Hearing loss in patients with vestibulotoxic reactions to gentamicin therapy.

OBJECTIVES: To determine whether patients with vestibulotoxic reactions to gentamicin have hearing thresholds worse than predicted by distributions of better-ear hearing thresholds in people of the same age and sex in the general population, and, if so, to measure the severity and audiometric pattern of that hearing loss. DESIGN: Retrospective case series from previously published prospective and retrospective studies of vestibular function in patients receiving gentamicin. SETTING: Tertiary neurotological practice. PATIENTS: Convenience sample of 33 consecutive patients seen for objective evidence of vestibulotoxic reactions after systemic gentamicin therapy. Twenty-five of 33 patients underwent valid and complete audiometry. MAIN OUTCOME MEASURES: Age- and sex-corrected better-ear pure tone thresholds, 0.5 to 6.0 kHz. The better-ear audiogram was defined in 2 ways: primarily, the audiogram of the ear with the better average threshold at 0.5, 1.0, and 2.0 kHz; secondarily, the composite audiogram taking the better threshold for each frequency. RESULTS: Patients exhibiting vestibulotoxic reactions to gentamicin therapy had hearing thresholds that were similar to those seen in the general population at 0.5, 3.0, and 6.0 kHz. Median thresholds were 6 to 7 dB worse than expected at 1.0 and 2.0 kHz (95% confidence intervals, 2-13 dB and 3-12 dB, respectively). The largest median difference was 15 dB at 4.0 kHz (95% confidence interval, 3-23 dB), but this difference was not significant for the more conservative composite definition of the better ear. CONCLUSIONS: Patients with vestibulotoxic reactions to gentamicin therapy have little additional hearing loss compared with the general population. Physicians should monitor both auditory and vestibular function when aminoglycosides, especially gentamicin, must be used.

Five-year surveillance of West Nile and eastern equine encephalitis viruses in Southeastern Virginia.

To investigate the occurrence of West Nile virus (WNV) and Eastern equine encephalitis virus (EEE) in southeastern Virginia, the Bureau of Laboratories at the Norfolk Department of Public Health (NDPH) analyzed mosquito pools and the sera of sentinel chickens from the southeastern Virginia area each year from 2000 to 2004. Mosquito pool supernatants were screened for the presence of viral RNA by conventional reverse transcription polymerase chain reaction (RT-PCR) and Taqman RT-PCR with the i-Cycler. Mosquito pools were also tested for virus activity by Vero cell culture. The primary enzootic vector of WNV was Culex (Cx.) pipiens and that of EEE was Culiseta (Cs.) melanura. During the five-year surveillance period, the peak minimum infection rates (MIRs) of WNV and EEE in these mosquito species were 2.7 (2002) and 0.9 (2001), respectively. In 2003, the MIRs in Cs. melanura for WNV and EEE were 0.24 and 0.56, respectively; and the MIR for WNV in Cx. pipiens was 0.64. In 2004, Cs. melanura was less active in the WNV transmission cycle (MIR = 0.07) than was Cx. pipiens (MIR = 1.8), and Cs. melanura was the only vector for EEE (MIR = 0.37). The trend was for EEE activity to peak in July; WNV activity peaked in August. Sentinel-chicken sera were tested for IgM antibodies, and peak IgM seroconversions to these arboviruses were recorded in August 2003 for WNV and in July 2003 for EEE. In 2004, the highest IgM seroconversions to EEE occurred later in August. The overall trend of arbovirus activity was greater in 2003 than in 2004.

Permanent gentamicin vestibulotoxicity.

OBJECTIVE: To determine the natural history of permanent gentamicin vestibulotoxicity. STUDY DESIGN: Retrospective; comparison of retrospective and prospective studies. SETTING: Tertiary neurotology clinic. Clinical research and technology center. SUBJECTS: Thirty-three subjects with permanent gentamicin-induced vestibulotoxicity. INTERVENTIONS: Medical records review, neurotologic examination, and vestibular and auditory function tests. MAIN OUTCOME MEASURES: Vestibular and auditory function test results at least 1 year after discontinuation of gentamicin, clinical examination results, serum gentamicin levels, and serum creatinine levels. RESULTS: Thirty-three subjects had vestibular function test results consistent with permanent gentamicin ototoxicity. All complained of dysequilibrium, 32 described oscillopsia, and 23 had tinnitus. All 33 subjects had complained of symptoms consistent with ototoxicity within 1 to 3 weeks of initiation of gentamicin therapy; however, gentamicin vestibulotoxicity was not recognized before hospital discharge in 32 of 33 subjects. Serum peak and trough gentamicin levels did not correlate with the development of vestibulotoxicity, nor did observance of recommended "safe" dosage ranges. Of 17 subjects whose serum creatinine levels were recorded, 6 experienced abnormal elevations in serum creatinine in conjunction with gentamicin use. CONCLUSION: Gentamicin can cause permanent vestibular and auditory ototoxicity. There is no safe dose of gentamicin. Serum gentamicin levels are of no value in predicting the onset, occurrence, or severity of vestibulotoxicity or cochleotoxicity. Termination of gentamicin on appearance of signs or symptoms of ototoxicity may reduce the incidence of permanent vestibular ototoxicity. When possible, other antibiotics should be administered.

Benign paroxysmal positional nystagmus in hospitalized subjects receiving ototoxic medications.

OBJECTIVE: To investigate the occurrence of benign paroxysmal positional nystagmus in subjects undergoing treatment with potentially ototoxic medications. STUDY DESIGN: Prospective and retrospective record reviews. SETTING: Tertiary referral neurotology clinic; clinical research and technology center. SUBJECTS: Ninety-nine hospitalized subjects undergoing treatment of infectious disease or carcinoma with potentially ototoxic medications. INTERVENTIONS: Records review, tests of vestibular function. MAIN OUTCOME MEASURE: Results of Hallpike positional tests for benign paroxysmal positional nystagmus (electro-oculography). RESULTS: Forty-one (41%) of 99 subjects were female and 58 (59%) were male. Age range was 15 to 73 years (mean, 47 years). Forty-nine (50%) of 99 subjects had an unequivocally positive Hallpike test for benign paroxysmal positional nystagmus in one or both ears. The occurrence of benign paroxysmal positional nystagmus in the Hallpike-positive population was distributed equally across age decades. Of the 49 subjects with benign paroxysmal positional nystagmus, 22 (44%) were female and 27 (56%) were male. CONCLUSIONS: Benign paroxysmal positional nystagmus is the most common cause of vertigo in the general population, including subjects receiving ototoxic drugs. Complaints of vertigo in subjects receiving ototoxic drugs therefore may or may not indicate onset of ototoxicity. Occurrence of benign paroxysmal positional nystagmus in subjects receiving ototoxic drugs was independent of gender or age. The high occurrence rate of benign paroxysmal positional nystagmus in subjects receiving potentially ototoxic medications is consistent with the observation that benign paroxysmal positional nystagmus occurs in combination with many pathologic conditions. Benign paroxysmal positional nystagmus presenting in subjects receiving ototoxic drugs may complicate the clinical identification of ototoxicity and obfuscate clinical decision-making processes.

Eye movement responses to active, high-frequency pitch and yaw head rotations in subjects with unilateral vestibular loss or posterior semicircular canal occlusion.

This study assessed the eye movement responses to active head rotation in six subjects with complete unilateral vestibular loss (UVL), five subjects with posterior canal plugging (PCP) and age- and sex-matched normal subjects. Subjects performed head rotations in the pitch and yaw planes at frequencies ranging from 2 to 6 Hz, while looking at an earth-fixed target. Vertical eye movement gains obtained in UVL, PCP and normal subjects were not significantly different. Vertical phases decreased with increasing head movement frequencies in both UVL and PCP subjects. Although this decrease produced significantly different vertical phases between UVL and normal subjects for head movements above 3.9 Hz, vertical phases in some normal subjects were similar to those obtained in UVL subjects. We conclude that active head oscillations in the pitch plane are not clinically useful for the detection of vertical canal impairment limited to one ear. As expected, UVL subjects showed reduced horizontal gains, and eye velocity asymmetries during active head rotation in the yaw plane. Results in some PCP subjects suggested possible minor impairments of horizontal vestibulo-ocular reflexes.