Factor In Sensorineural Hearing Loss Research Articles

A retrospective case-controlled study of 1490 consecutive patients presenting to a neuro-otology clinic to examine the relationship between blood lipid levels and sensorineural hearing loss.

This study set out to test the null hypothesis that the distribution of blood lipid levels is the same in a population with a sensorineural hearing loss (SNHL) as in a control population. Hyperlipidaemia has been implicated as an aetiological factor in SNHL; however, the majority of reports are retrospective, lack adequate controls, or are based on a series of cases which may represent incidental findings and not a true causal relationship. In all, 1490 consecutive patients who presented to a neuro-otology clinic were studied retrospectively. This group is exceptional in that all patients had had fasting lipid profiles done regardless of their presenting problem. Those with a mean SNHL > 25 dB (0.5, 1, 2 and 4 kHz) were compared with those with hearing thresholds < or = 25 dB. An analysis of variance was also done. The study group was also compared with the National Study of Hearing data set to add external validity. Simple correlations were found between hearing thresholds and many parameters such as blood pressure, fasting glucose, triglyceride or fasting cholesterol. Analysis of variance of the neuro-otology group, controlling for variables such as age and sex, showed no significant association between hearing and blood pressure, packed cell volume, mean corpuscular volume, fasting glucose, triglyceride or fasting cholesterol. However, when general linear interactive modelling was used to analyse hearing thresholds, raised total fasting cholesterol was associated with significantly better hearing threshold levels. This study leads to a rejection of the Null hypothesis that the distribution of lipid levels is the same in a population with a hearing loss as in a control population, as hearing thresholds were found to be significantly better in those with raised cholesterol levels.

Hereditary Hearing Loss - the Role of Environmental Factors

A large family with mid onset sensorineural hearing loss (HL) was used to study the effect of environmental factors on progression HL. Data from five-generations of one family were traced and 104 living members were included in the study. Audiograms were measured for 60 family members. We used an expert program to study the individual risk factors, which included the known risk factors for sensorineural HL. The pattern of inheritance in this HL family was autosomal dominant and 22 individuals were affected. The HL among affected individuals was symmetrical and varied from mild to severe. The mean age at onset of HL was 22 years. The mean deterioration of hearing at 2 kHz frequency was 1 dB/year. In the risk analysis the use of NSAID-analgetics and military noise exposure correlated with HL. There was no correlation between occupational and free time noise-exposure and HL. Analgetics may aggravate the HL in subjects with inherited HL. This type of genetic lesion is new and is not in those chromosomal areas already documented in the literature.

Sensorineural Hearing Loss in Children After Liver Transplantation

DEUTSCH, ELLEN S.; BARTLING, VICTORIA; LAWENDA, BRIAN; SCHWEGLER, JOHN; FALKENSTEIN, KATHLEEN; DUNN, STEPHEN Author Information

Sensorineural hearing loss in children after liver transplantation.

To investigate risk factors for sensorineural hearing loss (SNHL) in children after liver transplantation. Retrospective medical record review. Pediatric tertiary care hospital. One hundred twenty-five consecutive children who received liver transplants between March 1, 1987, and June 30, 1996. The presence of SNHL (bone conduction threshold of >35 dB of hearing loss in at least 1 frequency) and the cause of the liver abnormality in all 125 patients. In addition, among the subset of children who had biliary atresia and underwent transplantation before 2 years of age, the total dose (milligrams per kilogram of body weight) of aminoglycoside antibiotic medications (tobramycin sulfate, gentamicin sulfate, and amikacin sulfate) and of intravenous loop diuretic agents (furosemide) was compared between children with and without SNHL. Audiologic evaluations were available for 66 of 125 patients, 15 (12%) of whom have SNHL. Of 5 survivors with the short-bowel syndrome, 4 have severe to profound SNHL. Of 46 children who have biliary atresia and who underwent transplantation before 2 years of age, 8 (17%) have SNHL. Among the 26 evaluable children with biliary atresia undergoing liver transplantation before 2 years of age, logistic regression analysis revealed that the most important risk factor for SNHL was the cumulative dose of amikacin (P = .05). Children receiving liver transplants are at an increased risk for SNHL. Those with the short-bowel syndrome have the greatest prevalence of SNHL. Among the subset of children with biliary atresia receiving liver transplants before 2 years of age, statistical analysis demonstrates a dose-response relationship between the receipt of amikacin and the occurrence of SNHL.

Risk factors for childhood sensorineural hearing loss in the Oxford region.

We have used a comprehensive register of hearing-impaired children born in the former Oxford Health Region to study risk factors for sensorineural hearing loss. The occurrence of a wide variety of risk factors was documented from the case notes of 145 children; these were all the cases known at the time of the study with all degrees of hearing loss born between 1984 and 1988. Comparison with the normal Regional population showed that maternal age over 35 years and Asian ethnic origin were significant risk factors for congenital (non-acquired) hearing loss (odds ratio 1.7 and 2.5 respectively). Black/Asian children were also significantly more likely to have acquired losses. Low birthweight (below 2500 g) also gave a significantly increased risk, with an odds ratio of 4.5, rising to 9.6 for birthweight less than 1500 g. We also found that significantly more hearing-impaired cases were in lower social classes compared with the general population. A high proportion of cases (24%) had cranio-facial abnormalities (CFA), including many non-aural abnormalities and dysmorphic features, which therefore should be counted as high risk. Hearing losses acquired due to perinatal causes were almost all mild or moderate. Four factors-admission to special care baby unit for more than 72 hours, CFA, family history, and meningitis-accounted for 69% of all cases in this study. Targeted neonatal screening based on the first three factors, plus obligatory testing following meningitis, therefore, should be highly efficient at detecting deafness early.

Risk factors of sensorineural hearing loss in preterm infants.

Among 547 preterm infants of < or = 34 weeks gestation born between 1987 and 1991, 8 children (1.46%) developed severe progressive and bilateral sensorineural hearing loss. Perinatal risk factors of infants with hearing loss were compared with those of two control groups matched for gestation and birth weight and for perinatal complications. Our observations demonstrated an association of hearing loss with a higher incidence of perinatal complications. Ototoxicity appeared closely related to a prolonged administration and higher total dose of ototoxic drugs, particularly aminoglycosides and furosemide. Finally, we strongly recommend to prospectively and regularly perform audiologic assessment in sick preterm children as hearing loss is of delayed onset and in most cases bilateral and severe.

Risk factors for sensorineural hearing loss in extremely premature infants.

To identify potentially preventable risk factors for sensorineural hearing loss (SNHL) in extremely premature infants. A case control study of survivors with gestational age (GA) < 28 weeks or birthweight (BW) < 1000 g using data collected prospectively in our Neonatal Intensive Care Unit database. Each subject with bilateral SNHL > 40 dB was matched according to GA, BW and sex with two controls who had neither sensorineural nor conductive hearing loss. Infants with SNHL had increased mean (+/- s.d.) days ventilated (53 +/- 21 vs 37 +/- 23 days, P = 0.006) and in oxygen (107 +/- 44 vs 69 +/- 28 days, P = 0.02) compared with controls. The risk for SNHL was increased for infants who spent > 90 days in oxygen (OR 4.0 [95% CI 1.1-15.6]), had maximum FiO2 > 0.90 (5.6 [1.2-26.9]), minimum plasma Na < 125 mmol/L (5.6 [1.1-27.8] or maximum pH > 7.60 (5.6 [1.1-89.0]). Neither maximum serum bilirubin nor exposure to ototoxic drugs was associated with SNHL. Avoidance of severe hyponatraemia and extreme alkalosis, as well as use of surfactant to minimize the severity of hyaline membrane disease, may result in a decreased incidence of SNHL in extremely premature infants.

Hearing screening of high risk newborns.

Prospective screening of an extremely high risk group of 137 infants cared for in the Newborn Intensive Care Unit of the James Whitcomb Riley Hospital for Children was undertaken during 1983. Auditory brain stem responses (ABR) were obtained utilizing a clinical evoked potential system (Madsen 2250). Patients were selected for screening prior to discharge or transfer to the referring hospital on the basis of one or more of the following criteria: birth weight less than 1250 grams; birth weight less than 1500 grams and ventilatory support; significant depression at birth (Apgars less than 3 and 6 at 1 and 5 minutes, respectively); seizures, meningitis, and/or sepsis. Of the original 137 infants tested, 82 passed the initial ABR, 22 conditionally passed, and 34 failed. Eighty-two infants had follow-up behavioral and audiometric testing while 20 infants died and 35 were lost to follow-up. Four infants had severe sensorineural hearing loss, each of whom had failed the initial ABR. None of the infants who initially passed or conditionally passed the ABR had sensorineural hearing loss on follow-up testing. High risk factors for sensorineural hearing loss in the neonatal period included: intraventricular/periventricular hemorrhage, apnea, family history, major malformations of the head and neck, and possibly hyperbilirubinemia and congenital infection. No relationship of sensorineural hearing loss with very low birth weight, hyponatremia, infection, seizures, or medications was found. On the basis of these data, it is suggested that electrophysiologic hearing screening of a high risk population may be delayed until 3 to 6 months of age to improve specificity of testing.

Central auditory focus in neonatal hyperbilirubinemia using evoked potentials

Increase in bilirubin levels in neonates has been considered a risk factor for sensorineural hearing loss. Recent brainstem evoked potential (BEP) and electrocochleographic studies have suggested that the focus of the lesion is in the brainstem and not in the cochlea for those who have hearing loss. It was consequently postulated that every infant whose bilirubin levels are elevated have at least some temporary auditory brainstem involvement that would be reflected in the BEP waveform. All infants born in the hospital during June, July, and August, 1980 were given BEP testing using clicks at 70 and 30 dB EQSPL. Normal full term babies served as controls. For those infants, at 70 dB, wave I averaged 1.7 ms, wave III averaged 4.7 ms. and V averaged 7.0 ms. Infants with increasing bilirubin levels were recorded at 1/2‐day intervals. For all jaundice infants waves III and V increased in latency as the bilirubin level increased. Wave I did not change. Conduction time, between waves III and V was within the normal range, while conduction time betwen wave I and III was abnormal. Since wave I was always normal, hyperbilirubinemia was found to specifically affect wave III which is thought to reflect activity at the second and third synapes in the brainstem. Normal neural function beyond wave III was suggested.