Pediatric Annals

Otitis Media: Current Concepts in Diagnosis and Management

Stephen I Pelton, MD; Patricia Whitley, MD

Abstract

Acute otitis media (AOM) is an important disease in children representing the most frequent illness diagnosed in the pediatrician's office. A large epidemiologie study reported that by the age of three years, 7 1 % of the children had at least one episode of AOM and one-third of the children had three or more episodes (Table I).1 For the purpose of this review, acute otitis media refers to inflammation of the middle ear of infectious etiology associated with fluid in the middle ear cavity. The importance of prompt diagnosis, appropriate treatment, and careful followup of the child with AOM cannot be emphasized enough in view of the significant morbidity associated with middle ear effusion. Although supportive complications of otitis media such as mastoiditis and meningitis are now relatively uncommon, there is increasing concern about impairment of hearing associated with the presence of middle ear fluid and the effects of such hearing deficits on the development of the child.

EPIDEMIOLOGY AND PATHOPHYSIOLOGY

Acute otitis media occurs most commonly in the first two years of life with a higher frequency in males than females (Table 2). Factors which contribute to the increased incidence of acute otitis in this age group are most likely associated with anatomic or physiologic dysfunction of the eustachian tube. The allergic child has an additional risk factor for developing acute otitis media because of edema and increased mucous production in the nasopharynx which may obstruct the eustachian tube.3 Anatomical malformations, such as seen in children with cleft palate, are associated with dysfunction of the eustachian tube and otitis media is nearly universal in this population.

DIAGNOSIS

In the young child the symptoms of AOM are usually non-specific, ie, irritability, rhinorrhea, anorexia, lethargy, pulling at the ears, edematous nasopharyngeal mucosa. In the older child, earache or hearing loss may be the complaint. Otoscopie findings, however, are the only reliable diagnostic signs.

For optimum visualization of the tympanic membrane the external ear canal should be adequately cleared either by using a blunt curette or by lavaging with a syringe or Water-Pik apparatus. Extreme caution is necessary in cleaning the canals to prevent trau mat ization which may result in bleeding (thereby obscuring the tympanic membrane) and to prevent psychological trauma to the child.

The normal eardrum is a translucent, pearly graycolor which may become reddened with crying. A well-defined light reflex is not always evident. The eardrum should be freely mobile in response to positive and negative pressure by the pneumatoscope. Retracted tympanic membranes will have rebound mobility in response to negative pressure and none or reduced mobility with positive pressure. The tympanic membrane of AOM is usually hyperemic (or bluish), boggy and sometimes bulging, with loss of the light reflex and sometimes the presence of an air-fluid Une. The most significant sign is the loss or decrease in mobility of the tympanic membrane.

Table

The microbiology of AOM in the newborn issimilarto that of the older child with the exception that the gramnegative enteric bacilli, 5. aureus, and Groups ? and B beta-hemolytic Streptococci are more commonly isolated from the middle ear fluid of newborns. However, SP and non-typable HI are still the most frequent bactériologie agents isolated from the middle ear fluids of infants under six weeks of age (Table 4). S. aureus and gram-negative enteric bacilli are responsible for approximately 20% of cases.

The treatment of AOM in the neonate is comparable to that in the older child because the same pathogens, SP and HI, are predominant. However, concern for S. aureus and gram-negative enterics requires the clinician to consider broader spectrum antimicrobial therapy when: 1) the…

Acute otitis media (AOM) is an important disease in children representing the most frequent illness diagnosed in the pediatrician's office. A large epidemiologie study reported that by the age of three years, 7 1 % of the children had at least one episode of AOM and one-third of the children had three or more episodes (Table I).1 For the purpose of this review, acute otitis media refers to inflammation of the middle ear of infectious etiology associated with fluid in the middle ear cavity. The importance of prompt diagnosis, appropriate treatment, and careful followup of the child with AOM cannot be emphasized enough in view of the significant morbidity associated with middle ear effusion. Although supportive complications of otitis media such as mastoiditis and meningitis are now relatively uncommon, there is increasing concern about impairment of hearing associated with the presence of middle ear fluid and the effects of such hearing deficits on the development of the child.

EPIDEMIOLOGY AND PATHOPHYSIOLOGY

Acute otitis media occurs most commonly in the first two years of life with a higher frequency in males than females (Table 2). Factors which contribute to the increased incidence of acute otitis in this age group are most likely associated with anatomic or physiologic dysfunction of the eustachian tube. The allergic child has an additional risk factor for developing acute otitis media because of edema and increased mucous production in the nasopharynx which may obstruct the eustachian tube.3 Anatomical malformations, such as seen in children with cleft palate, are associated with dysfunction of the eustachian tube and otitis media is nearly universal in this population.

DIAGNOSIS

In the young child the symptoms of AOM are usually non-specific, ie, irritability, rhinorrhea, anorexia, lethargy, pulling at the ears, edematous nasopharyngeal mucosa. In the older child, earache or hearing loss may be the complaint. Otoscopie findings, however, are the only reliable diagnostic signs.

For optimum visualization of the tympanic membrane the external ear canal should be adequately cleared either by using a blunt curette or by lavaging with a syringe or Water-Pik apparatus. Extreme caution is necessary in cleaning the canals to prevent trau mat ization which may result in bleeding (thereby obscuring the tympanic membrane) and to prevent psychological trauma to the child.

The normal eardrum is a translucent, pearly graycolor which may become reddened with crying. A well-defined light reflex is not always evident. The eardrum should be freely mobile in response to positive and negative pressure by the pneumatoscope. Retracted tympanic membranes will have rebound mobility in response to negative pressure and none or reduced mobility with positive pressure. The tympanic membrane of AOM is usually hyperemic (or bluish), boggy and sometimes bulging, with loss of the light reflex and sometimes the presence of an air-fluid Une. The most significant sign is the loss or decrease in mobility of the tympanic membrane.

Table

TABLE 1INCIDENCE OF ACUTE OTITIS MEDIA IN BOSTON CHILDREN'

TABLE 1

INCIDENCE OF ACUTE OTITIS MEDIA IN BOSTON CHILDREN'

Table

TABLE 2FREQUENCY OF ACUTE OTITIS MEDIA IN THE PEDIATRIC WALK-IN CLINIC AT BOSTON CITY HOSPITAL3

TABLE 2

FREQUENCY OF ACUTE OTITIS MEDIA IN THE PEDIATRIC WALK-IN CLINIC AT BOSTON CITY HOSPITAL3

Figure 1. The type A tympanogram shows a peak at or near O mm HiO and is characteristic of normal or otosclerotic ears, but not of ears containing effusions. The type B tympanogram is an almost flat curve and is virtually pathognomonic of middle ear effusion (MEE). The type C tympanogram shows a peak at a negative pressure and indicates eustachian tube dysfunction, with difficulty in equalizing pressure between the middle ear and the atmosphere, but no significan! refationsnip can be stated between negative peaking and MEE. (Ghory, 1982)

Figure 1. The type A tympanogram shows a peak at or near O mm HiO and is characteristic of normal or otosclerotic ears, but not of ears containing effusions. The type B tympanogram is an almost flat curve and is virtually pathognomonic of middle ear effusion (MEE). The type C tympanogram shows a peak at a negative pressure and indicates eustachian tube dysfunction, with difficulty in equalizing pressure between the middle ear and the atmosphere, but no significan! refationsnip can be stated between negative peaking and MEE. (Ghory, 1982)

Tympanometry is a non-invasive diagnostic technique which is used to determine the compliance of the tympanic membrane and the middle ear. Through a probe snugly placed in the external ear canal, a fixed tone is delivered at a given intensity as the air pressure in the canal is varied from positive to negative. The tympanogram is a recording of the acoustic compliance of the middle ear, including the tympanic membrane, over a range of air pressures. Normal middle ear compliance is greatest when pressures are equal on both sides of the tympanic membrane. Middle ear effusion leads to decreased compliance of the tympanic membrane and a limited response to changes in air pressure is observed (Figure I).

Some investigators have observed normal tympanograms in young infants who have documented middle ear effusion. They claim this reflects the increased mobility of the infant canal. However, recent studies of tympanometry have demonstrated accuracy in detecting the presence of effusion in some children less than seven months of age.4

Table

TABLE 3BACTERIAL PATHOGENS ISOLATED FROM MIDDLE EAR FLUID IN 4,675 CHILDREN WITH ACUTE OTITIS MEDIA2

TABLE 3

BACTERIAL PATHOGENS ISOLATED FROM MIDDLE EAR FLUID IN 4,675 CHILDREN WITH ACUTE OTITIS MEDIA2

MICROBIOLOGIC DIAGNOSIS

Microbiologie diagnosis by tympanocentesis is not necessary in every case of AOM. Results from previous microbiologie studies in AOM have been so consistent that therapeutic decisions can be based on the bactériologie data from these studies. Microbiologie diagnosis by tympanocentesis in AOM is indicated in: 1) children with overwhelming sepsis in which case a culture of infected middle ear fluid might provide a specific pathogen; 2) children with persistent symptoms of AOM after more than 48 to 72 hours of antimicrobial therapy; 3) children with abnormal host defenses where unusual pathogens may be the causative agents; or 4) the neonate.

MICROBIOLOGY

Multiple studies have elucidated the microbiology of AOM based on cultures of middle ear fluid aspirates for bacteria, viruses, mycoplasmas, and chlamydia. Streptococcus pneumonias (SP) and HaemophUus influenzae (Hl) are the two most prevalent organisms in AOM. A recent review reported a 29-yearsummary of bactériologie data from 4,000 children with AOM (Table 3).2 SP was the most frequently isolated agent (33% of the cases) with types 19,23,6, 14,3, 18, 15, 9, 7, 4, and 1 accounting for 80% of the SP isolates.

Hl was isolated from 21% of cases with majority of strains (about 90%) being non-typable. Group A betahemolytic streptococcus, Branhamelia catarrhalis, Staphylococcus aureus, and gram-negative enteric bacilli were infrequently isolated from middle ear aspirates. B. catarrhalis, previously regarded as part of the normal skin and nasopharyngeal flora, has been recognized recently as a significant pathogen in children with acute otitis media. In an unpublished study, B. catarrhalis was isolated from 38 ( 19%) of 200 middle ear fluid cultures (Kovatch, WaId, Michael, unpublished data). Pure cultures of B. catarrhalis were obtained in 8% of the 200 cultures of middle ear fluid. The majority (76%) of these isolates were beta-lactamase producers and would be expected to be resistant to ampicillin and penicillin G. Future monitoring for the prevalence of B. catarrhalis in children with AOM and their sensitivity patterns will be necessary to determine the importance of this study.

In a review of the significance of viruses and mycoplasmas in either AOM or chronic otitis media, viruses were isolated from only 4.4% of middle ear fluids and only one Mycoplasma pneumoniae was isolated from the fluids of 771 patients/'6

TREATMENT

Selection of appropriate antimicrobial therapy is based upon several factors: 1) knowledge of the likely etiologic agents in AOM or recovery of a specific pathogen from middle ear fluid; 2) antibiotic penetration into middle ear fluid; 3) the in vitro efficacy of specific antibiotics against the organisms responsible for AOM; 4) a history of drug allergy; and 5) patient compliance.

Since SPaccountsforapproximately 33% and Hl, 20% of the pathogens isolated from middle ear effusions in AOM, the antibiotics selected for treatment of AOM should be efficacious against both SP and HI. The penicillins, cep halos porins, erythromycin, and trimethoprim-sulfamethoxazole (TM P-SM Z) are effective against SP. Ampicillin, amoxicillin, the sulfonamides, TMPSMZ, and cefaclor are effective against HI. Oral ampicillin at 50 to 75 mg/kg/day in four divided doses or amoxiciliin at 20 to 40 mg/kg,day in three divided doses is the recommended initial treatment for AOM. For the patient who is allergic to penicillin, erythromycin (25 to 50 mg, kg, day) in four divided doses in combination with sulfisoxazole (100 mg kg day in four divided doses) or trimethoprim in combination with sulfamethoxazole (8 and 40 mg/kg/day respectively in two divided doses) are recommended.7

Fifteen to 30% of non-typable Hl strains isolated from middle ear fluids are ampicUlin-resistant. In known or suspected cases of AOM due to ampicillin-resistant Hl, TMP-SMZ, erythromycin and sulfisoxazole, orcefaclor (40 rag/kg/day in three divided doses) is the treatment of choice. Since HI accounts for 20% of AOM and 15-30% of those isolates are ampicillin-resistant, only 3-6% of cases of AOM are due to resistant Hl. In our opinion, the problem of ampicillin-resistant HI is still small, and amp ici Hin or amoxicillin remains the drug of choice for initial therapy. However, with the emergence of betalactamase-producing B. catarrhalis as a pathogen, and the fluctuations in prevalence of ampicillin-resistant isolates of non-typable H. influenzae, knowledge of local resistance patterns for H. influenzae and B. caiarrhalis are necessary when considering initial antimicrobial therapy.

Additional therapy including antipyretics and analgesics may be helpful in alleviating some of the acute symptoms. Decongestants and antihistamines have not been demonstrated to be helpful in the treatment of AOM.8

CLINICAL COURSE

Resolution of AOM without antimicrobial therapy occurs in some children either by spontaneous perforation of the tympanic membrane or by discharging the contents of the middle ear cavity into the eustachian tube. Most children with AOM have significantly improved within 48 to 72 hours of antimicrobial therapy. For those children who are not improved, inadequate compliance or resistant organisms may be explanations for clinical and microbiologie failures.

A study of 43 children with otitis media and persistent systemic signs and symptoms at 48 hours after initiating therapy has recently been reponed. Results of culture of middle ear fluid in these children demonstrated sterile fluid or non-pathogens in 60%. In 20%, bacteria resistant to the prescribed therapy were recovered.9

We believe tympanocentesis to define the etiologic agent should be considered in children with AOM who are unimproved (ie, persistent fever) 48 to 72 hours after initiating antibiotic therapy. If tympanocentesis is not done the initial antibiotic regimen should be changed to one that would include therapy directed at ampicillinresistant HI, realizing that only 20% of these children truly have ampicillin-resistant isolates. TMP-SMZ, erythromycin-sulfisoxazole, or cefaclor would provide appropriate coverage.

Beta-lactamase producing B. catarrhalis, ormoderately resistant SP may also be explanations for children with otitis media who fail to respond to initial therapy.

Persistence of sterile middle ear fluid is a recognized pattern in AOM. In appropriately treated children 40% will not have cleared their effusions at four weeks after diagnosis. Although these children may be asymptomatic, they will continue to have abnormal pneumatic otoscopie examinations and abnormal tympanograms documenting the persistent middle ear effusion.

In children with persistent symptoms who appear toxic, further diagnostic studies, including a white blood cell count, blood culture, and lumbar puncture (if clinically indicated), should be performed to rule out possible complications, such as bacteremia and meningitis.

NEONATAL OTITIS MEDIA

The diagnosis of AOM in the neonate may not be recognized as readily as in the older child. The clinical picture includes non-specific symptoms characteristic of neonatal sepsis, ie, lethargy, hyperthermia, or jaundice. Examination of the tympanic membrane in the newborn should be performed as part of each work-up for sepsis. The normal newborn eardrum may be in an extreme oblique position and is opaque and thickened. Mobility of the tympanic membrane should exist after the first 24 hours of life when ventilation of the middle ear has occurred. Mobility of the canal walls may be mistaken for mobility of the tympanic membrane because of the oblique position of the tympanic membrane in relation to the wall of the external ear canal. In addition, the physician should keep in mind that the eardrum in the premature infant, especially under 1,000 g, may be immobile for prolonged periods of time. Immobility, along with inflammatory changes or perforation of the tympanic membrane, are diagnostic criteria for AOM in the newborn.

In one study, the incidence of middle ear effusion in an intensive care nursery was as high as 30%.'° Sixty percent of these middle ear fluids were culture positive for S. aureus or gram-negative enteric organisms. Our experience at Boston City Hospital revealed that middle ear effusion in the intensive care nursery was an infrequent event. Only three (7%) of 48 infants were thought to have middle ear effusions (by pneumatic otoscopy using an operating microscope). However, tympanocentesis performed on these three tympanic membranes failed to demonstrate middle ear effusion.

Jaffee reported the incidence of neonatal AOM in a Navajo population to be 18%, but the diagnosis was made by pneumatic otoscopy and not confirmed by tympanocentesis." However, at seven months of age, 61% of the babies who had poorly mobile drums at one to two days of life had abnormal drums and history of significant middle ear disease.

Table

TABLE 4BACTERIOLOGY OF ACUTE OTITIS MEDIA IN THE FIRST SIXWEEKS OF LIFE2

TABLE 4

BACTERIOLOGY OF ACUTE OTITIS MEDIA IN THE FIRST SIXWEEKS OF LIFE2

The microbiology of AOM in the newborn issimilarto that of the older child with the exception that the gramnegative enteric bacilli, 5. aureus, and Groups ? and B beta-hemolytic Streptococci are more commonly isolated from the middle ear fluid of newborns. However, SP and non-typable HI are still the most frequent bactériologie agents isolated from the middle ear fluids of infants under six weeks of age (Table 4). S. aureus and gram-negative enteric bacilli are responsible for approximately 20% of cases.

The treatment of AOM in the neonate is comparable to that in the older child because the same pathogens, SP and HI, are predominant. However, concern for S. aureus and gram-negative enterics requires the clinician to consider broader spectrum antimicrobial therapy when: 1) the child is less than two weeks of age; 2) the neonatal course has been complicated (ìe, prolonged intubation, prematurity, etc.); or 3) signs or symptoms of sepsis are present. In these situations, we perform tympanocentesis prior to initiating therapy with a penicillin and an aminoglycoside, and modify antimicrobial therapy dependent on the results of culture of the middle ear fluid.

MORBIDITY

The child with recurrent episodes of acute otitis media and /or persistent effusion in the middle ear cleft represents a special problem to the clinician. We have followed 2,500 children from three months through their third birthday in order to define the natural history and morbidity associated with recurrent or persistent disease. About one-third of children will have three or more episodes of acute disease by their third birthday. These findings are comparable to those of Drs. Howie and Ploussard who reported that one-third of children in their practice had two or more episodes before their first birthday, and 12% had six episodes before reaching school age. In addition to frequent episodes, many children have prolonged middle ear effusion following acute otitis. In two studies at Boston City Hospital, approximately 40% of children had persistent effusion at one month, 20% at two, 10% at three and 5% at four months post-infection.'6'17 Although the majority of these effusions resolve spontaneously, time spent with effusion during the first and second year of life may be considerable. In our studies, 2% of children spent more than six months in their first year and 7% of children spent more than six months in their second year with middle ear effusion (Klein JO, Teele DW, unpublished data).

Studies on hearing loss in association with middle ear effusion document a moderate conductive loss in most children. This loss appears to resolve when ventilation of the middle ear cleft returns. However, long periods of time spent with middle ear effusion and the accompanying hearing loss may impair speech, and delay language development and diminish performance in school. Dr. Jack Paradise of Pittsburgh has recently reviewed the many published studies evaluating the relationship between otitis media and developmental impairment. He concludes that no definitive impairment of a lasting nature has been proven. However, he also states that evidence is lacking that such episodes are entirely innocuous.18

In our studies, children with greater than 130 days of effusion in theirfirst three years of life had reduced scores on the Peabody Picture Vocabulary Test, as well as on tests of articulation when compared to a disease-free cohort.19

Lastly, the cost of otitis media must be considered. Children with three or more episodes of otitis media make twice as many (20 versus 10) office visits as their diseasefree controls in the first three years of life.

MANAGEMENT OF CHRONIC PROBLEMS OF MIDDLE EAR INFECTION

We believe children with chronic otitis media can be divided into two groups: those with recurrent episodes of acute infection in which the middle ear effusion resolves between episodes, and those with persistent effusion with or without acute exacerbations.

Children with multiple episodes of acute otitis media without prolonged effusion can usually be managed with a single dose of an antimicrobial agent given daily. Experience in Rochester, New York,20 Alaska, and our own unpublished observations support that a single dose, given daily, will usually prevent recurrences of signs of acute infection. Amoxicillin 20 mg/ kg/day, Sulfisoxazole 50 mg/kg/day, and Trimethoprim-Sulfamethoxazole 4 mg and 20 mg respectively/ kg/ day appear acceptable and have few side effects. Criteria for initiating therapy are three episodes of acute otitis occurring within a six-month period. In addition, we recommend prophylaxis in children less than six months of age who have had two episodes of acute otitis within a three-month period. These antimicrobial agents should be given over three to six months, dependent on historical information regarding the seasonal pattern in the child. Most often we find the winter months (December through March) to be the time of highest risk. Chemoprophylaxis may suppress acute symptoms while middle ear effusion persists. Therefore, these children require continued observation at approximately four to six week intervals. Myringotomy during the course of acute otitis does not appear to hasten resolution of disease and is used largely for bactériologie diagnosis and occasionally for pain relief.

Efficacy of pneumococcal vaccine is limited because of the failure of children less than two years of age to respond immunologically to the majority of type-specific polysaccharide antigens for those types most frequently associated with otitis media. Studies to date have been focused at children less than two years of age, and although protection against those antigens to which the children developed antibody was demonstrated, the overall number of episodes of otitis media was not significantly altered. Success of different antigenic formulations or dosage schedules will be necessary if the vaccine is to be useful in the child less than two years. In the older child (>2), efficacy is suggested by the single study in this age group.21 At present, we do not routinely use vaccine in children with recurrent episodes of otitis media.

Children with prolonged middle ear effusions are of more concern. Potential pathogens can be cultured from 25% of children less than three years of age with asymptomatic effusion. Although no controlled studies

have been reported, we believe it is reasonable to prescribe a full course of antimicrobial therapy for new effusions in this age group. In addition, in those children who suffer from frequent acute episodes of acute otitis, it is often difficult to discriminate between persistent effusion and incomplete resolution from prior episodes. In the latter group, "prophylactic" antibiotics will often prevent acute episodes and allow resolution of the effusion.

Oral decongestants or antihistamines, although widely used, do not appear to offer benefit for the child with persistent effusion in the several trials reported.22 We limit our use of decongestants to symptomatic therapy for the child with profuse rhinitis.

Corticosteroids might be expected to be of use either by anti-inflammatory action on the mucosa of the eustachian tube, allowing drainage, or by direct action on inflammation in the middle ear cleft. Three studies with short-term oral steroids suggest a beneficial effect on resolution of effusion. However, only one of these was double-blinded and controlled.23 Although these results warrant further clinical study, we do not believe they are sufficient to recommend such therapy, especially in light of the relapsing nature of this disease.

Surgical intervention has consisted of myringotomy alone, myringotomy with tube insertion (M&T) and/or adenoidectomy. Myringotomy alone does not appear to alter the duration of effusion. Myringotomy with tube insertion is effective for evacuation of fluid from the middle ear cleft and restoration of normal hearing. It is associated with complications such as otorrhea and tympanosclerosis, but does not appear to have long-term sequelae at present. The critical question is the timing of myringotomy and tube insertion. In our opinion, each child must be evaluated for hearing loss and speech development. In children with only mild hearing loss and normal speech development, effusions lasting three to six months can probably be tolerated. However, if significant hearing loss (greater than 40 db) or impaired speech development are present, earlier M&T seemsappropriate. Rarely will M&T be indicated for children with effusion for less than three months, since 90% of effusions will resolve if kept free from recurrent disease within this time period. It is the unusual child who should be permitted to persist with effusion beyond six months.

The role of adenoidectomy continues to be controversial. Some children with enlarged adenoids, recurrent otitis, and chronic effusion appear to benefit from surgical removal, while others do not. It is unclear howto identify which children will benefit from surgery. Studies in Pittsburgh by Drs. Bluestone, Stool and Paradise are now evaluating predictive factors for successful outcomes following adenoidectomy.

The problem of recurrent otitis and persistent effusion is large in scope, and the potential for long-term morbidity is considerable. We have reviewed interventions available to the clinician. However, we await further research on the relationship between frequent episodes of otitis media or prolonged middle ear effusion and language impairment, and more information of the safety and efficacy of available interventions before any therapeutic approach can be considered conclusively proven.

REFERENCES

1. Teelc DW, Klein JO. Rosner BA: Epidemiology of otitis media in children. Ann Otol Rhtnol Laryngol 1980: 89(Suppl 68):5.

2. Klein JO, Bluestone CD: Acute otitis media. Pediatrie Infectious Disease 1982: 1:66.

3. Klein JO: Middle ear disease in children. Hasp Proci July 1976. p 45.

4. Groothius JR. Sell SHW, Wright PF. et al: Otitis media in infancy: Tympanometric findings. Pediatrics 1979; 63:435.

5. Klein JO, Tecle DW: Isolation of viruses and mycoplasmas from middle ear effusions: A review. Ann Otol Rhtnol and Laryngol 1976; 85: 140.

6. Henderson FW. Collier AM. Sanyal MA. et al: A longitudinal study of respiratory viruses and bacteria in (he etiology of acute otitis media with effusion. V Engl J Med 1982; 306:1377.

7. Shurin PA. Pelton SI, Donner A. et al: Trimethaprim-sulfamethoxaüole compared with ampicillin in the treatment of acute otitis media. J Pe dial r 1980:96:1081.

8. Randall JE. Hendley JO: A decori gestant-antihistamine mixture in the prevention of otitis media in children with colds. Pediatrics 1979; 63:483.

9. Teele DW. Pelton Sl. Klein JO: Bacteriology of acute otitis media unresponsive to initial antimicrobial therapy. J Pediatr 1981: 98:537.

10. Berma n RA. Balkany TJ. Simmons MA: Otitis media in the neonatal intensive care unit. Pediatrics 1978; 62:198.

11. Jaffe BF. Hurtado F. Hurtado E: Tympanic membrane mobility in the newborn (with seven months follow-up). Laryngoscope 1970; 80:36.

12. Bland RD: Otitis media in the first six weeks oflife: Diagnosis, bacteriology and management. Pediatrics 1972; 49:187.

13. Shurin PA. Pelton Sl. Klein JO: Otitis media in t he newborn infant. A nnal.t of Otology, Rfit'nalogy. Laryngology 1976; 85:1.

14. Birman SA, Balkany TJ. Simmons MA: Otitis media in infants less than 12 weeks of age: Differing bacteriology among in-patients and out-patients. J Pedian 1978; 93:453.

15. Shurin PA. Howie VM. Pelton SI, et al: Bacterial etiology of otitis media during the first six weeks of life. J Pediatr 1978; 92:893.

16. Shurin PA. Pelton SI. Donner AL. et al: Persistence of middle ear effusion after acute otitis media in children. ?? EnglJ Med 1979: 300:1121.

17. Teele DW, Klein JO. Rosner BA: Epidemiology of otitis media in children. Ann Otol Rhino! Laryngol 1980: 89(Suppl 68):5.

18. Paradise J L: Otitis media during early life: How hazardous to development? A critical review of the evidence. Pediatrics 198 I: 68:869.

19. Teele DW, Klein JO. et al: Effects of persistent middle ear effusion on development of speech and language. Pediatr Re* 1981; 15:623.

20. Pen-in JM. Chamey E, MacWhinney JB Jr. el al: Sulfisoxa/ole as chemoprophylaxis for recurrent otitis media. A double-blind crossover study in pediatrie practice. N Eng! J Med 1974: 291:664.

21. Makela PH. Sibakov M. Herva E. et al: Pneumococcal vaccine and otitis media. Lancet 1980; 2:547.

22. Olson AL. Klein SW.Charney E, et al: Prevention and therapy of serous otitis media by oral decongestant: A double-blind study in pediatrie practice. Pediatrics 1978; 61:679.

23. Schwan? RH. Puglese J. Schwan? P: Use of a short course of prednisone for treating middle ear effusion. A double-blind crossover study. Ann Otol Rhino! Laryngol 1980; 89(Suppl 68):296.

BIBLIOGRAPHY

Paradise JL: Otitis media in infants and children. Pediatrics 1980: 65:917.

Bluestone CD: Otitis media in children: To treat or not to treat. A' Engl J Med 1982:306:1399

TABLE 1

INCIDENCE OF ACUTE OTITIS MEDIA IN BOSTON CHILDREN'

TABLE 2

FREQUENCY OF ACUTE OTITIS MEDIA IN THE PEDIATRIC WALK-IN CLINIC AT BOSTON CITY HOSPITAL3

TABLE 3

BACTERIAL PATHOGENS ISOLATED FROM MIDDLE EAR FLUID IN 4,675 CHILDREN WITH ACUTE OTITIS MEDIA2

TABLE 4

BACTERIOLOGY OF ACUTE OTITIS MEDIA IN THE FIRST SIXWEEKS OF LIFE2

10.3928/0090-4481-19830301-04

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