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Middle Ear, Acute Otitis Media, Medical Treatment
Updated: Jan 17, 2008
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.
Pathophysiology
Obstruction of the eustachian tube appears to be the most important antecedent event associated with 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. 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 usefulinfutureyears.
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 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
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Further Reading
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
