AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Background

Middle ear and eustachian tube inflammation are common denominators in various clinical conditions, namely, acute otitis media (AOM), chronic otitis media with effusion (COME), and eustachian tube dysfunction (ETD).

Pathophysiology

AOM can be described on the cellular and molecular level as a transudation of neutrophils, serum, and inflammatory mediators into the middle ear space. This transudation is associated with mucosal edema of the middle ear and bacterial or viral infection of the eustachian tube and middle ear space.

Chronic otitis media (COM) involves a transudation of serum with less cellularity of the effusion material. The inflammatory mediators are less destructive, and bacteria and viral antigens may be less prevalent.

Frequency

United States

Otitis media (OM) is the most common diagnosis made by office-based physicians of children younger than 15 years. OM is the most common reason children are prescribed antibiotics and the most common indication for surgery in children. OM accounted for 18% of physician visits from 1993-1995. Recent large prospective studies revealed that at least 90% of children have 1 or more episodes of middle ear effusion prior to age 2 years.

International

Rates of OM equal to or higher than rates in the United States are noted internationally, especially in less developed countries. A delay is evident in the peak incidence of OM in European children, which may be attributable to the fact that European children enter childcare at a later age.

Mortality/Morbidity

In the era of modern medicine, middle ear infection rarely leads to mortality, except in rare cases of intracranial spread of infection.

ETD and COME affect 70% of children by age 7 years and are common causes of childhood hearing loss. Morbidity from OM primarily stems from the effect on hearing. In most cases the conductive hearing loss is entirely reversible with medical or surgical treatment. Children may have a speech/language acquisition delay from recurrent AOM or COME. OM has not clearly been shown to affect the long-term acquisition of language skills in children; however, studies have predicted that early recurrent OM and COME may be predictive of future decreases in hearing as measured by school screening tests and a decrease in overall school achievement. These findings suggest a possible long-term effect on the central auditory pathway.

Race

American Indian and Native Alaskan children, including the Inuit, have higher rates of COM than whites. Hispanic children have higher rates of OM than either whites or African American children.

The prevalence of chronic suppurative OM is highest in Inuits of Alaska, Canada, and Greenland; Australian Aborigines; and in American Indians. High prevalence is also found in Pacific Islanders and Africans. Low prevalence is found in residents of Korea, India, and Saudi Arabia. The lowest prevalence is found in residents of the United States, United Kingdom, Denmark, and Finland.

Sex

Males have a higher prevalence of AOM and undergo myringotomies and tympanoplasties more frequently than females do.

Age

Middle ear dysfunction and ETD are more common in the pediatric age group. Peak incidence of OM is in the first 2 years of life.

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

History

• ETD: Symptoms usually follow the onset of an upper respiratory tract infection (URTI) or allergic rhinitis. Symptoms include aural fullness, difficulty popping ears, intermittent sharp ear pain, hearing loss, tinnitus, and dysequilibrium.
• OM: AOM can also be observed following URTI or secondary to any cause of eustachian tube inflammation or blockage. Symptoms include otalgia, hearing loss, fever, and dysequilibrium.
• COME: Symptoms include hearing loss, tinnitus, and dysequilibrium. COME is not associated with fever. Children may have speech/language delay.

Physical

Otoscopic findings of ETD are usually normal. The pathologic condition is more often observed on rhinoscopy, which can reveal nasal obstruction with either a deviated septum or hypertrophied inferior turbinates. Nasopharyngoscopy may reveal peritubal inflammation or a mass. Chronic ETD may reveal retraction pockets or atelectatic middle ear disease with incudostapediopexy having little or no middle ear aeration.

• AOM reveals an erythematous bulging tympanic membrane that is sluggish to pneumatic otoscopy and contains obscured landmarks. Fever may also be present.
• COM is associated with a dull-appearing tympanic membrane that is sluggish to pneumatic otoscopy. Always use pneumatic otoscopy because it greatly increases the accuracy of diagnosis. Tuning fork examination may reveal lateralization to the ipsilateral side in the absence of sensorineural hearing loss. Bone conduction is also greater than air conduction in the affected ear.

Causes

The prevailing theory of the development of middle ear inflammation and effusion has been that eustachian tube inflammation leads to the build up of bacteria and a resultant secondary bacterial infection of the middle ear space.

• URTIs caused by rhinovirus, respiratory syncytial virus, influenza virus, and adenovirus have been implicated in the pathophysiology of eustachian tube inflammation and middle ear inflammation.
• Most studies agree that viruses directly damage eustachian tube lining and can result in decreased mucociliary clearance.
• Recent studies suggest a more direct role of viruses in the development of middle ear inflammation. Research has demonstrated direct viral invasion of middle ear mucosa without evidence of bacterial secondary infection. Recent animal studies have concluded that the immune response to middle ear and eustachian tube viral infection continues to propagate the resultant inflammation long after clearance of viral antigen.
  • Purely immune-mediated cases of OM have been developed in animal studies.
  • Multiple cytokines have been investigated as contributing to OM and have been strated in middle ear effusions. These cytokines include interleukin-1beta, tumor necrosis factor-alpha, and gamma-interferon.
  • Other cytokines and cell surface markers have been described in animal studies, including interleukin-1alpha and intracellular adhesion molecule (ICAM).
  • This theory of a persistent sterile effusion following viral URTI gives credence to the expectant management of nonsevere OM as practiced in the Netherlands and elsewhere in Europe.
• Other theories include reflux of nasopharyngeal bacteria through the eustachian tube causing infection of the middle ear cleft.
• Streptococcus pneumoniae, nontypeable Haemophilus influenzae, and Moraxella catarrhalis are the most commonly isolated bacteria of middle ear infections. Less frequent isolates include group A streptococci, Staphylococcus aureus, and enteric bacteria found in newborns such as Escherichia coli, species of Klebsiella, Enterobacter, and Pseudomonas aeruginosa.
• Historically, allergy has been associated with the development of eustachian tube and middle ear inflammation; however, clear evidence has not been elucidated.
• Anatomic abnormalities, such as those observed in patients with cleft palate or other cranial facial abnormalities, may lead to middle ear and eustachian tube inflammation by a direct effect on eustachian tube function.
• Environmental factors, such as daycare attendance, passive smoke exposure, and pacifier usage, may contribute to nasopharyngeal and middle ear inflammation.
• The method of feeding infants may contribute to middle ear infection. Maternal immunoglobulin G (IgG) in breast milk may be protective against the development of middle ear infection. With breastfeeding, any detrimental effects of bottle feeding may be avoided, although conclusive data regarding these effects are unavailable.
• Gastroesophageal reflux has also been implicated as an etiological agent in the development of middle ear and eustachian tube inflammation. Nasopharyngeal pH has been noted to be lower in a subset of patients with adenoiditis and otalgia, although the degree of decreased pH required for pathology has not been standardized.

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Other Problems to be Considered

Hyperemia of vascular strip observed with crying child
Otitis externa
Bullous myringitis
Barotrauma
Laryngeal pharyngeal reflux

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Lab Studies

• Lab studies are seldom necessary unless the patient is being evaluated for a complication of OM.
• • In rare instances, tympanocentesis is performed, the specimen is cultured, and sensitivity tests are performed. These instances include refractory cases of AOM, neonates with severe OM, immunocompromised patients, and very ill children with OM.
  • A CBC count may be useful in a patient who appears toxic, and a lumbar puncture is useful if concerns of meningitis secondary to OM have arisen.

Imaging Studies

• Imaging studies are not typically applicable in cases of OM.
• • A CT scan of the temporal bones is useful to evaluate the temporal bone for extracranial complications of OM.
  • An MRI study is useful to evaluate for intracranial complications of OM.

Other Tests

• An impedance measurement (tympanogram) is an indirect measurement of eustachian tube and middle ear function that suggests the presence or absence of effusion or pressure in the middle ear space.
• • Type A tympanogram with little negative pressure suggests normal middle ear and eustachian tube function.
  • Type B tympanogram with low volume suggests middle ear fluid.
  • Type B tympanogram with a large volume suggests a patent tube or perforation. Small volume with visible perforation on exam suggests eustachian tube edema. Volume of 4-5 mL suggests a patent eustachian tube.
  • Type C tympanogram with high negative pressure suggests eustachian tube inflammation and dysfunction.
  • Type D tympanogram suggests a flaccid tympanogram with high negative pressure or ossicular discontinuity.
• Audiometry is critical in determining any temporary effects that middle ear fluid may have on hearing sensitivities.
• • The method of audiological examination depends on the patient's age. Infants younger than 6 months typically undergo behavioral observation audiometry, while children aged 6 months to 2.5 years typically undergo visual reinforcement audiology. Children older than 2.5 years undergo play audiometry, while older children are evaluated using standard testing with hand raising.
  • Middle ear effusions can produce mild-to-moderate levels of conductive hearing loss, although threshold testing may be normal. Children with middle ear effusions may demonstrate problems with auditory processing despite normal thresholds.

Procedures

• Myringotomy with tube placement is the primary treatment for persistent middle ear effusion. A tympanocentesis is useful for refractory cases of AOM and for research purposes.
• • Second-line surgical treatment of persistent OME involves adenoidectomy without tonsillectomy. Consider adenoidectomy in patients requiring a second set of ventilation tubes.
  • Mastoidectomy and tympanoplasty are also used to treat eustachian tube abnormalities and OM.

Histologic Findings

A bony and cartilaginous structure separated by a tubal isthmus forms the eustachian tube. The isthmus is smaller in children (about 2.4 mm x 0.8 mm) than in adults (about 4.3 mm x 1.7 mm). Analysis of human eustachian tube mucosa reveals that it is similar to respiratory epithelium, which is found elsewhere. The cartilaginous portion contains many seromucoid glands.

The middle ear mucosa consists of tall columnar cells near the tube and hypotympanum and cuboidal and simple squamous mucosal cells throughout the remainder of the middle ear. Collagen fibers, blood and lymph capillaries, and nerve fibers predominantly form the subepithelial space. A relative paucity of immunocompetent and seromucoid glands are found in the noninfected middle ear.

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical Care

• In the United States, AOM is typically treated with antibiotics. Treatment with amoxicillin for 10 days is the initial antibiotic selection, or Bactrim is substituted if the patient is allergic to penicillin. In Europe, a more conservative approach to treating AOM is used. Given the alarming increase in antibiotic resistance, the routine usage of antibiotics in the United States should be reconsidered.
• A recent meta-analyses from 30 articles written in English and 3 articles written in a language other than English revealed that AOM achieved complete clinical resolution without treatment 81% of the time as compared with resolution 95% of the time with the use of antimicrobials. Criteria for withholding or delaying antibiotic therapy for AOM include (1) patient older than 2 years, (2) normal host, (3) intact tympanic membrane, (4) at least 3-6 months since last episode of OM, (5) receptive parents, and (6) assurance of medical follow-up care.
• In the United States, OME can be treated with observation, antibiotics, or tympanostomy tube placement. Meta-analysis of controlled studies revealed only a 14% increase in resolution rate when antibiotics are given. Antibiotic suppression is not indicated for OME, and multiple courses of antibiotics have no proven benefit. Consider surgical intervention after 3-4 months of effusion with a 20 dB or greater hearing loss.
• ETD can be treated primarily with a combination of time, autoinsufflation (eg, an Otovent), and oral and nasal steroids (budesonide, mometasone, prednisone, methylprednisolone). Decongestants (eg, pseudoephedrine, oxymetazoline, phenylephrine) are also helpful, but not as useful for chronic ETD. Consider the cardiovascular effects of oral decongestants and the early development of tachyphylaxis observed with the use of nasal decongestants; limit the use of the decongestant to short-term symptomatic relief (ie, no more than 3-5 d). Nasal and oral antihistamines can also be beneficial in patients with allergic rhinitis. Leukotriene antagonists (eg, montelukast sodium [Singulair]) are helpful in some patients when oral steroids are not an option. Adequate control of laryngeal pharyngeal reflux helps to resolve ETD in patients with an associated peritubal inflammation from reflux. Proton pump inhibitors (esomeprazole magnesium [Nexium], rabeprazole [Aciphex], omeprazole [Prilosec]) administered twice adayare
  often used. Myringotomy with tube insertion is reserved for the refractory patient with debilitating symptoms.

Surgical Care

The primary surgical treatment of all types of OM is myringotomy with tube placement. The typical ventilation tube stays in place for a period of 8-12 months with closure of the perforation occurring after tube extrusion. In a small percentage of patients with poor eustachian tube function or other complicating factors, the perforation may persist.

• Adenoidectomy is indicated for refractory OME in children older than 4 years and in younger children when adenoid pathology is present (eg, chronic adenoiditis, adenoid hypertrophy).
• Tonsillectomy has not been shown to prevent OM either alone or in conjunction with adenoidectomy.
• Mastoidectomy, both canal wall up and canal wall down, can be used to treat complications of middle ear infection and ETD.

Consultations

Consult with an otolaryngologist if the patient has any evidence of complications of OM, if the effusion persists for longer than 3 months, if a 20 dB or greater hearing loss exists, or if a patient has more than 3 episodes of OM in 4 months or 6 episodes of OM in 1 year.

Neurosurgery consultation may be required for intracranial complications such as a brain abscess.

Activity

Patients with ETD must be careful when flying or diving because of the risk of barotrauma. Instruct patients with significant ETD to use oral and topical decongestants 30 minutes before landing. An Otovent may be used to assist with autoinsufflation in the treatment of ETD.

MEDICATION

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Antimicrobials are frequently chosen for the treatment of AOM and OME.

Topical nasal decongestants, oral decongestants, nasal steroids, and antihistamines can be used to treat ETD.

Drug Category: Antimicrobials

Used to eradicate middle ear bacteria and prevent mastoiditis in AOM and to help speed the resolution of inflammation and effusion in COME.

Drug Category: Oral decongestants

Used to decrease swelling of eustachian tube and sinus mucosa.

Drug Category: Nasal corticosteroids

Used to decrease perieustachian tube inflammation.

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Further Inpatient Care

• Inpatient care is seldom required for uncomplicated OM. Patients may need admission for IV antibiotics and surgical drainage for extracranial/intracranial complications of acute or chronic OM.

Further Outpatient Care

• After 3 months, re-evaluate patients treated conservatively for OME. Ninety percent of effusions that are going to clear without surgical treatment do so by 90 days. If no resolution of effusion occurs, consider myringotomy and ventilation tube insertion.

In/Out Patient Meds

• First-line antimicrobials used for OM include amoxicillin, trimethoprim/sulfamethoxazole, and erythromycin/sulfisoxazole. Despite the prevalence of resistant strains, the low cost and effectiveness in most patients supports continued use of these drugs.
• Second-line antimicrobials for OM include amoxicillin/clavulanate, cefuroxime, clarithromycin, and azithromycin. These antibiotics and others in their class offer a broader spectrum of coverage. A 2- to 3-week course of a second-line antibiotic has been shown to improve the resolution of OME in 15% more patients compared with no treatment at all. Multiple courses of antibiotics have shown no benefit.
• Pseudoephedrine is an ingredient found in oral decongestants. Oral decongestants are used in the treatment of ETD and can help decrease peritubal edema provoked by allergies or URI.
• Oxymetazoline is an ingredient found in topical decongestants. Topical decongestants can be used acutely for ETD but must be discontinued after a maximum of 5 days to prevent rebound swelling.
• Budesonide, fluticasone, beclomethasone, mometasone, triamcinolone, and flunisolide are steroids used in nasal sprays. Steroid nasal sprays are used in the hope of decreasing the peritubal edema on a long-term basis. These agents are most helpful in patients with allergic rhinitis.

Transfer

• Evaluation by an otolaryngologist is recommended for any signs of extracranial/intracranial complications or for chronic effusions with hearing loss.

Deterrence/Prevention

• Environmental modification is recommended.
  • Breastfeeding is recommended for at least 3-6 months. A meta-analysis reported a 13% reduction in the frequency of OM associated with breastfeeding for this period of time.
  • Smoking in proximity to the children is not recommended. Two meta-analyses reported the relative risks (1.2-1.7) of passive smoke in the development of OM.
  • Limit pacifier use to the moments when the child is falling asleep. A recent study revealed a 29% lower rate of AOM in children with limited pacifier usage.
  • Limit daycare exposure when possible; limited exposure can help decrease the frequent development of URTIs. Daycare enrollment is a greater risk factor for OM than parental smoking.
• Vaccination is the main form of prevention currently available.
  • Haemophilus influenzae type B vaccination is administered to infants for prevention of meningitis and other invasive infections. H influenzae type B causes only approximately 2% of OM. Nontypeable H influenzae accounts for a larger percentage of OM; however, a common antigen that would cross protect against the various strains of this bacteria has not been developed.
  • Heptavalent pneumococcal conjugate vaccines currently are administered to infants at age 2, 4, and 6 months with a booster dose administered at age 2 years. A significant reduction in OM caused by the serotypes contained in the vaccine was demonstrated in the recent Kaiser Permanente vaccine study.
  • A vaccine for Moraxella catarrhalis is currently being investigated. M catarrhalis has been isolated in approximately 10% of patients with AOM. URTI is the common denominator in many causes of OM.
  • Viral vaccines are currently under investigation including vaccines against adenovirus, respiratory syncytial virus, and influenza. A Finnish study investigating an influenza vaccine showed a reduction in the incidence of URTI and AOM in infants who attended daycare during an influenza epidemic.

Complications

• Tympanic membrane perforation
• Hearing loss
• Cholesteatoma
• Meningitis
• Brain abscess
• Subdural empyema
• Subperiosteal abscess
• Petrositis
• Labyrinthitis
• Sigmoid sinus thrombophlebitis
• Otitic hydrocephalus
• Facial paralysis
• Death

Prognosis

• Prognosis is excellent if infection is not permitted to spread beyond the middle ear and eustachian tube. Permanent sequelae are usually rare.

Patient Education

• Education of parents in the form of risk factor reduction is useful. Modifiable risk factors include breastfeeding exclusively for at least 3 months, avoidance of parental cigarette smoke, feeding the baby in an upright position, limiting pacifier usage to just when the infant is falling asleep, and avoidance of daycare attendance, if possible.

MISCELLANEOUS

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical/Legal Pitfalls

• As with any surgical procedure, if a complication arises following surgical treatment of OME, legal ramifications are possible. Be certain that the procedure can be backed up with evidence-based studies.

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

• Asbjornsen A, Holmefjord A, Reisaeter S, et al. Lasting auditory attention impairment after persistent middle ear infections: a dichotic listening study. Dev Med Child Neurol. Jul 2000;42(7):481-6. [Medline].
• Bernstein JM. Immunologic reactivity in the middle ear in otitis media with effusion. Otolaryngol Clin North Am. Aug 1991;24(4):845-58. [Medline].
• Black S, Shinefield H, Fireman B, et al. Efficacy, safety and immunogenicity of heptavalent pneumococcal conjugate vaccine in children. Northern California Kaiser Permanente Vaccine Study Center Group [see comments]. Pediatr Infect Dis J. Mar 2000;19(3):187-95. [Medline].
• Bluestone CD. Epidemiology and pathogenesis of chronic suppurative otitis media: implications for prevention and treatment. Int J Pediatr Otorhinolaryngol. Jan 1998;42(3):207-23. [Medline].
• Conrad DA. Should acute otitis media ever be treated with antibiotics?. Pediatr Ann. Feb 1998;27(2):66-7, 70-4. [Medline].
• Contencin P, Maurage C, Ployet MJ, et al. Gastroesophageal reflux and ENT disorders in childhood. Int J Pediatr Otorhinolaryngol. Jun 1995;32 Suppl:S135-44. [Medline].
• Contencin P, Narcy P. Nasopharyngeal pH monitoring in infants and children with chronic rhinopharyngitis. Int J Pediatr Otorhinolaryngol. Oct 1991;22(3):249-56. [Medline].
• Daly KA, Giebink GS. Clinical epidemiology of otitis media. Pediatr Infect Dis J. May 2000;19(5 Suppl):S31-6. [Medline].
• Doyle WJ, Alper CM, Buchman CA, et al. Illness and otological changes during upper respiratory virus infection. Laryngoscope. Feb 1999;109(2 Pt 1):324-8. [Medline].
• Haddad J Jr, Saiman L, San Gabriel P, et al. Nonsusceptible Streptococcus pneumoniae in children with chronic otitis media with effusion and recurrent otitis media undergoing ventilating tube placement. Pediatr Infect Dis J. May 2000;19(5):432-7. [Medline].
• Heikkinen T. Role of viruses in the pathogenesis of acute otitis media. Pediatric Infectious Disease Journal. 2000;19, No. 5:S17-23. [Medline].
• Ilicali OC, Keles N, Deger K, Savas I. Relationship of passive cigarette smoking to otitis media. Arch Otolaryngol Head Neck Surg. Jul 1999;125(7):758-62. [Medline].
• Meek RB 3rd, McGrew BM, Cuff CF, et al. Immunologic and histologic observations in reovirus-induced otitis media in the mouse. Ann Otol Rhinol Laryngol. Jan 1999;108(1):31-8. [Medline].
• Niemela M, Uhari M, Mottonen M, Pokka T. Costs arising from otitis media. Acta Paediatr. May 1999;88(5):553-6. [Medline].
• 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. Sep 2000;106(3):483-8. [Medline].
• Pichichero ME, Reiner SA, Brook I, et al. Controversies in the medical management of persistent and recurrent acute otitis media. Recommendations of a clinical advisory committee. Ann Otol Rhinol Laryngol Suppl. 2000;Aug;183:1-12. [Medline].
• Rinaldo A, Ferlito A. The pathology and clinical features of "glue ear": a review [In Process Citation]. Eur Arch Otorhinolaryngol. 2000;257(6):300-3. [Medline].
• Rovers MM, Zielhuis GA, Straatman H, et al. Prognostic factors for persistent otitis media with effusion in infants. Arch Otolaryngol Head Neck Surg. Nov 1999;125(11):1203-7. [Medline].
• Rovers MM, Straatman H, Ingels K, et al. The effect of ventilation tubes on language development in infants with otitis media with effusion: A randomized trial. Pediatrics. Sep 2000;106(3):E42. [Medline].
• Ruuskanen O, Arola M, Putto-Laurila A, et al. Acute otitis media and respiratory virus infections. Pediatr Infect Dis J. Feb 1989;8(2):94-9. [Medline].
• Shaw CB, Obermyer N, Wetmore SJ, et al. Incidence of adenovirus and respiratory syncytial virus in chronic otitis media with effusion using the polymerase chain reaction. Otolaryngol Head Neck Surg. Sep 1995;113(3):234-41. [Medline].
• Skull SA, Morris PS, Yonovitz A, et al. Middle ear effusion: rate and risk factors in Australian children attending day care. Epidemiol Infect. Aug 1999;123(1):57-64. [Medline].
• Takahashi M, Peppard J, Harris JP. Immunohistochemical study of murine middle ear and Eustachian tube. Acta Otolaryngol. Jan-Feb 1989;107(1-2):97-103. [Medline].
• US Otitis Media Guideline Panel, Stool SE, US Agency for Health Care Policy and Research. Otitis media with effusion in young children/Otitis Media Guideline Panel. Rockville, Md: US Dept. of Health and Human Services, Public Health Service;1994:Clinic practice gudeline, No. 12.
• Uhari M, Hietala J, Tuokko H. Risk of acute otitis media in relation to the viral etiology of infections in children. Clin Infect Dis. Mar 1995;20(3):521-4. [Medline].
• Wright CG, Meyerhoff WL. Pathology of otitis media. Ann Otol Rhinol Laryngol Suppl. May 1994;163:24-6. [Medline].
• Zielhuis GA, Gerritsen AA, Gorissen WH, et al. Hearing deficits at school age; the predictive value of otitis media in infants. Int J Pediatr Otorhinolaryngol. Aug 1O 1998;44(3):227-34. [Medline].

Article Last Updated: Mar 22, 2006