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Otitis Media Clinical Presentation

  • Author: Muhammad Waseem, MD, MS; Chief Editor: Ravindhra G Elluru, MD, PhD  more...
 
Updated: Mar 15, 2016
 

History

Acute otitis media (AOM), with or without effusion, should be suspected in children with a history of characteristic head-neck and general symptoms.

Common head and neck symptoms of AOM include the following:

  • Otalgia - Young children may exhibit signs of otalgia by pulling on the affected ear or ears or pulling on the hair; otalgia apparently occurs more often when the child is lying down (eg, during the night, during nap time), which may be due to increased eustachian tube dysfunction (ETD) when the child is in a recumbent position
  • Otorrhea - Discharge may come from the middle ear through a recently perforated tympanic membrane (TM), through a preexisting tympanostomy tube (TT), or through another perforation; for trauma patients, excluding a basilar skull fracture with associated cerebrospinal fluid (CSF) otorrhea is important
  • Concurrent or recent symptoms of upper respiratory infection (URI), such as cough, rhinorrhea, or sinus congestion

Common general symptoms include the following:

  • Two thirds of children with AOM have a history of fever, although fevers greater than 40°C are uncommon and may represent bacteremia or other complications
  • Irritability may be the sole early symptom in a young infant or toddler
  • A history of lethargy, although nonspecific, is a sensitive marker for sick children and should not be dismissed

Gastrointestinal (GI) tract symptoms may include the following:

  • Anorexia
  • Nausea
  • Vomiting
  • Diarrhea

Otitis media (OM) with effusion (OME) often follows an episode of AOM. Consider OME in patients with recent AOM in whom the history includes any of the following symptoms:

  • Hearing loss - Most young children cannot provide an accurate history; parents, caregivers, or teachers may suspect a hearing loss or describe the child as inattentive
  • Tinnitus - This is possible, though it is an unusual complaint from a child
  • Vertigo - Although true vertigo (ie, room-spinning dizziness) is a rare complaint in uncomplicated AOM or OME, parents may report some unsteadiness or clumsiness in a young child with AOM
  • Otalgia - Intermittent otalgia tends to worsen at night

OM treatment varies widely, depending on the duration of symptoms, past therapeutic failures, and severity of current symptoms.

Exposure to environmental risk factors is another important aspect of the history and includes the following:

  • Passive (ie, secondhand) exposure to tobacco smoke
  • Group daycare attendance
  • Seasonality - AOM prevalence is much higher in winter and early spring than in summer and early fall
  • Supine bottle feeding (ie, bottle propping)
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Physical Examination

Pneumatic otoscopy remains the standard examination technique for patients with suspected OM. When performed correctly, it is 90% sensitive and 80% specific for diagnosis of AOM, and its findings are more accurate than those of myringotomy.

Proper pneumatic otoscopy technique is crucial to distinguish AOM from OME because recommended therapies for these entities are significantly different. Studies show that most practitioners improperly perform otoscopic examinations. Almost one half of physicians never use pneumatic compression of the TM during routine otoscopic examination, and almost 30% use otoscopes with inadequate light sources.

Tympanometry, acoustic reflectometry, and audiometry are important adjunctive techniques with which to evaluate patients with middle ear effusion (MEE).

In addition to a carefully documented examination of the external ear and TM, examining the entire head and neck region of patients with suspected OM is important. Several congenital syndromes, craniofacial anomalies, and systemic diseases have increased incidence associated with OM, including cleft palate, Down syndrome, Treacher Collins syndrome (ie, mandibulofacial dysotosis), hemifacial microsomia, diabetes mellitus, human immunodeficiency virus (HIV) infection, and many types of mucopolysaccharidosis.

Pneumatic otoscopy

Under direct visualization, first remove any cerumen, which causes a limited and sometimes inaccurate view of the TM and inaccurate and confusing results on tympanometry and audiometry.

To move the TM, the ear speculum must create an air seal against the external auditory canal (EAC), which is seldom possible with a standard disposable speculum. All otoscope manufacturers sell inexpensive cuffed ear speculums to perform insufflation. A rubber sleeve over the speculum may reduce patient discomfort during the examination.

Usually, the TM is in the neutral position (ie, neither retracted nor bulging), pearly gray, translucent, and unperforated. It responds briskly to positive and negative pressure, indicating an air-filled space. Many older texts emphasize a TM "light reflex" in an otherwise normal ear. Because this reflex may be absent in entirely normal ears and present in ears with MEE, the light reflex does not help confirm or exclude an OM diagnosis.

Every examination should include an evaluation and description of the following four TM characteristics:

  • Color
  • Position
  • Mobility
  • Perforation

Color

A normal TM is a translucent pale gray. An opaque yellow or blue TM is consistent with MEE. Dark red indicates a recent trauma or blood behind the TM. A dark pink or lighter red TM is consistent with AOM or hyperemia of the TM caused by crying, coughing, or nose blowing.

The color of the eardrum is less important diagnostically than its position and mobility. Redness of the TM alone does not necessarily suggest AOM because crying, removal of cerumen with associated irritation of the auditory canal, coughing, nose blowing, and fever can all cause redness of the eardrum without a middle ear infection. Note that most children cry when their ears are examined.

A study of 85 infants showed that the otoscopic finding most predictive of AOM was a poorly mobile, bulging, yellow, and opacified TM. However, this appearance was noted in only 19% of patients. In another analysis, a slightly red TM in a normal position and with normal mobility had a predictive value of only 7% for AOM.

Position

The position of the TM (ie, bulging, retracted, neutral, full) is key to differentiating AOM from OME.[20] In AOM, the TM is usually bulging. In OME, the TM is typically retracted or in the neutral position.

Mobility

Abnormal movement of the TM during pneumatic otoscopy can suggest various conditions or disorders. Movement during negative pressure only suggests ETD. A TM that moves only slightly with both positive and negative pressure applied indicates the probable presence of middle ear fluid. No movement occurs with a TM perforation or a TT.

Studies show that the most consistent physical finding in patients with OME is impaired mobility of the TM during pneumatic otoscopy. Pay special attention to movement of retracted segments of the TM because immobility of these sections may indicate middle ear cholesteatoma in the retraction pockets.

Perforation

Single perforations are most common, but some patients may have multiple perforations.

Note the location and cause of the perforation. Perforations in the posterosuperior quadrant, which are the most difficult to detect, are important because they occasionally are associated with cholesteatoma. Pus or other fluid may drain through a perforation. Multiple perforations and otorrhea that does not yield pathogens on culture may indicate tuberculosis.

Adjunctive screening techniques

Adjunctive techniques help identify patients with asymptomatic OME, which may account for 10% of cases.

Tympanometry

Tympanometry (ie, impedance audiometry), the most commonly used adjunctive technique, measures changes in acoustic impedance of the TM/middle ear system with air pressure changes in the EAC.

Current recommendations call for screening tympanometry at the beginning of school and 1 year later to identify children aged 4-6 years with asymptomatic OME. Tympanometry screening has a high degree of sensitivity (>90%) but is not specific for OME. The test may yield false-positive results in children with a retracted TM or a thickened TM without effusion. Screening tests may also yield invalid results in children who have cerumen obstructing the external canal or who are crying during the examination.

Middle ear pressure more than –200 daPa or a flat tympanometric curve is classified as a failure.

Further physician evaluation is indicated in a child in whom tympanometry screening fails in both ears and who has at least a 20-dB hearing loss at 1, 2, or 4 kHz.

After 2 months, retest any child in whom tympanometry screening fails in one ear and hearing loss occurs (>20 dB). Also retest children in whom tympanometry screening fails in both ears, even without marked hearing loss (ie, <20 dB). A second screening failure should lead to physician evaluation. Assess the child's hearing, speech, and language and immediately start therapy to correct deficits.

Acoustic reflectometry

Acoustic reflectometry uses an acoustic otoscope to measure reflected sound from the TM; the louder the reflected sound, the greater the likelihood of an MEE. The breakpoint is defined as the level of sound reflectivity that correlates with the presence of MEE.

Acoustic reflectometry is rapid and easy to perform. Among its advantages over tympanometry is that an airtight seal of the EAC is unnecessary and that the test is unaffected by a crying patient or the presence of cerumen in the EAC. Despite these advantages, acoustic reflectometry has not been widely accepted by otolaryngologists because of the difficulty in setting standards to interpret test results.

Because no accepted breakpoint standards have been established, reported sensitivity and specificity vary according to the breakpoints set for each study. A low breakpoint leads to high sensitivity but low specificity. A high breakpoint leads to higher specificity but lower sensitivity.

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Complications

Mastoiditis

Mastoid infections have two forms: acute coalescent mastoiditis[21] and chronic mastoiditis with osteitis. Treatment for both types consists of a mastoidectomy.

Acute coalescent mastoiditis occurs when obstruction of the aditus (the small opening between the epitympanum and the mastoid antrum) creates a sealed space in the mastoid antrum (the air space in the mastoid portion of the temporal bone that communicates with the tympanic cavity and mastoid air cells). Acute infection of the fluid in this space usually occurs as an extension of middle ear infection. Diagnosis is confirmed with a computed tomography (CT) scan of the head that reveals loss of septation between mastoid air cells.

Chronic mastoiditis occurs when acute mastoiditis remains undetected, with subsequent changes in the mucosal lining of the mastoid air cells. Granulation tissue filled with inflammatory cells replaces the air spaces of the mastoid and middle ear, and bone necrosis with erosion may result, leading to an extracranial Bezold abscess (see the image below) or intracranial complication. Chronic mastoiditis may not be depicted on CT. Magnetic resonance imaging (MRI) reveals regions of nonspecific bright signal, consistent with inflammation.

Acute coalescent mastoiditis with a Bezold abscess Acute coalescent mastoiditis with a Bezold abscess in a young girl who presented with chronic right ear pain and multiple untreated middle ear infections.

Cholesteatoma

Cholesteatomas are cystlike expanding lesions of the temporal bone, lined by stratified squamous epithelium and containing desquamated keratin and purulent material. Their etiology is controversial. Although cholesteatoma development is complicated and incompletely understood, contributing factors include ETD, increased negative pressures in the middle ear, repeated infection, chronic MEE, loss of collagen fibers and structural support of the TM, collapse of the TM, and formation of chronic retraction pockets.

Diagnosis is difficult but can be made by an experienced clinician using a pneumatic otoscopic examination in patients with chronic middle ear disease and progressive conductive hearing loss.

Treatment is surgical excision or exteriorization. In very rare cases (eg, when the patient is not a surgical candidate because the cholesteatoma is secondary to a comorbid disease), repeated cleansing under a surgical microscope may temporarily control the cholesteatoma.

Labyrinthitis

Inflammation of the labyrinth produces vestibular and auditory symptoms. In patients with chronic OM (COM), bacteria may infiltrate the bony labyrinth and produce a condition of suppurative labyrinthitis. Acute symptoms include hearing loss and vertigo, which usually improve after the body goes through a phase of central compensation for the damaged vestibular organs. Prolonged labyrinth infection leads to vestibular end-organ damage and permanent hearing loss.

Diagnosis of labyrinthitis in patients with COM is most often retrospectively confirmed. Vertigo and sensorineural hearing loss in these patients is presumptive evidence for labyrinthitis.

In patients in whom hearing or vestibular function recovers, labyrinthitis is classified as serous rather than suppurative; recovery indicates that the bacteria never truly invaded the labyrinth and that the symptoms were caused by severe inflammation of the vestibular organs without bacterial invasion.

Labyrinthitis treatment includes intravenous (IV) antibiotics directed against the common pathogens in COM to limit damage to vestibular organs. Vestibular suppressants are used in the acute period to relieve dizziness and nausea.

Facial paralysis

In patients with invasive OM (especially OM with cholesteatoma), infection and inflammation of the facial nerve leads to edema and nerve fiber compression that causes facial paralysis. The facial nerve courses through the temporal bone in the fallopian canal, protected by bone and epineurium. Naturally occurring bony dehiscences of the fallopian canal and reactive osteitis (often due to cholesteatoma) place the facial nerve at risk in invasive OM.

The combination of OM with concurrent ipsilateral facial paralysis suggests an obvious diagnosis, but other entities in the differential diagnosis for acute facial paralysis should be considered. Treatment is immediate administration of IV antibiotics and/or surgical treatment of the cholesteatoma involving the facial nerve.

Meningitis

Meningitis is among the most common intracranial complications of OM, occurring in children with either AOM or COM. Fever accompanied by neck stiffness should immediately prompt a search for an intracranial complication. As with all intracranial complications, perform contrast-enhanced CT or MRI.

Lumbar puncture and examination of the cerebrospinal fluid (CSF) is mandatory in patients in whom meningitis is suspected. CSF leukocytosis, with low glucose and high protein and lactate levels, is characteristic of meningitis. Studies of the CSF should include Gram staining, culturing, and testing for bacterial antigens.

The treatment of choice is immediate administration of broad-spectrum IV antibiotics, followed by directed therapy based on CSF culture results. Some experts have reduced neurologic and auditory sequelae resulting from meningitis by administering dexamethasone early in the treatment course.

Epidural abscess

Epidural abscesses secondary to OM occur near the temporal bone. Infection extends to the epidural space through venous channels in the bone or by bone erosion. The most common routes for extension are through the thin bone of the tegmen to the middle cranial fossa or through the bone adjacent to the sigmoid sinus and posterior cranial fossa. Most intracranial complications are accompanied by a concomitant epidural abscess because of the pathways involved in OM spread.

Diagnosis relies on high clinical suspicion and is confirmed using contrast-enhanced CT or MRI. Treatment requires surgical exploration, with a cortical mastoidectomy and thinning of the bone overlying the tegmen tympani, sigmoid sinus, and posterior fossa to allow the epidural space to be seen. If granulation tissue or purulent fluid is discovered in the epidural space, continue removing bone until noninflamed dura is encountered.

Lateral sinus thrombophlebitis

Lateral and sigmoid sinuses are relatively unprotected from direct extension of infections from the middle ear and mastoid. Direct extension occurs secondary to bone erosion from osteitis or necrosis. Indirect extension occurs via retrograde thrombophlebitis of the mastoid emissary veins.

Obstruction of venous drainage by thrombosis can produce elevated intracranial pressure (ICP) and headache. Otitic hydrocephalous can complicate the course of lateral sinus thrombosis, leading to vision changes and sixth cranial nerve (CN VI) palsy. Septic emboli can disseminate the infection to distant body sites, and the constant bacteremia produces febrile episodes.

The classic clinical picture of high spiking fevers, headache, and active ear disease is rare.

Diagnosis of this complication relies on high clinical suspicion and is confirmed by MRI or contrast-enhanced CT demonstrating the thrombosis. Early administration of IV antibiotics and surgical exploration are the mainstays of therapy. After exposing the sigmoid sinus, a needle may be used to aspirate the sinus. If free-flowing blood returns, no further surgery is needed. If no blood returns, open and drain the sinus.

Brain abscess

Brain abscess is the first or second most common intracranial complication of COM. Most abscesses form in the temporal lobe or cerebellum, supporting the theory that brain abscesses associated with OM are probably caused by direct extension of infection and not hematogenous spread of bacteria.

In addition to fever from the infectious process, symptoms and signs of brain abscess relate to abscess location and the overall mass effect of the abscess. Headache, vomiting, and lethargy may indicate increased ICP. Significant localizing signs include seizures, hemiparesis, cranial nerve palsies, and aphasia. Abscesses in the temporal lobe or cerebellum can exist with relatively few early localizing symptoms.

Contrast-enhanced CT or MRI is the diagnostic study of choice. The initial therapy of choice is administration of broad-spectrum antibiotics. Consult with a neurosurgeon for decisions about abscess drainage. In some patients, mastoid surgery can be performed with a neurosurgical procedure. Otologic surgery can be delayed in patients who are less stable until neurologic stability is established.

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Contributor Information and Disclosures
Author

Muhammad Waseem, MD, MS Associate Professor of Emergency Medicine in Clinical Pediatrics, Associate Professor of Clinical Healthcare Policy and Research, Weill Medical College of Cornell University; Consulting Staff, Department of Emergency Medicine, Lincoln Medical and Mental Health Center

Muhammad Waseem, MD, MS is a member of the following medical societies: American Academy of Pediatrics, American College of Emergency Physicians, American Heart Association, Society of Critical Care Medicine, Society for Simulation in Healthcare, American Medical Association

Disclosure: Nothing to disclose.

Coauthor(s)

Muhammad Aslam, MD Associate Professor of Pediatrics, University of California, Irvine, School of Medicine; Neonatologist, Division of Newborn Medicine, Department of Pediatrics, UC Irvine Medical Center

Muhammad Aslam, MD is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Alan D Murray, MD Pediatric Otolaryngologist, ENT for Children; Full-Time Staff, Medical City Dallas Children's Hospital; Consulting Staff, Department of Otolaryngology, Children's Medical Center at Dallas, Cook Children's Medical Center; Full-Time Staff, Texas Pediatric Surgery Center, Cook Children's Pediatric Surgery Center Plano

Alan D Murray, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Otolaryngology-Head and Neck Surgery, American Society of Pediatric Otolaryngology, Society for Ear, Nose and Throat Advances in Children, American Academy of Pediatrics, American College of Surgeons, Texas Medical Association

Disclosure: Nothing to disclose.

Chief Editor

Ravindhra G Elluru, MD, PhD Professor, Wright State University, Boonshoft School of Medicine; Pediatric Otolaryngologist, Department of Otolaryngology, Dayton Children's Hospital Medical Center

Ravindhra G Elluru, MD, PhD is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery, American Academy of Pediatrics, American Bronchoesophagological Association, American College of Surgeons, American Medical Association, Association for Research in Otolaryngology, Society for Ear, Nose and Throat Advances in Children, Triological Society, American Society for Cell Biology

Disclosure: Nothing to disclose.

Acknowledgements

Orval Brown, MD Director of Otolaryngology Clinic, Professor, Department of Otolaryngology-Head and Neck Surgery, University of Texas Southwestern Medical Center at Dallas

Orval Brown, MD is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery, American Academy of Pediatrics, American Bronchoesophagological Association, American College of Surgeons, American Medical Association, American Society of Pediatric Otolaryngology, Society for Ear, Nose and Throat Advances in Children, and Society of University Otolaryngologists-Head and Neck Surgeons

Disclosure: Nothing to disclose.

Michael Jones, MD Consulting Staff, Department of Emergency Medicine, Brooke Army Medical Center

Disclosure: Nothing to disclose.

David Malis, MD Assistant Chief, Otolaryngology Service, Brooke Army Medical Center, Clinical Assistant Professor, Department of Otolaryngology-Head and Neck Surgery, The University of Texas Health Science Center at San Antonio

Disclosure: Nothing to disclose.

Leslie A Wilson, MD Chief, Well-Baby Clinic and Chronic Ear Clinic, Department of Pediatrics, Wilford Hall Air Force Medical Center

Disclosure: Nothing to disclose.

References
  1. Fireman P. Otitis media and eustachian tube dysfunction: connection to allergic rhinitis. J Allergy Clin Immunol. 1997 Feb. 99(2):S787-97. [Medline].

  2. Mittal R, Robalino G, Gerring R, Chan B, Yan D, Grati M, et al. Immunity genes and susceptibility to otitis media: a comprehensive review. J Genet Genomics. 2014 Nov 20. 41(11):567-81. [Medline].

  3. Patel JA, Nair S, Revai K, Grady J, Chonmaitree T. Nasopharyngeal acute phase cytokines in viral upper respiratory infection: impact on acute otitis media in children. Pediatr Infect Dis J. 2009 Nov. 28(11):1002-7. [Medline].

  4. Skovbjerg S, Roos K, Nowrouzian F, Lindh M, Holm SE, Adlerberth I, et al. High cytokine levels in perforated acute otitis media exudates containing live bacteria. Clin Microbiol Infect. 2009 Oct 14. [Medline].

  5. Bercin S, Kutluhan A, Yurttas V, Yalciner G, Bozdemir K, Sari N. Evaluation of laryngopharyngeal reflux in patients with suspected laryngopharyngeal reflux, chronic otitis media and laryngeal disorders. Eur Arch Otorhinolaryngol. 2008 May 21. [Medline].

  6. Lee SK, Yeo SG. Relationship between pediatric obesity and otitis media with effusion. Curr Allergy Asthma Rep. 2009 Nov. 9(6):465-72. [Medline].

  7. Rosch JW. Promises and pitfalls of live attenuated pneumococcal vaccines. Hum Vaccin Immunother. 2014 Oct 3. 10(10):3000-3. [Medline].

  8. Broides A, Dagan R, Greenberg D, Givon-Lavi N, Leibovitz E. Acute otitis media caused by Moraxella catarrhalis: epidemiologic and clinical characteristics. Clin Infect Dis. 2009 Dec 1. 49(11):1641-7. [Medline].

  9. Yilmaz T, Ceylan M, Akyon Y, et al. Helicobacter pylori: a possible association with otitis media with effusion. Otolaryngol Head Neck Surg. 2006 May. 134(5):772-7. [Medline].

  10. Harimaya A, Takada R, Hendolin PH, et al. High incidence of Alloiococcus otitidis in children with otitis media, despite treatment with antibiotics. J Clin Microbiol. 2006 Mar. 44(3):946-9. [Medline].

  11. de Miguel Martinez I, Macias AR. Serous otitis media in children: implication of Alloiococcus otitidis. Otol Neurotol. 2008 Jun. 29(4):526-30. [Medline].

  12. Tauriainen S, Oikarinen S, Taimen K, et al. Temporal relationship between human parechovirus 1 infection and otitis media in young children. J Infect Dis. 2008 Jul 1. 198(1):35-40. [Medline].

  13. Jones LL, Hassanien A, Cook DG, Britton J, Leonardi-Bee J. Parental smoking and the risk of middle ear disease in children: a systematic review and meta-analysis. Arch Pediatr Adolesc Med. 2012 Jan. 166(1):18-27. [Medline].

  14. Strachan DP, Cook DG. Health effects of passive smoking. 4. Parental smoking, middle ear disease and adenotonsillectomy in children. Thorax. 1998 Jan. 53(1):50-6. [Medline].

  15. Greenberg D, Hoffman S, Leibovitz E, Dagan R. Acute otitis media in children: association with day care centers - antibacterial resistance, treatment, and prevention. Paediatr Drugs. 2008. 10(2):75-83. [Medline].

  16. Elden LM, Coyte PC. Socioeconomic impact of otitis media in North America. J Otolaryngol. 1998. 27 Suppl 2:9-16. [Medline].

  17. Wanna GB, Dharamsi LM, Moss JR, Bennett ML, Thompson RC, Haynes DS. Contemporary Management of Intracranial Complications of Otitis Media. Otol Neurotol. 2009 Oct 31. [Medline].

  18. Paradise JL, Hoberman A, Rockette HE, Shaikh N. Treating Acute Otitis Media in Young Children: What Constitutes Success?. Pediatr Infect Dis J. 2013 Feb 21. [Medline].

  19. Williams CJ, Jacobs AM. The impact of otitis media on cognitive and educational outcomes. Med J Aust. 2009 Nov 2. 191(9):S69-72. [Medline].

  20. Shaikh N, Hoberman A, Kaleida PH, Rockette HE, Kurs-Lasky M, Hoover H, et al. Otoscopic signs of otitis media. Pediatr Infect Dis J. 2011 Oct. 30(10):822-6. [Medline].

  21. Lin HW, Shargorodsky J, Gopen Q. Clinical strategies for the management of acute mastoiditis in the pediatric population. Clin Pediatr (Phila). 2010 Feb. 49(2):110-5. [Medline].

  22. Dowell SF, Butler JC, Giebink GS, et al. Acute otitis media: management and surveillance in an era of pneumococcal resistance--a report from the Drug-resistant Streptococcus pneumoniae Therapeutic Working Group. Pediatr Infect Dis J. 1999 Jan. 18(1):1-9. [Medline].

  23. [Guideline] Lieberthal AS, Carroll AE, Chonmaitree T, Ganiats TG, Hoberman A, Jackson MA, et al. The diagnosis and management of acute otitis media. Pediatrics. 2013 Mar. 131 (3):e964-99. [Medline].

  24. Klein JO. Review of consensus reports on management of acute otitis media. Pediatr Infect Dis J. 1999 Dec. 18(12):1152-5. [Medline].

  25. Noel GJ, Blumer JL, Pichichero ME, Hedrick JA, Schwartz RH, Balis DA, et al. A Randomized Comparative Study of Levofloxacin Versus Amoxicillin/Clavulanate for Treatment of Infants and Young Children With Recurrent or Persistent Acute Otitis Media. Pediatr Infect Dis J. 2008 Jun. 27(6):483-489. [Medline].

  26. Fischer T, Singer AJ, Lee C, Thode HC Jr. National trends in emergency department antibiotic prescribing for children with acute otitis media, 1996-2005. Acad Emerg Med. 2007 Dec. 14(12):1172-5. [Medline].

  27. Stool SE, Berg AO. Otitis media with effusion in young children. Clinical practice guideline number 12. 1994.

  28. Rosenfeld RM. An evidence-based approach to treating otitis media. Pediatr Clin North Am. 1996 Dec. 43(6):1165-81. [Medline].

  29. [Guideline] Rosenfeld RM, Shin JJ, Schwartz SR, Coggins R, Gagnon L, Hackell JM, et al. Clinical Practice Guideline: Otitis Media with Effusion (Update). Otolaryngol Head Neck Surg. 2016 Feb. 154 (1 Suppl):S1-S41. [Medline]. [Full Text].

  30. Barclay L. Tympanostomy Tube Guideline Issued by Multidisciplinary Team. Available at http://www.medscape.com/viewarticle/807157. Accessed: July 9, 2013.

  31. Rosenfeld RM, Schwartz SR, Pynnonen MA, Tunkel DE, Hussey HM, Fichera JS, et al. Clinical practice guideline: tympanostomy tubes in children--executive summary. Otolaryngol Head Neck Surg. 2013 Jul. 149(1):8-16. [Medline].

  32. van Dongen TM, van der Heijden GJ, Venekamp RP, Rovers MM, Schilder AG. A trial of treatment for acute otorrhea in children with tympanostomy tubes. N Engl J Med. 2014 Feb 20. 370(8):723-33. [Medline].

  33. Bluestone CD. Role of surgery for otitis media in the era of resistant bacteria. Pediatr Infect Dis J. 1998 Nov. 17(11):1090-8; discussion 1099-100. [Medline].

  34. Prymula R, Peeters P, Chrobok V, et al. Pneumococcal capsular polysaccharides conjugated to protein D for prevention of acute otitis media caused by both Streptococcus pneumoniae and non-typable Haemophilus influenzae: a randomised double-blind efficacy study. Lancet. 2006 Mar 4. 367(9512):740-8. [Medline].

  35. Coker TR, Chan LS, Newberry SJ, Limbos MA, Suttorp MJ, Shekelle PG, et al. Diagnosis, Microbial Epidemiology, and Antibiotic Treatment of Acute Otitis Media in Children: A Systematic Review. JAMA. 2010 Nov 17. 304(19):2161-2169. [Medline].

  36. Norhayati MN, Ho JJ, Azman MY. Influenza vaccines for preventing acute otitis media in infants and children. Cochrane Database Syst Rev. 2015 Mar 24. 3:CD010089. [Medline].

  37. Foshee WS, Steele RW. Should prophylactic antibiotics be used for the otitis-media-prone child?. Pediatr Infect Forum. 2000. 2:2-7.

 
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Diagram of the normal tympanic membrane anatomy.
Healthy tympanic membrane.
Acute otitis media with purulent effusion behind a bulging tympanic membrane.
Chronic otitis media with a retraction pocket of the pars flaccida.
Cholesteatoma of the pars flaccida.
Central/pars tensa tympanic membrane perforation with a healthy middle ear membrane.
Central/pars tensa tympanic membrane perforation with a tympanostomy tube in place.
Various tympanostomy tube styles and sizes.
Initial presentation of a young girl with chronic right ear pain and multiple untreated middle ear infections.
Acute coalescent mastoiditis with a Bezold abscess in a young girl who presented with chronic right ear pain and multiple untreated middle ear infections.
A young girl who presented with chronic right ear pain and multiple untreated middle ear infections on the operating table for mastoidectomy and drainage of Bezold abscess.
Aspirating pus from the Bezold abscess for Gram staining, culturing, and sensitivity testing in a young girl who presented with chronic right ear pain and multiple untreated middle ear infections.
Surgical incision to aspirate pus in a young girl who presented with chronic right ear pain and multiple untreated middle ear infections.
Freer elevator demonstrating extension of an abscess cavity from the mastoid into the neck in a young girl who presented with chronic right ear pain and multiple untreated middle ear infections.
Incision is closed and a drain is placed in the abscess cavity in a young girl who presented with chronic right ear pain and multiple untreated middle ear infections.
Postoperative bandage in a young girl who presented with chronic right ear pain and multiple untreated middle ear infections.
The wound now appears clean and dry on postoperative day 4. This young girl initially presented with chronic right ear pain and multiple untreated middle ear infections.
Postoperative day 4: Mom is smiling. This young girl initially presented with chronic right ear pain and multiple untreated middle ear infections.
 
 
 
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