Medical and surgical management of otitis media in children

Otolaryngol Clin N Am 35 (2002) 811–825

Medical and surgical management of otitis media in children Jonathan A. Perkins, DO* Division of Pediatric Otolaryngology—Head and Neck Surgery, University of Washington and Children’s Hospital and Regional Medical Center, 4800 Sand Point Way NE/CH-62, Seattle, WA 98105, USA

Otitis media (OM) is the most frequent outpatient diagnosis for children seen by physicians and, consequently, the number one reason that outpatient antibiotics are prescribed in this age group. High prevalence of OM ensures that the annual expenditures on OM remain high, and that this condition is seen frequently by otolaryngologists. The past decade has brought significant changes in management recommendations for OM caused by multiple factors. Attention to treatment costs, treatment outcomes, understanding the natural history of OM, development of resistant bacteria, and preventative measures have all impacted the medical and surgical management of OM in children. In an effort to control health care costs, scrutiny of medical and surgical treatment outcomes are being applied to all aspects of health care. Excellent guidelines for OM management were published in 1994 by the Agency for Health Care Policy and Research (AHCPR) [1]. Subsequently, a comprehensive text on all aspects of evidence-based medicine as applied to OM has been published [2]. From these works and others, a logical framework for approaching OM has been created. At the same time, our understanding of OM pathophysiology has grown through molecular genetics and careful epidemiologic evaluations [3,4]. Despite our improved understanding of OM, treatment options remain the same: observation, antibiotic therapy, tympanostomy tube placement (TT), and adenoidectomy (Ad). This article will highlight recent clinical and basic science developments that impact decision-making in pediatric OM management, as this is the most important part of OM treatment.

* E-mail address: [email protected] (J.A. Perkins). 0030-6665/02/$ - see front matter Ó 2002, Elsevier Science (USA). All rights reserved. PII: S 0 0 3 0 - 6 6 6 5 ( 0 2 ) 0 0 0 5 1 - 8

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Definitions Otitis media is a condition in which there is a middle ear effusion (MEE) (Table 1). A MEE can be acutely symptomatic resulting in acute OM (AOM), or asymptomatic resulting in OM with effusion (OME). In both AOM and OME infectious (viral and bacterial), pathogens are present, meaning that both are ‘‘ear infections.’’ Children under age 2 are commonly affected by recurrent AOM (RAOM), which has been defined as 3 or more bouts of AOM in 6 months.

Treatment costs Estimates of annual costs related to AOM and OME are near $ 5 billion [5]. To prospectively analyze AOM treatment costs, direct and indirect parameters have been used. Direct costs are accrued by the illness and its treatment (ie, medications, physician fees). Indirect costs arise secondarily to the illness and its treatment (ie, time off from work, travel expenses). Prospective analysis of AOM treatment including both indirect and direct costs have determined that a single episode can cost as much as $1,330 [6]. In this analysis, it was discovered that at least 90% of these costs where indirect. Surgical treatment further adds to costs associated with OM. Of particular concern is that treatment costs can limit access to appropriate surgical therapy in some instances [7]. Treatment outcomes Natural history of OM An understanding of treatment outcomes must be based on an understanding of the natural history of a disease; this is definitely the case in OM [8]. Most children experience one episode of AOM in childhood [9]. AOM occurs most often between 6–12 months of age; following this the incidence decreases. RAOM is also common, with 10–19% of children havTable 1 Definitions for Otitis media Middle ear condition

Definition

MEE AOM

Fluid in the middle ear space MEE with symptoms and signs of inflammation (ie, otalgia, fever, irritability) MEE without symptoms or signs of inflammation Three or more episodes of AOM in 6 months MEE without symptoms for more than 3 months

OME RAOM Persistent OME

Abbreviations: AOM, acute Otitis media; MEE, middle ear effusion; OME, Otitis media with effusion; RAOM, recurrent acute Otitis media.

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ing three or more episodes of acute OM before age 1 [10]. Otitis media with effusion and has been seen in as many is 61% of children in day care [11]. Placebo-controlled clinical trials have demonstrated spontaneous resolution of up to 80% AOM episodes in the placebo group [12]. OME has been shown to resolve without therapy in 80–90% of patients in observational studies and the control group in randomized control trials [13,14]. This reality that OM resolves without therapy in the majority of patients changes our perception of treatment efficacy and requires large study populations to validate treatment efficacy. Risk factors for OM Another aspect of OM affecting treatment outcome that has been further clarified in the past few years are host and environmental risk factors (Table 2). Host factors associated with increased incidence of OM are patient age and genetics. Children who experience OM under age 1 are more likely to develop RAOM than those that do not [15]. Infants under 2 months with OM are more likely to develop OME than their peers [16]. Twin/ triplet studies have demonstrated significant genetic predisposition to both AOM and OME [4]. Significant environmental risk factors that increase OM are: large daycare settings, viral upper respiratory infections (URI), the presence of multiple siblings, passive smoke exposure, socioeconomic status, and pacifier use in daycare. Daycare settings with more than six children increase the risk of persistent OME 2.6 times as compared with children in home care [17]. This is thought to be secondary to an increased incidence of URI in these children from exposure to multiple viral pathogens. Indeed, multiple viruses have been detected in the MEE of AOM [18]. Children with multiple older siblings have had more RAOM as compared with their peers for this same reason. Passive smoke exposure is widely thought to increase OME; recent studies have found maternal smoking of more than 20 cigarettes a day increases the incidence of RAOM and OME [19–21]. It has been widely held that socioeconomic status limits prompt treatment of OM, but it may be an independent predictor of OM [22]. Finally, pacifier use in daycare has been shown to increase the incidence of RAOM by 25% [23].

Table 2 Risk factors: potentially increasing incidence Otitis media Intrinsic

Extrinsic

Patient age Male gender Atopic disease Immune deficiency Palate anomaly Craniofacial anomalies Genetic predisposition

Fall/winter season Upper respiratory infection Daycare Older siblings Passive smoke exposure Pacifier use in daycare Bottle feeding

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Medical therapy for OM Extensive work has been completed in recent years to brilliantly interpret the multiple clinical studies conducted over the past several decades that have evaluated medical therapy for OM. The following summarizes the conclusions that have been made [8]: (1) antibiotics have a small but statistically significant effect on AOM and OME, as well as OM prevention, (2) improved efficacy of broad-spectrum antibiotics as compared with standard therapy (ie, amoxicillin) has not been demonstrated, (3) oral and/or topical steroid use with or without antibiotics has no proven long-term therapeutic effect on OME [24], and (4) antihistamine decongestant medications do not hasten the resolution of OME. From this analysis of medical treatment outcomes for OM, specific treatment guidelines have been created that incorporate this understanding of medical therapy along with the known natural history of OM in the antibiotic era [8]. Surgical therapy for OM Outcomes of surgical therapy for OME (ie, TT and/or Ad) have been debated from many perspectives. The otolaryngologist is most interested in eliminating the consequences of OME (ie, hearing loss, language delay, and complications of chronic OM). The primary care physician has been concerned with the prevention of infectious complications of OM and avoiding unnecessary surgery [25]. TT improves hearing and patient symptoms, when they are functional, by eliminating a MEE. Additionally, there is a measurable improvement in quality of life in children with OM treated with TT [26]. For these reasons and others, the AHCPR OME guidelines, which apply to healthy children 1–3 years of age, recommend TT when bilateral OME is present for more than 3 months and bilateral hearing loss is present (hearing threshold 20 dB or greater) [1]. However, these guidelines are directed at healthy children from 1–3 years of age, without conditions associated with language delay (Table 3). Even though the AHCPR treatment parameters for OME are straightforward, the most controversial area surrounding TT and OME remains whether chronic OM causes language delay, and whether TT prevents language delay [27]. The AHCPR panelists in analyzing the literature did not find a consensus regarding the potential for OME to cause delayed language development, along with problems of inattentiveness and inappropriate behavior. Subsequently, several studies have attempted to determine if OME causes language delay or behavior/attention span problems in otherwise healthy children. Short-term gains in hearing from TT were not associated with improved language development in children under age 3 with OME, as compared with observation alone, in a randomized prospective trial [28]. These conclusions have been criticized because they were made from data primarily obtained from healthy children with unilateral OME, and

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Table 3 Host factors that potentially increase the risk of language delay with OM Eustachian tube dysfunction Overt cleft palate Submucous cleft palate Craniofacial anomaly Congenital conductive hearing loss Aural stenosis/atresia Ossicular malformation Neuro-developmental/behavioral issues Attention deficit disorder Autism, pervasive developmental delay Global developmental delay Mental retardation Chromosomal anomalies Sensorineural hearing loss Primary language delay

as hearing thresholds in the study population were not carefully assessed [29]. Because of this, these findings cannot be applied to children with bilateral OME or those having risk factors associated with language delay. Two smaller prospective studies have shown similar findings but also have had methodology issues that do not allow their conclusions to be applied broadly [30,31]. Interestingly, one of these studies pointed out that improvement in young children’s language skills was most strongly associated with the mother’s educational level. In contrast with these studies, long-term effects of childhood OME have adversely impacted reading ability, verbal IQ, and behavior in adolescence in a large birth cohort study [32]. Additionally a small prospective study has demonstrated adverse short-term behavioral and language consequences from delaying TT [33]. All of this points to the difficulty in measuring a demonstrable OM treatment effect on short term or long term language development [34,35]. Consequently there is still no consensus regarding the affect of OM on language development. It has been emphasized that children raised in a high income home will be exposed to more than triple the number of words by age 4 as compared with children who are not, demonstrating the many intangible factors that affect early language development in healthy children [27]. Quite possibly, the child’s home environment is of more importance in language development than improved hearing with tympanostomy tubes. Obviously, there are many unstudied scenarios in which OME may be very significant clinically. This would include children at high risk for language and behavioral problems (Table 3). Additionally, the average elementary school child faces a variety of environments where mild to moderate hearing loss may affect awareness, cognition, and school performance. When anticipating outcomes

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of treatment or observation, these other variables must be considered when planning treatment [34]. RAOM is frequently treated with TT. Following TT, the frequency of OM is decreased [36]. With the advent of bacterial resistance, TT can be used as a means of preventing OM in selected individuals [37]. In children needing a second set of TT, Ad is helpful in reducing the rate of RAOM [38]. The impact of TT on normal tympanic membrane (TM) has been evaluated in a number of studies. Myringosclerosis is associated with 40–50% of TT cases however, this is not detrimental to hearing [39,40]. When multiple TT are necessary, focal atrophy of the TM at the tube insertion site is present in up to 40% of TMs [41]. Even this does not adversely affect longterm tympanic membrane function, provided middle ear atelectasis does not develop [42]. Attic retraction pockets are associated with the duration of OME irregardless of TT [41]. Despite this good news, some physicians have pointed out that TTs may cause more complications than they prevent [27]. Infectious factors in OM Development of drug-resistant bacteria has changed the approach to OM treatment more than anything else in the past 10 years. Beta lactamase-producing Hemophilus influenza and drug-resistant Streptococcus pneumoniae (DRSP) are organisms that must be considered when treating AOM and OME. Resistance rates for DRSP are increasing, whereas the three most common bacterial OM pathogens remain the same [43]. It is important to note that S. pneumoniae is responsible for 50% of AOM. Because randomized controlled studies have demonstrated only a small improvement with antibiotic use and DRSP is common, how best to treat AOM and RAOM is debated [2]. Most experts advocate selective antibiotic use in these circumstances, but there are no prospective studies that clarify the most appropriate therapy in terms of therapy duration and dosage [44]. Detection of viral particles in AOM has furthered the argument against frequent antibiotic use for AOM or OME [18]. In children under age 2, viral URI are commonly associated with AOM. Some viruses such as respiratory syncytial virus (RSV) have been strongly implicated in AOM. Another point of interest is that MEE in OME have frequently not grown bacteria and that, when bacterial cultures show growth, the organisms are frequently drug-resistant [45]. Our understanding of bacterial behavior in OME has been changed by the detection of bacterial DNA and mRNA in long-standing MEE [3,46]. These findings imply that viable bacteria are present in MEE, even though they are not culturable. It has been suggested that MEE in persistent OME may be caused by facultative bacteria present in a biofilm. Because bacteria in a biofilm are resistant to standard antibiotic therapy, other treatments for OME may need to be developed [47]. Indeed, one small clinical trial utilized a nasal spray in an attempt to colonize the nasopharynx in Otitis-prone children with ‘‘good’’ bacteria [48]. The ‘‘good bacteria’’ con-

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sisted of alpha streptococci, which are part of the normal flora of the pharynx that have the ability to interfere with growth of common bacterial pathogens. Putting this together in a pathophysiologic model could happen as follows. The microbial environment within the nasopharynx and middle ear responds to changes induced by respiratory viruses (ie, mucosal cell damage), promoting bacterial overgrowth (ie, culturable bacteria). Once the acute infection ends, facultative bacteria persist in the middle ear in a biofilm. Because biofilms are highly susceptible to aerobic environments, TT (which increases middle ear aeration) may be the most effective means of eliminating bacteria in a MEE. Prevention of OM OM prevention has centered on modification of risk factors and vaccination. Stopping pacifier use in daycare has been shown to reduce the incidence of AOM by one third in children between 7–18 months of age as compared with controls [49]. This is the only extrinsic OM risk factor in which modification demonstrated a decrease in AOM. Modification of other OM risk factors are also clinically important and are recommended [2]. Because S. pneumoniae is the most frequent cause of AOM under age 2, the U.S. Food and Drug Administration (FDA) approval of the 7-valent pneumococcal conjugate vaccine has been met with enthusiasm [50]. This vaccine contains pneumococcal serotypes that cause 60% of pneumococcal AOM. In initial testing, using a randomized double-blinded clinical trial in more than 37,000 children, the incidence of AOM was reduced by 7% and TT by 20% [51]. Subsequent studies have reproduced the reduction in AOM and demonstrated a significant reduction in pneumococcal AOM [52]. Future work will address vaccination against the 83 known disease-causing pneumococcal serotypes, not in the 7-valent vaccine. Currently, this vaccine is recommended to be used in children: 2–23 months old; with sickle cell disease; with HIV infection; with immunodeficient conditions; Alaskan Native Americans, African-Americans; and children in group daycare [53]. It is debated whether widespread use of this vaccine before age 2 will actually increase the cost of OM treatment, as a series of three to four vaccines are necessary in this age group [54,55]. Additionally, there is concern that the 7 serotypes on this vaccine will be decreased through vaccination, but this will then allow some of the other 83 serotypes of S. pneumoniae to become more prevalent [56]. If this is the case, the net long-term affect of vaccination on AOM prevention by S. pneumoniae will be negligible. The Haemophilns influenzae type B conjugate vaccine (HIB) vaccine has not reduced the incidence of AOM. Influenza vaccination has reduced AOM by 30%, as compared with controls [57]. So the use of this vaccine in at-risk populations may reduce the frequency of AOM. Vaccines for RSV are not commercially available, but passively administered RSV antibody offered some protection against AOM [58,59].

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Treatment recommendations for OM Overview This article does not replace the comprehensive analysis of OM and its treatment that has been recently published [2]. The following recommendations are meant to emphasize the clinical importance of specific aspects of OM treatment that are relevant to otolaryngologists. In general, any OM treatment should attempt to conserve health care resources. This can best be accomplished by careful attention to treatment cost and outcome, as well as to a current understanding of OM pathophysiology and its application to therapeutic decisions.

AOM When approaching a child with AOM, several factors must be considered. The patient’s age, OM history, and daytime environment are arguably the most important. A child under age 2 with AOM and a history of OM before age 1 who is in full-time daycare attendance is at high risk for development of RAOM and/or OME. Whereas a child over age 2 with AOM, without a history of OM and not attending daycare is less likely to develop chronic OM. Consequently, in the first scenario, a first-line antibiotic (ie, amoxicillin) is recommended, whereas the second child might not require any antibiotic therapy. Why first-line antibiotics instead of broader spectrum drugs? The rate of spontaneous resolution for AOM is independent of the causative bacterial organism (ie, beta lactamase-producing organisms), and amoxicillin achieves much more effective levels against DRSP in MEE than broad-spectrum antibiotics [8]. Often, children over age 2 with AOM can be managed expectantly with supportive measures alone [60]. Though these are the current recommendations for AOM treatment, modification of physician practice and parenteral expectations has been difficult [34]. Along with the change in recommendation regarding empiric antibiotic use, the use of shorter courses of antibiotics is being practiced. There is no consensus as to the optimal dosing and duration of antibiotics for AOM, although a 5-day course seems as effective as 10 [44]. Future research efforts are necessary to answer questions more accurately regarding the optimal management of AOM in children of all ages [61]. In addition to selective antibiotic therapy, parental education regarding treatment effectiveness (ie, are antibiotics necessary?), the natural history of OM and OM prevention (ie, modification of extrinsic factors associated with OM) is essential [62]. Vaccination under age 2 is recommended because children in this age group are most prone to invasive pneumoccocal infection [53]. Adjunctive medical therapy (ie, antihistamine, decongestants, and steroids) is not recommended unless the patient has symptoms that are primarily treated with these medications (ie, nasal congestion) [1,2].

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When there are persistent fevers, otalgia after antibiotic therapy for AOM have been used for 24–48 hours; treatment failure may be present. A suppurative complication of OM or other infection is possible. In this situation, tympanocentesis for culture should be considered. Myringotomy does not appear to be more advantageous than antibiotics alone [63]. RAOM If the patient develops RAOM despite optimal primary treatment and prevention, other therapy may be necessary [8]. Again, patient age and daytime environment are important considerations. If not previously obtained, audiometric evaluation is necessary. Additionally, children with RAOM and conditions that predispose them to sequelae of OM (ie, language delay) must be treated aggressively. These children should be offered TT because of increased prevalence of language delay in this population. Children without these risks may benefit from careful observation and treatment of each episode of AOM, particularly if the patient’s extrinsic risk factors can be changed. Thankfully, RAOM decreases in frequency in healthy children over age 2. The routine use of prophylactic antibiotics for RAOM is now discouraged because increased treatment cost, lack of efficacy, and promotion of bacterial resistance [64]. Currently, three antibiotic regimes are recommended for RAOM or persistently symptomatic AOM: amoxicillin/ clavulanate in combination with amoxicillin (80–90 mg/kg/day amoxicillin, cefuroxime (30 mg/kg/day), or ceftriaxone (IM 1–3 doses) [65,66]. If this is ineffective, then TT should be considered. TT significantly decreases the incidence of AOM and the symptoms associated with AOM [36]. Delayed otorrhea associated with TT is usually successfully treated with topical drops alone, eliminating the need for oral antibiotics in many cases [67]. Ad in this population is not usually necessary when TT are first placed. If subsequent sets of TT are necessary, then this procedure should be considered [38]. OME OME is the most frequent reason for TT placement. Selecting appropriate patients for TT can be difficult, and careful analysis of each patient is essential. As in any OM treatment, patient selection is based on age, analysis of risk factors, and evidence for problems associated with persistent OME (ie, language delay, TM retraction). The most important indicator for TT is the duration of OME; when the MEE has been present for more than 6 months, it is unlikely to resolve on its own and is associated with an increased incidence of attic retraction [41,68] (Table 4). Preoperative parenteral counseling should focus on conveying realistic short-and long-term expectations for the procedure. This is one of the key ingredients in making the perception of TT placement successful [26]. In selected asymptomatic patients (ie, unilateral OME), no treatment may be necessary, provided

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Table 4 OME duration and tympanostomy tubes OME duration

Probability of spontaneous resolution

TT

<3 months 3–6 months

High Intermediate

>6 months

Low

No Placed on individualized basis Yes

TT, tympanostomy tube placement.

careful follow-up is accomplished. When OME is bilateral and associated with hearing loss (conductive and/or sensorineural), TT are the most effective means of MEE removal, improving hearing and quality of life in affected children [69]. This is especially important in older elementary age children learning to read [70]. As no demonstrable long-term effect of any medical therapy alone has been demonstrated, medical therapy is not advised for OME [2]. The type of tympanostomy tube used is varied based on duration of OME and presence of eustachian tube dysfunction. Short-acting ventilation tubes are sufficient in most children without craniofacial anomalies or a cleft palate. This reduces the risk of delayed otorrhea and persistent TM perforation [71]. In children with abnormal eustachian tube anatomy, one should consider using long-acting ventilation tubes to prevent the need for multiple TT. Ad has been shown to decrease the recurrence of OME after ventilation tubes are extruded [72]. The exact indications for laser myringotomy in OME and RAOM remain to be determined in a large randomized clinical trial [73]. Special mention needs to be made of infants with OME. This is now seen in increasing frequency because of widespread hearing screening of infants in some states. OME in creates a conductive hearing making otoacoustic emission testing abnormal. It is felt that amniotic fluid and debris in the neonate’s middle ear predispose the infant to persistent MEE [74]. As most infants are asymptomatic, a period of watchful waiting is recommended. In the unusual circumstance that an infant develops AOM, careful monitoring is essential because of the risk of progression to RAOM or OME [15,16]. In either situation, if a MEE does not resolve after 4–6 months, then TT is necessary, so that the OME is eliminated and hearing thresholds can be established with. Complications of OM Infectious complications of OM, such as acute mastoiditis, lateral sinus thrombosis, and petrous apicitis are uncommon [75]. Acute mastoiditis still occurs and there is some concern that it is increasing in frequency because of DRSP, but retrospective reports do not confirm this [76–78]. This condition is usually the first manifestation of OM in children under 4 years of age [79].

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With the excellent diagnostic accuracy of high-resolution CT, MR imaging, and MR angiography, these conditions can be managed medically in selected individuals. Patients who are not clinically toxic, or without significant bony erosion of the temporal bone or signs of septic thrombophlebitis, can be managed carefully with TT and culture-directed parenteral antibiotic therapy [80]. In cases where this is not effective, then a mastoidectomy or other temporal bone procedure is necessary [81,82]. Other articles in this issue will discuss technical aspects of surgical management of complications of OM. Summary OM, though frequent and seemingly simple to evaluate and manage, remains a treatment challenge. Increasingly sophisticated clinical trials assessing OM medical treatment efficacy and outcome have demonstrated that many treatment regimens that were commonly used a decade ago are no longer recommended. Surgical therapy for OM, though remaining the same, has come under intense scrutiny from several angles but still plays a central role for this disease. Given the multiple facets of OM, its frequency, and its potential to cause short- and long-term morbidity in children, the next decade is sure to bring further treatment innovations. References [1] Stool SE, Berg AO, Berman S, et al. Otitis media in young children. Rockville, MD: Agency for Health Care Policy and Research, Public Health Service, US Department of Health and Human Services; 1994. Clinical Practice Guideline #12. [2] Rosenfeld RM, Bluestone C. Evidence-based otitis media. ed 1. Hamilton, Ontario (BC): Decker Inc.; 1999. [3] Post JC, Preston RA, Aul JJ, Larkins-Pettigrew M, Rydquist-White J, Anderson KW, et al. Molecular analysis of bacterial pathogens in otitis media with effusion. JAMA 1995; 273:1598–604. [4] Casselbrant ML, Mandel EM, Fall PA, Rockette HE, Kurs-Lasky M, Bluestone CD, et al. The heritability of otitis media: a twin and triplet study. JAMA 1999;282:2125–30. [5] Gates GA. Cost-effectiveness considerations in otitis media treatment. Otolaryngol Head Neck Surg 1996;114:525–30. [6] Alsarraf R, Jung CJ, Perkins J, Crowley C, Alsarraf NW, Gates GA. Measuring the indirect and direct costs of acute otitis media. Arch Otolaryngol Head Neck Surg 1999; 125:12–8. [7] Kogan MD, Overpeck MD, Hoffman HJ, Casselbrant ML. Factors associated with tympanostomy tube insertion among preschool-aged children in the United States. Am J Public Health 2000;90:245–50. [8] Rosenfeld RM. An evidence-based approach to treating otitis media. Pediatr Clin North Am 1996;43:1165–81. [9] Teele DW, Klein JO, Rosner B. Epidemiology of otitis media during the first seven years of life in children in greater Boston: a prospective, cohort study. J Infect Dis 1989;160: 83–94. [10] Kero P, Piekkala P. Factors affecting the occurrence of acute otitis media during the first year of life. Acta Paediatr Scand 1987;76:618–23.

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[11] Casselbrant ML, Brostoff LM, Cantekin EI, Flaherty MR, Doyle WJ, Bluestone CD, et al. Otitis media with effusion in preschool children. Laryngoscope 1985;95:428–36. [12] Rosenfeld RM, Vertrees JE, Carr J, Cipolle RJ, Uden DL, Giebink GS, et al. Clinical efficacy of antimicrobial drugs for acute otitis media: metaanalysis of 5400 children from thirty-three randomized trials. J Pediatr 1994;124:355–67. [13] Teele DW, Klein JO, Rosner BA. Epidemiology of otitis media in children. Annals of Otology, Rhinology, & Laryngology 1980;89(Suppl):5–6. [14] Rosenfeld RM, Post JC. Meta-analysis of antibiotics for the treatment of otitis media with effusion. Otolaryngol Head Neck Surg 1992;106:378–86. [15] Jero J, Virolainen A, Virtanen M, Eskola J, Karma P. Prognosis of acute otitis media: factors associated with poor outcome. Acta Otolaryngol 1997;117:278–83. [16] Marchant CD, Shurin PA, Turczyk VA, Wasikowski DE, Tutihasi MA, Kinney SE. Course and outcome of otitis media in early infancy: a prospective study. J Pediatr 1984; 104:826–31. [17] Rasmussen F. Protracted secretory otitis media. The impact of familial factors and daycare center attendance. Int J Pediatr Otorhinolaryngol 1993;26:29–37. [18] Pitkaranta A, Virolainen A, Jero J, Arruda E, Hayden FG. Detection of rhinovirus, respiratory syncytial virus, and coronavirus infections in acute otitis media by reverse transcriptase polymerase chain reaction. Pediatrics 1998;102:291–5. [19] Etzel RA, Pattishall EN, Haley NJ, Fletcher RH, Henderson FW. Passive smoking and middle ear effusion among children in day care. Pediatrics 1992;90:228–32. [20] Ilicali OC, Keles N, Deger K, Savas I. Relationship of passive cigarette smoking to otitis media. Arch Otolaryngol Head Neck Surg 1999;125:758–62. [21] Stathis SL, O’Callaghan DM, Williams GM, Najman JM, Andersen MJ, Bor W. Maternal cigarette smoking during pregnancy is an independent predictor for symptoms of middle ear disease at five years’ postdelivery. Pediatrics 1999;104:16. [22] Paradise JL, Rockette HE, Colborn DK, Bernard BS, Smith CG, Kurs-Lasky M, et al. Otitis media in 2253 Pittsburgh-area infants: prevalence and risk factors during the first two years of life. Pediatrics 1997;99:318–33. [23] Niemela M, Uhari M, Mottonen M. A pacifier increases the risk of recurrent acute otitis media in children in day care centers. Pediatrics 1995;96:884–8. [24] Butler CC, van Der Voort JH. Steroids for otitis media with effusion: a systematic review. Arch Pediatr Adolesc Med 2001;155:641–7. [25] Kleinman LC, Kosecoff J, Dubois RW, Brook RH. The medical appropriateness of tympanostomy tubes proposed for children younger than 16 years in the United States. JAMA 1994;271:1250–5. [26] Rosenfeld RM, Bhaya MH, Bower CM, Brookhouser PE, Casselbrant ML, Chan KH, et al. Impact of tympanostomy tubes on child quality of life. Arch Otolaryngol Head Neck Surg 2000;126:585–92. [27] Berman S. Management of otitis media and functional outcomes related to language, behavior, and attention: is it time to change our approach? Pediatrics 2001;107: 1175–6. [28] Paradise JL, Feldman HM, Campbell TF, Dollaghan CA, Colborn DK, Bernard BS, et al. Effect of early or delayed insertion of tympanostomy tubes for persistent otitis media on developmental outcomes at the age of three years. N Engl J Med 2001;344:1179–87. [29] Rosenfeld RM. Effect of early or delayed tympanostomy-tube insertion for persistent otitis media. N Engl J Med 2001;345:465–6. [30] Minter KR, Roberts JE, Hooper SR, Burchinal MR, Zeisel SA. Early childhood otitis media in relation to children’s attention-related behavior in the first six years of life. Pediatrics 2001;107:1037–42. [31] Rovers MM, Krabbe PF, Straatman H, Ingels K, van der Wilt GJ, Zielhuis GA. Randomised controlled trial of the effect of ventilation tubes (grommets) on quality of life at age 1–2 years. Arch Dis Child 2001;84:45–9.

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[32] Bennett KE, Haggard MP, Silva PA, Stewart IA. Behaviour and developmental effects of otitis media with effusion into the teens. Arch Dis Child 2001;85:91–5. [33] Wilks J, Maw R, Peters TJ, Harvey I, Golding J. Randomised controlled trial of early surgery versus watchful waiting for glue ear: the effect on behavioural problems in preschool children. Clinical Otolaryngology & Allied Sciences 2000;25:209–14. [34] Klein JO. Management of otitis media: 2000 and beyond. Pediatr Infect Dis J 2000;19:383–7. [35] Butler CC, MacMillan H. Does early detection of otitis media with effusion prevent delayed language development? Arch Dis Child 2001;85:96–103. [36] Casselbrant ML, Kaleida PH, Rockette HE, Paradise JL, Bluestone CD, Kurs-Lasky M, et al. Efficacy of antimicrobial prophylaxis and of tympanostomy tube insertion for prevention of recurrent acute otitis media: results of a randomized clinical trial. Pediatr Infect Dis J 1992;11:278–86. [37] Rosenfeld RM. Surgical prevention of otitis media. Vaccine 2000;19(Suppl 1):S134–139. [38] Paradise JL, Bluestone CD, Colborn DK, Bernard BS, Smith CG, Rockette HE, et al. Adenoidectomy and adenotonsillectomy for recurrent acute otitis media: parallel randomized clinical trials in children not previously treated with tympanostomy tubes. JAMA 1999;282:945–53. [39] Goldstein NA, Roland JT, Sculerati N. Complications of tympanostomy tubes in an inner city clinic population. Int J Pediatr Otorhinolaryngol 1996;34:87–99. [40] Maw AR. Development of tympanosclerosis in children with otitis media with effusion and ventilation tubes. J Laryngol Otol 1991;105:614–7. [41] Maw AR, Bawden R. Tympanic membrane atrophy, scarring, atelectasis and attic retraction in persistent, untreated otitis media with effusion and following ventilation tube insertion. Int J Pediatr Otorhinolaryngol 1994;30:189–204. [42] Li Y, Hunter LL, Margolis RH, Levine SC, Lindgren B, Daly K, et al. Prospective study of tympanic membrane retraction, hearing loss, and multifrequency tympanometry. Otolaryngol Head Neck Surg 1999;121:514–22. [43] Butler JC, Hofmann J, Cetron MS, Elliott JA, Facklam RR, Breiman RF. The continued emergence of drug-resistant Streptococcus pneumoniae in the United States: an update from the Centers for Disease Control and Prevention’s Pneumococcal Sentinel Surveillance System. J Infect Dis 1996;174:986–93. [44] Pichichero ME. Short course antibiotic therapy for respiratory infections: a review of the evidence. Pediatr Infect Dis J 2000;19:929–37. [45] Sutton DV, Derkay CS, Darrow DH, Strasnick B. Resistant bacteria in middle ear fluid at the time of tympanotomy tube surgery. Annals of Otology, Rhinology & Laryngology 2000;109:24–9. [46] Rayner MG, Zhang Y, Gorry MC, Chen Y, Post JC, Ehrlich GD. Evidence of bacterial metabolic activity in culture-negative otitis media with effusion. JAMA 1998;279:296–9. [47] Costerton JW, Stewart PS, Greenberg EP. Bacterial biofilms: a common cause of persistent infections. Science 1999;284:1318–22. [48] Roos K, Hakansson EG, Holm S. Effect of recolonisation with ‘‘interferring’’ alpha streptococci on recurrences of acute and secretory otitis media in children: randomised placebo controlled trial. BMJ 2001;322:210–2. [49] Niemela M, Pihakari O, Pokka T, Uhari M. Pacifier as a risk factor for acute otitis media: A randomized, controlled trial of parental counseling. Pediatrics 2000;106:483–8. [50] Giebink GS. The prevention of pneumococcal disease in children. N Engl J Med 2001; 345:1177–83. [51] Black S, Shinefield H, Fireman B, Lewis E, Ray P, Hansen JR, et al. Efficacy, safety and immunogenicity of heptavalent pneumococcal conjugate vaccine in children. Northern California Kaiser Permanente Vaccine Study Center Group. Pediatr Infect Dis J 2000;19:187–95. [52] Eskola J, Kilpi T, Palmu A, Jokinen J, Haapakoski J, Herva E, et al. Efficacy of a pneumococcal conjugate vaccine against acute otitis media. N Engl J Med 2001;344: 403–9.

824

J.A. Perkins / Otolaryngol Clin N Am 35 (2002) 811–825

[53] Overturf GD. American Academy of Pediatrics. Committee on Infectious Diseases. Technical report: prevention of pneumococcal infections, including the use of pneumococcal conjugate and polysaccharide vaccines and antibiotic prophylaxis. Pediatrics 2000;106:367–76. [54] Lieu TA, Ray GT, Black SB, Butler JC, Klein JO, Breiman RF, et al. Projected costeffectiveness of pneumococcal conjugate vaccination of healthy infants and young children. JAMA 2000;283:1460–8. [55] Weycker D, Richardson E, Oster G. Childhood vaccination against pneumococcal otitis media and pneumonia: an analysis of benefits and costs. Am J Manag Care 2000;6: S526–535. [56] Lavin A. A pneumococcal conjugate vaccine and acute otitis media. N Engl J Med 2001; 344:1719–20. [57] Belshe RB, Mendelman PM, Treanor J, King J, Gruber WC, Piedra P, et al. The efficacy of live attenuated, cold-adapted, trivalent, intranasal influenzavirus vaccine in children. N Engl J Med 1998;338:1405–12. [58] Anderson LJ. Respiratory syncytial virus vaccines for otitis media. Vaccine 2000; 19(Suppl 1):S59–65. [59] Simoes EA, Groothuis JR, Tristram DA, Allessi K, Lehr MV, Siber GR, et al. Respiratory syncytial virus-enriched globulin for the prevention of acute otitis media in high risk children. J Pediatr 1996;129:214–9. [60] Takata GS, Chan LS, Shekelle P, Morton SC, Mason W, Marcy SM. Evidence assessment of management of acute otitis media: I. The role of antibiotics in treatment of uncomplicated acute otitis media. Pediatrics 2001;108:239–47. [61] Chan LS, Takata GS, Shekelle P, Morton SC, Mason W, Marcy SM. Evidence assessment of management of acute otitis media: II. Research gaps and priorities for future research. Pediatrics 2001;108:248–54. [62] Finkelstein JA, Davis RL, Dowell SF, Metlay JP, Soumerai SB, Rifas-Shiman SL, et al. Reducing antibiotic use in children: a randomized trial in 12 practices. Pediatrics 2001;108:1–7. [63] Engelhard D, Cohen D, Strauss N, Sacks TG, Jorczak-Sarni L, Shapiro M. Randomised study of myringotomy, amoxycillin/clavulanate, or both for acute otitis media in infants. Lancet 1989;2:141–3. [64] Guillemot D, Carbon C, Balkau B, Geslin P, Lecoeur H, Vauzelle-Kervroedan F, et al. Low dosage and long treatment duration of beta-lactam: risk factors for carriage of penicillin-resistant Streptococcus pneumoniae. JAMA 1998;279:365–70. [65] Pichichero ME. Recurrent and persistent otitis media. Pediatr Infect Dis J 2000;19: 911–6. [66] Leibovitz E, Piglansky L, Raiz S, Press J, Leiberman A, Dagan R. Bacteriologic and clinical efficacy of one day vs. three day intramuscular ceftriaxone for treatment of nonresponsive acute otitis media in children. Pediatr Infect Dis J 2000;19:1040–5. [67] Goldblatt EL, Dohar J, Nozza RJ, Nielsen RW, Goldberg T, Sidman JD, et al. Topical ofloxacin versus systemic amoxicillin/clavulanate in purulent otorrhea in children with tympanostomy tubes. Int J Pediatr Otorhinolaryngol 1998;46:91–101. [68] Williamson IG, Dunleavey J, Bain J, Robinson D. The natural history of otitis media with effusion: a three-year study of the incidence and prevalence of abnormal tympanograms in four South West Hampshire infant and first schools. J Laryngol Otol 1994;108:930–4. [69] Maw R, Bawden R. Spontaneous resolution of severe chronic glue ear in children and the effect of adenoidectomy, tonsillectomy, and insertion of ventilation tubes (grommets). BMJ 1993;306:756–60. [70] Bennett KE, Haggard MP. Behaviour and cognitive outcomes from middle ear disease. Arch Dis Child 1999;80:28–35. [71] Goode RL. Long-term middle ear ventilation with T tubes: the perforation problem. Otolaryngol Head Neck Surg 1996;115:500–1.

J.A. Perkins / Otolaryngol Clin N Am 35 (2002) 811–825

825

[72] Gates GA, Avery CA, Cooper Jr JC, Prihoda TJ. Chronic secretory otitis media: effects of surgical management. Annals of Otology, Rhinology & Laryngology 1989;138(Supplement):2–32. [73] Szeremeta W, Parameswaran MS, Isaacson G. Adenoidectomy with laser or incisional myringotomy for otitis media with effusion. Laryngoscope 2000;110:342–5. [74] Palva T, Northrop C, Ramsay H. Effect of amniotic fluid cellular content on attic aeration pathways: histologic observations of infants aged 2 to 4 months. Am J Otol 2000;21:62–70. [75] Go C, Bernstein JM, de Jong AL, Sulek M, Friedman EM. Intracranial complications of acute mastoiditis. Int J Pediatr Otorhinolaryngol 2000;52:143–8. [76] Antonelli PJ, Dhanani N, Giannoni CM, Kubilis PS. Impact of resistant pneumococcus on rates of acute mastoiditis. Otolaryngol Head Neck Surg 1999;121:190–4. [77] Bahadori RS, Schwartz RH, Ziai M. Acute mastoiditis in children: an increase in frequency in Northern Virginia. Pediatr Infect Dis J 2000;19:212–5. [78] Luntz M, Brodsky A, Nusem S, Kronenberg J, Keren G, Migirov L, et al. Acute mastoiditis–the antibiotic era: a multicenter study. Int J Pediatr Otorhinolaryngol 2001; 57:1–9. [79] Ghaffar FA, Wordemann M, McCracken Jr GH. Acute mastoiditis in children: a seventeen-year experience in Dallas, Texas. Pediatric Infectious Disease Journal 2001;20: 376–80. [80] Harley EH, Sdralis T, Berkowitz RG. Acute mastoiditis in children: a 12-year retrospective study. Otolaryngol Head Neck Surg 1997;116:26–30. [81] Kaplan DM, Kraus M, Puterman M, Niv A, Leiberman A, Fliss DM. Otogenic lateral sinus thrombosis in children. Int J Pediatr Otorhinolaryngol 1999;49:177–83. [82] Syms MJ, Tsai PD, Holtel MR. Management of lateral sinus thrombosis. Laryngoscope 1999;109:1616–20.