormalities of the central auditory pathways.

We have used animal models of long term neonatal cochlear hearing loss to study developmental plasticity of the central auditory pathways. Newborn chinchilla pups and feline kittens were treated with the ototoxic drug amikacin, so as to induce basal lesions in the cochlea. At maturity these animals were used in single unit electrophysiological mapping studies, in which the cochleotopic organization of primary auditory cortex (of the cat) and the inferior colliculus of the midbrain (in the chinchilla) were mapped. We have observed, both in the midbrain and auditory cortex, massive reorganization of frequency representation. Most striking were the presence of large monotonic regions (i.e. large areas in which all neurons have similar tuning properties). Cochlear lesions which involve inner hair cells clearly modify the normal development of cochleotopic representation in the midbrain and cortical regions. We suggest that similar abnormal patterns of frequency representation will exist in human subjects with long term neonatal hearing loss.

Ciprofloxacin. Use as a topical otic preparation.

Most common topical otic preparations have been shown to cause sensorineural hearing loss and hair-cell damage in experimental animals. Ciprofloxacin is a relatively new fluoroquinolone with excellent activity against Pseudomonas and methicillin-resistant Staphylococcus aureus. Recent studies have shown oral ciprofloxacin to be effective in the treatment of chronic serous otitis media and malignant external otitis. However, this drug has never been used as a topical otic preparation. Thirty-five albino female guinea pigs were used to investigate the ototoxicity of topical ciprofloxacin hydrochloride. Bilateral transbullae drug delivery tubes were placed and auditory brain-stem response thresholds were recorded at 20, 16, 8, and 4 kHz before treatment and 21 days after the completion of treatment. Two groups of guinea pigs were used. In group 1 (positive controls), five guinea pigs had 0.1 mL of neomycin sulfate administered in one ear while the opposite (control) ear received 0.1 mL of 0.9% sodium chloride solution; in group 2, 30 guinea pigs received 0.75% ciprofloxacin ophthalmic solution and 0.9% sodium chloride solution in the control ear. All drugs were given twice a day for 7 consecutive days. All results were evaluated with paired, two-tailed t test and Hotelling's T2 test, and calculation of power was performed on all nonsignificant results. No significant ototoxic reaction was observed; small increases in hearing thresholds occurred at 4 (5.65 +/- 8.25 dB [mean +/- SD]) and 8 kHz (3.70 +/- 6.63 dB [mean +/- SD]) in the ciprofloxacin-treated ears; however, no significant hair-cell loss was seen.(ABSTRACT TRUNCATED AT 250 WORDS)

[Deafness, induced by sodium ethacrynate in guinea pigs, alleviated by microwave treatment]. / Amélioration de la surdité induite par l'étacrynate de sodium chez le cobaye, à l'aide d'un traitement par micro-onde.

Microwave is used to treat temporal hearing loss caused by intravenous injection of the ethacrynic acid in guinea pigs. The recovery of hearing is much faster in the treated groups than in the control group. The article proposes possible mechanism of the effects against the ethacrynic acid induced deafness and assume that the result of this research can provide an experimental basis for treatment of some perceptive deafness due to ischemia of stria vascularis of the cochlea.

High-dose cisplatin treatment: hearing loss and plasma concentrations.

Fifty-four patients with metastatic cancer were followed audiometrically during high-dose (100-120 mg/m2) cisplatin chemotherapy. Eighty-one percent of the patients showed significant changes in air-conduction hearing thresholds after completion of therapy. Thirteen percent sustained a significant hearing handicap. An interindividual variation was found, ranging from severe hearing loss after the first course to unaffected hearing after three courses. The ototoxic effect was not increased by pre-existing hearing loss, but was slightly increased by age. The risk was determined more by the amount of the single dose than by the cumulative dose. The further ototoxic effect could not be predicted on the basis of the audiogram after the first course. Peak plasma concentration of platinum was measured in eight patients, and no ototoxic changes were noted below a concentration of 1 microgram/L.

[Evaluation of auditory function in homozygous beta-thalassemia]. / Valutazione della funzione uditiva nella beta-talassemia omozigote.

We examined the auditory function of 29 subjects affected by homozygous beta-thalassemia, managed with an high transfusion scheme and regularly treated with 40-60 mg/kg/day of desferrioxamine. A group of 29 healthy subjects is studied as control. We found conductive hearing defect in 8 thalassemics (6 bilateral) and sensory-neural hearing loss at high frequencies in 4. Thalassemic patients showed more auditory impairment than controls, an higher incidence of tonsillar hypertrophy, adenotonsillitis and submandibular lymph-node enlargement.

Beta blockers and loss of hearing.

Loss of hearing in a 43 year old man during treatment with metoprolol was dose related and disappeared within a few months after the drug had been stopped. The hearing impairment was of mixed type, with an air bone gap without any disorder of the middle ear observable by conventional clinical methods. Similar scattered reports from international sources on loss of hearing during treatment with beta blockers are also presented.

Auditory toxicity effects of long-term cis-dichlorodiammineplatinum II therapy in genitourinary cancer patients.

To determine the auditory toxicity effects of long-term cis-dichlorodiammineplatinum II therapy, pure tone hearing thresholds were measured prior to therapy and repeated before each subsequent treatment. CDDP was given by a slow intravenous drip method at a low dose of 1 mg/kg body weight, with 37.5 gm mannitol, once a week for six treatments and every 3 weeks thereafter. From a group of 173 genitourinary cancer patients treated, 50 male patients were selected who received at least 12 months of CDDP with no active conductive ear pathology, and whose audiograms obtained at baseline, 6th weeks, 26th weeks, and 52nd weeks of treatment were all available for comparison. Pure tone threshold levels deteriorated across time particularly by the 52nd week and at the higher frequencies. Threshold differences across time were statistically significant and within a linear trend. Of the 50 cases, 30% showed suspect or no ototoxicity, 26% mild, 32% moderate, 2% marked, and 4% showed severe ototoxic changes. Of the two cases who developed severe ototoxicity, one showed complete recovery. There was partial recovery in 26% and no recovery in 54%. Individual variability in susceptibility to and recovery from ototoxicity necessitates systematic audiometric monitoring throughout the therapy.