eMedicine Specialties > Otolaryngology and Facial Plastic Surgery > Middle Ear & Mastoid

Middle Ear, Acute Otitis Media, Medical Treatment

John D Donaldson, MD, FRCS(C), FAAP, FACS, Chairman, Board of Directors, Lee Memorial Health System; President-elect, Florida Pediatric Society

Updated: Sep 28, 2009

Introduction

Background

In America, acute otitis media (AOM) is the most common affliction necessitating medical therapy for children younger than 5 years. The total annual cost to society for this disease and for otitis media with effusion (OME) runs into the billions of dollars. Yet, despite research into prevention and therapy, the costs of this disease continue to rise while the incidence remains unabated. The emergence of antimicrobial-resistant bacteria requires reevaluation of the traditional management of otitis media (OM).

AOM is defined by convention as the first 3 weeks of a process in which the middle ear shows the signs and symptoms of acute inflammation. OME is defined as the presence of fluid in the middle ear with accompanying conductive hearing loss and without concomitant symptoms or signs of acuity. OME is classified as subacute when it persists from 3 weeks to 3 months after the onset of AOM and is classified as chronic thereafter.

Tympanic membrane of a person with 12 hours of ear pain, slight tympanic membrane bulge, and slight meniscus of purulent effusion at bottom of tympanic membrane. Reproduced with permission from Isaacson G: The natural history of a treated episode of acute otitis media. Pediatrics. 1996; 98(5): 968-7.

Pathophysiology

Obstruction of the eustachian tube appears to be the most important antecedent event associated with acute otitis media (AOM). The vast majority of AOM episodes are triggered by an upper respiratory tract infection (URTI) involving the nasopharynx. The infection is usually of viral origin, but allergic and other inflammatory conditions involving the eustachian tube may create a similar outcome. Inflammation in the nasopharynx extends to the medial end of the eustachian tube, creating stasis and inflammation, which, in turn, alter the pressure within the middle ear. These changes may be either negative (most common) or positive, relative to ambient pressure. Stasis also permits pathogenic bacteria to colonize the normally sterile middle ear space by direct extension from the nasopharynx by reflux, aspiration, or active insufflation.

The response is the establishment of an acute inflammatory reaction characterized by typical vasodilatation, exudation, leukocyte invasion, phagocytosis, and local immunological responses within the middle ear cleft, which yields the clinical pattern of AOM.

In a minority of otitis-prone children, the eustachian tube is patulous or hypotonic. Children with neuromuscular disorders or abnormalities of the first or second arch are most likely "too open" and are predisposed to reflux of nasopharyngeal contents into the middle ear cleft. To become pathogenic in hollow organs, such as the ear or sinus, most bacteria must adhere to the mucosal lining. Viral infections that attack and damage mucosal linings of respiratory tracts may facilitate the ability of the bacteria to become pathogenic in the nasopharynx, eustachian tube, and middle ear cleft. This postulation might explain the recovery of viral antigens from middle ear aspirates in children with AOM, while only rarely is the actual virus isolated. Data have also been presented indicating that mucosal damage by endotoxins secreted by bacterial invaders may similarly enhance the adhesion of pathogens to mucosal surfaces.

Etiology and Microbiology - The Role of the Virus

Viral infection in the nasopharynx with subsequent inflammation of the orifice and mucosa of the eustachian tube has long been understood as part of the pathogenesis of AOM, although the complete role of the virus is not fully understood. Concurrent or antecedent URTIs are identified in at least a quarter of all attacks of AOM in children, but the virus itself seldom appears as the pathogen in the middle ear. Clements has shown that the administration of trivalent influenza A vaccine decreases the frequency of AOM during the influenza season.²⁰ Viruses have been recovered with increasing frequency as techniques to identify them by direct culture and by indirect means (eg, enzyme-linked immunosorbent assay) have improved. On direct culture, the yield is less than 10%, with the respiratory syncytial virus (RSV) recovered most frequently; the influenza virus is a distant second.

When an enzyme-linked immunosorbent assay is performed on middle ear aspirates, the presence of viral antigens is detected in approximately a quarter of the samples. RSV is the virus most frequently detected by this method. The presence of viruses in the middle ear effusion may influence the outcome of therapy for OM. Results of outcome studies have been mixed, ranging from no effect to evidence of prolongation of acuity and effusion when viruses are present in persons with AOM.

Respiratory syncytial virus

Because of the strong association of RSV with AOM, the practitioner must be familiar with this pathogen. Most commonly, RSV is associated with bronchiolitis and pneumonia in very young persons, but it may cause acute respiratory disease in persons of any age group. In northern climates, RSV is normally identified during annual epidemics in the winter and early spring, but it should be considered in any neonate with lethargy, irritability, or apnea, with or without OM. In older infants and children, respiratory symptoms are usually more prominent, making diagnosis easier.

A large RNA paramyxovirus, RSV was identified early as a pathogen that appeared to create long-term pulmonary complications, primarily asthma, in up to half the infants with bronchiolitis. RSV may be particularly lethal for children with congenital heart disease, cystic fibrosis, immunodeficiency, bronchopulmonary dysplasia, or prematurity of less than 37 weeks gestational age. RSV-specific intravenous immunoglobulin prophylaxis is recommended only for high-risk children. When treating a child with concomitant pneumonia or other systemic disease and OM, the practitioner must ensure appropriate diagnosis and management of all aspects of the child's illness. Drainage of the ear by tympanocentesis or myringotomy for culture and therapy may be necessary in some cases. Drainage is mandatory in neonates who are septic or in children who are immunosuppressed.

Bacterial Pathogens in Acute Otitis Media

Pathogenic bacteria are recovered from the middle ear effusion in at least half the children with AOM, and bacterial DNA or cell wall debris is found in another quarter to a third of specimens previously classified as sterile. Four bacteria, ie, Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, and Streptococcus pyogenes, are responsible for the preponderance of episodes of AOM in persons older than 6 weeks. Other bacteria recovered and implicated in AOM include Staphylococcus aureus, Streptococcus viridans, and Pseudomonas aeruginosa.

The emergence of resistance to antimicrobial agents is of increasing importance in the management of AOM and other bacterial illnesses. The various mechanisms used by bacteria to confer this resistance will be delineated as the common pathologic agents linked to AOM are described.

S pneumoniae

This bacterium is the most common etiologic agent responsible for AOM and for invasive bacterial infections in children of all age groups. S pneumoniae is a gram-positive diplococcus with 90 identified serotypes (classified based on the polysaccharide antigen), the frequency of which varies between age groups and geography. Upon direct culture, various studies have shown these bacteria to be responsible for 29-40% of isolates, but pneumococcal antigens are recovered from approximately a third of those cultures classified as sterile. Pneumococcal infections are probably responsible for at least half the episodes of AOM. Serotypes 4, 6B, 9V, 14, 18C, 19F, and 23F are responsible for most invasive pneumococcal disease in America; in ear aspirates from patients with AOM, serotypes 19 (23%), 23 (12.5%), 6 (12%), 14 (10%), 3 (8.5%), and 18 (6%) are isolated most commonly. The polyvalent pneumococcal vaccine confers immunity to approximately 85% of those serotypes responsible for AOM.

Until recently, this bacterium was susceptible to almost all common antibiotics, including penicillin G, erythromycin, and even most sulfonamides. Alteration of the cell wall's penicillin-binding protein has led to widespread resistance to beta-lactam compounds, macrolides, and sulfonamides by alteration of the antimicrobial target. These mutations are termed multidrug-resistant strains. Resistance rates as high as 40% have been reported for these 3 therapeutic antimicrobial groups. Serotypes 6B, 9V, 14, 19A, 19F, and 23F have the highest frequency of resistance to penicillin.

Ceftriaxone, cefotaxime, rifampin, and vancomycin still appear to have therapeutic efficacy, as does immunization with polyvalent pneumococcal vaccine for prevention. Unfortunately, polysaccharide antigens are not immunogenic early in life. To overcome this problem, conjugated antigens, in which the polysaccharide antigen is attached to a protein carrier, may be administered to induce production of antibodies to these bacterial capsular polysaccharides. Some conjugated antigens (eg, vaccinations for H influenzae type b [Hib]) are in widespread use.

A heptavalent vaccine to S pneumoniae is now in widespread use and appears to have made an impact on the number of cases of invasive pneumococcal disease. This vaccine confers long-term immunity to 7 of the most common and invasive strains. Emerging evidence suggests that other serotypes are beginning to be recovered more frequently in ear and sinus infections. This might render the vaccine less useful in future years.

H influenzae

In middle ear aspirates from patients with AOM, H influenzae is the second most frequently isolated bacterium and is responsible for approximately 20% of episodes in preschool children. The frequency may be higher in otitis-prone children, older children, and adults who have received the pneumococcal vaccine. The bacterium is a small, pleomorphic, gram-negative coccobacillus. Those bacteria encapsulated with a polysaccharide coating are classified into 6 distinct types (a-f), while nonencapsulated types are termed nontypeable and are responsible for the great majority of AOM episodes. (The nonencapsulated strains have been subtyped biochemically and antigenically, but, to date, this classification has limited clinical application).

Traditionally, Hib has been found responsible for most invasive illnesses attributed to these bacteria and for meningitis, epiglottitis, and septicemia. Hib accounts for only 10% of all episodes of AOM in which H influenzae is recovered. In areas of the world where the aforementioned Hib-conjugated vaccine is administered early in life, risks from this potentially lethal strain have greatly diminished. Antimicrobial resistance by these bacteria is almost exclusively (95%) caused by the formation of a single enzyme, triethylenemelamine 1 lactamase, and, in some series, is formed by as many as 40% of all nontypeable strains. This resistance is overcome relatively easily by using blocking agents, extended-coverage cephalosporins, broad-spectrum macrolides, or sulfonamides.

H influenzae may participate more widely than previously demonstrated in head and neck infections. One of the principle mechanisms is related to the ability of the bacterium to hide and recover from antibiotic action by forming a biofilm. This is a mucous complex in which the bacteria hides from actions noted. Research has focused on enhancing penetration and/or dissolving the biofilm protection.

M catarrhalis

In the mid 1970s, this common organism was classified as nonpathogenic in middle ear infections, although, when previously known as Neisseria catarrhalis, it constituted approximately 10% of all isolates from middle ear aspirates. At that time, M catarrhalis was almost universally susceptible to ampicillin-type penicillins. Twenty years and 2 name changes later (ie, N catarrhalis to Branhamella catarrhalis to M catarrhalis), it is isolated in up to a quarter of children with AOM, and resistance to the ampicillin-type beta-lactams is almost universal.

M catarrhalis is a gram-negative diplococcus and is considered part of the normal flora of the human upper respiratory tract. Resistance is conferred by the secretion of multiple isoenzymes of lactamase, which may be plasmid or chromosomal in origin and which may be inducible (ie, present only in low levels until a substrate is provided). More than 1 isoenzyme may be secreted by a single bacterium. To date, almost all forms are blocked by clavulanic acid, and most are still susceptible to sulfonamides, lactamase-stable cephalosporins, or broad-spectrum macrolides. M catarrhalis is often found to coexist with other airway pathogens. The lactamases (cephalosporinases) that M catarrhalis secretes may protect those other bacteria from antimicrobial agents to which the second target pathogen might ordinarily be susceptible.

S pyogenes

This bacterium, group A streptococci (GAS), while still occupying the fourth spot in frequency of isolates from ears with AOM, has shown a steady decline in frequency of recovery from the ear and in virulence over the past half-century. Similarly, a substantial decline in the major complications of streptococcal infection, rheumatic fever, glomerulonephritis, and scarlet fever has occurred. GAS may be associated with streptococcal toxic shock syndrome, which may include coagulopathy, soft tissue necrosis or fasciitis, desquamating rash, and liver or renal involvement. GAS, a gram-positive coccus, is primarily a pathogen of the pharynx, with more than 80 distinct M-protein strains identified. Currently, with the improvement in primary care and the availability of rapid identification tests, early aggressive treatment is normally instituted against this bacterium, which has shown minimal ability to develop resistance to antimicrobial agents.

Acute necrotic OM was associated with scarlet fever in the early 1900s; however, the condition was also associated with measles, pneumonia, and influenza. Generally, the patient was extremely ill with the systemic component of the disease and presented with a spontaneous perforation shortly after the onset of otalgia.

Early inspection of the ear would show the perforation to be moderate to large; within days, significant evidence of tissue necrosis would be observed, perhaps including the entire tympanic membrane, ossicles, tympanic mucoperiosteum, or the bone of the mastoid air cells. The patient would demonstrate a marked conductive hearing loss, although sensorineural loss was not uncommon. Pathologically, the ear showed a marked paucity of the normal vascular proliferation associated with an inflammatory reaction. Instead, a complete loss of the vascularity normally associated with vasculitis or toxin exposure occurred. Healing was never normal; tissue was replaced by epithelial invasion or scar tissue formation.

In industrialized societies, acute necrotic OM is now primarily of historic interest. The disease is still reported in aboriginal populations living in areas where modern medicine has not yet penetrated. Interestingly, according to historical research by Robin Brown, Thomas Edison appears to have experienced the sequelae of this condition.

For acute coalescent mastoiditis, GAS also appeared to be the most prominent organism recovered from patients with this condition in the preantibiotic era. In the 1990s, GAS relinquished this distinction to S pneumoniae, but they remain prominent pathogens when this disease is encountered in very young persons.

Other aerobic pathogens

Except in neonates and children with chronic disease, few other pathogens have been demonstrated in aspirates from the middle ears of immunologically intact individuals. S aureus is rarely recovered, except in Japan, where studies indicate a somewhat higher incidence (up to 10%). Mycobacterium tuberculosis is most often associated with chronic OM, but it should be considered when a patient presents with painless otorrhea as an initial complaint. Consider any patient with a compromised immune system at risk for such an opportunistic infection. Chlamydia pneumonia has been shown to be an uncommon but significant pathogen in persons with AOM and responds only to macrolide therapy.

Anaerobic bacteria

Anaerobic bacteria have been recovered from the middle ears of children with AOM, but the data do not support a prominent role for these microorganisms in persons with OM, at least in the acute form. When recovered from ears of children with AOM, the anaerobic pathogen most often is not the sole pathogen cultured.

Acute otitis media in the neonatal period

In the perinatal period, the gram-negative bacteria Escherichia coli, Enterococcus species, and group B S pyogenes are the most common etiological agents responsible for sepsis and meningitis. These agents are often recovered from the middle ear, although the total percentage is probably less than 10% of neonates with AOM. S pneumoniae remains the most common pathogen responsible for AOM in all age groups, including neonates. The nonencapsulated H influenzae and nontypeable varieties may be invasive in these infants and constitute the second most common pathogens recovered from the ear. Because bacteremia is common in all neonates with AOM, tympanocentesis should be performed for both diagnosis and therapy in any infant with signs of AOM or generalized sepsis and any middle ear effusion.

Immunology in Acute Otitis Media

Immunological activity may play a significant role in the frequency of AOM and its outcome. While most research has focused on the immunological aspects of OME, certain relationships between AOM and the patient's immune status have been demonstrated. First, the production of antibodies may promote the clearance of a middle ear effusion following an acute attack. Second, previous exposure or immunization may have a preventative role by suppressing colonization of the nasopharynx by pathogens. Third, the formation of antibodies during an attack may prevent or modify future attacks. Unfortunately, antibodies to both S pneumoniae and H influenzae are of the polysaccharide type and develop late unless conjugated to proteins. Finally, minor and/or transient immunological defects may give rise to recurrent OM.

Much attention has been focused on the immunoglobulins and the patient's ability to form them. Immunoglobulin G2 and immunoglobulin G4 are responsible for immunity against polysaccharide antigens; deficiencies in the formation of these antibodies invariably lead to OM. Many patients with Down syndrome have been demonstrated to have decreased function of immunoglobulin A, immunoglobulin G2, and/or immunoglobulin G4, partially explaining their increased risk for chronic rhinitis and OM.

The immunologic aspects of AOM are not confined to the middle ear. The nasopharynx plays an important role in the pathogenesis of AOM, and immunologic modifications in this lymphoid tissue provide some protection from pathogens by preventing their adherence to mucosal surfaces. The presence of nasopharyngeal immunoglobulin A antibodies to pneumolysin toxin released by pneumococcal autolysis appears to protect against invasion by healthy pneumococci. Conversely, not all immunoglobulins in the nasopharynx are protective. Bernstein describes effects of immunoglobulin E hypersensitivity or hyperimmune effects on the eustachian tube mucosa. The allergic response in the nasopharyngeal end of the eustachian tube promotes stasis and the subsequent formation of a middle ear effusion.

If immunological therapy to prevent AOM is to be found, successful development of vaccines that are effective against non-typeable H influenzae and all serotypes of S pneumoniae is necessary. Some progress is being reported on isolating antigens in the former group. A summary of current vaccine research by the National Institute of Health (NIH) is available.¹

Frequency

United States

Seventy percent of all children experience one or more attacks of acute otitis media (AOM) before their second birthday. A recent study from Pittsburgh prospectively followed urban and rural children for the first 2 years of life.² The study indicates that children experience incidence rates of middle ear effusion episodes of approximately 48%, 79%, and 91% at age 6 months, 1 year, and 2 years, respectively. The peak incidence of AOM is in children aged 3-18 months. Some infants may experience their first attack shortly after birth and are considered otitis prone, ie, at risk for recurrent OM. In the Pittsburgh study, the incidence was highest among poor urban children.

International

The difference in incidence between nations is influenced by racial, socioeconomic, and climatic factors.

Mortality/Morbidity

Death is rare in the era of modern medicine.

Race

Definite racial differences exist in the incidence of AOM. Native Americans and Inuit have very high rates of acute and chronic ear infection, while African Americans appear to have a slightly lower rate than white children living in the same communities.

Sex

The incidence is slightly higher in boys than in girls.

Age

Children aged 6-11 months appear particularly susceptible to AOM, with frequency declining around age 18-20 months. A small percentage of children develop this disease later in life, often in the fourth and early fifth year. After the eruption of permanent teeth, incidence drops dramatically, although some otitis-prone individuals continue to have acute episodes into adulthood. Occasionally, an adult with no previous history of ear disease, but with an acute viral URTI, presents with AOM.

Clinical

History

The history of AOM varies with age, but a number of constant features manifest during the otitis-prone years. Irritability or feeding difficulties may be the only indication of a septic focus in the neonate. Older children begin to demonstrate a consistent presence of fever (with or without a coexistent URTI) and otalgia or ear tugging. These latter symptoms are not entirely exclusive to AOM; teething pain or pharyngitis (particularly coxsackievirus infection) can mimic these symptoms. In older children and adults, hearing loss becomes a constant feature of AOM and OME, with reports of ear stuffiness noted even before the detection of middle ear fluid. Otalgia without hearing loss or fever is observed in adults with external otitis, dental abscess, or pain referred from the temporomandibular joint. Orthodontic appliances often elicit referred pain as the dental occlusion is altered.

Physical

A thorough clinical examination has no substitute. Pneumatic otoscopy is the standard of care in the diagnosis of AOM and chronic OM. In acute disease, the tympanic membrane normally demonstrates signs of inflammation, beginning with reddening of the mucosa and progressing to the formation of purulent middle ear effusion and poor tympanic mobility. The tympanic membrane may bulge in the posterior quadrants, and the superficial epithelial layer may exhibit a scalded appearance. Perforation of the tympanic membrane is not unusual as the process advances, most frequently in posterior or inferior quadrants. Prior to or instead of a single perforation, an opaque serumlike exudate is sometimes seen oozing through the entire tympanic membrane.

With perforation and in the absence of a coexistent viral infection, the patient generally experiences rapid relief of pain and fever. The discharge initially is purulent, although it may be thin and watery or bloody; pulsation of the otorrhea is common. Otorrhea from acute perforation normally lasts 1-2 days before spontaneous healing occurs. Otorrhea may persist if the perforation is accompanied by mucosal swelling or polypoid changes, which can act as a ball valve. Other considerations include the following:

• Bullous myringitis
  • Pneumatic otoscopy is an important diagnostic tool when differentiating AOM from acute bullous myringitis. The latter, in its purest form, manifests 10-14 days following a viral infection and causes severe localized otalgia without middle ear effusion.
  • The bullae or blebs may contain serous or hemorrhagic fluid and may extend onto the adjacent canal wall. Pain is relieved by puncturing the bleb. Similar blebs may occur in association with AOM.
  • These patients demonstrate more systemic symptoms and continue to have pain associated with purulent middle ear effusion, which persists following rupture of the blebs.
• Immunosuppressed patients
  • Remember that the above descriptions are for patients who are immunocompetent. Children who are immunosuppressed, particularly those undergoing chemotherapy, may not manifest the typical inflammatory responses described.
  • In these patients, the simultaneous appearance of systemic sepsis and a serous middle ear effusion might be the only indicators of AOM.
• Danger signs of possible impending complications: These include (1) sagging of the posterior canal wall, (2) puckering of the attic, and (3) swelling of postauricular areas with loss of the skin crease.
• Systemic examination considerations
  • A finding of AOM does not relieve the practitioner of the responsibility to search for coexistent related or unrelated conditions. This responsibility is particularly important when antimicrobial agents are prescribed, in order to ensure appropriate simultaneous coverage of coexistent infections such as AOM with streptococcal pharyngitis or mycoplasmal pneumonia.
  • Transtympanic measurements of temperature in children with middle ear effusions have been shown to be inconsistent. Accordingly, measure body temperature via oral, rectal, or axillary methods.

Causes

The following are proven risk factors for OM:

• Patient factors
  • Prematurity and low birth weight
  • Young age
  • Early onset
  • Family history
  • Race - Native American, Inuit, Australian aborigine
  • Altered immunity
  • Craniofacial abnormalities
  • Neuromuscular disease
  • Allergy
• Environmental factors
• Day care
• Crowded living conditions
• Low socioeconomic status
• Tobacco and pollutant exposure
• Use of pacifier
• Prone sleeping position
• Fall or winter season
• Not breastfed, prolonged bottle use

Differential Diagnoses

External Ear, Infections

Other Problems to Be Considered

External otitis
Dental pain
Temporomandibular joint pain
Acute viral pharyngitis
Trauma to the ear

Workup

Laboratory Studies

Culture and sensitivity of a specimen from a fresh perforation or a tympanocentesis may be helpful.

Imaging Studies

CT scanning may be necessary to determine if a complication has occurred; otherwise, imaging studies are unnecessary. MRI might be more appropriate to diagnose suspected intracranial complications.

Other Tests

• Audiometry
  • All children with AOM have conductive hearing loss associated with the middle ear effusion; consequently, testing in the acute phase is probably unhelpful.
  • Tympanometry may assist in the diagnosis of middle ear effusion but, for the skilled pneumatic otoscopist, is seldom necessary.

Procedures

• Perform tympanocentesis in the following patients:
  • Neonates younger than 6 weeks with AOM
  • Patients who are immunocompromised
  • Patients in whom adequate antimicrobial treatment has failed
  • Patients with a complication that requires a culture for adequate therapy

Treatment

Medical Care

AOM has been described as a self-limiting disease provided the patient does not develop a complication. This is an old reference, but in the new millennium, practitioners are forced to observe the lessons of history because these may serve as our models of life without effective antimicrobial agents. Presently, a chorus of advocates recommends withholding antibiotic therapy for patients with AOM under terms such as watchful waiting or wait-and-see. As expected from long-known data, most of these children do well, but a recent study from England observes that the rate of mastoiditis increased in children at a rate that is, essentially, the inverse of the decrease in prescriptions for acute otitis.

Despite these advocates, the overwhelming consensus remains that antibiotics are the initial therapy of choice for AOM for 3 very valid reasons. First, after the institution of antibiotic therapy, a marked decline in the suppurative complications of AOM is noted. Second, practitioners cannot predict with certainty which patients will develop complications. Third, studies have demonstrated that the use of antibiotics improves patient outcomes in both the early and late phases of AOM.

Recently, some order has been brought to the discussions of antibiotic use under the auspices of the Centers for Disease Control and Prevention and by the Agency for Health Care Policy and Research, both agencies of the US government. The Centers for Disease Control and Prevention published 6 principles of appropriate antibiotic use in an attempt to bring precepts of good public health and responsible therapy to the discussion while minimizing the selection of resistant strains of bacteria within the community. These principles are listed below.

• Principles for judicious use of antimicrobials in the treatment of AOM
  • Classify episodes of OM as AOM or OME.
  • Antimicrobials are indicated for treatment of AOM; however, diagnosis requires documented middle ear effusion and signs or symptoms of acute local or systemic illness.
  • Uncomplicated AOM may be treated with a 5- to 7-day course of antimicrobials in certain patients older than 2 years.
  • Antimicrobials are not indicated for the initial treatment of OME; treatment may be indicated if effusions persist for longer than 3 months.
  • Persistent OME after therapy for AOM is expected and does not require re-treatment with antimicrobials.
  • Reserve antimicrobial prophylaxis for controlling recurrent AOM, defined as 3 or more distinct, well-documented episodes in 6 months or 4 or more episodes in 12 months.
• Antibiotic therapy
  • Selection of an antibiotic, in the absence of culture results obtained from tympanocentesis, should have 2 objectives. First, the antibiotic should cover most of the common bacterial pathogens detailed earlier in this article. Second, the antibiotic must be individualized for the child with regard to allergy, tolerance, previous exposure to antibiotics, cost, and community resistance levels.
  • The duration of therapy is also somewhat empiric, and data indicate that significant numbers of children do not receive prescribed antibiotics beyond relief of acute symptoms. Ten to 14 days of therapy has been traditional and is convenient for office scheduling, but it may not necessarily be more efficacious than 5 days of therapy, or even 2 days.
  • Studies have demonstrated that short-duration therapy may not be appropriate in children younger than 2 years who appear prone to failure even after 14 days of therapy. Mandel showed that when an effusion-free ear is the prime objective, 20 days of antibiotic therapy achieves improved outcomes versus 10 days of therapy or placebo. However, after 90 days, no difference in the groups existed and recurrence was not prevented by the additional therapy.
  • The administration of prescribed antimicrobials may differ from recommendations for the same antibiotic when used for soft tissue infections.
  • Pulse-dosing antibiotics, when administered for infections of hollow organs, such as the ear or sinuses, appear to have efficacy due to poorly understood antimicrobial mechanisms, increased compliance on the part of the patient or parent, and slower penetration into and removal from middle ear effusion.
  • Subminimal serum levels of antibiotics have been shown to disrupt adhesive bonds between bacteria and mucosal cell walls and to provide a postantibiotic effect, in which the reproduction of bacteria is disrupted for a period of hours after exposure to antibiotics. Similarly, a leukocyte-enhancing action has been demonstrated at these low concentrations. When used in this manner, a marked variation in the effectiveness of individual antibiotics and susceptibility for the various etiologic agents exists.
  • Generally, beta-lactam antibiotics are most successful against gram-positive pathogens for both disruption of adhesion and postantibiotic effect.
  • Amoxicillin (erythromycin/sulfisoxazole in patients who are allergic to penicillin) remains the initial treatment of choice in children with AOM.
  • With the emergence of resistant strains, the practitioner may need to select an alternative antimicrobial therapy from either a broad-spectrum beta-lactamase–resistant cephalosporin or a combination drug such as amoxicillin-clavulanate or trimethoprim-sulfamethoxazole. Combination therapy may help prevent the emergence of resistance by mutation, provided the pathogen is initially sensitive to both components. Efficacy and dosages for selected antimicrobials are provided in the Medication section.
  • With the emergence of multidrug-resistant S pneumoniae (MDRSP), oral therapy consisting of amoxicillin and amoxicillin-clavulanate may have efficacy when the total amoxicillin dose reaches 80-100 mg/kg/d.
  • If a child does not respond to an antibiotic within 48 hours and concurrently develops local and systemic signs of toxicity, this may indicate resistance to the selected drug. Treatment options include an empirical change of antimicrobial agent or a drainage procedure with culture. Failure to improve with antibiotic therapy may indicate coexistent viral infection in children with prolonged acute symptoms.
• Other medical therapies
  • Analgesics and antipyretics have a definite role in the symptomatic management of AOM.
  • Decongestants and antihistamines do not appear to have efficacy either early or late in the acute process, although they may relieve coexistent nasal symptoms.
  • Systemic steroids have no demonstrated role in the acute phase.

Surgical Care

Tympanocentesis and myringotomy are the procedures used to treat AOM.

• Tympanocentesis, in its purest form, is a diagnostic procedure that gives the clinician access to acute or chronic middle ear effusions for culture and other evaluations.
  • Generally, perform tympanocentesis without anesthesia, after sterilization of the ear canal with isopropyl alcohol or povidone-iodine solution (Betadine). Insert a needle through the anterior portion of the tympanic membrane, and aspirate the contents of the middle ear into a sterile trap for identification of microbes and their properties.
  • Consider tympanocentesis in (1) children who are immunosuppressed or immunocompromised, (2) neonates with AOM (they are more likely to have an unusual or more invasive pathogen), (3) patients in whom antimicrobial therapy has failed and who continue to experience local or systemic signs of sepsis, and (4) patients who have had a complication of AOM in conjunction with attempts to recover the etiological agent from other sites (eg, cerebrospinal fluid, blood).
  • Additionally, tympanocentesis remains a valuable research tool in the evaluation of new antimicrobial agents for efficacy in AOM and for identification of host defense mechanisms or flaws in the middle ear immunochemistry.
• A tympanocentesis may be converted to a myringotomy and become therapeutic by enlarging the hole in the tympanic membrane, often by spreading the edges with microalligator forceps or suction tip. Instilling antibiotic drops and suctioning the middle ear are possible through the myringotomy. Typically, the patient experiences prompt relief of local symptoms. Culture results must be obtained before extension of the incision.
• The use of a carbon dioxide laser in myringotomy on children with AOM has been promoted widely and directly to the consumer by the manufacturers of these instruments; proponents claim to have ushered in a new treatment for AOM without the use of antimicrobials. While undoubtedly a boon to the otolaryngologist who is less technically adept, emerging studies demonstrate little or no change in efficacy over standard myringotomy.
• If the patient has a suppurative complication of the temporal bone and requisite prolonged drainage seems likely, the insertion of a tympanostomy tube may be needed. In most instances, general anesthesia or sedation is necessary in older children because topical anesthesia is relatively ineffective in acutely inflamed tympanic membranes. With increasing antimicrobial resistance, surgical intervention in the form of tympanostomy tube placement can be expected to increase in the coming years, after having fallen into disfavor in the past 2 decades when resistance was less of a factor. In the author's practice, children younger than 15 months and those who attend day care centers are most likely to require surgery.

Consultations

Consultation is seldom necessary, although some otolaryngologists might be more comfortable having the pediatrician provide all the primary care.

Medication

Antibiotics are the only medications with demonstrated efficacy in the management of AOM. Most antibiotics can be administered once or twice daily to improve compliance and to avoid the necessity of sending medication to school or day care centers. The following list excludes medications that have reduced activity against common pathogens or that have significant adverse effects without other redeeming features to warrant inclusion.

Antibiotics

Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.

Amoxicillin (Amoxil, Trimox, Wymox)

DOC for management of AOM. Interferes with synthesis of cell wall mucopeptides during active multiplication, resulting in bactericidal activity against susceptible bacteria.

Dosing

Adult

250-500 mg PO q8h

Pediatric

90 mg/kg/d PO q8-12h for all initial therapy for AOM

Interactions

Reduces efficacy of oral contraceptives

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dose in renal impairment; may enhance risk of candidiasis

Amoxicillin/clavulanate (Augmentin)

Combination drug that includes a blocking agent (clavulanic acid).

Dosing

Adult

250-500 mg amoxicillin with 62.5-125 mg clavulanate PO q8h

Pediatric

90 mg/kg/d PO of Amoxicillin component for recurrent AOM

Interactions

Coadministration with warfarin or heparin increases risk of bleeding

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Give for a minimum of 10 d to eliminate organism and prevent sequelae (eg, endocarditis, rheumatic fever); following treatment, perform cultures to confirm eradication of streptococci

Erythromycin ethylsuccinate/sulfisoxazole (E.E.S. 400)

Doses supplied in 200 mg/5 mL (erythromycin) and 600 mg/5 mL (sulfisoxazole). Widely used for individuals who are penicillin-sensitive. Well absorbed from GI tract but best administered on full stomach to avoid GI upset.

Dosing

Adult

Not used

Pediatric

50 mg/kg/d of erythromycin component divided PO q8-12h

Interactions

Coadministration may increase toxicity of theophylline, digoxin, carbamazepine, and cyclosporine; may potentiate anticoagulant effects of warfarin; coadministration with lovastatin and simvastatin increases risk of rhabdomyolysis

Contraindications

Documented hypersensitivity; hepatic impairment

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in liver disease; estolate formulation may cause cholestatic jaundice; adverse GI effects are common (give doses pc); discontinue use if nausea, vomiting, malaise, abdominal colic, or fever occur

Trimethoprim/sulfamethoxazole (Bactrim, Bactrim DS, Septra, Septra DS)

Inhibits bacterial growth by inhibiting synthesis of dihydrofolic acid.

Dosing

Adult

160 mg TMP with 800 mg SMZ PO bid

Pediatric

8 mg/kg TMP with 40 mg/kg SMZ PO divided q12h

Interactions

May increase PT when used with warfarin (perform coagulation tests and adjust dose accordingly); coadministration with dapsone may increase blood levels of both drugs; coadministration of diuretics increases incidence of thrombocytopenia purpura in elderly persons; phenytoin levels may increase with coadministration; may potentiate effects of methotrexate in bone marrow depression; hypoglycemic response to sulfonylureas may increase with coadministration; may increase levels of zidovudine

Contraindications

Documented hypersensitivity; megaloblastic anemia due to folate deficiency

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Discontinue at first appearance of skin rash or sign of adverse reaction; obtain CBC counts frequently; discontinue therapy if significant hematologic changes occur; goiter, diuresis, and hypoglycemia may occur with sulfonamides; prolonged IV infusions or high doses may cause bone marrow depression (if signs occur, give 5-15 mg/d leucovorin); caution in folate deficiency (eg, chronic alcoholism, elderly persons, those receiving anticonvulsant therapy, those with malabsorption syndrome); hemolysis may occur in persons with G-6-PD deficiency; AIDS patients may not tolerate or respond to TMP-SMZ; caution in renal or hepatic impairment (perform urinalyses and renal function tests during therapy); give fluids to prevent crystalluria and stone formation

Cefixime (Suprax)

By binding to one or more of the penicillin-binding proteins, arrests bacterial cell wall synthesis and inhibits bacterial growth.

Dosing

Adult

400 mg PO qd or divided bid

Pediatric

8 mg/kg PO qd or divided bid

Interactions

Coadministration of aminoglycosides increase nephrotoxicity; probenecid may increase effects

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dose in renal impairment

Cefuroxime Axetil (Ceftin)

Second-generation cephalosporin that maintains gram-positive activity of first-generation cephalosporins; adds activity against Proteus mirabilis, H influenzae, E coli, Klebsiella pneumoniae, and M catarrhalis.
Condition of patient, severity of infection, and susceptibility of microorganism determine proper dose and route of administration.

Dosing

Adult

250-500 mg PO q12h

Pediatric

15-30 mg/kg/d PO divided q12h

Interactions

Disulfiramlike reactions may occur when alcohol is consumed within 72 h of administration; may increase hypoprothrombinemic effects of anticoagulants; may increase nephrotoxicity in patient receiving potent diuretics (eg, loop diuretics); coadministration with aminoglycosides increase nephrotoxic potential

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Administer half dose if creatinine clearance is 10-30 mL/min and one-quarter dose if <10 mL/min; fungal and microorganism overgrowth may occur with prolonged therapy

Cefprozil (Cefzil)

Binds to one or more of the penicillin-binding proteins, which, in turn, inhibits cell wall synthesis and results in bactericidal activity.

Dosing

Adult

250-500 mg PO q12h

Pediatric

15-30 mg/kg/d PO divided q12h

Interactions

Probenecid increases effect; coadministration with furosemide and aminoglycosides increases nephrotoxic effects

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dosage in renal impairment

Cefpodoxime (Vantin)

Indicated for management of infections caused by susceptible mixed aerobic-anaerobic microorganisms.

Dosing

Adult

100-200 mg PO q12h

Pediatric

10 mg/kg/d PO divided q12h

Interactions

Alcoholic beverages consumed <72 h after administration may produce disulfiramlike reactions; may increase hypoprothrombinemic effects of anticoagulants; coadministration with potent diuretics (eg, loop diuretics) and aminoglycosides may increase nephrotoxicity

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Reduce dosage by half if creatinine clearance is 10-30 mL/min and by three quarters if <10 mL/min; bacterial or fungal overgrowth of nonsusceptible organisms may occur with prolonged or repeated therapy

Cefdinir (Omnicef)

Third-generation cephalosporin indicated for treatment of uncomplicated skin infections.

Dosing

Adult

600 mg PO qd or divided bid

Pediatric

14 mg/kg PO qd or divided bid

Interactions

May increase hypoprothrombinemic effects of anticoagulants; coadministration with potent diuretics (eg, loop diuretics) and aminoglycosides may increase nephrotoxicity

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Reduce dosage by half if creatinine clearance is 10-30 mL/min and by one quarter <10 mL/min; bacterial or fungal overgrowth of nonsusceptible organisms may occur with prolonged or repeated therapy

Clindamycin (Cleocin HCl)

Lincosamide for treatment of serious skin and soft tissue staphylococcal infections. Also effective against aerobic and anaerobic streptococci (except enterococci). Inhibits bacterial growth, possibly by blocking dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest.

Dosing

Adult

600-1800 mg/d PO divided q6-8h

Pediatric

10-25 mg/kg/d PO divided q6-8h

Interactions

Increases duration of neuromuscular blockade induced by tubocurarine and pancuronium; erythromycin may antagonize effects; antidiarrheals may delay absorption

Contraindications

Documented hypersensitivity, blood dyscrasias

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dose in severe hepatic dysfunction; no adjustment necessary in renal insufficiency; associated with severe and possibly fatal colitis by allowing overgrowth of Clostridium difficile

Clarithromycin (Biaxin)

Inhibits bacterial growth, possibly by blocking dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest.

Dosing

Adult

250-500 mg PO q12h

Pediatric

15 mg/kg/d PO divided q12h

Interactions

Toxicity increases with coadministration of fluconazole and pimozide; effects decrease and adverse GI effects may increase with coadministration of rifabutin or rifampin; may increase toxicity of anticoagulants, cyclosporine, tacrolimus, digoxin, omeprazole, carbamazepine, ergot alkaloids, triazolam, and HMG CoA-reductase inhibitors
Plasma levels of certain benzodiazepines may increase, prolonging CNS depression; arrhythmias and increase in QTc intervals occur with disopyramide; coadministration with omeprazole may increase plasma levels of both agents

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Coadministration with ranitidine or bismuth citrate not recommended with CrCl <25 mL/min; give half dose or increase dosing interval if CrCl <30 mL/min; diarrhea may be sign of pseudomembranous colitis; superinfections may occur with prolonged or repeated antibiotic therapies

Azithromycin (Zithromax)

Broad-spectrum macrolide antibiotic. Absorption markedly reduced when taken with food.

Dosing

Adult

500 mg on day 1; then 250 mg/d on days 2-5

Pediatric

10 mg/kg on day 1; then 5 mg/kg on days 2-5

Interactions

May increase toxicity of theophylline, warfarin, and digoxin; effects are reduced with coadministration of aluminum and/or magnesium antacids; nephrotoxicity and neurotoxicity may occur when coadministered with cyclosporine

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Site reactions can occur with IV route; bacterial or fungal overgrowth may result with prolonged antibiotic use; may increase hepatic enzymes and cholestatic jaundice; caution in patients with impaired hepatic function, prolonged QT intervals, or pneumonia; caution in hospitalized, geriatric, or debilitated patients

Ceftriaxone (Rocephin)

Third-generation cephalosporin. Manufacturer has heavily promoted IM use of this drug to physicians and directly to the public for routine treatment of AOM. Subsequently, MDRSP resistance has emerged, making this less effective in many communities. Author believes this drug is best reserved for IV use for management of severe infections. Avoid widespread use for AOM.

Dosing

Adult

1-2 g/d IM for 3 d

Pediatric

50 mg/kg/d IM for 3 d

Interactions

Probenecid may increase levels; coadministration with ethacrynic acid, furosemide, and aminoglycosides may increase nephrotoxicity

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dose in renal impairment; caution in breastfeeding and allergy to penicillin

Follow-up

Further Outpatient Care

• Reexamine patients within 48 hours if no evidence of decreasing acuity manifests, if symptoms become more severe, or at anytime a complication becomes evident. Otherwise, follow-up care is normally scheduled 10-14 days after the acute event.
• Persistent middle ear effusion should be expected at the initial follow-up visit; statistically, only 30% of patients show complete resolution. In the absence of acuity, further treatment is unwarranted, but the patient should be scheduled to return at intervals until the effusion resolves.

Deterrence/Prevention

• Children with recurrent AOM have no effusion within the middle ear cleft between attacks of acute disease. Management of this condition is confined to the following 7 options:
  • Episodic management: Each episode is considered a new attack and is treated with antibiotics; the patient is monitored until the episode resolves.
  • Immunotherapy: Preventative treatment involves the administration of a conjugated heptavalent pneumococcal vaccine. Recent studies indicate that while the vaccine is intended to combat invasive effects in infants, immunized children have a reduced incidence of AOM, a reduced need for antibiotic therapy or tympanostomy tubes, and a reduced risk of invasion or hearing loss.³ No vaccine exists for nontypeable H influenzae. Correspondingly, research has been commenced on immunization against the common viruses that induce AOM, ie, RSV, adenoviruses, influenzae A and B viruses, and rhinoviruses.
  • Antibiotic prophylaxis: This option is becoming less popular as resistant strains emerge. Amoxicillin and sulfisoxazole have both been used extensively. The former has better coverage against S pyogenes but may promote nasopharyngeal colonization with beta-lactam–resistant pneumococci and H influenzae. Reserve prophylaxis for otitis-prone children who are younger than 2 years or in day care and who have had 3 or more attacks in a 6-month period. Both amoxicillin and sulfisoxazole can cause serum sickness reactions.
  • Tympanostomy tube placement: This decreases episodes of AOM. Ventilation has been used more frequently when evidence of MDRSP exists. In the author's practice, resistance is noted most frequently in infants and children aged 6-14 months who are in day care. Tympanostomy tubes are also beneficial in children with recurrent AOM and coexistent reactive airway disease and should be considered when recurrent episodes of AOM destabilize control of other systemic conditions. Examples include alterations in seizure thresholds, otitic hydrocephalus, or control of diabetes. Similarly, early tympanostomy tube placement might be considered for children with sensorineural hearing loss, speech development abnormalities, or learning dysfunction to give the child a consistent hearing model.
  • Control of rhinitis: Control of nasal inflammation in children, whether caused by an allergy or recurrent infection, appears to decrease the recurrence of AOM. Trials are being conducted to determine the efficacy of topical nasal steroids for decreasing middle ear disease, in an attempt to confirm anecdotal information that supports this treatment modality.
  • Environmental manipulation: Some of the risk factors discussed under epidemiology can be removed by such efforts as alteration of child care arrangements, provision of a tobacco-free living space, and cessation of bottle use in children older than 1 year.
  • Adenoidectomy: In children with recurrent AOM, adenoidectomy has demonstrated efficacy. However, determining which children will benefit from this treatment modality is not yet possible. Few pediatric otolaryngologists recommend adenoidectomy initially over tympanostomy tube placement alone, unless coexistent nasal symptoms are present. The procedure might be considered for older children who require replacement of their tympanostomy tubes.

Complications

• The complications of AOM are classified by location as the disease spreads beyond the mucosal structures of the middle ear cleft. Complications are as follows:
  • Intratemporal - Perforation of the tympanic membrane, acute coalescent mastoiditis, facial nerve palsy, acute labyrinthitis, petrositis, acute necrotic otitis, or development of chronic OM
  • Intracranial - Meningitis, encephalitis, brain abscess, otitis hydrocephalus, subarachnoid abscess, subdural abscess, or sigmoid sinus thrombosis
  • Systemic - Bacteremia, septic arthritis, or bacterial endocarditis

Prognosis

• With effective antibiotic therapy, the systemic signs of fever and lethargy should begin to dissipate, along with the localized pain, within 48 hours.
  • Note that middle ear effusion and conductive hearing loss can be expected to persist well beyond the duration of therapy, with up to 70% of children expected to have middle ear effusion after 14 days, 50% at 1 month, 20% at 2 months, and 10% after 3 months, irrespective of therapy.
  • Children with fewer than 3 episodes are 3 times more likely to resolve with a single course of antibiotics, as are children who develop AOM in nonwinter months.
  • In most instances, persistent middle ear effusion can merely be observed without antimicrobial therapy; however, a second course of either the same antibiotic or a drug of a different mechanism of action may be warranted to prevent a relapse before resolution.
  • Expect patients to recover the conductive hearing loss associated with AOM.

Patient Education

• For excellent patient education resources, see eMedicine's Headache Center and Teeth and Mouth Center. Also, visit eMedicine's patient education articles Sinus Infection and Teething.

Miscellaneous

Medicolegal Pitfalls

• Medicolegal problems associated with AOM are rare. Problems are primarily related to failure to diagnose and/or appropriately manage a complication of AOM.

Multimedia

Media file 1: Healthy tympanic membrane.

Media file 2: Tympanic membrane of a person with 12 hours of ear pain, slight tympanic membrane bulge, and slight meniscus of purulent effusion at bottom of tympanic membrane. Reproduced with permission from Isaacson G: The natural history of a treated episode of acute otitis media. Pediatrics. 1996; 98(5): 968-7.

References

1. Xin-Xing Gu, M.D. National Institutes of Health. National Institute on Deafness and other Communication Disorders. Available at http://www.nidcd.nih.gov/research/scientists/gux.asp.

2. Paradise JL, Rockette HE, Colborn DK, et al. Otitis media in 2253 Pittsburgh-area infants: prevalence and risk factors during the first two years of life. Pediatrics. Mar 1997;99(3):318-33. [Medline].

3. Fireman B, Black SB, Shinefield HR, et al. Impact of the pneumococcal conjugate vaccine on otitis media. Pediatr Infect Dis J. Jan 2003;22(1):10-6. [Medline].

4. American Academy of Pediatrics. Group A streptococcal infections. In: Red Book: Report of the Committee on Infectious Diseases. 27^th ed. Elk Grove Village, Ill: 2006:610-620.

5. American Academy of Pediatrics. Haemophilus influenzae infections. In: Red Book: Report of the Committee on Infectious Diseases. 27^th ed. Elk Grove Village, Ill: 2006:310-3318.

6. American Academy of Pediatrics. Pneumococcal infections. In: Red Book: Report of the Committee on Infectious Diseases. 27^th ed. Elk Grove Village, Ill: 2006:525-537.

7. American Academy of Pediatrics. Respiratory syncytial virus. In: Red Book: Report of the Committee on Infectious Diseases. 27^th ed. Elk Grove Village, Ill: 2006:560-566.

8. Arola M, Ruuskanen O, Ziegler T, et al. Clinical role of respiratory virus infection in acute otitis media. Pediatrics. Dec 1990;86(6):848-55. [Medline].

9. Arola M, Ziegler T, Ruuskanen O. Respiratory virus infection as a cause of prolonged symptoms in acute otitis media. J Pediatr. May 1990;116(5):697-701. [Medline].

10. Barenkamp SJ, Shurin PA, Marchant CD, Karasic RB, Pelton SI, Howie VM. Do children with recurrent Haemophilus influenzae otitis media become infected with a new organism or reacquire the original strain?. J Pediatr. Oct 1984;105(4):533-7. [Medline].

11. Berman S, Roark R. Factors influencing outcome in children treated with antibiotics for acute otitis media. Pediatr Infect Dis J. Jan 1993;12(1):20-4. [Medline].

12. Bernstein JM. The role of IgE-mediated hypersensitivity in the development of otitis media with effusion. Otolaryngol Clin North Am. Feb 1992;25(1):197-211. [Medline].

13. Block SL. Causative pathogens, antibiotic resistance and therapeutic considerations in acute otitis media. Pediatr Infect Dis J. Apr 1997;16(4):449-56. [Medline].

14. Bluestone CD. State of the art: definitions and classifications. In: Lim DJ, ed. Recent Advances in Otitis Media with Effusion. Philadelphia, Pa: BC Decker; 1984:. 1-4.

15. Bluestone CD, Klein JO. Epidemiology. In: Otitis Media in Infants and Children. 2nd ed. Philadelphia, Pa: WB Saunders; 1988:. 31-43.

16. Bluestone CD, Klein JO. Otitis media, atelectasis, and eustachian tube dysfunction. 2nd ed. Philadelphia, Pa: WB Saunders; 1988:. 39-72.

17. Bluestone CD, Klein JO. Otitis media, atelectasis, and eustachian tube dysfunction. In: Bluestone CD, Stool SE, eds. Pediatric Otolaryngology. 2nd ed. Philadelphia, Pa: WB Saunders; 1990:. 320-487.

18. Byrns PJ, Bondy J, Glazner JE, Berman S. Utilization of services for otitis media by children enrolled in Medicaid. Arch Pediatr Adolesc Med. Apr 1997;151(4):407-13. [Medline].

19. Chonmaitree T, Owen MJ, Patel JA, et al. Effect of viral respiratory tract infection on outcome of acute otitis media. J Pediatr. Jun 1992;120(6):856-62. [Medline].

20. Clements DA, Langdon L, Bland C, Walter E. Influenza A vaccine decreases the incidence of otitis media in 6- to 30- month-old children in day care. Arch Pediatr Adolesc Med. Oct 1995;149(10):1113-7. [Medline].

21. Culpepper L, Froom J. Routine antimicrobial treatment of acute otitis media: is it necessary?. JAMA. Nov 26 1997;278(20):1643-5. [Medline].

22. Daigler GE, Markello SJ, Cummings KM. The effect of indoor air pollutants on otitis media and asthma in children. Laryngoscope. Mar 1991;101(3):293-6. [Medline].

23. Doern GV. Trends in antimicrobial susceptibility of bacterial pathogens of the respiratory tract. Am J Med. Dec 29 1995;99(6B):3S-7S. [Medline].

24. Donaldson JD, Martin GF, Maltby CC, Seywerd EB. The efficacy of pulse-dosed antibiotic therapy in the management of persistent otitis media with effusion. J Otolaryngol. Jun 1990;19(3):175-8. [Medline].

25. Dowell SF, Marcy M, Phillips WR. Otitis media - Principles of judicious use of antimicrobial agents. Pediatrics. 1998;101(1-2):165-71.

26. Duncan B, Ey J, Holberg CJ, et al. Exclusive breast-feeding for at least 4 months protects against otitis media. Pediatrics. May 1993;91(5):867-72. [Medline].

27. Gaillat J. [Clinical manifestations of Chlamydia pneumoniae infections]. Rev Med Interne. 1996;17(12):987-91. [Medline].

28. Gannon MM, Haggard MP, Golding J. Sleeping position: a new environmental risk for otitis media? Abstract of Sixth International Symposium on Recent Advances in Otitis. Ft. Lauderdale, Fla; 1995.

29. Gliklich RE, Eavey RD, Iannuzzi RA, Camacho AE. A contemporary analysis of acute mastoiditis. Arch Otolaryngol Head Neck Surg. Feb 1996;122(2):135-9. [Medline].

30. Greenfield BJ, Selesnick SH, Fisher L, et al. Aural tuberculosis. Am J Otol. Mar 1995;16(2):175-82. [Medline].

31. Hando S, Nonomura N, Niijima H, et al. Adherence of Haemophilus influenzae to middle ear mucosa injured by killed H. influenzae. Auris Nasus Larynx. 1992;19(2):69-74. [Medline].

32. Loh RK, Harth SC, Thong YH, Ferrante A. Immunoglobulin G subclass deficiency and predisposition to infection in Down's syndrome. Pediatr Infect Dis J. Aug 1990;9(8):547-51. [Medline].

33. Mandel EM, Casselbrant ML, Rockette HE, et al. Efficacy of 20- versus 10-day antimicrobial treatment for acute otitis media. Pediatrics. Jul 1995;96(1 Pt 1):5-13. [Medline].

34. Marx J, Osguthorpe JD, Parsons G. Day care and the incidence of otitis media in young children. Otolaryngol Head Neck Surg. Jun 1995;112(6):695-9. [Medline].

35. Niemela M, Uhari M, Mottonen M. A pacifier increases the risk of recurrent acute otitis media in children in day care centers. Pediatrics. Nov 1995;96(5 Pt 1):884-8. [Medline].

36. Palva T, Lehtinen T. Pneumococcal antigens and endotoxin in effusions from patients with secretory otitis media. Int J Pediatr Otorhinolaryngol. Dec 1987;14(2-3):123-8. [Medline].

37. Paradise JL. Short-course antimicrobial treatment for acute otitis media: not best for infants and young children. JAMA. Nov 26 1997;278(20):1640-2. [Medline].

38. Poehling KA, Szilagyi PG, Grijalva CG, Martin SW, LaFleur B, Mitchel E. Reduction of frequent otitis media and pressure-equalizing tube insertions in children after introduction of pneumococcal conjugate vaccine. Pediatrics. Apr 2007;119(4):707-15. [Medline].

39. Reed BD, Lutz LJ, Zazove P, Ratcliffe SD. Compliance with acute otitis media treatment. J Fam Pract. Nov 1984;19(5):627-32. [Medline].

40. Roberton DM, Colgan T, Ferrante A, Jones C, Mermelstein N, Sennhauser F. IgG subclass concentrations in absolute, partial and transient IgA deficiency in childhood. Pediatr Infect Dis J. Aug 1990;9(8 Suppl):S41-5. [Medline].

41. Rosenfeld RM. What to expect from medical treatment of otitis media. Pediatr Infect Dis J. Sep 1995;14(9):731-7; quiz 738. [Medline].

42. Rosenfeld RM, Culpepper L, Doyle KJ. Clinical practice guideline: Otitis media with effusion. Otolaryngol Head Neck Surg. May 2004;130(5 Suppl):S95-118. [Medline].

43. Rovers MM, Glasziou P, Appelman CL, Burke P, McCormick DP, Damoiseaux RA. Predictors of pain and/or fever at 3 to 7 days for children with acute otitis media not treated initially with antibiotics: a meta-analysis of individual patient data. Pediatrics. Mar 2007;119(3):579-85. [Medline].

44. Shambaugh GE, Glasscock ME. Pathology and clinical course of inflammatory diseases of the middle ear. In: Surgery of the Ear. 3rd ed. WB Saunders Co;1980:191, 200-207.

45. Shimamura K, Shigemi H, Kurono Y, Mogi G. The role of bacterial adherence in otitis media with effusion. Arch Otolaryngol Head Neck Surg. Oct 1990;116(10):1143-6. [Medline].

46. Shurin PA, Howie VM, Pelton SI, Ploussard JH, Klein JO. Bacterial etiology of otitis media during the first six weeks of life. J Pediatr. Jun 1978;92(6):893-6. [Medline].

47. Shurin PA, Rehmus JM, Johnson CE, Marchant CD, Carlin SA, Super DM. Bacterial polysaccharide immune globulin for prophylaxis of acute otitis media in high-risk children. J Pediatr. Nov 1993;123(5):801-10. [Medline].

48. Stenstrom R, Bernard PA, Ben-Simhon H. Exposure to environmental tobacco smoke as a risk factor for recurrent acute otitis media in children under the age of five years. Int J Pediatr Otorhinolaryngol. Aug 1993;27(2):127-36. [Medline].

49. Stool SE, Berg AO, Berman S. Otitis Media with Effusion in Young Children (Clinical Practice Guideline Number 12). AHCPR Publication No. 94-0622. Bethesda, Md: U.S. Agency for Health Care Policy and Research; July, 1994.

50. Sung BS, Chonmaitree T, Broemeling LD, et al. Association of rhinovirus infection with poor bacteriologic outcome of bacterial-viral otitis media. Clin Infect Dis. Jul 1993;17(1):38-42. [Medline].

51. Takata GS, Chan LS, Shekelle P, Morton SC, Mason W, Marcy SM. Evidence assessment of management of acute otitis media: I. The role of antibiotics in treatment of uncomplicated acute otitis media. Pediatrics. Aug 2001;108(2):239-47. [Medline].

52. Teele DW, Klein JO, Rosner B. Epidemiology of otitis media during the first seven years of life in children in greater Boston: a prospective, cohort study. J Infect Dis. Jul 1989;160(1):83-94. [Medline].

53. The Annals of Otology, Rhinology & Laryngology. Workshop on epidemiology of otitis media. Ann Otol Rhinol Laryngol Suppl. Jul 1990;149:1-60. [Medline].

54. Virolainen A, Jero J, Kayhty H, et al. Nasopharyngeal antibodies to pneumococcal pneumolysin in children with acute otitis media. Clin Diagn Lab Immunol. Nov 1995;2(6):704-7. [Medline].

55. Wald ER. Anaerobes in otitis media and sinusitis. Ann Otol Rhinol Laryngol Suppl. Sep 1991;154:14-6. [Medline].

56. Wald ER. Otitis media and sinusitis: a clinical update. Clin Updates Pediatr Infect Dis. 1995;1:1-4.

Keywords

acute otitis media, AOM, OM, acute suppurative otitis media, acute otitis, otitis media with effusion, OME, chronic otitis media, COM, ear infection, ear ache, eustachian tube destruction, upper respiratory infection, URI, upper respiratory tract infection, URTI, bacterial ear infection, viral ear infection, Streptococcus pneumoniae, S pneumoniae, Haemophilus influenzae, H influenzae, Moraxella catarrhalis, M catarrhalis, Streptococcus pyogenes, S pyogenes, Staphylococcus aureus, S aureus, Streptococcus viridans, S viridans, Pseudomonas aeruginosa, P aeruginosa, staph infection, strep infection, otorrhea, ear bacteremia, middle ear effusion, otalgia, ear tugging, tympanocentesis, myringotomy

Contributor Information and Disclosures

Author

John D Donaldson, MD, FRCS(C), FAAP, FACS, Chairman, Board of Directors, Lee Memorial Health System; President-elect, Florida Pediatric Society
John D Donaldson, MD, FRCS(C), FAAP, FACS is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery, American Academy of Pediatrics, American College of Surgeons, and American Society of Pediatric Otolaryngology
Disclosure: Nothing to disclose.

Medical Editor

Carol A Bauer, MD, FACS, Associate Professor of Surgery, Division of Otolaryngology-Head and Neck Surgery, Southern Illinois University School of Medicine
Carol A Bauer, MD, FACS is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery, American Neurological Association, and Society of University Otolaryngologists-Head and Neck Surgeons
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Gregory C Allen, MD, Assistant Professor, Department of Otolaryngology-Head and Neck Surgery, University of Colorado School of Medicine
Gregory C Allen, MD is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery, American Academy of Pediatrics, American Cleft Palate/Craniofacial Association, American College of Surgeons, American Laryngological Rhinological and Otological Society, American Medical Association, Christian Medical & Dental Society, and Colorado Medical Society
Disclosure: Nothing to disclose.

CME Editor

Christopher L Slack, MD, Otolaryngology-Facial Plastic Surgery, Private Practice, Associated Coastal ENT; Medical Director, Treasure Coast Sleep Disorders
Christopher L Slack, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, and American Medical Association
Disclosure: Nothing to disclose.

Chief Editor

Arlen D Meyers, MD, MBA, Professor, Department of Otolaryngology-Head and Neck Surgery, 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, and American Head and Neck Society
Disclosure: Covidien Corp Consulting fee Consulting; US Tobacco Corporation unstricted gift unknown; Axis Three Corporation Ownership interest Consulting; Omni Biosciences Ownership interest Consulting; Sentegra Ownership interest Board membership; Syndicom Ownership interest Consulting; Oxlo  Consulting; Medvoy Ownership interest Management position

Clinical guidelines

Cincinnati Children's Hospital Medical Center. Evidence based clinical practice guideline for medical management of acute otitis media in children 2 months to 13 years of age. Cincinnati (OH): Cincinnati Children's Hospital Medical Center; 2004 Oct. 16 p.

University of Michigan Health System (UMHS). Otitis media. Ann Arbor (MI): University of Michigan Health System (UMHS); 2007 July. 12 p.

© 1994- by Medscape.
All Rights Reserved
(http://www.medscape.com/public/copyright)