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Hearing Screening Outcomes in Infants of Pregestational Diabetic Mothers

Posted on: Tuesday, 20 September 2005, 03:00 CDT

Purpose: Hearing screening results for newborns of diabetic mothers were compared with those of nondiabetic controls.

Method: This study was a retrospective chart review of mothers with pregestational diabetes mellitus and their neonates (n = 73) who received newborn hearing screening between January 1, 2000, and May 1, 2002. A group of nondiabetic mothers and their infants (n = 73), with birth dates that matched the diabetic group, served as controls. A 2-tiered hearing screening protocol, employing distortion product otoacoustic emission (DPOAE) and automated auditory brainstem response (A-ABR) screening techniques, was used.

Results: The DPOAE screening failure rate was 5.5% (4/73) for babies in the nondiabetic control group and 11.0% (8/73) for infants of diabetic mothers; this difference was not statistically significant. The A-ABR failure rate was 9.1% (1/11) for the diabetic group compared with 0% (0/4) for the controls, but the A-ABR was measured for only a small number of participants in each group. The frequency of premature birth and abnormal birth weight was significantly greater for the infants of diabetic mothers compared with controls.

Conclusions: Given the greater frequency of prematurity and abnormal birth weight in the population of neonates born to diabetics, additional research using A-ABR is recommended.

Key Words: pregestational diabetes mellitus, newborn hearing screening, distortion product otoacoustic emissions, automated auditory brainstem response

In this article, we present preliminary findings on hearing screening outcomes for a sample of neonates and their diabetic mothers. Many of the physiological perturbations and complications associated with diabetes mellitus (DM) in pregnancy have the potential to affect both the developing inner ear and brain of the diabetic conceptus. Thus, peripheral and central auditory processing may be altered, and offspring of diabetics may be at risk for developing communication and learning disorders.

During early development, intellectual and psychomotor impairments have been reported for infants of diabetics, and longitudinal studies demonstrate that the detrimental effects of this maternal disease can persist into later childhood (Churchill, Berendes, & Nemore, 1969; Hod et al., 1999; Levy-Shiff, Lerman, Har- Even, & Hod, 2002; Stehbens, Baker, & Kitchell, 1977; Stenninger, Flink, Eriksson, & Sahlen, 1998). Significant correlations between intellectual and psychomotor performance and maternal metabolic derangement have also been shown, although in some studies the developmental outcome scores fell within the normal range (Levy- Shiff et al., 2002; Rizzo et al., 1995; Rizzo, Metzger, Burns, & Burns, 1991; Rizzo, Ogata, Dooley, Metzger, & Cho, 1994). Research exploring the relationship between verbal and nonverbal abilities in this population is limited. Sells, Robinson, Brown, and Knopp (1994) found similar intelligence scores but significant differences between all groups on the Communication subscale of the Vineland Adaptive Behavior Scales and the Peabody Picture Vocabulary Test; the worst performance results were obtained for offspring of poorly controlled diabetic mothers, followed by the well-controlled diabetic group, and then nondiabetic controls. Auditory function and communication disorders in this population remain relatively unexplored.

Hyperglycemia is common to all forms of DM. Two major categories of DM are defined by the etiology and pathogenesis of this metabolic disease. Type 1 is caused by a deficiency in insulin secretion by the pancreas, and Type 2 results from both insulin resistance at the tissue level and insufficient insulin secretion to overcome this resistance. The prevalence of DM continues to increase and is estimated to affect 10%-14% of the adult population in the United States (Centers for Disease Control and Prevention, 2001; The Expert Committee on the Diagnosis and Classification of Diabetes Mellitus, 2000). Although the devastating effects of this disease are well documented, the health status of infants resulting from a diabetic pregnancy has received less attention. However, the Centers for Disease Control and Prevention estimate that 1.85 million American women of childbearing age are diabetic and that "diabetes during pregnancy, regardless of type, puts both a woman and her unborn child at risk for negative health outcomes" (Centers for Disease Control and Prevention, 2001, p. 10). Pregnant women first diagnosed with DM during pregnancy have gestational DM, a temporary condition that typically resolves after delivery. Gestational DM occurs in about 4% of all pregnancies and accounts for 90% of all diabetic pregnancies. The remaining 10% are women with pregestational Type 1 or Type 2 DM; the prevalence of this form of diabetic pregnancy is approximately 0.1%-0.3% (Centers for Disease Control, 2001; The Expert Committee on the Diagnosis and Classification of Diabetes Mellitus, 2000). Current clinical practice involves screening for DM during pregnancy and early treatment with insulin and/or diet therapy. As a result, perinatal mortality and congenital malformations, the major sequelae of maternal DM, have been reduced significantly (Damm & Molsted-Pedersen, 1989; Hadden, 1999; J. F. Pedersen, 1977; Suhonen, Hiilesmaa, & Teramo, 2000).

Medical treatment and nutritional therapy, even when mothers achieve a clinically acceptable level of glycemic control, do not restore normal physiology (American Diabetes Association, 2000). DM, even in the well-controlled diabetic pregnancy, modifies the maternal levels of glucose, lipids, and amino acids and therefore the availability of these essential fuels to the developing fetus (Grace, Susa, Gruppuso, & Widness, 1984; Freinkel, 1980; Kalkhoff, 1991; Silverman, Purdy, & Metzger, 1996). Despite early treatment, these disturbances in maternal metabolism and the intrauterine environment can persist and have been linked to perinatal conditions, birth complications, and long-term developmental disturbances in children of diabetics (Farquhar, 1969; Jovanovic- Peterson et al., 1991; Petersen, Pedersen, Greisen, Pedersen, & Molsted-Pedersen, 1988; Schwartz & Teramo, 2000; Sells et al., 1994; Silverman et al., 1996; Stehbens et al., 1977; Stenninger et al., 1998; Vohr, McGarvey, & Tucker, 1999; Yamashita et al., 1996).

Several conditions and complications common to the diabetic pregnancy are also known indicators for neonatal hearing loss and thus have the potential to alter the developing auditory system (Joint Committee on Infant Hearing, 1994, 2000; Kalkhoff, 1991; Schwartz & Teramo, 2000). Craniofacial anomalies are among the congenital malformations that can occur in offspring of diabetics (Becerra, Khoury, Cordero, & Erickson, 1990; Ewart-Toland et al., 2000). Chronic intrauterine hypoxia and ischemia (Kelemen, 1955, 1960; Madsen, 1986; Nylund, Lunell, Lewander, Persson, & Sarby, 1982; Teramo et al., 1987; Widness et al., 1981), delayed fetal lung development (Hallman & Teramo, 1979), and respiratory distress have been reported (Robert, Neff, Hubbell, Taeusch, & Avery, 1976; Schwartz & Teramo, 2000). Abnormal birth weight, particularly macrosomia, occurs frequently and carries with it an increased risk of birth asphyxia and fetal distress (Hod et al., 1996; Schwartz & Teramo, 2000; Stenninger, Scollin, & Aman, 1991; Stevenson et al., 1982; Weintrob, Karp, & Hod, 1996). Intrauterine growth retardation and low birth weight have also been found more frequently in this population, particularly in mothers with poor glycemie control during pregnancy (Petersen et al., 1988). Hyperbilirubinemia is also more common in newborns of diabetics (Stevenson, 1987; Taylor et al., 1963). These various complications and conditions often require the use of potentially ototoxic pharmacological therapies (i.e., aminoglycoside antibiotics, loop diuretics) and ventilation therapy. Poor maternal glucose control increases perinatal exposure to these deleterious conditions (Grace, 1989; Kalkhoff, 1991; Schwartz & Teramo, 2000).

Few studies have focused specifically on the auditory function of infants born to diabetic mothers. Traditionally, the teratogenic effects of maternal DM have been of primary concern, with early research indicating a significantly higher rate of congenital malformations in this population (Becerra et al., 1990; Mills, 1982; Molsted-Pedersen & Pedersen, 1985; L. M. Pedersen, Tygstrup, & Pedersen, 1964). With respect to inner ear development and hearing, craniofacial anomalies in particular are indicative of potential auditory disorders (Hayes, 1994). Craniofacial anomalies have not been classically linked to maternal DM (Martinez-Frias, 1994). However, various craniofacial anomalies including ear abnormalities can occur in combination with other malformations and have recently been described as part of the oculoauriculovertebral complex in patients with a history of maternal DM (Ewart-Toland et al., 2000; Grix, 1982). Hearing loss occurred in 43% of the patients in this series, and screening for this complex was recommended for all diabetics (Ewart-Toland et al., 2000).

With better management of maternal DM, the severity of thedisease during the first trimester has improved, and the prevalence of congenital malformations has decreased concomitantly (Damm & Molsted- Pedersen, 1989; Suhonen et al., 2000). However, it is well established that most infants with congenital hearing loss do not exhibit craniofacial malformations. Until recently, offspring of diabetics without craniofacial anomalies or other hearing risk factors were not assessed routinely for auditory system function. Because hearing deficits of cochlear or neural origin are not obvious in the neonate, even when these deficits are severe, hearing impaired neonates, including those of DM mothers, were not identified at birth. For this reason, universal newborn hearing screening has now become the recommended practice, and in birthing facilities with universal hearing screening, infants of diabetic mothers are now tested routinely (Joint Committee on Infant Hearing, 2000).

The advent of universal newborn hearing screening has provided us the opportunity to study hearing screening outcomes in this population. In the two-tiered hearing screening protocol used in this study, infants received an initial otoacoustic emission (OAE) hearing screening; those who did not pass the OAE or were considered high risk received an auditory brainstem response (ABR) hearing screening. The aim of this preliminary study was to compare hearing screening results in newborns of pregestational diabetic mothers with those of nondiabetic controls.

Method

Participants

This is a retrospective study of 73 pregestational diabetic women and their newborns and 73 nondiabetic controls and their offspring. All cases for study were drawn from the population of neonates who received newborn hearing screening at the Good Samaritan Hospital (Cincinnati, OH) between January 1, 2000, and May 1, 2002 (n = 10,603). Infants of nondiabetic mothers, with birth dates that matched those in the diabetic group, served as control subjects and were randomly selected from the hospital population. In the sample of maternal DM infants, 12.3% (9/73) were cared for in the neonatal intensive care unit (NICU) compared with 3.0% (2/73) of infants in the control group. All remaining infants were cared for in the well baby nursery.

Screening Protocols and Methods

All newborns at the Good Samaritan Hospital were screened for hearing loss according to the established hospital protocols. A two- tiered hearing screening protocol, employing distortion product OAE (DPOAE) and automated ABR (A-ABR) screening techniques, was used. Infants in the well baby nursery received A-ABR if they did not pass the DPOAE screen or developed hyperbilirubinemia; infants in the NICU routinely received both DPOAE and A-ABR screening.

The DPOAE screening result of "Pass" or "Refer" was obtained with the handheld Bio-logic AudX II hearing screening device and using the manufacturer's screening and in-the-ear calibration protocols (Bio-logic Systems). The DPOAE (2F1-F2) screening was performed at four frequencies (F2: 2, 3, 4, and 5 kHz). The F2:F1 ratio was 1.22 with intensities of 65 dB SPL for F1 and 55 dB SPL for F2. Signal averaging was performed in the frequency domain. The stopping rules for averaging included the following criteria: (a) minimum DPOAE amplitude of -10 dB SPL, (b) DPOAE 8 dB or more than the noise floor amplitude, (c) noise amplitude of-17 dB SPL, and (d) maximum averaging time of 10 s artifact-free. Noise was calculated as the average amplitude of 100 Hz above and 100 Hz below the DPOAE frequency. The "Pass" criteria for a given test frequency were as follows: (a) DPOAE amplitude greater than 6 dB above the noise floor; (b) minimum DPOAE amplitudes of-6 dB SPL for F2 at 5 kHz, -5 dB SPL for F2 at 4 kHz, -8 dB SPL for F2 at 3 kHz, and -7 dB SPL for F2 at 2 kHz; (c) maximum DPOAE amplitudes of 39 dB SPL at all F2 frequencies; and (d) maximum noise floor amplitudes of 14 dB SPL at all F2 frequencies. The overall "Pass" criteria for a given ear required that all of these conditions be met for three of the four F2 test frequencies.

The ALGO 2 Newborn Hearing Screener (Natus Medical) was used to perform the A-ABR hearing screening using the manufacturer's disposable earphone couplers and disposable electrodes. Both ears were tested simultaneously with 35 dB nHL alternating 100-s clicks presented at repetition rates of 37/s for the right ear and 34/s for the left ear. The number of stimulus presentations varied from a minimum of 500 to a maximum of 15,000. The ALGO 2 screening result of "Pass" or "Refer" was based on the likelihood ratio of 160 calculated from responses obtained for blocks of 500 sweeps and compared with an internal template; if the criterion likelihood ratio was not reached within 15,000 stimulus presentations, then the screening result was a "Refer."

Universal newborn hearing screening was not required in Ohio during the period of the study (mandated in 2004). All parents or guardians of infants who did not pass the Good Samaritan Hospital hearing screening were counseled to seek follow-up reassessment by an audiologist. A list of facilities that could perform this follow- up service was provided, as required by state law.

Statistics

The chi-square test was used to determine whether the frequencies of abnormal DPOAE screening test results, gestational age, and birth weight were significantly different between the maternal DM and control groups. Statistical analyses of A-ABR outcomes were not performed because of the small number of cases.

The study protocol was approved by the Good Samaritan Hospital and University of Cincinnati Human Subjects Institutional Review Board.

Results

During the study period, 10,603 newborns at Good Samaritan Hospital were screened for hearing. Of this group 0.7% (73) were identified as infants of mothers with pregestational DM. For the well baby nursery population, annual hospital referral rate data during the study period indicate average hearing screening failure rates of 3.7% and 14.0% for DPOAE and A-ABR, respectively. As shown in Table 1, the DPOAE screening failure rate for babies in our randomly selected nondiabetic control group was comparable at 5.5% (4/73). The DPOAE screening failure rate for the infants of the diabetic mothers was greater at 11.0% (8/73), but the difference between groups was not statistically significant (χ^sup 2^ = 0.82, p = .37). Seven of the 8 participants in the diabetic group who failed the initial DPOAE screening test were tested with A-ABR. Of these, 1 participant did not pass this subsequent A-ABR screen. The 4 newborns in the control group who failed the DPOAE screen all passed the A-ABR follow-up screen (see Table 2).

Table 1. DPOAE screening failure rates by group and nursery.

Table 3. Frequency of prematurity and abnormal birth weight by group.

According to the two-tier screening protocol, infants in the well baby nursery who fail the DPOAE screening test receive an A-ABR follow-up screening test (see Table 2). In the well baby nursery, 6 DM group participants received the A-ABR follow-up screening; 1 failed this screening. For the control group, all 4 of the babies who failed the initial DPOAE were in the well baby nursery, and all passed the subsequent A-ABR test.

NICU babies at the Good Samaritan Hospital, even those who pass the DPOAE screening test, are considered to be at higher risk for hearing loss and therefore receive both the DPOAE and A-ABR tests routinely. In this study, 5 of the babies born to DM mothers were cared for in the NICU and received the A-ABR screen. Two of these had failed the initial DPOAE test, but all 5 passed the subsequent A- ABR test (an additional 4 NICU babies from the DM group passed the DPOAE screen but did not receive the A-ABR). For the control group, only 2 infants were cared for in the NICU; both passed the DPOAE and A-ABR screening tests.

Infants born before 37 weeks gestational age are considered premature. In our control group, 9.6% (7/73) were premature. There was an overrepresentation of premature infants in the maternal DM group at 24.7% (18/73) compared with the nondiabetic controls; this group difference was statistically significant (χ^sup 2^ = 4.83, p = .03; see Table 3).

The distribution of birth weight was also different between groups, as shown in Table 3. Eleven percent (8/73) of the maternal DM group had an abnormally low birth weight (<2,500 g) compared with 5.5% (4/73) of the controls. Abnormally high birth weights were also found for infants born to diabetic mothers. Twenty-two percent (16/ 73) of babies in the maternal DM group had birth weights greater than 4,000 g compared with 11.0% (8/73) of the control group. The frequency of abnormal birth weight was significantly greater for the infants of diabetic mothers compared with controls (χ^sup 2^ = 4.46, p = .04).

Table 2. A-ABR screening failure rates by group and nursery.

Table 4. DPOAE failure rate as a function of group and gestational age.

With respect to the DPOAE screening test results, the distribution of failure rate appears to be similar across gestational age and birth weight for both groups. DPOAE failure rates as a function of gestational age and birth weight are presented in Tables 4 and 5. Due to the small sample size in each category, statistical analyses were not performed.

Discussion

The long-term objectives of our research program are to identify whether infants of diabetic mothers are at risk for auditory system impairment and communication disorders. The specific aim of this study was to examine the results of a two-tiered hearing screening protocol in a consecutive series of infants born to mothers with pregestational DM. We found that 11.0% of infants of diabetic mothers failed to pass the DPOAE screening test compared with 5.5% of the nondiabetic control infants. Although these hearing screening outcomes show that infants exposed to DM during pregnancy have a slightly highe\r DPOAE referral rate, this trend was not statistically significant. The referral rate for the A-ABR was also higher than for the DM group compared with controls, but the number of infants screened was insufficient to draw conclusions.

Little is known about the hearing abilities of infants born to diabetic mothers. In a recent retrospective study of 27 children with craniofacial anomalies and a history of maternal DM, 9 exhibited hearing loss: 4 with mixed or sensorineural losses, 2 with conductive losses, and 3 with unspecified hearing losses. Auditory assessment methods were not described, making it impossible to determine whether the origin of the loss was cochlear or retrocochlear for those with a sensorineural component (Ewart- Toland et al., 2000). Gratz, Pollack, and Zimmerman (1981) provide two case reports of children who were born to diabetic mothers and who presented with ipsilateral facial palsy and deafness associated with hypoplasia of the internal auditory canal, suggesting a retrocochlear component to the hearing loss. In early studies of DM during pregnancy, temporal bone histological findings for two fetuses of diabetic mothers indicated appropriate structural development but with hemorrhaging in the cochlea and eighth nerve. However, in each case the DM was severe, requiring termination of the pregnancy during the second trimester (Kelemen, 1955, 1960).

Table 5. DPOAE failure rate as a function of group and infant birth weight.

Several conditions, each a consequence of physiological perturbations associated with maternal DM, may combine synergistically to form a hostile environment for the developing fetus and newborn. The general health of the fetus before delivery may be an important contributor to neonatal outcome (Langer & Conway, 2000; Weintrob et al., 1996). The progeny of the diabetic mother is exposed to adverse conditions during development because maternal DM disrupts the intrauterine environment. DM during pregnancy modifies the maternal levels of glucose, lipids, and amino acids and therefore the availability of these essential substrates to the developing fetus (Crace et al., 1984; Freinkel, 1980; Kalkhoff, 1991; Silverman et al., 1996). These derangements in the fetal fuel supply and the complications associated with DM in pregnancy can affect the developing brain of the diabetic conceptus.

Common perinatal complications of the diabetic pregnancy include abnormal birth weight and prematurity (Schwartz & Teramo, 2000; Weintrob et al., 1996). In our study, we found a significant difference in the birth weight distribution between groups. The maternal DM group had more participants of abnormal birth weight, including the high, low, and very low birth weight categories. A statistically significant difference in the number of premature babies was also found between groups, with prematurity being more prevalent for the infants of diabetic mothers. Macrosomia, or excessive fetal growth, is now the most frequent perinatal complication of DM in pregnancy. The number of macrosomic (>4,000 g) babies was significantly greater in our maternal DM group, despite the fact that babies of the diabetic mothers were more frequently premature. Our results are similar to those reported in the literature, with prematurity and abnormal birth weight being common neonatal outcomes of maternal DM (Kalkhoff, 1991; Schwartz & Teramo, 2000; Weintrob et al., 1996).

In addition to abnormal birth weight and prematurity, complications associated with perinatal hypoxia and ischemia and hyperbilirubinemia are recognized as risk factors for hearing loss and occur more frequently in infants born to diabetic mothers, particularly those with poor glycemic control during pregnancy (Schwartz & Teramo, 2000; Weintrob et al., 1996). Metabolic derangements associated with maternal DM include hyperglycemia and alterations in long chain polyunsaturated fatty acids (LCPUFAs) and micronutrient levels of calcium, magnesium, and iron. Although not recognized as hearing risk factors per se, these variables could work alone or in combination to affect the structure and function of the developing cochlea and auditory nervous system.

OAEs are generated by the outer hair cells, thus providing information about preneural aspects of cochlear function, while the ABR arises from the auditory nerve and brainstem pathways. However, both screening techniques are influenced by peripheral auditory function, and the OAEs in particular depend on normal middle ear function for adequate acoustic stimulation, and recording of this response. Our results indicate no significant difference between DPOAE screening outcomes for infants of diabetic mothers and participants in the nondiabetic control group. This suggests that the middle ear status is similar for both groups and that the outer hair cells of the cochlea are fairly resistant to the effects of DM during pregnancy.

Until recently it was thought that sensorineural hearing loss invariably involved a cochlear lesion, with loss or damage to the outer hair cells. The presence of robust OAEs, and therefore normal outer hair cell function, in a subset of hearing impaired patients with absent or abnormal auditory nerve and brainstem responses has provided the basis for a disorder known as auditory neuropathy (or auditory dys-synchrony). The potential site of auditory system dysfunction in patients with this clinical picture may be the inner hair cell, auditory nerve, and/or the synapse between these cells (Berlin et al., 1998; Rapin & Gravel, 2003; Starr, Picton, Sininger, Hood, & Berlin, 1996). With current techniques (OAE and ABR), it is not possible to delineate inner hair cell dysfunction from damage to primary auditory neurons. However, both cell types, in addition to the central auditory pathways, might be vulnerable to maternal DM during development, with the specific pathology dependent on the nature of the metabolic derangements present in utero.

Common etiologies in infants with auditory neuropathy are hypoxia, ischemia, and hyperbilirubinemia (Rance et al., 1999). This is particularly intriguing for our research, because, as noted above, these conditions are also common to infants of diabetic mothers. Hypoxia and ischemia, as well as reduced levels of calcium and magnesium, have all been implicated in pathophysiological mechanisms affecting different cochlear cells and tissues (Borg, 1997; Gunther, Rebentisch, Vormann, Konig, & Ising, 1988; Ikeda, Kobayashi, Takasaka, Yumita, & Furukawa, 1987; Ikeda, Kusakarai, Kobayashi, & Saito, 1987). For example, animal models of hypoxia reveal inner hair cell damage with preserved outer hair cells and OAEs (Shirane & Harrison, 1987). It is possible that selective inner hair cell damage occurs in offspring of diabetic mothers. This is a limitation of our study because if the inner hair cells were selectively damaged in our diabetic group, the DPOAE screening technique would be insensitive to this cochlear lesion.

ABR and behavioral studies in human neonates and animal models all suggest that the auditory system is susceptible to alterations in LCPUFAs (Amin, Merle, Orlando, Dalzell, & Guillet, 2000; Auestad, Stockard-Sullivan, Innis, Korsak, & Edmond, 2003; Bourre, Durand, Erre, & Aran, 1999; Unay et al., 2004), iron deficiency (Algarin, Peirano, Garrido, Pizarro, & Lozoff, 2003; Cankaya et al., 2003), hypoxia (Borg, 1997; Jiang, 1998; Rehn et al., 2002; Sohmer & Freeman, 1991), and hyperbilirubinemia (Shapiro, 2003). All are metabolic perturbations or perinatal conditions that occur frequently as a consequence of maternal DM, yet little is known about the status of the auditory nerve and central auditory system of infants of DM mothers. In our study, A-ABRs were abnormal for 9.1% (1/11) but were measured for only a small number of participants in our maternal diabetic group (11/73). Kountakis, Skoulas, Phillips, and Chang (2002), in a prospective study of hearing risk factors, studied a sample of 746 infants who failed the Joint Committee on Infant Hearing (JCIH) risk factor screening protocol. From this sample, 9 infants were born to mothers with a history of DM. Of the infants in this maternal diabetic group, 4 (44.4%) failed a follow-up ABR screen. The incidence of abnormal ABRs is higher than in our study, but it is also biased because all participants had failed the JCIH screening and thus had one or more JCIH hearing risk factors in addition to the history of maternal DM. Kountakis et al. (2002) proposed that maternal DM be considered a new risk factor for hearing loss. However, given the limitations of each study, it is difficult to draw conclusions about auditory nerve or brainstem function in babies born to diabetic mothers.

Summary and Conclusions

The proportion of women with maternal DM, and thus the number of infants exposed to this disease in utero, is increasing dramatically. This is a particularly dangerous situation for certain ethnic groups (Hispanic, African American) with a greater predisposition for acquiring this disease and who are less likely to seek treatment for their DM (Centers for Disease Control and Prevention, 2001). This investigation provides the first study of hearing screening outcomes in a consecutive series of neonates born to diabetic mothers. Our findings indicate that a history of maternal DM does not significantly increase the neonatal DPOAE screening failure rate. Although our A-ABR screening measures indicate possible abnormalities, additional research is needed to determine whether the auditory nerve and central pathways are compromised in this population.

We propose that infants born to diabetics deserve special attention by the research community as a potential "at risk" group. The question posed in this proposal, whether DM during pregnancy adversely affects fetal auditory system development, is a crucial one. Hypoxia, hyperbilirubinemia, LCPUFA alterations, and ir\on deficiencies have all been implicated as pathological mechanisms that compromise the developing nervous system or auditory nerve, rather than the outer hair cells. These complications are hallmarks of the diabetic pregnancy and increase the risk for neurodevelopmental disorders in general and auditory system dysfunction in particular. The danger is that infants of diabetic mothers may pass a DPOAE screening, have many of the above complications, and yet be lost to follow-up if not identified as being potentially at risk. This is particularly true if the complications are subclinical (i.e., are mild and do not meet the precise requirements to qualify as a hearing risk factor) and additive.

Future prospective studies are planned to examine the relationship between metabolic perturbations during the diabetic pregnancy and auditory system function in infants born to affected mothers. A comparison of infants born to mothers with gestational DM and those born to mothers with pregestational DM is necessary to determine whether the type of DM has an impact on infant outcomes. Because gestational DM is usually considered less severe, early identification and surveillance of metabolic control during pregnancy may be less rigorous compared with those with known pregestational DM. Although the literature on potential risk factors to infant hearing suggests that the developing auditory system may be compromised by maternal DM, it is necessary to determine whether this is the case, and if so, to define the nature of the auditory impairment.

Acknowledgments

The authors thank B. Sutherland and L. Markesbury for assistance with data collection.

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Received November 14, 2004

Accepted May 2, 2005

DOI: 10.1044/1059-0889(2005/008)

Susan G. Stanton

Elizabeth Ryerson

Shana L. Moore

University of Cincinnati, Cincinnati, OH

Maureen Sullivan-Mahoney

Good Samaritan Hospital, Cincinnati, OH

Sarah C. Couch

University of Cincinnati, Cincinnati, OH

Contact author: Susan G. Stanton, Communication Sciences and Disorders, 344 French E Bldg., CAHS, 202 Goodman Avenue, Cincinnati, OH 45267-0379. E-mail: susan.stanton@uc.edu

Copyright American Speech-Language-Hearing Association Jun 2005

Source: American Journal of Audiology

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