Diagnosis and management of spontaneous cerebrospinal fluid-middle ear effusion and otorrhea.

OBJECTIVES/HYPOTHESIS: Spontaneous leak of cerebrospinal fluid (CSF) into the middle ear can occur in adults without a history of temporal bone trauma or fracture, meningitis, or any obvious cause. Therefore, clues may be lacking that would alert the otolaryngologist that fluid medial to an intact eardrum, or fluid emanating from an eardrum perforation, is likely to be CSF fluid. A review of relevant medical literature reveals that herniation of the arachnoid membrane through a tegmen defect may be congenital, or CSF leak may occur when dynamic factors (i.e., brain pulsations or increases in intracranial pressure) produce a rent in the arachnoid membrane. Because tegmen defects may be multiple rather than single, identifying only one defect may not be sufficient for achieving definitive repair. Data on nine cases of spontaneous CSF leak to the ear in adult patients from four medical centers are presented and analyzed to provide collective information about a disorder that can be difficult to diagnose and manage. STUDY DESIGN: Retrospective review of nine cases of spontaneous CSF middle ear effusion/otorrhea. RESULTS: The majority of patients presented with symptoms of aural fullness and middle ear effusion. Many developed suspicious clear otorrhea only after insertion of a tympanostomy tube. Two patients had multiple defects in the tegmen and dura, and five patients had meningoencephaloceles confirmed intraoperatively. Five patients underwent combined middle cranial fossa/transmastoid repair. Materials used in repair included temporalis fascia, free muscle graft, Oxycel cotton, calvarial bone, pericranium, bone wax, and fibrin glue. CONCLUSIONS: CSF middle ear effusion/otorrhea can develop in adults without a prior history of meningitis or head trauma or any apparent proximate cause. Although presenting symptoms can be subtle, early suspicion and confirmatory imaging aid in establishing the diagnosis. Because surgical repair by way of a mastoid approach alone can be inadequate if there are multiple tegmen defects, a middle fossa approach alone, or in combination with a transmastoid approach, should be considered in most cases.

Management of middle ear hemangiomas.

Hemangioma rarely presents as an isolated middle ear lesion. Because congenital hemangiomas usually regress spontaneously, surgical excision is not always necessary. However, a hemangioma in the middle ear can be complicated by infection and hearing impairment. We present 2 cases to show contrasting management strategies, both with successful outcomes. Two children who presented with unilateral otitis media were found to have concomitant mesotympanic hemangiomas on examination. The first child was asymptomatic and subsequently had an incisional biopsy, confirming the suspected diagnosis. The residual tumor then involuted over the following year. The second child, however, developed chronic otitis media refractory to medical therapy and required surgical removal of the entire hemangioma. Once a tissue diagnosis is made, middle ear hemangiomas can be managed expectantly (ie, wait for spontaneous resolution) or surgically. If growth of a middle ear hemangioma appears to be causing complications refractory to conservative therapy, then early surgical excision may be indicated.

Accuracy and usefulness of radiographic assessment of cervical neck infections in children.

OBJECTIVE: To determine the accuracy and usefulness of computed tomography (CT) in diagnosis and management of lateral and deep neck infections METHODS: An 11-year retrospective review of 110 children (age range 1 months to 17 years) was conducted at a tertiary care children's hospital. RESULTS: Fifteen patients treated medically (8 with cellulitis, 7 with early abscess) improved. Of the remaining 95 patients who had 107 cervical sites drained surgically, CT predicted accurately operative findings in 81 (76%) cases (72 with abscess, 9 with cellulitis). In the 26 (24%) cases with discrepancy between CT interpretation and operative findings, the most common problem was differentiating early abscess from cellulitis with 18 false positives (no abscess at surgery). In 8 cases, CT diagnosis other than abscess was made (4 cellulitis, 1 inflammatory mass, 1 hematoma, 1 lymphangioma, and 1 tumour); however, when the patients were operated on because of lack of improvement, an abscess was found. CONCLUSIONS: Although CT is helpful both in determining the presence and location of neck infections in children, the CT scan is less helpful in differentiating abscess from lymphadenitis, cellulitis, and some complex cervical masses.

Genetics and molecular biology of deafness. Update.

This article discusses the latest research in the molecular biology and genetics of hearing impairment and its importance to otolaryngologists. Recent research has led to the discovery of many of the genes and gene products that are responsible for hereditary hearing impairment. State mandated screening of newborn infants for hearing loss ensures that a large number of hearing-impaired children will be detected at a very early age. Additionally, these children often will be referred to the otolaryngologist for evaluation of the hearing impairment. It is the otolaryngologist who must gather a detailed family history and perform a thorough physical examination to fully assess the cause of the hearing impairment. In taking the family history, it is important to note that the diagnosis of a hereditary hearing impairment often involves the evaluation of a large-sized family that has a history of hearing disorders. A history of an affected individual in a small family does not necessarily support a diagnosis of hearing impairment in later affected offspring because of the small sample size. Often, a hearing impairment that is part of a syndrome may not be detected because the physical findings associated with a syndrome are subtle in a young infant. For example, the white forelock seen in patients with Waardenburg's syndrome type I cannot be visualized in the infant who lacks hair. Additionally, some patients with syndromic hearing impairment do not present with physical findings, but rather they exhibit abnormal laboratory studies. Additional points to remember include the following: As infectious iatrogenic causes of hearing impairment decrease, the relative incidence of hereditary hearing impairment will increase. Hereditary hearing impairment can present as an isolated finding, or in association with a number of anomalies recognizable as a syndrome. The study of genetics and molecular biology has led to the identification of genes associated with hearing impairment and will allow for future screening and possible therapy for the hearing-impaired. The screening of newborns for hearing impairment using the techniques of molecular biologists and geneticists will result in early identification and appropriate intervention for those at risk for hereditary hearing impairment. An understanding of the syndromic and nonsyndromic causes of hereditary hearing impairment can help the otolaryngologist make a diagnosis and provide appropriate audiologic and educational management to the patient.

Genetics and molecular biology of deafness.

With increased emphasis on early detection of hearing impairment, more babies are likely to be referred at younger ages to otolaryngologists for evaluation. With a diminution in the number of infants who have hearing impairment as a result of such factors as maternal infection, neonatal sepsis, or ototoxicity, the relative importance of detecting a genetic cause of newborn hearing impairment is likely to increase. Therefore, the otolaryngologist must become familiar with common causes of hereditary hearing impairment and the ways in which the newborn should be evaluated for hereditary hearing impairment. Advancements are rapidly being made in the ability to detect genes that cause hearing impairment, and we are now on the threshold of discovering ways to use gene therapy to prevent or treat hereditary deafness.

Intralabyrinthine schwannomas.

OBJECTIVE: To describe characteristic features of intralabyrinthine schwannomas (ISs) that may be used to distinguish them from other otologic disorders with similar symptoms so that appropriate evaluation and management can be instituted. STUDY DESIGN: This study was a retrospective case review. SETTING: This study was conducted at a university-affiliated urban tertiary care medical center and a university medical center in the same city. PATIENTS: Seven patients with ISs were included in this study. INTERVENTIONS: Tumor removal versus observation and monitoring with periodic magnetic resonance imaging (MRI) scans was investigated. MAIN OUTCOME MEASURES: Hearing, vertigo, and tumor growth were measured. RESULTS: Four of seven patients with ISs underwent surgical excision with no evidence of tumor recurrence. The remaining three patients are being followed-up with repeat MRI that has demonstrated minimal or no tumor growth. CONCLUSIONS: ISs can be detected in early stages if MRI is performed in patients with unilateral sensorineural hearing loss without vertiginous symptoms typical of Meniere's disease. Although complete surgical excision can be achieved readily with labyrinthectomy, observation and monitoring with rep--MRI is an option for some patients.

A stepwise approach to the diagnosis and treatment of hereditary hearing loss.

What To Do Do suspect a genetic cause in all cases of hearing loss. Do develop a working knowledge of common types of HHI that you may draw on to aid in diagnosis. Do think of HHI when the audiogram reveals a hearing loss with a "cookie bite" configuration. Do refer the infant to a geneticist in cases where you suspect a syndromic HHI, a nonsyndromic HHI, and in cases of "cryptogenic" hearing loss where an underlying HHI may be present. Often, the associated symptoms are subtle and best detected by a professional who deals with these issues on a daily basis. Do get the infant or family plugged into an audiologist or otolaryngologist and speech pathologist who will preferably work as a team to maximize aural rehabilitation and ensure serial follow-up. It is never too early to fit a child with hearing aids. Do refer to the HHIRR center at Boys Town. Do refer to the correct "deaf" organization or "blind-deaf" organization. Do think about working up other siblings or family members. Do keep in mind that some members of the "deaf society" may regard deafness as an alternative lifestyle and may not be amenable to their child's referral for additional workup and aural rehabilitation. What Not To Do Do not assume the child is deaf and nothing can be done. Do not wait until the child is older to refer to an otolaryngologist, speech therapist, and audiologist. Do not order a sonogram. Do not order a temporal bone CT scan on newborns. Do not forget about other siblings who may have a similar pathology. Do not forget that some forms of HHI can present beyond infancy. The pediatrician is the front line and can play a major role in the diagnosis, workup, and treatment of HHI. Armed with the proper degree of suspicion, careful elicitation of family history, meticulous physical examination, evaluation of the audiogram, and adequate fund of knowledge of common types of genetic deafness, the pediatrician can make a timely diagnosis and appropriate referrals. This avoids delay in detection of significant hearing impairment and the associated lack of essential skills in speech, language, and social interaction. No child is too young to have some type of hearing assessment. Early detection and intervention are best done with a multidisciplinary team approach with a neonatologist or pediatrician, audiologist, speech therapist, and otolaryngologist. In the future, blood tests using genetic probes may be available to screen for many types of HHI.

Otologic manifestations of Wolf-Hirschhorn syndrome.

OBJECTIVE: To determine if haploinsufficiency for chromosome 4p16.3 in Wolf-Hirschhorn syndrome (WHS) is associated with cochlear hearing loss. DESIGN: Case series. SETTING: Tertiary care center. PATIENTS: Six patients with WHS were identified through a database and charts were retrospectively reviewed. MAIN OUTCOME MEASURES: Presence of sensorineural hearing loss as assessed by brainstem auditory evoked response. RESULTS: One of the 6 patients had sensorineural hearing loss. Three of the 6 patients had chronic otitis media with effusion and underwent bilateral tympanostomy tube placement; 2 of these 3 had cleft lip and palate, and 1 had a bifid uvula. One of the 6 patients had spontaneous nystagmus. Five of the 6 patients had preauricular and/or auricular abnormalities. CONCLUSIONS: More than 25 genes for nonsyndromic hereditary hearing impairment have been mapped. One of these genes, DFNA6, was identified through linkage analysis of a family with dominant, progressive, low-frequency sensorineural hearing loss. DFNA6 maps to chromosome 4p16.3, a region that is partially deleted in patients with WHS. In our series, we identified the second patient with WHS in the literature with bilateral sensorineural hearing loss. The incidence and type of otologic findings are consistent with those reported in the literature. Analysis of patients with chromosomal rearrangements represents one strategy toward identifying candidate genes for genetic hearing impairment.

Management of oropharyngeal trauma in children.

OBJECTIVE: To determine the indications for admission, requisite imaging studies, and urgent medical or surgical intervention. DESIGN: We retrospectively reviewed the charts of 26 children (age range, 5 months to 14 years) who were seen by the otolaryngology service in the emergency department at the Children's National Medical Center, Washington, DC, from 1985 to 1993 and who were diagnosed as having oropharyngeal trauma. We specifically looked for common findings in the history and physical examination on initial presentation to predict the necessary steps in evaluation and management. SETTING: Tertiary care pediatric referral center. RESULTS: Indications for admission were (1) concern about neurologic injury, (2) concern about vascular injury, (3) radiographic evidence of retropharyngeal free air or abscess, (4) pneumomediastinum, and (5) unreliable adult supervision at home. Six patients required surgery; 3 underwent retropharyngeal aspiration or incision and drainage procedures; 2 required neck explorations; and 1, who had an impaled foreign body in the parapharyngeal space, underwent surgical extraction. There were no vascular, neurologic, or other permanent injuries. CONCLUSIONS: Oropharyngeal trauma may result in palatal and posterior pharyngeal wall injury requiring closure of lacerations and management of retropharyngeal free air. Rarely does an injury lead to retropharyngeal abscess or significant pneumomediastinum. Lateral oropharyngeal injuries require increased concern about potential neurovascular impairment. However, neither the mechanism of injury nor the degree of injury correlates with the potential for neurovascular sequelae. Since neurovascular involvement may not become clinically apparent until days or weeks after the incident, admission for observation alone should be based on the distance from the patient's home to the hospital and on the level of reliable adult supervision. Indications for medical and surgical treatment of internal carotid artery thrombosis remain controversial.

Relative incidence and alternative approaches for surgical drainage of different types of deep neck abscesses in children.

OBJECTIVES: To determine the relative frequency of retropharyngeal abscesses (RPAs) vs lateral pharyngeal abscesses (LPAs) and to analyze alternative approaches for surgical drainage. DESIGN: Retrospective chart review. SETTING: Tertiary care children's hospital. PATIENTS: Seventy pediatric patients who were evaluated, admitted, and treated for presumed deep neck abscesses (RPAs and LPAs) between January 1, 1986, and December 31, 1996. INTERVENTION: Intravenous antibiotic therapy and surgical drainage. MAIN OUTCOME MEASURE: Clinical resolution of the abscess. RESULTS: Fifty-eight patients were evaluated with computed tomographic scan. Thirteen of these patients did not have surgical intervention. Of 12 patients diagnosed as having an isolated RPA, all had intraoral surgical drainage and 9 had evidence of pus at surgery. Twenty-one patients had an isolated LPA. Sixteen of these underwent intraoral drainage and 5 underwent external drainage. Purulence was found at surgery in 14 and 2 patients, respectively. The remaining 12 patients had a combination of RPA and LPA. Eight patients underwent intraoral drainage, and 4 patients required both intraoral and external approaches. Purulence was found at surgery in 5 and 4 patients, respectively. Of the 12 patients who were not evaluated with computed tomographic scan, two thirds were treated prior to 1987. Six of these 12 patients underwent surgical drainage via an intraoral approach, and 4 of the 6 patients had pus. The remaining 6 improved without surgery. CONCLUSIONS: Most deep neck abscesses in children are located in the retropharyngeal or in the lateral pharyngeal space medial to the great vessels. Therefore, most can be managed successfully with intraoral rather than external drainage. External approaches are better reserved for those abscesses that are lateral to the great vessels or that involve multiple spaces. In this patient population, LPAs were more commonly seen than RPAs.

Benign lesions of the external auditory canal.

Benign mass lesions of the external auditory canal, such as exostoses and osteomas, are common findings on physical examination but most often do not require treatment. The differential diagnosis of lesions in the external auditory canal, however, should not be limited to those benign processes discussed here, but should also include infectious, dermatologic, congenital, and malignant processes.

Balancing pediatric otolaryngology training for fellows and residents at a children's hospital.

OBJECTIVE: To determine the feasibility of providing surgical, endoscopic, and patient contact experience of high educational value at a children's hospital sufficient for adequately training contemporaneously both residents in otolaryngology-head and neck surgery and fellows in pediatric otolaryngology. DESIGN: Retrospective review of operating room case logs and assignment of cases based on arbitrary perception of inherent case complexity and skill and experience that are required to manage the case. SETTING: Tertiary care children's hospital located in a major metropolitan area. MAIN OUTCOME MEASURES: (1) Volume of surgical and endoscopic cases assigned retrospectively to junior resident, senior resident, or fellow. (2) Score on newly developed self-assessment skill list in pediatric otolaryngology. RESULTS: During 1 year, there were 3224 surgical and endoscopic procedures performed in the operating room. Of the total number of procedures, only 44 (1.4%) were designated as being exclusively assigned for hands-on experience to a fellow, but 380 (11.8%) were appropriate for both a senior resident and a fellow and therefore were apportioned in an alternating fashion. A self-assessment instrument has been developed to assess competency and comfort in the management of otolaryngic disorders, both surgical and nonsurgical, in children. CONCLUSIONS: The volume and assortment of surgical and endoscopy cases at a tertiary care children's hospital can provide the basis for a rich, practical hands-on experience for residents and fellows. Since few surgical or endoscopic cases require pediatric fellowship training for mastery, becoming a pediatric otolaryngologist depends on acquiring skills and competence that exceed the technical skills acquired in the operating room.

Laryngomalacia. The search for the second lesion.

OBJECTIVES: To determine the necessity of rigid endoscopy in the diagnosis and management of laryngomalacia and its associated synchronous airway lesions (SALs), to analyze the incidence of SALs associated with laryngomalacia and their significance, and to determine the need for epiglottoplasty in management of laryngomalacia. DESIGN: Retrospective medical chart review. SETTING: Tertiary care children's hospital. PATIENTS: Two hundred thirty-three patients with a primary diagnosis of laryngomalacia on flexible fiberoptic laryngoscopy treated at the Children's National Medical Center, Washington, DC, from January 1, 1984, to June 30, 1994. INTERVENTION: Evaluation and treatment of laryngomalacia and associated SAL by flexible fiberoptic laryngoscopy, radiographic studies, rigid endoscopy, and other surgical procedures. MAIN OUTCOME MEASURES: Resolution of airway symptoms from laryngomalacia and associated SAL. RESULTS: Ninety patients (38.6%) underwent rigid endoscopy, and 12 patients (5.2%) required epiglottoplasty. Synchronous airway lesions were discovered in 44 patients (18.9%). Eleven patients (4.7%) had SALs that wre considered clinically significant; nine (3.9%) of these required surgical intervention. CONCLUSIONS: Rigid endoscopy in evaluation of an infant with laryngomalacia is rarely necessary. Clinically significant SALs requiring surgical intervention are uncommon. Surgical intervention for laryngomalacia also is rarely necessary.

Delayed diagnosis and fate of congenital cholesteatoma (keratoma).

OBJECTIVE: To analyze clinical presentation, modes of detection, growth pattern, operative findings, and results of surgery in children 3 years old or older who had extensive congenital cholesteatoma (keratoma). DESIGN: Survey, case series. SETTING: Two academically affiliated medical centers: a children's hospital and an eye, ear, and throat hospital, both located in major metropolitan cities. PATIENTS: Twenty-five children selected according to specified criteria. INTERVENTION: Tympanomastoid surgery, ie, canal wall up and canal wall down, some with ossicular reconstructive surgery. MAIN OUTCOME MEASURE: Audiologic assessment (speech reception threshold) and recurrence (recidivism) of cholesteatoma. RESULTS: Incidence of recidivism, 52%. Hearing maintained within the range of normal to mild hearing impairment postoperatively in 91% of the patients for whom complete data are available. CONCLUSIONS: Congenital cholesteatoma may grow for years without causing signs or symptoms and, having grown without early detection, can extend to involve the epitympanum and mastoid antrum, cause ossicular erosion, and even extend to the middle cranial fossa. To adequately remove a congenital cholesteatoma that has gone undetected for many years, exposure of the anterior epitympanum is often necessary and removal of both the body of the incus and the head of the malleus often is required. Since congenital cholesteatoma usually develops in a child with a well-pneumatized mastoid that would create a large mastoid bowl if exteriorized, the otologic surgeon is likely to hesitate in using the canal wall down mastoidectomy technique. Alternatives to the canal wall down mastoidectomy technique, which can achieve reasonably good hearing results and avoid creation of a large mastoid bowl, include planned two-stage canal wall up surgery or canal preservation with primary reconstruction and close follow-up with otomicroscopy and serial computed tomographic scans.

Further elucidation of the genomic structure of PAX3, and identification of two different point mutations within the PAX3 homeobox that cause Waardenburg syndrome type 1 in two families.

Waardenburg syndrome is an autosomal dominant disorder characterized by sensorineural deafness and pigmentary disturbances. Previous work has linked the disease to PAX3 on chromosome 2, and several mutations within the highly conserved paired-box and octapeptide motifs, but not the homeobox, have been reported. In this report, we have used the published cDNA sequence to further define the genomic structure of PAX3, using inverse PCR. We have identified exon/intron boundaries between exons 5 and 6 and between exons 6 and 7. Further, we have identified the first two mutations within the homeobox in two different families with type 1 Waardenburg syndrome. The first is a point mutation (G-->T) at the first base of exon 6, which substitutes phenylalanine for valine. In another family, we have identified a point mutation (C-->G) within the homebox, in exon 6, which substitutes a glycine for arginine at a highly conserved site. The homeodomain is important in binding of DNA and in effecting transcriptional control. These mutations likely result in structural change within the homeodomain that either change the DNA-binding specificity of the homedomain or reduce the affinity of the PAX3 protein for DNA. These homeodomain mutations should aid in elucidating the role of the homeodomain in the function of the PAX3 protein.

Enlarged vestibular aqueduct and sensorineural hearing loss in childhood.

OBJECTIVE: To determine if all children with enlarged vestibular aqueducts (EVAs) have development of uniform progressive sensorineural hearing loss (SNHL). To determine whether the size of the EVA correlates with severity, frequencies involved, and stability of SNHL. To determine if the audiologic pattern of SNHL correlates with likelihood of progression of SNHL. DESIGN: Retrospective study. SETTING: Children's National Medical Center, Washington, DC, a tertiary care center with a large otologic practice. PATIENTS: Fifteen children (26 ears) with EVA on computed tomographic scan. METHODS: History, physical examination, computed tomographic scans, and serial audiograms were reviewed. Factors analyzed included age at diagnosis, audiometric configuration (high tone, midtone, low tone, flat), degree of hearing loss at presentation, length of follow-up, and presence of associated inner ear anomalies. RESULTS: Nine ears had progressive SNHL, 16 ears had stable SNHL, and 1 ear had profound SNHL. The predominant audiologic configuration was flat. The audiogram configuration does not correlate with progression of SNHL. The size of the vestibular aqueduct does not correlate with the level, type, or progression of SNHL. CONCLUSION: Our study failed to uncover factors that might be predictive of progression of hearing loss. We conclude that until a better understanding of the natural history and pathophysiologic condition of EVAs is achieved, there is no surgical or other intervention that can be demonstrated as being efficacious.

A new nonsyndromic X-linked sensorineural hearing impairment linked to Xp21.2.

X-linked deafness is a rare cause of hereditary hearing impairment. We have identified a family with X-linked dominant sensorineural hearing impairment, characterized by incomplete penetrance and variable expressivity in carrier females, that is linked to the Xp21.2, which contains the Duchenne muscular dystrophy (DMD) locus. The auditory impairment in affected males was congenital, bilateral, profound, sensorineural, affecting all frequencies, and without evidence of radiographic abnormality of the temporal bone. Adult carrier females manifested bilateral, mild-to-moderate high-frequency sensorineural hearing impairment of delayed onset during adulthood. Eighteen commercially available, polymorphic markers from the X chromosome, generating a 10-15-cM map, were initially used for identification of a candidate region. DXS997, located within the DMD gene, generated a two-point LOD score of 2.91 at theta = 0, with every carrier mother heterozygous at this locus. Recombination events at DXS992 (located within the DMD locus, 3' to exon 50 of the dystrophin gene) and at DXS1068 (5' to the brain promoter of the dystrophin gene) were observed. No recombination events were noted with the following markers within the DMD locus: 5'DYS II, intron 44, DXS997, and intron 50. There was no clinical evidence of Duchenne or Becker muscular dystrophy in any family member. It is likely that this family represents a new locus on the X chromosome, which when mutated results in nonsyndromic sensorineural hearing loss and is distinct from the heterogeneous group of X-linked hearing losses that have been previously described.

Locus heterogeneity for Waardenburg syndrome is predictive of clinical subtypes.

Waardenburg syndrome (WS) is a dominantly inherited and clinically variable syndrome of deafness, pigmentary changes, and distinctive facial features. Clinically, WS type I (WS1) is differentiated from WS type II (WS2) by the high frequency of dystopia canthorum in the family. In some families, WS is caused by mutations in the PAX3 gene on chromosome 2q. We have typed microsatellite markers within and flanking PAX3 in 41 WS1 kindreds and 26 WS2 kindreds in order to estimate the proportion of families with probable mutations in PAX3 and to study the relationship between phenotypic and genotypic heterogeneity. Evaluation of heterogeneity in location scores obtained by multilocus analysis indicated that WS is linked to PAX3 in 60% of all WS families and in 100% of WS1 families. None of the WS2 families were linked. In those families in which equivocal lod scores (between -2 and +1) were found, PAX3 mutations have been identified in 5 of the 15 WS1 families but in none of the 4 WS2 families. Although preliminary studies do not suggest any association between the phenotype and the molecular pathology in 20 families with known PAX3 mutations and in four patients with chromosomal abnormalities in the vicinity of PAX3, the presence of dystopia in multiple family members is a reliable indicator for identifying families likely to have a defect in PAX3.

Management of otitis media and the New Agency for Health Care Policy and Research Guideline.

In these times of increasing dominance of managed care and diminishing autonomy for practitioners of medicine, any government pronouncement can be viewed as yet another of many annoyances. For otolaryngologists who yearn for the days when there were not so many intermediaries involved in patient care, the newly issued Clinical Practice Guideline, Otitis Media with Effusion in Young Children (see reference 2 for highlights) may seem more of an ominous threat than anything remotely beneficial. However, given the inexorable changes that are occurring, the Agency for Health Care Policy and Research (AHCPR) otitis media guideline is probably going to be more helpful than harmful.