OTITIS MEDIA
Jerome O. Klein
Acute otitis media (AOM) is defined as an acute illness marked by the presence of middle ear fluid and inflammation of the mucosa that lines the middle ear space. Otitis media with effusion (OME) is defined by the presence of middle ear fluid without acute signs of illness and usually follows AOM but may also occur as a result of barotrauma or allergy. Synonyms for OME include serous otitis, secretory otitis, glue ear, and middle ear catarrh. Less common chronic variations of otitis media include permanent perforation of the tympanic membrane, and perforation or retraction of the tympanic membrane with trapped epithelium that is unable to spontaneously clear desquamated debris, forming a cholesteatoma. This may occur in the presence of an intact tympanic membrane. Both perforations and cholesteatoma may be associated with recurrent foul-smelling otorrhea, termed chronic suppurative otitis media.
Infection may spread from the middle ear space to contiguous structures such as the mastoid air cells, the petrous bone, and the inner ear. For detailed discussions of the various facets of infections of the middle ear, the reader is referred to the text Otitis Media in Infants and Children by the author and Charles D. Bluestone1 and two Clinical Practice Guidelines: Diagnosis and Management of Acute Otitis Media2 and Otitis Media with Effusion,3 prepared by the American Academy of Pediatrics (AAP) and the American Academy of Family Physicians.
EPIDEMIOLOGY AND GENETICS
Incidence of Otitis Media
Otitis media is a disease of infancy and early childhood. Acute otitis media (AOM) is the most frequent reason that children visit health care facilities in the first 3 years of life and has been one of the most frequent reasons that physicians prescribe antimicrobial agents for infants and children. The peak age-specific attack rate of AOM occurs between 6 and 18 months. Children who have had little or no experience with otitis media by age 3 are unlikely to have subsequent severe or recurrent disease. On average, children have 1.2 and 1.1 episodes of AOM in the first and second years of life, respectively.6 By age 3, children may be categorized into three groups based on diagnoses of AOM: approximately one third have had no episodes of AOM; one third have had one or two episodes; and one third have had three or more episodes.5
Otitis media with effusion (OME) is even more common than AOM. Up to 90% of school age children have OME at some time. In the first year of life, > 50% of children experience OME, increasing to > 60% by 2 years of age. Most episodes resolve spontaneously within 3 months but about 30% of children have recurrent episodes of OME, and 5% to 10% of these episodes persist for 1 year or longer.2
The more severe suppurative complications are infrequent in developed countries where access to medical care is readily available, although these complications are still a frequent cause of morbidity in developing countries. It is unclear whether early prescribing of antibiotics has been responsible for decreasing the incidence of mastoiditis in developed countries.
Risk Features for Acute Otitis Media
Age at first episode of acute otitis media (AOM) is significantly associated with recurrent episodes. Males have a higher incidence of single and recurrent episodes of AOM than do females.6
Genetic predisposition to AOM is suggested by the aggregation of cases in families. A meta-analysis by Uhari and colleagues identified an increase in risk if any other member of the family had had AOM.7Severe and recurrent disease may be associated with genetically determined features, such as skull configuration, or by overt or subtle immunologic defects. Studies of the incidence of otitis media in twins indicate that there is a strong genetic component to the amount of time with otitis media with effusion and the number of episodes of AOM; there was a strong correlation between members of monozygotic twins compared with dizygotic sets.8
Selected racial groups, many in developing countries or hostile environments, appear to be otitis prone. Native Americans and Alaskan and Canadian Inuit infants and children have a high incidence of severe AOM and suppurative complications. A prevalence study of an Apache community found the presence of draining ear or perforation in 8.4% of patients of all ages.9 Several survey studies indicate that African American children have less otitis media than white children11,12 but it is unclear if this is explained by underdiagnosis in the African American community due to less access to medical care, or to difference in the position of the bony eustachian tube among races.12
The increased number of infants and young children in daycare groups has resulted in an increase in respiratory infections, including AOM. Children in daycare not only have more episodes of AOM than children in home care but have more surgical procedures; a study of Pittsburgh children who were observed from birth noted that myringotomy and tympanostomy tube placements were performed in 21% of children in group daycare and in only 3% of children in home care by the second year of life.13 The more children in the daycare group, the more exposures to respiratory pathogens brought to the daycare from the household of each child.
Breast-feeding has been documented to prevent nasopharyngeal colonization14 as well as respiratory infections including AOM.6 Altered host defenses may play a role in recurrent and severe AOM. Among the host issues are anatomic defects (cleft palate, cleft uvula, submucous cleft); alteration of normal physiologic defenses (patulous eustachian tube); congenital or acquired immunologic deficiencies (decreased or absent immunoglobulins, chronic granulomatous disease); malignant neoplasmas that may alter the anatomy of the upper respiratory tract; and drugs that suppress immune processes. An increased incidence of AOM also occurs in children with Down syndrome16 and in children with AIDS.17
Environmental factors, including passive cigarette smoking and environmental pollutants, have come under increased scrutiny as agents responsible for structural and physiologic changes in the respiratory tree.
PATHOPHYSIOLOGY
The middle ear system includes the nasopharynx, the eustachian tube, the middle ear space, and the adjacent structures, including the mastoid air cells and inner ear (see Fig. 369-1). The middle ear is a narrow box or cleft: the vertical and anterior-posterior diameters measure about 15 mm; the transverse diameter measures 2 to 6 mm; and the tympanic membrane diameter is 10 mm (eFig. 243.1 ). The size of the middle ear cavity and the ossicles are the same at birth as in the adult. In infancy, the eustachian tube is short, wide, and in a straight position, permitting easy access of nasopharyngeal flora into the middle ear space. With increasing age, the eustachian tube elongates, narrows, and assumes an oblique position, corresponding to a decrease in the incidence of otitis media as age increases.
The normal physiologic functions of the eustachian tube include pressure regulation or ventilation of the middle ear, which equilibrates gas pressure in the middle ear with atmospheric pressure; protection of the middle ear by anatomic, immunologic, and mucociliary defenses; and clearance or drainage of secretions produced within the middle ear via mucociliary activity and muscular clearance. In acute otitis media (AOM) and otitis media with effusion, one or more of these eustachian tube functions is impaired.
Most episodes of AOM involve the following sequence of events:
1. Congestion of the mucosa of the upper respiratory tract, including the nares, nasopharynx, and eustachian tube (ET), usually due to respiratory viral infection;
2. Swelling of the mucosa of the ET, resulting in obstruction of the narrowest portion of the tube, the isthmus;
3. Obstruction of the ET tube, which results in negative middle ear pressure and accumulation of secretions formed normally by the middle ear mucosa; the mucosa secretions have no egress and fill the middle ear space;
4. Viruses and bacteria that colonize the upper respiratory tract are aspirated or insufflated into the middle ear and multiply in the middle ear fluid, causing a suppurative infection, acute otitis media.
Although appropriate antimicrobial agents sterilize the middle ear infection, fluid may persist in the middle ear for weeks to months. The mean duration of middle ear effusion after an episode of AOM is approximately 23 days, with 10% persisting after 12 weeks (eFig. 243.2 ).
CAUSATIVE ORGANISMS
Our understanding of microbiology of acute otitis media (AOM) has been documented by needle aspiration (tympanocentesis) of the middle ear abscess. The results of many studies have been uniform in demonstrating the dominance of Streptococcus pneumoniae and nontypable Haemophilus influenzae and a minor role for Moraxella catarrhalis. Respiratory viruses alone or combined with bacterial pathogens are present in many middle ear fluids of children with AOM.
Our understanding of the microbiology of AOM is undergoing change based on recognition of new microbiologic phenomena such as biofilms and new microbiologic techniques such as polymerase chain reaction (PCR). The introduction of the pneumococcal conjugate vaccine (PCV7), has led to a decrease in number of episodes of AOM due to vaccine sero-types with resultant increased proportion of nonvaccine pneumococcal serotypes and nontypable H influenzae.
Although there are 90 antigenically distinct serotypes of S pneumoniae, relatively few types are responsible for most AOM. In recent surveys, the most common types responsible for AOM in order of decreasing frequency were types 19F, 23, 14, 6B, and 3.1 PCV7 includes the major serotypes responsible for invasive disease and AOM but lacks coverage for type 3, which is included in a 13-serotype investigational conjugate vaccine (Wyeth Vaccines).
H influenzae was first identified as an important pathogen of acute otitis media (AOM) in the 1940s; for reasons that remain unclear, earlier studies identified the pathogen in few cases or not at all. Studies of children with AOM since the introduction of PCV7 suggest that nontypable H influenzae may replace the pneumococcus as the most frequently isolated pathogen of AOM.23,24 Although H influenzae was considered to be restricted in importance to AOM in preschool children, the organism has been found of equal importance in older children, adolescents, and adults. H influenzae is the primary pathogen in the unique conjunctivitis–acute otitis media syndrome.25
M catarrhalis has been identified in up to 27% of middle ear fluid aspirates of children with AOM but most studies suggest an incidence of less than 10%.26
During the preantibiotic era, otitis media due to group A streptococcus (GAS) was frequently associated with scarlet fever and was often of a destructive form. GAS was the most prevalent organism in cultures taken at myringotomy for acute otitis media (AOM) and the most frequent cause of mastoid infection.27 In recent years, AOM due to GAS is uncommon. A recent survey of the experience of investigators in Beersheva, Israel, identified GAS in 3.1% of 11,311 episodes of AOM28
A variety of microorganisms have been infrequently identified in AOM as the sole focus of infection or part of a systemic or respiratory illness. Mycoplasma pneumoniae has been documented as a cause of bullous myringitis but has rarely been associated with AOM. Chlamydia pneumoniae has been identified in patients with pharyngitis, bronchitis, and pneumonia but infrequently with otitis media. Diphtheritic otitis media may accompany diphtheritic croup and nasopharyngitis; complications are frequent, including destruction of the tympanic membrane and ossicles and invasion of contiguous structures including the mastoid air cells, the temporal bone, and the labyrinth. Mycobacterium tuberculosis is characterized by a painless, watery otorrhea through single or multiple perforations of the tympanic membrane. When acute otitis media occurs as the only apparent focus of tuberculous infection, the disease is usually due to ingestion of infected cow’s milk.
The clinical history suggests that viral infection frequently is the initial event in the development of AOM (see Chapter 241). Respiratory viruses have been isolated from the nasopharynx of up to 50% of children with AOM.29Viruses, viral antigens, and virus presence by polymerase chain reaction have been identified in middle ear fluids alone or in combination with bacterial pathogens.
ACUTE OTITIS MEDIA
CLINICAL FEATURES
Children with acute otitis media (AOM) have rapid onset of nonspecific signs and symptoms including fever, irritability, headache, apathy, anorexia, vomiting, and diarrhea. Fever occurs in one third to two thirds of children with AOM but temperatures of 40°C or more are unusual unless accompanied by invasive bacterial disease or foci elsewhere.
Specific signs of AOM include the following: Patients may experience otalgia or ear pain. In infants, pulling at the ear or irritability may be the only sign of ear pain. Otalgia may also result from external otitis or from disease in the temporomandibular joint, teeth, or pharynx. Earache is not universal in AOM; about one fifth of children in a pediatric practice with AOM did not complain of ear pain, and most of the children were older than age 2.32
The pain is due to pressure of the increasing suppuration in the middle ear and is relieved when the pressure leads to ischemia of the central vessels in the capillary bed of the tympanic membrane. Persistent ischemia leads to necrosis of the tympanic membrane, with rupture and discharge of the contents of the middle ear abscess and virtual elimination of the otalgia. Otorrhea or discharge from the middle ear occurs, following rupture of the tympanic membrane. Parents often report that a child who had cried with pain was relieved and bloody pus was observed on the pillow or pajamas. However, the tympanic membrane is so vascular that the site of perforation may not be evident within 24 hours, and the re-sealed membrane may result in reaccumulation of the purulent middle ear fluid.
Hearing loss is a frequent sign in young infants and may be expressed by verbal children or detected by a parent who sees the child not responding to spoken voice.
Purulent conjunctivitis has been associated with acute otitis media due to nontypable H influenzae. The conjunctivae are injected with pain; there is tearing or purulent discharge associated with signs and symptoms of AOM.23
Swelling about the ear may be due to malignant external otitis media with spread of the infection to the contiguous skin and soft tissues. Rarely, a diabetic or immunocompromised patient may present with pseudomonal otitis externa that spreads via the fissures of Santorini to affect the skull base, and may present with pain and cranial nerve palsies. This condition is known as malignant otitis externa and carries a high mortality rate if not appropriately treated. Postauricular swelling may indicate disease of the mastoid, including periostitis or subperiosteal abscess.
Less common signs and symptoms of acute otitis media include vertigo, nystagmus, and tinnitus.
Otitis media with effusion may be silent in its presenting symptomatology and may be an incidental finding. There may be subjective symptoms such as mild balance disturbance, especially in younger children, or a change in a child’s behavior. The major symptom and concern is hearing loss (see Complications and Outcomes).
DIAGNOSIS
The diagnosis of acute otitis media (AOM) is based on three elements: (1) abrupt onset of signs and symptoms of middle ear inflammation; (2) presence of middle ear effusion identified by any of the following: bulging of the tympanic membrane (TM), limited or absent mobility of the tympanic membrane, or otorrhea; and (3) signs or symptoms of middle ear inflammation such as erythema of the TM or otalgia.2
Normal and abnormal findings on otoscopic examination are shown in Figure 243-1. The otoscopic examination should include evaluation of the position, color, and degree of translucency and mobility of the tympanic membrane. The normal eardrum should be in the neutral position. Mild retraction of the TM usually indicates the presence of negative middle ear pressure, an effusion, or both. Severe retraction of the TM identifies high negative pressure associated with middle ear effusion (MEE). Fullness or bulging of the TM is caused by increased middle ear pressure or MEE.
The normal TM has a ground-glass appearance and is translucent. The otoscopist should be able to look through the TM and visualize the middle ear landmarks. A blue or yellow color identifies MEE seen through a translucent TM. A red TM may indicate inflammation but may also identify engorgement of the blood vessels of the TM caused by crying, sneezing, or nose blowing. The diagnosis of AOM is often made with some uncertainty, particularly in infants and young children due to difficulty with adequate examination of the TM for confirmation of MEE.
FIGURE 243-1. A: Normal tympanic membrane. B: Early acute otitis media (AOM). A mildly erythematous tympanic membrane is seen with a small purulent effusion in the middle ear. C: Acute otitis media (AOM). The middle ear is filled with purulent material behind an erythematous bulging tympanic membrane. D: Otitis media with effusion (OME). A clear amber-colored effusion with a single air-fluid level is seen in the middle ear behind an otherwise normal tympanic membrane. E: Otitis media with effusion (OME). A clear amber-colored effusion with multiple air-fluid levels is seen in the middle ear behind an otherwise normal tympanic membrane. F: Bullous myringitis. A large fluid-filled bulla is seen distorting the surface of the tympanic membrane. This can result from viral or bacterial infections and usually resolves spontaneously. (From Knoop KJ, Stack LB, Storrow AB, Thurman RJ. The Atlas of Emergency Medicine. 3rd ed. New York: McGraw-Hill, 2010. Photo contributor: Richard A. Chole, MD, PhD.)
Pneumatic otoscopy is the most feasible and cost-effective method for diagnosis of AOM and otitis media with effusion. Mobility of the TM is identified by pressure applied to the rubber bulb attached to the pneumatic otoscope. The normal or air-filled middle ear is identified by a brisk movement inward with slight positive pressure and outward with slight negative pressure. MEE or high negative pressure within the middle ear dampens movement of the TM. Movement of the TM is best seen in the posterosuperior quadrant of the TM.
Tympanometry and acoustic reflectometry can supplement penuamtic otoscopy (see Chapter 369). Tympanometry involves varying the pressure in the external canal accompanied by a probe tone. A graphic presentation, the tympanogram, provides information on middle ear pressure and the presence of an air-filled or fluid-filled middle ear space.1 Because tympanometry and pneumatic otoscopy require a seal in the external canal for a few seconds, they may be difficult to perform in the young infant who is irritable due to ear pain. Acoustic reflectometry accompanied by spectral gradient analysis determines the probability of MEE by measuring the response of the eardrum to a frequency sweep in the audible range of 1.8 to 4.4 kHz and provides information on the probability of an air- or a fluid-filled middle ear space.33
MEE can also be demonstrated by needle aspiration, tympanocentesis, observation of fluid in the external canal, or evidence of pus on the pillow or bedding of the child as a result of tympanic membrane perforation.
TREATMENT
Infants and children who are diagnosed with acute otitis media (AOM) traditionally have been treated with an antimicrobial agent with efficacy against the three major bacterial pathogens: S pneumoniae, nontypable H influenzae, and M catarrhalis. An option of withholding therapy and observing the child may be considered for the child who has uncomplicated AOM with mild to moderate signs and symptoms and/or uncertain diagnosis and is older than age 2.
Many children with a diagnosis of AOM do not benefit from antimicrobial agents, including those whose diagnosis is uncertain, those whose AOM is due to a viral pathogen, and those who have AOM due to a bacterial pathogen that resolves spontaneously. Data from double tympanocentesis studies (aspiration at the time of diagnosis of AOM and 3 to 5 days later) in children treated with placebo revealed that approximately 50% of children who had nontypable H influenzae in the initial culture had sterile cultures in the later aspirate, and approximately 20% of children who had S pneumoniae in the initial culture had sterile cultures in the second aspirate.34,35 In many Western European communities, the practice is to withhold antimicrobial agents initially from children diagnosed with AOM. Although a number of clinical trials support an initial observation period, most of these studies have significant flaws in design and execution.2 The 2004 Clinical Practice Guideline suggested criteria for children with AOM who may be initially observed rather than treated with an antimicrobial drug. This includes children older than age 6 months whose diagnosis is uncertain, and children older than age 2 years who do not have severe disease (defined as moderate to severe otalgia or fever equal to or greater than 39°C in whom follow-up can be ensured and antibacterial agents started if symptoms persist or worsen). AOM is a treatable disease in all other children2 (Table 243-1).
Selection of antimicrobial agents is based on clinical and microbiology efficacy, acceptability (eg, taste and texture) of the oral preparation, absence of side effects and toxicity, and convenience of dosing schedule and cost. As of September 2008, 19 drugs have been approved by the US Food and Drug Administration (FDA) for treatment of AOM. Two types of eardrops, ofloxacin otic and ciprofloxacin with dexamethasone, are approved for acute otorrhea in children who have tympanostomy tubes in place.
The drugs of choice for patients who are being treated initially or who have failed initial management with antibacterial agents are listed in Table 243-2. Amoxicillin is the drug of choice for treatment of AOM in patients with a temperature less than 39°C and/or severe otalgia because it continues to be effective, safe, and relatively inexpensive. A dosage of 80 to 90 mg/kg/d in 2 doses provides concentration of the drug in the middle ear sufficient to inhibit susceptible and intermediate nonsusceptible strains of S pneumoniae and many resistant strains. Following administration of antibacterial agents, clinical stabilization should occur during the initial 24 hours, and clinical improvement by 48 to 72 hours. If initially febrile, defervescence usually is observed within 48 to 72 hours. If initial therapy fails (lack of clinical improvement), or the child has a temperature greater than 39°C, and/or moderate or severe otalgia at presentation, the American Academy of Pediatrics (AAP) recommends amoxicillin clavulanate, cefuroxime axetil, or a single dose of intramuscular ceftriaxone.2 A macrolide (erythromycin plus sulfisoxazole, azithromycin, or clarithromycin) is the preferred for therapy of acute otitis media in children who are allergic to β-lactam antimicrobial agents. Duration of therapy is based on data from clinical trials and tradition. The AAP recommends a 10-day course for the oral antimicrobial agents,2 except for azithromycin, which is approved for 1-, 3-, and 5-day courses. The FDA has approved shorter courses of other selected drugs; efpodoxime and cefinir are approved for 5-day courses.
Table 243–1. Guidelines for Management of Acute Otitis Media—American Academy of Pediatrics and American Academy of Family Physicians
The clinical course of the child who is treated with an effective antimicrobial agent results in significant resolution of acute signs and symptoms within 48 to 72 hours. Persistent ear pain or systemic signs, including fever, indicate a need for reevaluation for persistent AOM or foci elsewhere. The child may need change in antimicrobial therapy or a myringotomy. The myringotomy results in immediate relief by draining the abscess and provides information about the pathogen. Myringotomy should be considered for the child who is toxic, who has severe suppurative or nonsuppurative complications (eg, mastoiditis or facial nerve palsy), who fails to improve on repeated antibiotic therapy, or who has an underlying immunodeficiency.
AOM may be associated with severe pain as the middle ear abscess expands and presses against the tympanic membrane. The 2004 American Academy of Pediatrics Clinical Practice Guideline recommended that assessment of pain be included in management of acute otitis media and recommended acetaminophen or ibuprofen for mild to moderate pain and codeine or analogs or myringotomy for severe pain.2
Antihistamines have not been shown to be of any value in management of AOM and may prolong the duration of middle ear effusion.36 Similarly, nasal and oral decongestants administered alone or in combination with an antihistamine may provide symptomatic relief from the effects of nasal congestion but are ineffective for treatment of AOM or otitis media with effusion (OME).2 A short course of systemic corticosteroid therapy is of uncertain efficacy in management of OME in children and is not recommended for infants and children with OME because of its unproven efficacy and potential side effects.2
Table 243–2. Recommended Antibacterial Agents for Treatment of Acute Otitis Media
Surgical management of AOM includes tympanocentesis (needle aspiration of the middle ear infection), myringotomy (an incision in the anterior-inferior quadrant of the tympanic membrane that drains the middle ear abscess), and adenoidectomy. Myringotomy should be considered when the child has acute mastoiditis, labyrinthitis, facial paralysis, or an intracranial suppurative complication such as meningitis. Myringotomy and placement of a tympanostomy tube is extensively used for children with persistent otitis media with effusion and recurrent acute otitis media.3 Adenoidectomy for management of severe and recurrent AOM and OME has been shown to be of value in selected children age 2 and older but remains controversial.2
ACUTE OTITIS MEDIA ASSOCIATED WITH TYMPANOSTOMY TUBES
In a child with tympanostomy tubes, acute otitis media (AOM) may still occur, presenting as a discharging ear, usually without pain or fever. Although this may occur as a result of contaminated water penetrating the tympanostomy tube to enter the middle ear space (eg, bath water, pool water), it is much more likely to occur as a result of a concurrent upper respiratory tract infection. Treatment with antibiotic eardrops is usually effective, although systemic antibiotics (amoxicillin ± clavulanate) may also be indicated, especially if there is a tenacious exudate that may interfere with appropriate administration of the eardrops. A recent advance has been the introduction of quinilone antibiotic eardrops (Floxin, Ciloxan), which are extremely effective, well tolerated, and nonototoxic. An antibiotic and steroid combination eardrop (Cipro HC) may be utilized if desired. However, for antibiotic eardrops to be effective, they must penetrate the tympanostomy tube to reach the middle ear space. Most formulations require at least 7 drops per application to penetrate into the middle ear space. Tragal pumping is important to improve penetration. A proportion of children with recurrent ear discharge may have bacterial colonization of the tympanostomy tube itself, usually because of a bacterial biofilm, which may be extremely resistant to bacterial eradication. In such circumstances, removal of the tympanostomy tube may be required.
OTITIS MEDIA WITH EFFUSION
The likelihood of spontaneous resolution of otitis media with effusion (OME) varies depending upon the cause and duration. After an episode of acute otitis media (AOM), 75% to 90% of residual OME resolves within 3 months, and about 25% of OME of unknown duration in 2-to 4-year-old children resolves within 3 months. If OME is asymptomatic it is likely to resolve spontaneously and intervention is unnecessary. The laterality, duration, and presence and severity of associated symptoms should be documented at periodic reevaluations (every 3 to 6 months). Hearing should be evaluated if the effusion persists for 3 months or longer, and at any time that language, learning problems, or a significant hearing loss is suspected (see Complications and Outcomes below). Children who are otherwise well should be reevaluated at 3- to 6-month intervals until the effusion is no longer present, significant hearing loss is identified, or structural abnormalities of the middle ear are suspected. Medical therapies including antihistamines, decongestants, antimicrobials, and corticosteroids are not beneficial. There is no clear evidence showing a benefit of allergy management for treatment of OME.
Surgical treatment with tympanostomy tubes has been recommended to avoid developmental sequelae due to hearing deficits caused by persistent OME in early childhood. However, a large randomized controlled study that included children with bilateral effusions for > 90 days, or unilateral effusions for > 135 days showed no developmental benefit of early treatment compared to observation with surgical treatment only when bilateral effusion persisted > 6 months and unilateral effusion > 9 months.41 Despite these observations, existing recommendations still suggest that surgery can be considered for children with OME lasting 4 months or longer, or if there is recurrent or persistent OME in children at risk for inadequate follow-up, and in those in whom structural damage to the tympanic membrane or middle ear exists. Tympanostomy tubes are recommended as the initial surgery. Adenoidectomy should not be performed unless a distinct indication exists. If repeat surgery is performed, adenoidectomy plus myringotomy, with or without tube insertion, is recommended.
COMPLICATIONS AND OUTCOMES
Hearing Loss
Hearing loss is the most common complication of otitis media and can be conductive, sensorineural, or both. Some degree of conductive hearing loss is present whenever fluid fills the middle ear space. In acute otitis media, the loss is usually between 15 and 40 dB; the average loss due to acute otitis media or otitis media with effusion is 27 dB.38 Hearing returns to normal thresholds with resolution of the middle ear effusion. Negative pressure in the middle ear, in the absence of middle ear effusion, can also be a cause of hearing loss. Reversible or irreversible sensorineural hearing loss can occur during acute otitis media (AOM) or otitis media with effusion (OME). Reversible sensorineural loss is due to increased tension and stiffness of the round window membrane. Permanent sensorineural hearing loss is most likely due to the spread of infection or products of inflammation through the round window membrane into the labyrinth, development of a perilymphatic fistula in the oval or round window, or suppurative complications such as labyrinthitis or meningitis. Hearing testing is recommended when OME persists for 3 months or longer, or at any time that language delay, learning problems, or a significant hearing loss is suspected (see Chapter 369).
Effect of Otitis Media on Development of the Child
Middle ear effusion and the resulting conductive hearing loss may result in decreased perception of language, impaired development of speech and language, lower scores on tests of cognitive abilities, and poor performance in school. Many studies have been performed relating experience with AOM and OME and developmental outcomes,40 but the differences in design of the studies and inconsistencies of the results limit conclusions about the effect of otitis media on development. Paradise and colleagues found that early placement of ventilating tubes in children with prolonged time spent with middle ear fluid did not measurably improve developmental outcomes at age 3 years.41
Suppurative Complications
Chronic suppurative otitis media (CSOM) occurs when episodes of recurrent acute otitis media are untreated or inadequately treated; a perforation of the tympanic membrane persists and there is chronic infection of the middle ear and mastoid. The hallmark of CSOM is a purulent, mucoid, or serious discharge through the persistent perforation. CSOM is a major health problem in many developing countries but is of particular concern in regions and populations with limited access to medical care, including the Inuits of Alaska, Canada, and Greenland; Australian Aborigines; and Native Americans.
Extension of infection from suppurative AOM into the mastoid air cells is frequent; the mastoid infection resolves with treatment of AOM but in some cases may progress to an acute periosteitis or osteitis. Labyrinthitis may follow the spread of infection from the middle ear into the cochlear and vestibular organs, resulting in sensorineural hearing loss and/or vertigo.
Intracranial complications of otitis media include meningitis, epidural abscess, subdural empyema, brain abscess, dural sinus thrombosis, and otitic hydrocephalus. Suppurative meningitis and other intracranial complications usually follow invasive bacterial infection but may also occur as a result of spread from the middle ear mastoid infection through the dura. The pus can proceed to accumulate between the dura of the brain and the cranial bone (epidural abscess) or the potential space between the dura and the arachnoid (subdural empyema) or progress to the meninges to cause meningitis.
Nonsuppurative Complications
Nonsuppurative complications of acute otitis media include facial paralysis, avascular necrosis of the long process of the incus with an associated conductive hearing loss, atelectasis of the middle ear (with and without a retraction pocket), adhesive otitis media, tympano-sclerosis, and cholesteatoma.
Although the facial nerve normally travels in a bony canal in its complicated course through the middle ear, up to 55% of individuals have small areas where the bony covering is incomplete, particularly in the area of the oval window. Inflammation may cause edema of the exposed facial nerve as it passes through the middle ear, compromising its venous return within the surrounding bony canal and resulting in peripheral facial nerve palsy. Although full recovery of facial nerve function can be expected in virtually all cases, it is usually recommended that the patient have insertion of a tympanostomy tube and be started on systemic antibiotic therapy. A tympanostomy tube not only serves to drain pus but also allows for antibiotic and steroid eardrops to be placed directly into the middle ear space.
Cholesteatomas may be due to chronic negative middle ear pressure that retracts a portion of the tympanic membrane, inhibiting the natural epithelium migration of desquamated squamous debris. This can then become wet, and infected, producing foul-smelling otorrhea and/or an expansile mass lesion that can cause local bony erosions. In a patient with a history of chronic otorrhea, pneumatic otoscopy may demonstrate retraction of the TM or granulation tissue or debris within a retraction pocket. However, the diagnosis of cholesteatoma is best made with otomicroscopy using an operating microscope. Computed tomography scanning of the temporal bone may provide further information on the size of the lesion. Aside from otorrhea, symptoms may include conductive hearing loss due to ossicular erosion, sensorineural hearing loss or disequilibrium due to vestibular involvement. Treatment is surgical.
PREVENTION
Parents may reduce exposure of the infant to transmission of infectious agents and decreasing risk factors for acute otitis media by adhering to a few techniques: breast-feeding, making the home a smoke-free environment; discouraging pacifier use, using family or small-group out-of-home daycare, and maintaining simple but effective hygienic procedures such as appropriate hand-washing.
The rationale for chemoprophylaxis to prevent AOM is that a modified dose of antimicrobial agents administered during the respiratory season will decrease the rate or intensity of colonization of the upper respiratory tract by bacterial pathogens.37 The physician must weigh the benefits of decreased risk of infections against the risk of development of resistant bacteria and possible adverse events of the drug. There is an abundant literature about use of chemoprophylaxis to prevent new episodes of acute otitis media, and most studies identify benefits.1,37 Candidates to consider for prophylaxis include children who have had three episodes of AOM in 6 months or four episodes in 12 months. Both amoxicillin and trimethoprim-sulfamethoxazole have been used in various clinical trials, but when the two drugs have been compared, amoxicillin has had superior results. Half of the therapeutic dose is administered in 1 dose/day; the drug is provided during the respiratory season, usually from the fall through early spring. Occasional episodes of acute otitis media may occur in the child who is on chemoprophylaxis; therapy for these children should include an alternative agent such as parenteral ceftriaxone or amoxicillin-clavulanate.
The 7-valent pneumococcal conjugate vaccine (PCV7) is immunogenic in infants beginning at age 2 months and has demonstrated efficacy in prevention of invasive disease as well as pneumonia and otitis media.38,39 The vaccine reduced the number of episodes of otitis media and number of otitis media visits by 7.0% and 7.8%, respectively, and reduced the number of procedures for placement of ventilating tubes by 23%. Children who received the pneumococcal vaccine had more episodes of AOM due to nonvaccine pneumococcal serotypes and nontypable H influenzae (eTable 243.1 ). The reasons why PCV7 was more effective in preventing invasive pneumococcal disease than in preventing vaccine serotype pneumococcal otitis is uncertain, but higher concentrations of serum antibody may be necessary to prevent the local mucosal diseases such as acute otitis media and pneumonia.
OTITIS EXTERNA
Colin Rudolph
The healthy external ear is a self-cleaning environment with antibacterial protection. The medial two-thirds of the external ear canal is bony with a thin layer of skin closely adherent to the bone and with no cerumen glands. The outer third of the external canal is cartilaginous with a much thicker layer of skin and fibrous tissue including extensive glandular elements. Cerumen (wax) is a protective antibacterial and waterproofing agent produced by the cerumen glands of the outer third of the external ear canal.
PATHOPHYSIOLOGY
The two most common causes of otitis externa are trauma and water exposure. The most common forms of trauma include cotton-tip applicators, fingernails, foreign bodies, and insects, which may be especially irritating. Water exposure may cause desquamation of squamous epithelium, with water absorption by retained wax predisposing to otitis externa. A patient may have a predisposition to water trapping if there are canal exostoses (bony overgrowths) partly occluding the canal, usually secondary to excessive cold-water exposure (surfer’s ear). About 30% of otitis externa is caused by water exposure and 30% by trauma, and in 30% of cases, there is no obvious predisposition. The remaining 10% have less common etiologies including skin disorders such as eczema or dermatitis, which may result in recurrent problems with external otitis. Occasionally there may be an infection of the sebaceous glands of the outer third of the ear canal with formation of a furuncle, a small staphylococcal abscess with symptoms disproportionate to its size.
Vesicles of the tympanic membrane (bullous myringitis) may be associated with a Mycoplasma infection, and vesicles of the ear canal may be associated with herpes zoster infection. In Ramsey-Hunt syndrome, these are associated with vesicular eruptions on the soft palate and facial nerve palsy. Rarely there may be pathologic cerumen retention with ballooning of the bony ear canal, termed keratitis obturans, which may also be associated with an underlying ciliary dyskinesia. Bacterial otitis externa is most commonly associated with Staphylococcus aureus or Pseudomonas aeruginosa. Cases resistant to treatment may have an underlying fungal or yeast infection, frequently Candida albicans.
DIAGNOSIS
In its initial stages, externa otitis usually presents with itching and a sensation of fullness in the ear. This rapidly progresses to severe pain (otalgia) and associated ear discharge (otorrhea). Blockage of the external ear canal can cause a conductive hearing loss. Unlike acute otitis media, movement of the pinna will greatly exacerbate the pain. Fever is unusual. On physical examination, there may be frank discharge from the ear, and otoscopy may be limited by pain because of an inflamed and swollen external ear canal. In severe cases, the external ear canal may be swollen completely shut. If a furuncle is present, there will be localized swelling and erythema with extreme pain on palpation of the affected area. Whenever possible it is advisable to inspect the tympanic membrane to ensure that there is no underlying cause for the discharge, such as chronic suppurative otitis media or a perforation following acute otitis media. This may not be possible at initial assessment because of edema of the external ear canal and associated pain on inspection.
TREATMENT
Otitis externa requires prompt treatment of both the infective organism and the underlying cause. Treatment is simpler if commenced before the canal is so inflamed that it is swollen shut. Foreign bodies should be removed and debris in the ear canal removed with irrigation, swabbing, or suction. Use of cotton-tip applicators should be discontinued, and swimming should cease. The steroid component is important to alleviate the inflammation, pain, and swelling but should be discontinued in the presence of a fungal otitis externa. Oral antibiotics are rarely needed but should be used when otitis externa is persistent, when associated otitis media may be present, or when local or systemic spread has occurred. Treatment usually leads to resolution of symptoms within 2 to 3 days. Treatment should be continued for 5 days following cessation of symptoms. Antibiotic and steroid combination eardrops should be administered, initially several times per day. If the external canal is extremely edematous, placement of an otowick, sponge, or small piece of ribbon gauze in the external canal is useful to assure antibiotic penetrance. Systemic antibiotics are also warranted if there is surrounding cellulitis of the soft tissues adjacent to the ear or cervical adenitis. Adequate analgesia is warranted, and in severe cases, narcotic administration may be justifiable.
If otitis externa is unresponsive to initial treatment, a microbiological sample for culture and sensitivity should be obtained. The most likely organisms under these circumstances are multiple drug-resistant Pseudomonas aeruginosa or fungi. Quinolone eardrops are usually the most effective treatment for Pseudomonas, and anti-fungal drops or cream are indicated for yeast or fungal otitis.
A furuncle may require topical and systemic antistaphylococcal antibiotics, and if the abscess is pointing, then drainage with an 18-gauge needle may dramatically alleviate the pain associated with this condition. Once the acute infection has resolved, it is prudent to reassess the ear to ensure that there is no underlying predisposition to infection such as eczema or a cholesteatoma. Most experts recommend that individuals with acute otitis externa refrain from participation in water sports for seven to 10 days but some permit competitive swimmers to resume swimming within 2 to 3 days if the pain has entirely resolved. Alternatively, some allow swimming with well-fitting ear plugs.
COMPLICATIONS
Pain and conductive hearing loss are the most common temporary symptoms associated with otitis externa. Rarely in cases with recurrent otitis externa, particularly if associated with an underlying skin condition, a canal stenosis may develop, which in turn may further exacerbate the predisposition to otitis externa. A canal stenosis is not an easily treated condition and will usually require surgical intervention.
Rarely, a diabetic or immunocompromised patient may present with pseudomonal otitis externa that spreads via the fissures of Santorini to affect the temporal and adjacent bones. This condition is known as necrotizing or malignant otitis externa and carries a high mortality rate if not treated aggressively. Symptoms include severe otalgia and otorrhea. Typical findings include the presence of granulation tissue in the external auditory canal, especially at the bone-cartilage junction. Diagnosis requires culture of ear secretions and pathologic exam of the granulation tissue. Computed tomography scanning or bone scanning can be helpful. Treatment includes prolonged antibiotic therapy, local treatment of the auditory canal, reduction of immunosuppression if possible, and surgery in selected cases.
PREVENTION
In individuals predisposed to otitis externa, prophylactic measures may be taken to prevent recurrence. This may include treatment of underlying skin conditions, regular toilet of the external ear canal to prevent water trapping, surgical removal of bony exostoses, and use of alcohol eardrops after swimming to promote drainage of water from the ear. Persons who swim frequently can use a barrier to protect their ears from water but ear plugs can act as a local irritant. A tight-fitting bathing cap may offer protection. Other prophylactic measures such as drying the ears with a hair dryer and avoiding manipulation of the external auditory canal may help prevent recurrence.