7/1/13

Otitis Media Clinical Presentation

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Otitis Media Clinical Presentation

Author: Muhammad Waseem, MD, MS; Chief Editor: Glenn C Isaacson, MD, FACS, FAAP more... Updated: Apr 1, 2013

History
Suspect acute otitis media (AOM), with or without effusion, in children with a history of the following symptoms: Head and neck 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 ETD when the child is in a recumbent position. Otorrhea: Discharge may come from the middle ear through a recently perforated TM, through a preexisting TT, or through another perforation. For trauma patients, excluding a basilar skull fracture with associated cerebrospinal fluid (CSF) otorrhea is important. Headache Concurrent or recent URI symptoms (eg, cough, rhinorrhea, sinus congestion) General Two thirds of children with AOM have a history of fever, although fevers greater than 40C 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. GI tract: Symptoms include anorexia, nausea, vomiting, and diarrhea. 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, although 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 widely varies based 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 exposure (ie, secondhand) to tobacco smoke Group daycare attendance Seasonality: AOM prevalence is much higher in winter and early spring than in summer and early fall.
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Supine bottle feeding (ie, bottle propping)

Physical
Pneumatic otoscopy remains the standard examination technique for patients with suspected OM. When performed correctly, this technique is 90% sensitive and 80% specific for diagnosis of AOM, and findings are more accurate than with 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 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. Below are examination techniques used in the diagnosis of OM.

Pneumatic otoscopy examination

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 4 TM characteristics: 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. 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. 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
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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 for OM: Adjunctive techniques help identify patients with asymptomatic OME, which may comprise 10% of cases. 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 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. No accepted breakpoint standards have been established, so 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.

Causes
A multitude of host, infectious, allergic, and environmental factors contribute to OM development. Host factors Immune system: The immature immune systems of infants or the impaired immune systems of patients with congenital immune deficiencies, HIV infection, or diabetes may be involved in the development of OM. OM is an infectious disease that prospers in an environment of decreased immune defenses. The interplay between pathogens and host immune defense plays a role in disease progression. Patel et al (2009) found higher interleukin (IL)6 levels in patients with OM who also had influenza and adenoviral infections, whereas IL-1-beta (IL-1-beta) levels were higher in patients who developed OM following URI.[2] In another study, Skovbjerg et al (2009) found that middle ear effusions with culturable pathogenic bacteria were associated with higher levels of IL-1beta, IL-8, and IL-10 than sterile effusions.[3] Familial (genetic) predisposition: Although familial clustering of OM has been demonstrated in studies that examined genetic associations of OM, separating genetic factors from environmental influences has been difficult. No specific genes have been linked to OM susceptibility. As with most disease processes, effects of environmental exposures on genetic expression probably play an
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important role in OM pathogenesis. Mucins: The role of mucins in OME has been described. Mucins are responsible for gel-like properties of mucus secretions. The middle ear mucin gene expression is unique compared with the nasopharynx. Abnormalities of this gene expression, especially upregulation of MUC5B in the ear, may have a predominant role in OME. Anatomic abnormality: Children with anatomic abnormalities of the palate and associated musculature, especially the tensor veli palantini, exhibit marked ETD and have higher risk for OM. Specific anomalies that correlate with high prevalence of OM include cleft palate, Crouzon syndrome or Apert syndrome, Down syndrome, and Treacher Collins syndrome. Physiologic dysfunction: Abnormalities in the physiologic function of the ET mucosa, including ciliary dysfunction and edema, increase the risk of bacterial invasion of the middle ear and the resultant OME. Children with cochlear implants have a high incidence of OM, especially chronic OM and cholesteatoma formation. One study described a relationship between laryngopharyngeal reflux and chronic OM (COM); the authors concluded that reflux work-up should be performed as part of COM investigations, and, if reflux is confirmed, reflux treatment should be initiated in addition to treatment of primary disease.[4] Vitamin A deficiency is associated with pediatric upper respiratory infections and AOM. Obesity has been linked to an increased incidence of OM, although the causal factor is unknown. Speculations include alteration of intrinsic cytokine profile, increased gastroesophageal reflux with alterations of the oral flora, and/or fat accumulation; all of these have been linked with an increased incidence of OM. Conversely, OM may increase the risk of obesity by altering the taste buds.[5] Infectious factors Bacterial pathogens The most common bacterial pathogen in AOM is Streptococcus pneumoniae, followed by nontypeable Haemophilus influenzae and Moraxella catarrhalis . These 3 organisms are responsible for more than 95% of all AOM cases with a bacterial etiology. In infants younger than 6 weeks, gram-negative bacilli (eg, Escherichia coli, Klebsiella species, and Pseudomonas aeruginosa) play a much larger role in AOM, causing 20% of cases. S pneumoniae and H influenzae are also the most common pathogens in this age group. Staphylococcus aureus has also been found as a pathogen in this age group in some studies, but more recent studies suggest that the flora in these young infants may be that of usual AOM in children older than 6 weeks. Many experts had proposed that the MEE associated with OME was sterile because cultures of middle ear fluid obtained by tympanocentesis often did not grow bacteria. This view is changing as newer studies show 30-50% incidence of positive results in middle ear bacterial cultures in patients with chronic MEE. These cultures grow a wide range of aerobic and anaerobic bacteria; S pneumoniae, H influenzae, M catarrhalis, and group A streptococci are the most common. M catarrhalis induced AOM differs from AOM caused by other bacterial pathogens in several ways. It is characterized by higher a proportion of mixed infections, younger age at the time of diagnosis, lower risk of spontaneous perforation of the tympanic membrane, and an absence of mastoiditis.[6] Further evidence for the presence of bacteria in the MEE of patients with OME was provided by studies using polymerase chain reaction (PCR) assay to detect bacterial DNA in MEE samples that were determined to be sterile using standard bacterial culture techniques. In one such study using PCR assay, 77.3% of the MEE samples had positive results for one or more common AOM pathogens (eg, S pneumoniae, H influenzae, M catarrhalis ). In chronic suppurative OM, the most frequently isolated organisms include P aeruginosa, S aureus, Corynebacterium species, and Klebsiella pneumoniae. An unanswered question is whether these pathogens invade the middle ear from the nasopharynx via the ET (as do the bacteria responsible for AOM) or whether they enter through the perforated TM or a TT from the EAC. The role of Helicobacter pylori in children with OME has been increasingly recognized. Evidence that this agent might be responsible for OME comes from its isolation from middle ear and tonsillar and adenoidal tissue in patients with OME. Alloiococcus otitidis is a newly recognized species of gram-positive bacterium that has been recently discovered as a pathogen associated with OME.[7, 8] This organism is the most frequent bacterium in AOM, as well as in OME. It has also been detected in patients who had been treated with antibiotics, such as beta-lactams or erythromycin, suggesting that these agents may not be sufficiently effective to eliminate this organism. Further investigation is
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needed to reveal the clinical role of the organism in OM. Viral pathogens Because acute viral URI is a prominent risk factor for AOM development, most investigators have suspected a role for respiratory viruses in AOM pathogenesis. Many studies have substantiated this suspicion by showing how certain respiratory viruses can cause inflammatory changes to the respiratory mucosa that lead to ETD, increased bacterial colonization and adherence, and, eventually, AOM. Studies have also shown that viruses can alter the host-immune response to AOM, thereby contributing to prolonged middle ear fluid production and development of chronic OME. The viruses most commonly associated with AOM are respiratory syncytial virus (RSV), influenza viruses, parainfluenza viruses, rhinovirus, and adenovirus. Human parechovirus 1 (HPeV1) infection is associated with OM and cough in pediatric patients.[9] OM developed in 50% of 3-month follow-up periods that yielded evidence of HPeV1 infection but in only 14% of the HPeV1-negative periods; in recurring OM, the middle ear fluid samples were positive for HPeV in 15% of episodes. Factors related to allergies The relationship between allergies and OM remains unclear. In children younger than 4 years, the immune system is still developing, and allergies are unlikely to play a role in recurrent AOM in this age group. Although much evidence suggests that allergies contribute to the pathogenesis of OM in older children, extensive evidence refutes the role of allergies in the etiology of middle ear disease. The following is a brief list of evidence for and against the etiologic role of allergy in OM: Many patients with OM have concomitant allergic respiratory disease (eg, allergic rhinitis, asthma). Many patients with OM have positive results to skin testing or radioallergosorbent testing (RAST). Although mast cells are found in the middle ear mucosa, most studies fail to show significant levels of immunoglobulin E (IgE) or eosinophils in the MEE of patients with OM. OM is most common in the winter and early spring, yet most major allergens (eg, tree and grass pollens) peak in the late spring and early fall. Most patients with concomitant OM and allergy show no marked improvement in middle ear disease with aggressive allergy management, despite marked improvements to nasal and other allergy-related symptoms. Environmental factors Infant feeding methods Many studies report that breastfeeding protects infants against OM. The most recent and best of these studies indicates that this benefit is evident only in children who are breastfed exclusively for the first 3-6 months of life. Breastfeeding of this duration reduces the incidence of OM by 13%. The protective effects of breastfeeding for the first 3-6 months persist 4-12 months after breastfeeding ceases, possibly because delaying onset of the first OM episode reduces recurrence of OM in these children. Passive smoke exposure Many studies have shown a direct relationship between passive smoke exposure and risk of middle ear disease. A recent systematic review of 45 publications dealing with OM and parental smoking showed pooled odds ratios of 1.48 (95% confidence interval [CI] of 1.08-2.04) for recurrent OM, 1.38 (95% CI of 1.23-1.55) for MEE, and 1.3 (95% CI of 1.3-1.6) for AOM.[10] Group daycare attendance Daycare centers create close contact among many children, which increases the risks of respiratory infection, nasopharyngeal colonization with pathogenic microbes, and OM. Many researchers have used meta-analysis to confirm that exposure to other young children (including siblings) in group daycare settings is a major risk factor for OM.[11] A metaanalysis reported that care outside the home conferred a 2.5-fold risk for OM. Other critical reviews of studies on OM and group childcare show heightened odds ratios of 1.6-4.0:1 for center care versus home care. Children who attend daycare centers frequently acquire antibacterial-resistant organisms in their nasopharynx, leading to AOM that may be refractory to antibacterial treatment. American Academy of Pediatrics and American Academy of Family Physicians' guidelines recommend high-dose amoxicillin/clavulanic acid as the antibiotic of choice in the treatment of AOM in children who attend daycare.
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Socioeconomic factors: Socioeconomic status encompasses many independent factors that affect both the risk of OM and the likelihood that OM will be diagnosed.[12] In general, lower socioeconomic status confers higher risk for environmental exposure to parental smoking, bottle-feeding, crowded group daycare, crowded living conditions, and viruses and bacterial pathogens. Compared with children from middle-income and high-income families, children from lower socioeconomic groups use health care resources less frequently, which decreases the likelihood that OM cases will be diagnosed.

Contributor Information and Disclosures

Author Muhammad Waseem, MD, MS Associate Professor of Emergency Medicine in Clinical Pediatrics, 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, and American Medical Association Disclosure: Nothing to disclose. Coauthor(s) Muhammad Aslam, MD Assistant Professor of Pediatrics, Harvard Medical School; Staff Physician, Division of Newborn Medicine, Department of Pediatrics, Massachusetts General Hospital Muhammad Aslam, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Medical Association, Massachusetts Medical Society, and Southern Medical Association Disclosure: Nothing to disclose. Specialty Editor Board 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. 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, Medical Center of Lewisville, 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 is a member of the following medical societies: Alpha Omega Alpha, American Academy of Otolaryngology-Head and Neck Surgery, American Academy of Pediatrics, American College of Surgeons, American Society of Pediatric Otolaryngology, Society for Ear, Nose and Throat Advances in Children, and Texas Medical Association Disclosure: Nothing to disclose. Daniel Rauch, MD, FAAP Director, Pediatric Hospitalist Program, Associate Professor, Department of
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Pediatrics, New York University School of Medicine Daniel Rauch, MD, FAAP is a member of the following medical societies: Ambulatory Pediatric Association, American Academy of Pediatrics, and Society of Hospital Medicine Disclosure: Baxter Honoraria Consulting Chief Editor Glenn C Isaacson, MD, FACS, FAAP Professor of Otolaryngology-Head and Neck Surgery and Pediatrics, Temple University School of Medicine Glenn C Isaacson, MD, FACS, FAAP 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 Laryngological Rhinological and Otological Society, American Society of Pediatric Otolaryngology, and Society of University Otolaryngologists-Head and Neck Surgeons Disclosure: Covidien Honoraria Consulting Additional Contributors The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors, Michael Jones, MD, David Malis, MD, and Leslie Wilson, MD, to the development and writing of this article.

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