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Hearing impairment

A hearing impairment is a decrease in one's ability to hear (i.e. perceive auditory information). While some cases of hearing loss are reversible with medical treatment, many lead to a permanent disability (often called deafness). more...

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If the hearing loss occurs at a young age, it may interfere with the acquisition of spoken language and social development. Hearing aids and cochlear implants may alleviate some of the problems caused by hearing impairment, but are often insufficient. People who have hearing impairments, especially those who develop a hearing problem later in life, often require support and technical adaptations as part of the rehabilitation process.

Causes

There are four major causes of hearing loss: genetic, disease processes affecting the ear, medication and physical trauma.

Genetic

Hearing loss can be inherited. Both dominant and recessive genes exist which can cause mild to profound impairment. If a family has a dominant gene for deafness it will persist across generations because it will manifest itself in the offspring even if it is inherited from only one parent. If a family had genetic hearing impairment caused by a recessive gene it will not always be apparent as it will have to be passed onto offspring from both parents.

Dominant and recessive hearing impairment can be syndromic or nonsyndromic. Recent gene mapping has identified dozens of nonsyndromic dominant (DFNA#) and recessive (DFNB#) forms of deafness.

  • The most common type of congenital hearing impairment in developed countries is DFNB1, also known as Connexin 26 deafness or GJB2-related deafness.
  • The most common dominant syndromic forms of hearing impairment include Stickler syndrome and Waardenburg syndrome.
  • The most common recessive syndromic forms of hearing impairment are Pendred syndrome, Large vestibular aqueduct syndrome and Usher syndrome.

Disease or illness

  • Measles may result in auditory nerve damage
  • Meningitis may damage the auditory nerve or the cochlea
  • Autoimmune disease has only recently been recognised as a potential cause for cochlear damage. Although probably rare, it is possible for autoimmune processes to target the cochlea specifically, without symptoms affecting other organs. Wegener's granulomatosis is one of the autoimmune conditions that may precipiate hearing loss.
  • Presbyacusis is deafness due to loss of perception to high tones, mainly in the elderly. It is considered a degenerative process, and it is poorly understood why some elderly people develop presbyacusis while others do not.
  • Mumps (Epidemic parotitis) may result in profound sensorineural hearing loss (90 dB or more), unilateral (one ear) or bilateral (both ears).
  • Adenoids that do not disappear by adolescence may continue to grow and may obstruct the Eustachian tube, causing conductive hearing impairment and nasal infections that can spread to the middle ear.
  • AIDS and ARC patients frequently experience auditory system anomalies.
  • HIV (and subsequent opportunistic infections) may directly affect the cochlea and central auditory system.
  • Chlamydia may cause hearing loss in newborns to whom the disease has been passed at birth.
  • Fetal alcohol syndrome is reported to cause hearing loss in up to 64% of infants born to alcoholic mothers, from the ototoxic effect on the developing fetus plus malnutrition during pregnancy from the excess alcohol intake.
  • Premature birth results in sensorineural hearing loss approximately 5% of the time.
  • Syphilis is commonly transmitted from pregnant women to their fetuses, and about a third of the infected children will eventually become deaf.
  • Otosclerosis is a hardening of the stapes (or stirrup) in the middle ear and causes conductive hearing loss.

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Nonsurgical home treatment of middle ear effusion and associated hearing loss in children, Part I: clinical trial
From Ear, Nose & Throat Journal, 9/1/05 by Daniel S. Arick

Abstract

We conducted a randomized, controlled clinical trial to investigate the efficacy of treatment of persistent middle ear effusion (MEE) and associated hearing loss with a modified Politzer device used in the home setting over a 7-week period. Efficacy was determined by comparing pre- and posttherapy air-conduction thresholds, tympanometric peak pressures, and otoscopic findings. The study group was made up of 94 children (174 ears), aged 4 to 11 years, who had at least a 2-month history of MEE and associated hearing loss. At study's end, patients in the treatment group experienced statistically significant improvements in all measured outcomes; no significant improvements were seen in the control group in all measured outcomes. At study's end, the hearing sensitivity of 73.9% of the treated ears was within normal limits, compared with only 26.7% of the control ears. These findings demonstrate that home treatment of children with persistent MEE and associated hearing loss with the modified Politzer device is highly efficacious.

Introduction

Methods of managing middle ear effusion (MEE) have included (1) periodic observation during efforts to reduce environmental risk factors, (2) decongestants, (3) anti histamines, (4) corticosteroid therapy, (5) antimicrobial agents, (6) myringotomy with or without placement of tympanostomy tubes, (7) adenoidectomy with or without tonsillectomy, either alone or in combination with myringotomy with or without placement of tympanostomy tubes, and (8) insufflation of the eustachian tube/middle ear system by the Valsalva maneuver or the Politzer method.

The efficacy of treatment with drugs or surgery has been questioned. For example, Cantekin et al concluded that decongestant and antihistamine treatment was not beneficial in the management of MEE. (1) In a meta-analysis of 33 studies, Williams et al concluded that the beneficial effect of antimicrobial treatment is minor and only short-term. (2)

If medication fails, most otolaryngologists resort to surgical placement of tympanostomy tubes. (3) One survey showed that 40% of otolaryngologists believe that tubes are used too frequently. (4,5) There are several arguments against the surgical treatment of MEE with tympanostomy tubes:

* MEE resolves spontaneously in 80 to 90% of children within 3 months. (6,7)

* A significantly negative tympanometric peak pressure (TPP) may persist after surgical treatment with tympanostomy tubes. (8)

* Ventilation tubes frequently fall out prematurely, often in 4 to 7 months. (9,10) In such cases, 40% of patients experience a recurrence of MEE, (3) and 33 to 75% undergo repeat surgery to replace them. (10,11)

* The risk of one or more episodes of otorrhea following tube placement is three times higher than the risk following simple myringotomy.

* Patent tubes allow bacteria, viruses, and allergens to migrate into the middle ear cavity. (12)

* Other reported complications of tympanostomy tube placement include (1) tympanic membrane retraction, (2) postsurgical infection, (3) localized foreign-body reaction, (4) granulation, (5) hyalinization, (6) tympanosclerosis, (7) temporary or permanent hearing impairment of varying degrees, (8) persistent tympanic membrane perforation, (9) dislocation of the tube into the middle ear cavity, (10) tube blockage, and (11) cholesteatoma. (6,13,14)

A clinical practice guideline published in 2004 advises that antibiotics and decongestants are ineffective medical approaches to the treatment of MEE. (7) Likewise, antimicrobials, with or without corticosteroids, are not recommended for the routine treatment of MEE because they do not provide long-term benefits, although they may confer some short-term benefits. This guideline recommends that children who have MEE that has persisted for 4 months or longer and who have persistent hearing loss or other signs and symptoms should be considered for surgical insertion of tympanostomy tubes.

Insufflation of the eustachian tube/middle ear system involves forcing air under pressure through the eustachian tube (retrograde approach) and into the middle ear. The assumption underlying this approach is that frequent repetition of this procedure over a short period of time (on the order of days) can result in the normalization of negative middle ear pressure and the elimination of MEE. The two most common methods of insufflation are the Valsalva maneuver and the Politzer method. The Valsalva maneuver involves performing forced nasal expiration with the nose and lips closed. The Politzer method involves inserting the tip of a rubber air bulb into a patient's nostril, simultaneously compressing the other nostril with a finger, and having the patient swallow as the rubber bulb is compressed.

Valsalva maneuver. Cantekin et al evaluated the Valsalva maneuver in 66 children between 2 and 6 years of age who had recurrent or chronic otitis media and functioning tympanostomy tubes. (15) None of these children was able to open the eustachian tube with the Valsalva maneuver. The failure of the Valsalva maneuver was attributed to excessive tubal compliance in this age group.

One modification of the Valsalva maneuver involves inserting a balloon into one nostril while compressing the other nostril. (16) When the maneuver is successful, the balloon is inflated. Blanshard et al evaluated the balloon modification of the Valsalva maneuver in 85 children, aged 3 to 10 years, who had bilateral MEE and who were candidates for surgical placement of tympanostomy tubes. (17) Approximately one-half of these children were treated with autoinflation (experimental group), and the remainder were assigned to a control group. Patients in the experimental group achieved a beneficial effect after 2 to 4 weeks of autoinflation. The disadvantages of autoinflation in this study included difficulty in performing the procedure, as 43% of the experimental group performed it irregularly and 12% were unable to perform it at all.

Because of its limitations, the Valsalva maneuver does not hold promise as a treatment for otitis media with effusion and related conditions.

Politzer method. The Politzer method (politzerization) was patterned after an inflation technique described by Shea. (18) Schwartz et al modified the Politzer method by forcing air through the nostril with a 1-oz infant nasal syringe equipped with a plastic tip that was inserted into a nostril. (19) In a controlled study, they measured the effectiveness of politzerization by performing tympanometry 5 and 10 minutes after politzerization in 24 adults and children with MEE and associated tympanic membrane retraction. In the active-treatment group, the mean shift in TPP following politzerization was -9 mm [H.sub.2]O.

An important advantage that the Politzer method has over the Valsalva maneuver is that the forced air is initiated by an external source. The limitations of the Politzer apparatus and modifications thereof include (1) their cumbersome design, (2) a failure to produce continuous and nonfluctuant air-pressure flow, (3) a failure to coordinate the air-pressure stream with swallows, and (4) an absence of air-pressure and air-flow volume controls, which might lead to the generation of either harmful or ineffective air pressures into the middle ear via the nose. Politzerization has generally not been well accepted by patients, and it traditionally has not been suitable for use in the home setting. These limitations are attributable to the design of the currently existing Politzer devices rather than to any facet of the method itself.

An optimum insufflation device would (1) be portable, (2) be operable by a patient or parent, (3) allow for coordination of the air-pressure stream with swallows, and (4) be equipped with air-pressure and air-volume flow controls so that air pressures introduced into the middle ear through the nose are sufficient yet not harmful. (20,21)

We designed a modified Politzer autoinsufflation device that overcomes the aforementioned limitations of extant devices (figure 1). (20,21) Our handheld, battery-operated device emits controlled air pressure and flow that can be adjusted according to the patient's age and magnitude of hearing loss. (20,21) We conducted two earlier studies of treatment with a device very similar to this and found that approximately 75% of patients with MEE and associated hearing loss recovered following treatment. (20,21) However, a major limitation of these studies was that patients were required to come to a physician's office for treatment 2 or 3 times a week over a period of 6 to 7 weeks. This routine placed a burden on patients in terms of convenience and direct and indirect costs.

[FIGURE 1 OMITTED]

In an attempt to obviate the disadvantages of office-based politzerization, we conducted a National Institutes of Health--supported, randomized, controlled study of the feasibility of using our modified Politzer device to treat persistent MEE and associated hearing loss in the home setting. Efficacy was determined by comparing changes in pretherapy (pretest) and posttherapy (posttest) air-conduction thresholds, TPPs, and otoscopic findings.

Patients and methods

Instrumentation. Our modified Politzer device was very similar to the one that we used in our previous two studies. (20,21) The federal Food and Drug Administration has classified our modified apparatus as a 510(k) prescriptive medical device. The device emits a controlled air pressure and volume velocity sufficient to effect improvement (based on the results of our feasibility study) without discomfort. The device has two settings. Setting 1 delivers an air pressure of 5.2 psi at a volume velocity of 1,524 ml/min; setting 2 delivers an air pressure of 2.5 psi at a volume velocity of 1,690 ml/min (figure 2).

[FIGURE 2 OMITTED]

Patients. More than 600 children were referred to the Center for Auditory Research at Brooklyn (N.Y.) College for possible inclusion in the study. Suitable candidates were those who had furnished informed consent and who satisfied six study criteria: (1) age 4 to 11 years, (2) at least a 2-month history of MEE and associated hearing loss as documented by a physician, (3) pure-tone air-conduction thresholds of 20 dB HL or more at 3 frequencies between 500 and 4,000 Hz with air-bone gaps of 15 dB or more at these frequencies or pure-tone air-conduction thresholds of 25 dB HL or more at 2 frequencies between 500 and 4,000 Hz with air-bone gaps of 15 dB or more at these frequencies at the final pretest, (4) a TPP of -100 daPa or less at the final pretest, (5) an otologic diagnosis of MEE at the final pretest, and (6) an absence of enlarged adenoids, acute otitis media, and other ear abnormalities at the final pretest otologic examination.

Procedures. Treatment was initiated on the day of the final pretest. Each patient's parent administered the treatment twice daily--in the morning before breakfast and in the evening after supper--alternating nostrils with each treatment. During each treatment, the patient was instructed to be in a sitting position. To deliver therapy, the parent inserted a pediatric probe tip (coupled to the device) into one nostril while compressing the other nostril with a finger. Each participant had his or her own device. The parent was given alcohol-soaked wipes and instructed to clean the tip before each use. The child then held a small amount of water in the mouth without swallowing it. The parent then turned on the device, thereby introducing air flow into the nostril at a constant volume velocity. After 1 or 2 seconds of air flow, the parent asked the child to swallow the water.

Parents were provided with a daily log to foster and track compliance. Most patients were seen in the office for monitoring at least once near the midpoint of the treatment period, which lasted 7 weeks.

Initially, the air pressure was set to 5.2 psi. As the study progressed, a small proportion of the children (~3 to 4%) in the experimental group, particularly those whose hearing had been improving markedly, began to experience a slight discomfort during sensations of ear popping at this setting; none had experienced any discomfort at this setting at the beginning of the study. The discomfort appeared to reflect a decrease in the fluid level of the middle ear. In response, we modified the device to incorporate a second air-pressure setting of 2.5 psi. Lowering the psi from 5.2 to 2.5 resolved the discomfort. This circumstance forced us to modify our protocol so that the device was set at 2.5 psi for younger children ([less than or equal to] 7 yr) during the first week and increased to 5.2 psi (if tolerated) for the remainder of the study. For older children (>7 yr), the device was set to 5.2 psi throughout the study. In both of these age groups, the setting was lowered to 2.5 psi if any participant experienced discomfort.

Audiometry was performed by audiologists certified by the American Speech-Language-Heating Association and licensed by New York State. Otologic evaluations were performed by board-certified otolaryngologists with at least 15 years of experience. Audiologic evaluations (air- and bone-conduction threshold testing and tympanometry) and otolaryngologic evaluations (otoscopy) were performed upon enrollment in the study and 4 weeks after the completion of the treatment (i.e., 11 wk following study entry). However, parents were advised to discontinue treatment if a child developed a cold or upper respiratory infection and to complete the treatment after the cold or upper respiratory infection resolved. As a result, a small number of children were seen later than 11 weeks after study entry.

The patients in the control group did not undergo sham treatment with a dummy device because their parents would have immediately recognized it as such. These parents were instructed to contact the investigators immediately if they noticed any worsening of hearing status.

Audiologists were blinded to each patient's otologic findings, and otolaryngologists were blinded to each patient's audiometric findings. At the posttest, audiologists and otolaryngologists were blinded to each patient's disease status. The statistician was blinded as to whether test results were obtained before or after therapy and to the disease status of each patient.

Sample size determination was made using power formulae for Student's t tests. (22) To achieve a power of 90% or more for each of our hypotheses, the sample size to be recruited was 110 (55 for each group, a number calculated to include a possible 10% attrition rate). An alpha level of 0.05 was used for all statistical tests. For statistical analysis, an absent TPP was coded as -450 daPa.

All patients in the control group who had not spontaneously recovered by the posttest were given the option of receiving treatment with the study device upon the conclusion of their involvement in the study. The outcomes of these controls will be presented in another report.

Results

A total of 94 children (174 ears), aged 4 to 11 years, met the inclusion criteria and were entered into the study. Of this group, 47 patients (88 ears) were randomly assigned to the experimental group and 47 patients (86 ears) were assigned to the control group.

Compliance. Complete compliance with the treatment protocol was demonstrated by 46 of the 47 experimental patients (97.9%), based on inspection of their daily logs and our assessment of their familiarity with the device; in the remaining patient, compliance was judged to be moderate. Our device appeared to be easy to use at home and was well tolerated by patients and parents.

Air-conduction thresholds and TPPs. For each ear, the mean pretest air-conduction thresholds for the experimental and control groups were similar--that is, within 3.0 dB at 500 Hz, 5.1 dB at 1,000 Hz, 4.2 dB at 2,000 Hz, and 1.4 dB at 4,000 Hz (table 1). At the pretest, the mean 4-frequency pure-tone average (PTA) in the experimental group was 29.6 in the right ear and 32.6 dB HL in the left ear; in the control group, the mean for both ears was 29.3 dB HL. Overall, the mean PTAs in both ears in both groups were symmetrical to within 3.3 dB.

The mean pretest TPPs in both ears in both groups were symmetrical to within 40.3 daPa (table 1). All posttest mean air-conduction thresholds in the experimental group were less than 20 dB HL. By contrast, in the control group, all but 1 posttest mean air-conduction threshold were higher than 20 dB HL. The exception was seen at 2,000 Hz in the left ear, where the mean threshold was 17.6 dB HL; in the right ear at that frequency, the mean (20.7) was only slightly higher than 20 dB HL.

Comparisons of the pre- and posttest measures for each ear in each group were obtained using paired Student's t tests. In the experimental group, these comparisons revealed statistically significant improvements (p < 0.001) in mean air-conduction thresholds across the entire frequency range in both ears (table 2). No statistically significant improvements in mean air-conduction thresholds occurred at any frequency or in either ear in the control group (p > 0.05). Likewise, the experimental group experienced statistically significant improvements (p < 0.001) in mean TPPs in both ears, while no such improvements were seen in the control group (p > 0.05).

Comparisons of the differences in scores (posttest minus pretest) for each ear between the two groups were obtained using independent sample Student's t tests (assuming equal variances). These comparisons revealed statistically significant differences (p < 0.001) between the two groups in the difference scores throughout all frequencies in both ears, indicating that all mean improvements in air-conduction thresholds from pre- to posttest in the experimental group were significantly greater than those for the control group (table 3). Similarly, the mean posttest improvement in TPP in the right ear in the experimental group was significantly greater (p < 0.03) than that in the right ear in the control group. In the left ear, the contrast was even more striking (p < 0.001), as the results reflected not merely an improvement in mean TPP in the left ear in the experimental group, but an actual deterioration in mean TPP in the left ear in the control group. Although the observed difference in change in the mean TPPs from pre- to posttest between the two groups was greater in the left ear (181.1 daPa) than the right ear (75.5 daPa), there is no reason to conclude that the true effect is different for the two ears. However, these values are only point estimates of the differences in mean change scores, and the confidence intervals overlap substantially. Therefore, the apparent discrepancy between the results in the right and left ears is not statistically significant.

Hearing sensitivity. Overall, hearing sensitivity returned to within normal limits in at least one ear in 40 of the 47 patients (85.1%) in the experimental group, compared with only 15 of the 47 patients (31.9%) in the control group (table 4). In terms of the number of ears, recovery was seen in 65 of 88 experimental ears (73.9%) and 23 of 86 control ears (26.7%).

At the pretest, bilateral hearing loss was present in 41 experimental patients; at the posttest, heating had been restored to within normal limits in at least one ear in 37 patients (90.2%). Of these 37 patients, 25 (67.6%) achieved normal hearing in both ears and 12 (32.4%) in one ear. In the control group, 39 patients had a bilateral hearing loss at the pretest, and 12 (30.8%) achieved restoration of hearing. Of these 12 controls, 8 (66.7%) regained hearing in both ears and 4 (33.3%) regained hearing in one ear.

If we define a significant hearing loss for this age group as a PTA of 35 dB HL or more, 38 of the 88 experimental ears (43.2%) and 41 of the 86 control ears (47.7%) demonstrated such a hearing loss at the pretest. At the posttest, only 3 of the 38 experimental ears (7.9%) still had a PTA of 35 dB HL or more, compared with 36 of the 41 control ears (87.8 %).

Otoscopic findings. We examined the relationship between hearing sensitivity in the 65 experimental ears that had achieved normal hearing at the posttest and findings on pneumatic otoscopy. Normal tympanic membrane mobility was seen in 49 of these ears (75.4%), moderate mobility in 12 (18.5 %), and no mobility in 4 (6.2%). Thus, either normal or moderate mobility was observed in 61 of the 65 ears (93.8%). This finding further substantiates the efficacy of our device for improving middle ear function and hearing sensitivity in children with MEE. The absence of tympanic membrane mobility in 4 normal ears suggests that an immobile eardrum is not necessarily associated with hearing loss.

Follow-up. Upon completion of participation in the study, all parents were advised to notify us if they or others noticed any change in hearing status. The parents of 6 children who had improved following active treatment did contact us. One child developed MEE and hearing loss after 3 months; his hearing sensitivity was restored to within normal limits by an additional 2 weeks of treatment. Another parent called after 7 months, and we found that the child had developed recurrent MEE and hearing loss; this child's hearing also returned after an additional 2 weeks of treatment. Another parent called after 9 months, but her child's hearing sensitivity was found to be normal.

Calls from 3 other parents--2 of which came more than 1 year after treatment--indicated that tympanostomy tubes had been placed in 2 children. One of these children had already received 2 sets of tubes prior to enrollment in our study. Following the study, the child's hearing sensitivity and otologic status, which had been monitored by an otologist, had remained within normal limits for 1 year. Subsequently, however, the child experienced a recurrence of MEE and associated hearing loss, and a third set of tubes was inserted. Nevertheless, MEE with hearing loss recurred again 3 months later. The patient underwent a repeat course of home treatment with our device, and his hearing began to improve. Two children were diagnosed with enlarged adenoids; 1 underwent an adenoidectomy without tympanostomy tube placement and his hearing returned to normal, while the other underwent an adenoidectomy with insertion of tympanostomy tubes.

We also placed telephone calls to 10 randomly selected parents of children in the experimental group. These calls were made 12 to 18 months following the completion of the child's participation in the study. All of these parents reported satisfaction with the outcome of the treatment.

Discussion

The results of our investigation indicate that twice-daily home treatment of persistent MEE and associated hearing impairment over a period of 7 weeks with a modified Politzer device that controls air flow and air pressure is highly efficacious in children aged 4 to 11 years. All mean posttest air-conduction thresholds and TPPs were markedly better than the mean pretest values in the experimental group but not in the control group; the pre- and posttest differences in the experimental group were statistically significant (p < 0.001). Also, the differences between groups in the mean change from pre- to posttest were significant for all air-conduction and TPP measures, and these improvements were markedly greater in the experimental group.

The Agency for Health Care Policy and Research's Otitis Media Guidelines Panel recommends that candidacy for surgical placement of tympanostomy tubes in children with persistent MEE should be based on the presence of a hearing loss. (7) In our study, hearing impairment was present in all ears in both groups at the pretest. Hearing sensitivity was judged to be within normal limits if the air-conduction thresholds were less than 20 dB HL at any of 3 frequencies or less than 25 dB HL at either of 2 frequencies.

Although posttest hearing sensitivity did not improve to within normal limits in either ear in 7 of the 47 experimental patients (14.9%), reports by parents, teachers, and patients themselves indicated that these patients' listening and attention behaviors suggested that some degree of improvement in hearing status had occurred during treatment. It is possible that their hearing sensitivity actually did improve during treatment only to subsequently deteriorate because of a recurrence of MEE prior to the posttest; the posttest was not performed until 4 weeks after the completion of treatment. In a pilot study that we conducted prior to this investigation, audiologic evaluations were performed immediately before and after treatment, and we observed immediate improvement in heating sensitivity in all patients after each administration. These pilot data support our hypothesis that the 7 treatment failures were attributable to the lag between the end of treatment and the posttest. The audiologic, otologic, and demographic characteristics of the 7 experimental patients whose hearing was not restored were no different from the data on those whose hearing did recover to within normal limits. We also considered the possibility that the duration of treatment was insufficient for these 7 patients, and we offered them a 2- to 3-week extension. The results of the extended treatment will be reported in a separate article.

In conclusion, the results of our study indicate that the use of our modified, automated Politzer device for the home treatment of MEE in children aged 4 to 11 years was highly successful. Marked improvement was reflected by evaluations of pure-tone air-conduction thresholds, TPPs, and tympanic membrane mobility at the posttest 4 weeks following the completion of treatment. Future research is needed to generalize findings to children younger than 4 years, to teenagers, and to adults. Further study is also needed to explore long-term outcomes. Still, our anecdotal observations suggest that there is indeed a long-term benefit.

Acknowledgments

The authors thank Carol Ann Silverman, PhD, and Michele B. Emmer, PhD, for their valuable contributions.

References

(1.) Cantekin EI, Mandel EM, Bluestone CD, et al. Lack of efficacy of a decongestant-antihistamine combination for otitis media with effusion ("secretory" otitis media) in children. Results of a double-blind, randomized trial. N Engl J Med 1983;308:297-301.

(2.) Williams RL, Chalmers TC, Stange KC, et al. Use of antibiotics in preventing recurrent acute otitis media and in treating otitis media with effusion. A meta-analytic attempt to resolve the brouhaha. JAMA 1993;270:1344-51.

(3.) Schmidt MA. Childhood Ear Infections. Berkeley, Calif.: North Atlantic Books, 1990.

(4.) Armstrong BW, Armstrong RB. Chronic nonsuppurative otitis media. Comparison of tympanostomy tubes and medication versus ventilation. Ann Otol Rhinol Laryngol 1981;90:533-6.

(5.) Froom J. Otitis media. J Fam Pract 1982;15:743-5, 750, 755.

(6.) Mandel EM, Rockette HE, Bluestone CD, et al. Myringotomy with and without tympanostomy tubes for chronic otitis media with effusion. Arch Otolaryngol Head Neck Surg 1989; 115:1217-24.

(7.) Rosenfeld RM, Culpepper L, Doyle KJ, et al; American Academy of Pediatrics Subcommittee on Otitis Media with Effusion; American Academy of Family Physicians; American Academy of Otolaryngology-Head and Neck Surgery. Clinical practice guideline: Otitis media with effusion. Otolaryngol Head Neck Surg 2004;130(5 suppl):S95-118.

(8.) Holmquist J, Renvall U. Middle ear ventilation in secretory otitis media. Ann Otol Rhinol Laryngol 1976;85(suppl 25): 178-81.

(9.) Barfoed C, Rosborg J. Secretory otitis media. Long-term observations after treatment with grommets. Arch Otolaryngol 1980; 106:553-6.

(10.) Mawson SR, Fagan P. Tympanic effusions in children. Long-term results of treatment by myringotomy, aspiration, and indwelling tubes (grommets). J Laryngol Otol 1972;86:105-19.

(11.) Kokko E. Chronic secretory otitis media in children. A clinical study. Acta Otolaryngol Suppl 1974;327:1-44.

(12.) Gates GA, Avery C, Prihoda TJ, Holt GR. Delayed onset post-tympanotomy otorrhea. Otolaryngol Head Neck Surg 1988;98:111-5.

(13.) Valtonen H, Tuomilehto H, Qvarnberg Y, Nuutinen J. A 14-year prospective follow-up study of children treated early in life with tympanostomy tubes: Part 1: Clinical outcomes. Arch Otolaryngol Head Neck Surg 2005; 131:293-8.

(14.) Tos M, Poulsen G. Secretory otitis media. Late results of treatment with grommets. Arch Otolaryngol 1976; 102:672-5.

(15.) Cantekin El, Bluestone CD, Parkin LP. Eustachian tube ventilatory function in children. Ann Otol Rhinol Laryngol 1976;85(suppl 25):171-7.

(16.) Stangerup SE, Sederberg-Olsen J, Balle V. Autoinfiation as a treatment of secretory otitis media. A randomized controlled study. Arch Otolaryngol Head Neck Surg 1992; 118:149-52.

(17.) Blanshard JD, Maw AR, Bawden R. Conservative treatment of otitis media with effusion by autoinflation of the middle ear. Clin Otolaryngol Allied Sci 1993;18:188-92.

(18.) Shea JJ. Autoinflation treatment of serous otitis media in children. J Laryngol Otol 1971;85:1254-8.

(19.) Schwartz DM, Schwartz RH, Redfield NP. Treatment of negative middle ear pressure and serous otitis media with Politzer's technique. An old procedure revisited. Arch Otolaryngol 1978; 104:487-90.

(20.) Silman S, Arick D. Efficacy of a modified politzer apparatus in management of eustachian tube dysfunction in adults. J Am Acad Audiol 1999;10:496-501.

(21.) Arick DS, Silman S. Treatment of otitis media with effusion based on politzerization with an automated device. Ear Nose Throat J 2000;79:290-2, 294, 296.

(22.) Cohen J. Statistical Power Analysis for the Behavioral Sciences. New York: Academic Press, 1977.

Reprint requests: Dr. Shlomo Silman, Center for Auditory Research, Brooklyn College, CUNY, 2900 Bedford Ave., Brooklyn, NY 11210. Phone: (718) 951-4869; fax: (718) 951-4363; e-mail: ssilman@brooklyn.cuny.edu

This study was conducted at the Brooklyn (N.Y.) College Center for Auditory Research and at Arisil Instruments of Brooklyn. This research was supported by a grant (No. 5R44DC003613-03) from the Small Business Innovation Research Program, National Institute on Deafness and Other Communication Disorders, National Institutes of Health to Arisil Instruments. Dr. Arick and Dr. Silman were the principal investigators.

Daniel S. Arick, MD, FACS; Shlomo Silman, PhD

Dr. Arick is on the attending staff of the Department of Otolaryngology-Head and Neck Surgery, New York Eye & Ear Infirmary, New York City. Dr. Silman is with the Center for Auditory Research, Brooklyn College, City University of New York, Brooklyn.

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