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Middle Ear, Eustachian Tube, Inflammation/Infection Clinical Presentation

  • Author: Robert B Meek, MD; Chief Editor: Arlen D Meyers, MD, MBA  more...
 
Updated: Apr 20, 2015
 

History

See the list below:

  • Eustachian tube dysfunction (ETD): Symptoms usually follow the onset of an upper respiratory tract infection (URTI) or allergic rhinitis.[4] Symptoms include aural fullness, difficulty popping ears, intermittent sharp ear pain, hearing loss, tinnitus, and dysequilibrium.
  • Otitis media (OM): acute otitis media (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.
  • Chronic otitis media with effusion (COME): Symptoms include hearing loss, tinnitus, and dysequilibrium. Chronic otitis media with effusion (COME) is not associated with fever. Children may have speech/language delay.
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Physical

Otoscopic findings of eustachian tube dysfunction (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 eustachian tube dysfunction (ETD) may reveal retraction pockets or atelectatic middle ear disease with incudostapediopexy having little or no middle ear aeration.

  • Acute otitis media (AOM) reveals an erythematous bulging tympanic membrane that is sluggish to pneumatic otoscopy and contains obscured landmarks. Fever may also be present.
  • Chronic otitis media (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.
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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 otitis media (OM) have been developed in animal studies.
    • Multiple cytokines have been investigated as contributing to otitis media (OM) and have been started 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 otitis media (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.[5]
  • 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.[6] 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.
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Contributor Information and Disclosures
Author

Robert B Meek, MD 

Robert B Meek, MD is a member of the following medical societies: American Academy of Otolaryngic Allergy, American Academy of Otolaryngology-Head and Neck Surgery, Association for Research in Otolaryngology

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

Arlen D Meyers, MD, MBA Professor of Otolaryngology, Dentistry, and Engineering, University of Colorado School of Medicine

Arlen D Meyers, MD, MBA is a member of the following medical societies: American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, American Head and Neck Society

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Cerescan;RxRevu;SymbiaAllergySolutions<br/>Received income in an amount equal to or greater than $250 from: Symbia<br/>Received from Allergy Solutions, Inc for board membership; Received honoraria from RxRevu for chief medical editor; Received salary from Medvoy for founder and president; Received consulting fee from Corvectra for senior medical advisor; Received ownership interest from Cerescan for consulting; Received consulting fee from Essiahealth for advisor; Received consulting fee from Carespan for advisor; Received consulting fee from Covidien for consulting.

Acknowledgements

Ari J Goldsmith, MD Chief of Pediatric Otolaryngology, Long Island College Hospital; Associate Professor, Department of Otolaryngology, Division of Pediatric Otolaryngology, State University of New York Downstate Medical Center

Ari J Goldsmith, MD is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery, American Medical Association, and Medical Society of the State of New York

Disclosure: Nothing to disclose.

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Anatomy of the external and middle ear.
 
 
 
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