Karen J Doyle

Clinical Practice Guideline: Otitis Media with Effusion

The clinical practice guideline on otitis media with effusion (OME) provides evidence-based recommendations on diagnosing and managing OME in children. This is an update of the 1994 clinical practice guideline “Otitis Media With Effusion in Young Children,” which was developed by the Agency for Healthcare Policy and Research (now the Agency for Healthcare Research and Quality). In contrast to the earlier guideline, which was limited to children aged 1 to 3 years with no craniofacial or neurologic abnormalities or sensory deficits, the updated guideline applies to children aged 2 months through 12 years with or without developmental disabilities or underlying conditions that predispose to OME and its sequelae. The American Academy of Pediatrics, American Academy of Family Physicians, and American Academy of Otolaryngology- Head and Neck Surgery selected a subcommittee composed of experts in the fields of primary care, otolaryngology, infectious diseases, epidemiology, hearing, speech and language, and advanced practice nursing to revise the OME guideline. The subcommittee made a strong recommendation that clinicians use pneumatic otoscopy as the primary diagnostic method and distinguish OME from acute otitis media (AOM). The subcommittee made recommendations that clinicians should (1) document the laterality, duration of effusion, and presence and severity of associated symptoms at each assessment of the child with OME; (2) distinguish the child with OME who is at risk for speech, language, or learning problems from other children with OME and more promptly evaluate hearing, speech, language, and need for intervention in children at risk; and (3) manage the child with OME who is not at risk with watchful waiting for 3 months from the date of effusion onset (if known), or from the date of diagnosis (if onset is unknown). The subcommittee also made recommendations that (4) hearing testing be conducted when OME persists for 3 months or longer, or at any time that language delay, learning problems, or a significant hearing loss is suspected in a child with OME; (5) children with persistent OME who are not at risk should be reexamined at 3- to 6-month intervals until the effusion is no longer present, significant hearing loss is identified, or structural abnormalities of the eardrum or middle ear are suspected; and (6) when a child becomes a surgical candidate, tympanostomy tube insertion is the preferred initial procedure. Adenoidectomy should not be performed unless a distinct indication exists (nasal obstruction, chronic adenoiditis); repeat surgery consists of adenoidectomy plus myringotomy, with or without tube insertion. Tonsillectomy alone or myringotomy alone should not be used to treat OME. The subcommittee made negative recommendations that (1) population-based screening programs for OME not be performed in healthy, asymptomatic children and (2) antihistamines and decongestants are ineffective for OME and should not be used for treatment; antimicrobials and corticosteroids do not have long-term efficacy and should not be used for routine management. The subcommittee gave as options that (1) tympanometry can be used to confirm the diagnosis of OME and (2) when children with OME are referred by the primary clinician for evaluation by an otolaryngologist, audiologist, or speech-language pathologist, the referring clinician should document the effusion duration and specific reason for referral (evaluation, surgery), and provide additional relevant information such as history of AOM and developmental status of the child. The subcommittee made no recommendations for (1) complementary and alternative medicine as a treatment for OME based on a lack of scientific evidence documenting efficacy and (2) allergy management as a treatment for OME based on insufficient evidence of therapeutic efficacy or a causal relationship between allergy and OME. Last, the panel compiled a list of research needs based on limitations of the evidence reviewed. The purpose of this guideline is to inform clinicians of evidence-based methods to identify, monitor, and manage OME in children aged 2 months through 12 years. The guideline may not apply to children older than 12 years because OME is uncommon and the natural history is likely to differ from younger children who experience rapid developmental change. The target population includes children with or without developmental disabilities or underlying conditions that predispose to OME and its sequelae. The guideline is intended for use by providers of health care to children, including primary care and specialist physicians, nurses and nurse practitioners, physician assistants, audiologists, speech-language pathologists, and child development specialists. The guideline is applicable to any setting in which children with OME would be identified, monitored, or managed. This guideline is not intended as a sole source of guidance in evaluating children with OME. Rather, it is designed to assist primary care and other clinicians by providing an evidence-based framework for decision-making strategies. It is not intended to replace clinical judgment or establish a protocol for all children with this condition, and may not provide the only appropriate approach to diagnosing and managing this problem. (Otolaryngol Head Neck Surg 2004;130:S95.)

Neonatal Hearing Screening with Otoscopy, Auditory Brain Stem Response, and Otoacoustic Emissions

A study was performed to investigate the relationship between external and middle ear factors and hearing screening results by auditory brain stem response (ABR) and transient evoked otoacoustic emissions (EOAEs). The ears of 200 well newborns aged 5 hours to 48 hours underwent screening by ABR and EOAEs, followed by otoscopic examination. The pass rates for ABR and EOAE screening were 88.5% and 79%, respectively. On otoscopic examination, 13% (53 of 400) ears had occluding vernix obscuring the view of the tympanic membrane. Cleaning of vernix was attempted in ears that failed ABR or EOAE screening. Seventeen ears that failed ABR were cleaned, and 12 (71%) of them passed repeat ABR. Thirty-three ears that failed EOAE screening were cleaned, and 22 (67%) of them passed repeat emissions testing. Cleaning vernix increased the pass rates for ABR and EOAE screening to 91.5% and 84%, respectively. Decreased tympanic membrane mobility was found in 9% of ears that could be evaluated otoscopically. Increased failure rates for both ABR and EOAE screening were found in infant ears with decreased tympanic membrane mobility, but significance testing could not be performed because of inadequate sample size. Prevalence of occluding external canal vernix and middle ear effusion as a function of increasing infant age were studied. Implications for newborn hearing screening are discussed.

Otogenic cavernous sinus thrombosis

S e p t i c thrombosis of the dural venous sinuses was a fairly common complication of otitis media in the preantibiotic era. This dire complication frequently led to the patient’s death, either through overwhelming sepsis or intracranial complication. A small incidence of otogenic dural sinus thrombosis persists today, generally occurring in those patients whose ear infections have not been treated with specific antimicrobial therapy. The sigmoid sinus is the dural venous structure most frequently involved in otologic infection. Propagation of sigmoid sinus thrombosis (SST) via the petrosal sinuses to the cavernous sinus has been rarely reported in the literature. We present a recent case of otogenic cavernous sinus thrombosis (CST) that illustrates the contemporary diagnosis and management of this rare complication.

Audiologic findings in unilateral deafness resulting from contralateral pontine infarct

Audiologic findings in unilateral deafness resulting from contralateral pontine infarct KAREN JO DOYLE, MD, PhD, CYNTHIA FOWLER, PhD, and ARNOLD STARR, MD, Irvine and Long Beach, California F o c a l brain stem infarction has been uncommonly associated with unilateral sensorineural hearing loss (SNHL). Kumar et al. (1986) 1 found a single case of brain stem infarction among 200 cases of unilateral SNHL. Previous case reports of unilateral S N H L after brain stem infarct have been the result of lesions of the ipsilateral cochlear nuclei in the dor- solateral medulla. 2,3 Wada and Starr (1983) 4 deter- mined that an experimentally produced lesion of the lateral lemniscus produced a unilateral contralateral abnormality in the N 3 portion of wave III of the auditory brain stem response (ABR) in guinea pigs. We report a case of unilateral S N H L after a con- tralateral focal pontine infarct verified by magnetic resonance imaging (MRI) and A B R testing. CASE REPORT A 63-year-old man with a history of hypertension was admitted to the Veterans Administration Medical Cen- ter-Long Beach in June 1994 with a urinary tract infec- tion. During his admitting physical examination, a neuro- logic examination was performed that revealed a right- sided hearing loss. The neurologic examination was otherwise normal. He reported that he had had a stroke in April 1994 and had spent several days in another hospital. The records and MRI scans from that hospital- ization were obtained. The admission physical examina- tion from April revealed a blood pressure of 170/86, a central right facial palsy, a right-sided hearing loss, nys- tagmus (direction not given), and unsteady gait. Labora- tory examination revealed normal cerebrospinal fluid chemistries and cell counts and negative VDRL. The MRI From the Divisions of Otolaryngology-Head and Neck Sur- gery and Audiology (Drs. Doyle and Fowler), Veterans Administration Medical Center; and the Departments of Otolaryngology-Head and Neck Surgery (Drs. Doyle and Fowler) and Neurology (Dr. Starr), University of California Irvine. Received for publication April 28, 1995; revision received June 27, 1995; accepted July 17, 1995. Reprint requests: Karen Jo Doyle, MD, PhD, Department of Otolaryngology-Head and Neck Surgery, University of Cali- fornia Irvine Medical Center, Bldg. 25, Route 81, 101 The City Dr., Orange, CA 02668. OTOI.A~YNGOI. HZAO NECK SUnG 1996;114:482-6. from April 1994 demonstratd a dorsally located infarct involving the medial left portion of the upper pons, as well as ischemic changes of the periventricular deep white matter (Figs. 1 and 2). He was referred 3 weeks after the stroke to the Audi- ology Department for evaluation of his right-sided hearing loss. Audiogram revealed a fiat, severe SNHL in the right ear and a moderate high-frequency SNHL above 2000 Hz in the left ear (Fig. 3). Speech discrimination was 0% in the right ear and 92% in the left ear. Acoustic reflexes were absent in the right ear. ABR was performed with condensation and rarefaction dicks presented 10/second at 95 dB nSL (Fig. 4). In the left ear, all components were identified, and their intercomponent times were within normal limits. In the right ear, wave I was present for condensation clicks at 1.98 msec, and no other waves were identified. Transient and distortion-product otoacoustic emissions (OAEs) were performed. In the right ear, tran- sient emissions were present with energy present through 3000 Hz with 81% reproducibility, similar to those ob- tained from the left ear (Fig. 5). Distortion-product OAEs (2F2 - F1 = 1.221; F1 = 70 dB SPL; F2 = 70 dB SPL) were present across frequencies in the right ear and through F2 = 3000 Hz in the left ear. Repeat MRI with gadolinium of the internal auditory canals was performed, and they were normal. DISCUSSION Although we used the combined term sensorineu- ral hearing loss, the majority of patients with S N H L have lesions of the sensory apparatus, whereas neu- ral lesions, including spiral ganglion degeneration, eighth nerve lesions, and central auditory pathway lesions from the cochlear nuclei to the temporal cortex, are found less frequentlyJ A m o n g the causes of hearing loss, cerebrovascular infarction of the auditory pathways has been described infrequently. A 1986 report of 200 cases of unilateral S N H L found 42 individuals with confirmed retrocochlear lesions, of which there was one lesion adjacent to the co- chlear nucleus and a second patient with a pontine lesion? The most commonly found central lesions in that study were cerebellopontine angle tumors, cen- tral nervous system lues, and multiple sclerosis. Lownie and Parnes (1991) 2 found two cases of ipsi- lateral S N H L caused by infarcts of the cerebellum

PATHOGENESIS OF OTITIC HYDROCEPHALUS : CLINICAL EVIDENCE IN SUPPORT OF SYMONDS' (1937) THEORY

&tic hydrocephalus was described first by Quincke in 1896,’ who defined it as signs of increased intracranial pressure associated with normal cerebrospinal fluid (CSF) composition on lumbar puncture and called it “serous meningitis.” He believed that it was caused by increased secretion of CSF by the choroid plexus in response to a number of conditions, including sinusitis, tonsillitis, and otitis media. It was Symonds who coined the term otitic hydrocephalus in 1931 and outlined the clinical features of the syndrome: signs and symptoms of increased intracranial pressure (headache, vomiting, and papilledema), without abscess formation and with nonpathologic CSF findings, associated with otitis media.’ Symonds based his diagnosis on physical findings and lumbar puncture results. With the advent of ventriculography, it was discovered that the ventricles are not enlarged in otitic hydrocepha l u ~ , ~ but the name has persisted to the present day. In a second paper, Symonds in 19374 carefully outlined the possible pathophysiologic mechanisms involved in the formation of otitic hydrocephalus. Using available clinical and postmortem information, Symonds deduced the pathologic basis of the syndrome to be infection of the lateral sinus, with retrograde extension of thrombophlebitis to the superior sagittal sinus and resultant blockage of the arachnoid villi producing elevated CSF pressure. He emphasized that otitic hydrocephalus could occur in

THE EFFECTS OF SIGNAL PROCESSING BY THE HOUSE–URBAN SINGLE‐CHANNEL STIMULATOR ON AUDITORY PERCEPTION ABILITIES OF PATIENTS WITH COCHLEAR IMPLANTS

The House-Urban single-channel cochlear implant (CI) was first implanted in a patient in 1972 after an extensive investigation of multiple-electrode hardwired systems in three patients. The major goal in the design of the singlechannel, single-electrode system was to provide a prosthesis that was safe, had a high degree of clinical efficacy, and was biologically stable. To begin, we should consider the rationale that forms the basis for the engineering decisions which resulted in the present House-Urban CI. There are three key components of the House-Urban CI device that will be briefly reviewed: (1) bandpass filtering of the input speech spectrum; (2) amplitude modulation of a 16-kHz carrier wave; and (3) transmission of the AM signal to the implanted electrodes via a magnetic induction coil system. The design of the input filter section is based on data collected from patients using speech and environmental sound tests, as well as subjective evaluations under everyday listening conditions. The 3-dB downpoints for the lowand high-frequency cutoffs of the filter are 200 and 4000 Hz, respectively. Our experience has demonstrated that lowering the low-frequency cutoff results in interference and annoyance due to environmental sound with no improvement in speech discrimination or environmental sound recognition. Increasing the high-frequency cutoff above 4 kHz also does not improve performance with this CI system. The amplitude-modulated high-frequency carrier system was originally selected because (1) it was believed that there would be negligible net DC; (2) it allowed efficient energy transfer across the skin via the induction coils; and ( 3 ) it allowed frequency coding over the entire speech spectrum with little effect from the induction coil transfer characteristics. The decision to use a 16-kHz carrier signal was based primarily on threshold considerations and patient preference. A magnetic induction system was designed for transmitting signals from the processor to the implanted electrodes since it was believed that to be useful as a long-term clinical device, that is, to avoid tissue reaction and rejection, the connection should not protrude through the skin. It was also felt that by keeping the implanted device as simple as possible, with a minimum of implanted electronic components, the chance of internal device failure would be substantially reduced. From the standpoint of safety and clinical efficacy these bioengineering decisions have stood the test of time.

Features from normal and sensorineural listeners' nonsense syllable test errors.

Identification errors for initial consonants of consonants vowels-consonants-vowels from lists A and B of the Nonsense Syllable Test were analyzed for 10 normal-hearing and 8 sensorineural hearing-impaired listeners. The Nonsense Syllable Test stimuli were presented binaurally through earphones at 6 increasing sensation levels. Listeners verbal responses were recorded and transcribed, converted to symmetric confusion matrices, and submitted to analysis of individual differences scaling for symmetrical matrices. Results from 2- through 5-dimensional analyses revealed that voicing, place of articulation, frication, and sibilancy were the salient features used by both listener types in their perceptions of the initial consonants. Findings suggest that consideration of composition of the stimulus set is important when assessing a listeners response to specific speech discrimination tests.

09:30: Expression Patterns in the Injured Cochlea Microenvironment

ynx and the contribution of individual structures (palate/tonsils, tongue, epiglottis, and lateral pharyngeal walls) to upper airway obstruction. Test-retest reliability was determined separately for the blinded and unblinded surgeons based on the agreement between the surgeon’s ratings for the two DISE procedures. RESULTS: Twenty-eight patients (6 female; 22 male) were studied with DISE. Preoperative polysomnography findings included a mean apnea-hypopnea index of 33.3 16.4 and a lowest oxygen saturation was 78.4 8.4%. For the DISE ratings, there was moderate-good agreement (weighted kappa 0.41-0.63) for the degree of obstruction at the level of the palate and hypopharynx. Agreement regarding the contribution of individual structures was moderate-good (Cohen’s kappa 0.44-0.71). Greater agreement was demonstrated for the unblinded surgeon ratings. CONCLUSIONS: The inter-rater reliability of DISE is moderate-good.

10:06: Endoscopic Microvascular Decompression

t-test were used for analysis. RESULTS: No significant difference was found for high frequency hearing loss, DPOAE, ABR and MLR in the users. High frequency hearing loss was seen in subjects using the phone for more than 4 years (P 0.040). Users with complaints like aural fullness or tinnitus had prolonged I-III interpeak latency compared to those with no complaints (P 0.04). There was a significant difference in Pa wave amplitude values between the users and the controls on the left side (P 0.015). CONCLUSIONS: Long-term use of mobile phones may cause inner ear damage. Presence of ear symptoms like fullness may be an early warning sign.

11:24: Diagnostic Parameters of Video Pneumatic Otoendoscope

idiopathic, progressive sensorineural hearing loss (SNHL). 3. Appreciate that diagnostic work-up for all cases of idiopathic SNHL should include syphilis serology. 4. Understand that treatment of otosyphilis with intravenous penicillin stabilizes hearing. 5. Establish the prevalence of spirochete-associated labyrinthine disease in patients with idiopathic, progressive SNHL and, thus, to determine whether routine testing for spirochetes is appropriate. METHODS: A retrospective review of patients presenting to a university outpatient otology clinic with idiopathic, progressive SNHL between 1998 and 2006 was conducted. Cases with SNHL attributable to other causes were excluded. All cases underwent nonspecific and specific serological testing for syphilis, and screening for Lyme disease. Audiometric assessments and MRI brain scans were performed. RESULTS: The study cohort consisted of 185 subjects (mean age 56.3 years, range 18-89). Otosyphilis was diagnosed in 9 cases (4.9%). One of the 9 (11.1%) had a negative syphilis screening test but a positive confirmatory test. Otosyphilis cases received a two-week course of intravenous penicillin and all exhibited stabilized hearing. Lyme disease was not detected. CONCLUSIONS: All patients with idiopathic, progressive SNHL should undergo confirmatory tests for syphilis. Use of screening tests is discouraged as these have low specificity. Intravenous penicillin is effective in preventing disease progression. There were no cases of Lyme-induced hearing loss in the Lyme-endemic study area and routine testing for this disease is not recommended.