Marx: Rosen's Emergency Medicine, 7th ed.

Otitis media (OM) is the most common diagnosis made by U.S. physicians for children younger than 15 years old.^[1] In 2002, 16.7 million visits were made to physician offices across the country for OM with an estimated 2.65 million visits made to emergency departments (ED), making it the sixth most common ED discharge diagnosis.^[2] Over 80% of children will have at least one episode of acute otitis media (AOM) during their lifetime, and by age 3 up to 40% will have at least three episodes during the first 3 years of life.^[3] The financial repercussions are enormous; one estimate is that $5 billion per year is spent on the evaluation, treatment, and socioeconomic effects of OM.^[4] The most frequent outpatient use of antimicrobials in the United States is for OM, with the number of prescriptions increasing from 12 million in 1980 to more than 23.6 million in 1992.

Male gender, day care attendance, parental smoking, pacifier use, and a family history of middle ear disease have been implicated as risk factors. ^{[5] [6]} Children with anatomic abnormalities, such as cleft palate and Down syndrome, have a higher rate of OM, probably because of eustachian tube abnormalities. Some immunocompromised patients, including patients with HIV, may have recurrent OM as an initial symptom of their underlying disease. OM and upper respiratory infections occur primarily in the winter. Breast-feeding seems to be protective.^[7]

Otitis media is broadly defined as inflammation of the inner ear and is a continuum of disease. Acute otitis media is defined as the signs and symptoms of an acute infection, with evidence of effusion; this has also been called acute suppurative, or purulent, OM. Otitis media with effusion (OME) has effusion without signs or symptoms of an acute infection; additional descriptive terms include serous, mucoid, nonsuppurative, or secretory OM. OME is classified further into acute (<3 weeks), subacute (3 weeks to 3 months), and chronic (>3 months). Chronic OM, or chronic suppurative otitis media, refers to chronic discharge from the ear through perforation of an intact membrane. Recurrent OM is defined by three or more episodes over 6 months or four episodes in 1 year.

Eustachian tube dysfunction is the central theme of most theories of AOM pathogenesis. The eustachian tube, between the middle ear cavity and the nasopharynx, ventilates the middle ear to equilibrate pressure, allows for middle ear drainage, and provides protection from nasopharyngeal secretions. In children, it measures approximately 18 mm and is almost horizontal. As individuals age, the eustachian tube widens, doubles in length, becomes more vertically oriented, and stiffens (which may explain the decreased incidence of AOM in adults). Normally, the tube is collapsed, but it opens during yawning, chewing, and swallowing.

The eustachian tube may become either mechanically or functionally obstructed, decreasing middle ear ventilation. Examples of mechanical obstruction include inflammations from an upper respiratory infection, hypertrophied adenoids, and a cleft palate.^[8] Functional obstruction from persistent tubal collapse occurs primarily in young children, who have less fibrocartilage support of the medial eustachian tube than older children or adults.^[8] It has been postulated that this dysfunction results in negative middle ear cavity pressure, causing a transudate of fluid that combines with the reflux of nasopharyngeal secretions and bacteria.

The most common causes of bacterial infection in children are Streptococcus pneumoniae, Haemophilus influenzae (primarily nontypeable), and Moraxella (Branhamella) catarrhalis. Streptococcus pyogenes, Staphylococcus aureus, and gram-negative bacteria are much less common.^[9] Adult infection involves similar organisms. In OME, there is a greater proportion of H. influenzae and a higher percentage of sterile effusions.^[10] Viruses also have been found in the middle ear aspirates of children with OM and are found in anywhere from 5 to 16%. ^{[11] [12] [13]} The advent of reserve transcriptase polymerase chain reaction technology for viral identification has improved, and it is likely that an even greater number of viral agents will be found. Some authors believe that viral infection is the cause of the inflammatory reaction in most cases and antibiotics are not necessary. Respiratory syncytial virus is the most common virus, but parainfluenza, influenza, enterovirus, rhinovirus, and adenovirus have also been found in the middle ear aspirates of children. ^{[10] [11]} Viruses have contributed to poor treatment outcome by increasing middle ear inflammation, decreasing neutrophil function and decreasing antibiotic penetration into the middle ear.^[14]

In young children, it was believed that gram-negative organisms and S. aureus were the causative organisms. Although these bacteria may be the causes in intubated patients or patients in the neonatal intensive care unit, healthy newborns tend to be infected by the same pathogens as healthy older children.^[15] Bullous myringitis presents with bullae on the tympanic membrane and may be present in up to 5% of cases of OM in children less than 2 years.^[16] Although previously thought to be caused by Mycoplasma pneumoniae, culturing middle ear aspirates in this condition generally grows the usual organisms that cause AOM and M. pneumoniae is uncommon. ^{[16] [17]}

Over 70% of children presenting with purulent conjunctivitis may have OM, a symptom complex described as the otitis-conjunctivitis syndrome,^[18] which is predominantly caused by H. influenza.^[19] Other, less likely organisms that can cause AOM include Mycobacterium tuberculosis (primarily in children) and Chlamydia trachomatis (most commonly seen in children younger than 6 months old with pneumonia).^[20]

Conjugate pneumococcal vaccine has been effective in markedly reducing invasive disease in young children and decreasing the incidence of OM.^[21] It is estimated that its use would decrease the number of visits to the pediatrician for OM by 1 million, and the number of children receiving tympanostomy tubes might decrease by 500,000.^[22] The vaccine may be responsible for an increase in gram-negative and virulent β-lactamase-producing organisms in middle ear effusions, primarily in patients who have recently been treated. ^{[23] [24] [25]}

Up to 5 to 10% of the general pediatric population may be at risk for developing four or more episodes of OM in the first year of life; these children are generally called otitis-prone.^[26] They may have subtle immunologic abnormalities^[26] or a greater baseline colonization of virus and bacteria than the general population.^[27]

OM may be manifested by a multitude of symptoms, such as cough, poor appetite, diarrhea, vomiting, fever, and pulling at ears, all of which are nonspecific. Older children may be able to verbalize pain, but otalgia is not universally present. In OM, pain usually precedes otorrhea, in contrast to OME, in which pain accompanies the drainage. Children often have associated upper respiratory tract infections. Fever may be present, but in one large series, a temperature of 38.3° C or greater was present in only 26% of the episodes, with only 4% having a fever of 40°C or greater.^[28] Some authorities have modified the definition to include otoscopic findings of acute inflammation regardless of symptoms; with this definition, one third of cases are not accompanied initially by acute symptoms.^[29]

The auricle and external canal should be inspected for signs of erythema, discharge, or tenderness. If the canal is occluded with cerumen, an ear curette with direct visualization may be successful in clearing the canal. If not, the placement of 3% hydrogen peroxide or emulsifying drops, followed by gentle irrigation, may cleanse the canal.

The tympanic membrane (TM) may be bulging (as in AOM), neutral, or retracted as seen in chronic OME.^[30] The color may be red, pink, yellow, or a normal pearly gray or translucent. The presence of erythema in itself does not indicate infection because crying or fever may cause hyperemia; however, a TM that is distinctly red (defined as hemorrhagic, strongly or moderately red) suggests AOM.^[30]

Landmarks that should be visible include the pars flaccida, the malleolus, and the light reflex below the umbo.^[30] The TM may have air-fluid levels, may have bubbles behind the TM, or may be completely opacified, all of which indicate middle ear effusion. The lack of mobility is one of the most sensitive indicators of middle ear effusion. In fact, mobility in response to insufflation should raise serious doubt as to the diagnosis of AOM. A TM that is cloudy, bulging, and distinctly immobile indicates AOM.^[30] In OME, the TM often is retracted, with the malleolus being particularly prominent. The landmarks all may be obscured in the presence of significant fluid. A comparison examination of the other ear may help in confirming suspected infection.

In neonates, the TM appears thickened and opaque normally in the first few weeks of life, and the TM is in a highly oblique position. With tympanostomy tubes, in the absence of infection, the TM may have decreased mobility, altered landmarks, opacity, or dullness. If the tube is patent, erythema and discharge may indicate infection. If not, erythema, bulging of the TM, and immobility indicate AOM.

Before the use of antibiotics, there was a 20% incidence of complications from AOM, with mastoiditis and otic meningitis being relatively common.^[31] Complications are either intratemporal or intracranial, occurring in both adults and children. The development of either complication of OM is thought to occur by one of three mechanisms: (1) direct extension of infection through bone weakened by osteomyelitis or cholesteatoma; (2) retrograde spread of infection by thrombophlebitis; or (3) extension of infection along preformed pathways, such as the round or oval windows or through dehiscences that are the result of congenital malformations.^[32] The use of antibiotics has led to a reduction of all complications to less than 1%.^[33]

Hearing impairment is the most common complication in OM. Almost all children with OM have a temporary conductive hearing loss; sensorineural deficit occurs less commonly, probably as a spread of infection through the round window. This deficit may contribute to the association of OM with decreased or delayed speech, language, or cognitive development.

TM perforation occurs most commonly at the pars tensa and usually resolves spontaneously. It may persist for a longer period, resulting in a chronic perforation, chronic OM, or both.^[20] Chronic OM refers to inflammation of the middle ear that persists for 6 weeks or longer^[34] accompanied by discharge through perforation of an intact membrane. It may occur spontaneously or through tympanostomy tubes. The pathogenesis is multifactorial, and the most commonly involved causal organisms are Pseudomonas aeruginosa, S. aureus, gram-negative organisms, and anaerobes. Whereas acute otitis and its complications are more common in younger children, complications secondary to chronic OM are more common in older children and adults.^[35] Topical antibiotics are an effective treatment.^[36] Systemic treatment should be reserved for patients showing signs of complicated or invasive infections or signs of systemic disease.^[34] Cholesteatoma is an accumulation of keratin-producing squamous epithelium in the middle ear and may result in erosion of bone within the middle ear cavity. It is seen most often in OME, in which retraction of the TM is a common problem and its presence may alter the courses of some treatment therapies.

Labyrinthitis occurs when infection spreads to the cochlear and vestibular apparatus, usually through the round or oval windows. Serous labyrinthitis results when bacteria from the middle ear spread into the labyrinth space, resulting in a mixed conductive-sensorineural hearing loss and vestibular symptoms. Suppurative labyrinthitis is the development of purulence directly into the labyrinth as a result of bacterial invasion through the round window or around the annular ligament of the round window. It generally begins suddenly with mixed hearing loss and vestibular symptoms and is generally more severe than the serous form.^[32]

The facial nerve courses through the middle ear, and facial paralysis is a known complication in OM. The exact mechanism is unknown, but it may be due to infection, surrounding osteitis, facial nerve swelling, demyelination of the facial nerve from bacterial toxins, or facial nerve ischemia.^[37] Infectious eczematoid dermatitis may result from the otorrhea of OM, with perforation or tympanostomy tubes infecting the external auditory canal. Treatment involves otic suspension (not solution). Although caution is urged with these products, the incidence of adverse effects is small.^[38]

Meningitis is the most common intracranial complication for AOM, resulting from hematogenous spread and direct invasion. Brain abscesses are most commonly due to chronic otitis and are the second most common intracranial complication.^[39] They generally result from hematogenous extension secondary to thrombophlebitis but can result from erosion as well.^[35] Causative organisms include Proteus, Pseudomonas, Staphylococcus aureus, Streptococcus pneumoniae, and anaerobes. ^{[40] [41]} Symptoms include headache, fever, vomiting, and mental status changes.

An extradural abscess may result from destruction of bone adjacent to the dura by cholesteatoma, infection, or both. Subdural empyema is a collection of fluid between the dura and arachnoid membrane as a result of infection or venous thrombophlebitis. Focal otic encephalitis is an edematous or inflamed area in the brain from a complication of OM, extradural abscess, or sinus dural thrombophlebitis.

Lateral venous sinus thrombosis occurs when the mastoid infection comes in contact with the sinus wall, which inflames the adventitia and penetrates the venous wall. Thrombosis and embolization occur. The classic presentation is the presence of high spiking fevers in a “picket fence” pattern, chills, earache, headache, and mastoid and neck tenderness.

Antibiotics are the primary treatment for all complications of OM. Myringotomy with or without tympanostomy tube placement ensures drainage of the middle ear and makes specimens available for culture.^[42] Operative treatment may be required in the presence of intratemporal complications with abscess formation or intracranial complications, or when chronic OM or cholesteatoma is a cause of the acute complications. ^{[42] [43]}

Pneumatic otoscopy to confirm immobility of the TM is an important part of diagnosis in all cases (see earlier discussion). Tympanocentesis is aspiration of the middle ear effusion to identify causative organisms and is rarely indicated in the ED. Indications include patients with AOM who are seriously ill or appear toxic, are unresponsive to therapy, are younger than 4 weeks old, are immunocompromised, are receiving antimicrobials, or have suppurative complications.

OM usually does not cause a significantly high fever; in approaching a febrile, ill-appearing infant, the physician should investigate other causes for the fever. If a child or adult complains of otalgia, additional considerations or possibilities include OME, trauma, foreign bodies, and complications of OM such as mastoiditis. Ear pain also may be referred from the teeth, sinuses, throat, or temporomandibular joint.

Although more than 16 antibiotics have been approved by the Food and Drug Administration for OM, few have shown efficacy against all of the main causative pathogens.^[4] Concern about the rising rates of antibacterial resistance and the growing costs of antibacterial prescriptions has focused the attention of the medical community and the general public on the need for judicious use of bacterial agents.^[44] Based on this and other factors, the American Academy of Pediatrics, the American Academy of Family Physicians, the Agency for Healthcare Research and Quality, and the Southern California Evidence Based Practice Center met to develop guidelines for the diagnosis and management of AOM to assist physicians in providing a framework for clinical decision making. These guidelines apply specifically to an otherwise healthy child between the ages of 2 months and 12 years without underlying conditions that may alter the natural course of acute AOM ( Table 70-1 ).^[4] Making a diagnosis of AOM requires three findings: (1) history of acute onset, (2) signs of middle ear effusion (including TM immobility), and (3) signs or symptoms of middle ear inflammation (see Table 70-1 ).

Because over 80% of cases of AOM resolve spontaneously,^[45] the use of observation versus antibiotics has been advocated.^[46] Several European countries have practiced this approach of “watchful waiting” for 48 hours for a number of years, with a resulting lower rate of antibiotic-resistant bacteria.^[47] Although somewhat controversial, this approach has been met with acceptance by a majority of patients and physicians. ^{[47] [48]} It has been successful in an ED setting^[49] but has not yet become standard practice.^[50]

The decision to treat is based on the age of the patient and certainty of the diagnosis.^[44] The guidelines recommend an age-stratified approach that incorporates the age with a combination of diagnostic certainty and illness severity. Observation is an option in children older than 2 years, unless the child has severe otalgia or temperature of 39° C or greater ( Table 70-2 ). In children 6 months to 2 years old, treatment recommendations are based on the certainty of the diagnosis and severity of illness, with recommended observation if the diagnosis is uncertain. The guidelines recommend treatment in children younger than 6 months old. Observation recommendations are based on the degree of severity, reliability of the caregivers, and ability for close follow-up. If there is concern about the ability to get follow-up, parents can be given a prescription to be filled if the patient does not improve in 48 hours—a so-called safety net.^[51]

There is evidence that immediate antibiotic therapy for children younger than 2 years with severe symptoms results in a more rapid resolution of symptomatic disease and a reduced rate of treatment failure or relapse. ^{[52] [53]} The potential risk of complications must be balanced against the side effects of antibiotic use, which may include allergic reactions, gastric upset, accelerated bacterial resistance, and unfavorable changes in the bacterial flora.^[54]

Amoxicillin's cost, efficacy, safety profile, and palatability continue to make it a good first-line agent. It can be given twice a day at a dosage of 80 to 90 mg/kg/day. This higher concentration is effective against susceptible and intermediate resistant strains of Streptococcus pneumoniae. In patients who are allergic to penicillin, the guidelines distinguish between those with type I sensitivity (urticaria or anaphylaxis) and those with non-type I sensitivity, but second- and third-generation cephalosporins have little cross reactivity.^[55] Patients should be reevaluated in 3 days if the treatment fails. Treatment failure is defined by lack of clinical improvement in signs and symptoms, such as ear pain; fever; and TM findings of redness, bulging, or otorrhea. Treatment should include agents effective against the β-lactamase-producing organisms H. influenzae and M. catarrhalis. Recommended agents include amoxicillin-clavulanate (using 80–90 mg/kg/day of the amoxicillin component), oral cefuroxime axetil, and intramuscular ceftriaxone. Although ceftriaxone has been as effective as amoxillicin in patients with a history of vomiting, poor compliance, and a lack of follow-up,^[56] a 3-day regimen may improve its effectiveness.^[57] If treatment failure occurs within the first 28 days, recommended antibiotics are the same as at 3 days.

Patients who have been on antibiotics in the prior month should receive high-dose amoxicillin, high-dose amoxicillin-clavulanate, or cefuroxime axetil as the initial treatment. Cefdinir may be preferred over cefuroxime because of its more pleasing taste, which can equate to improved compliance.^[4] Treatment failures at 3 days should be treated with intramuscular ceftriaxone or clindamycin, with tympanocentesis strongly encouraged. Clindamycin should be used only for treatment of S. pneumoniae because it is not effective against either H. influenzae or M. catarrhalis. ^{[4] [9]} Treatment failures within 1 month should be treated with high-dose amoxicillin-clavulanate, cefuroxime axetil, or intramuscular ceftriaxone.^[57]

Trimethoprim-sulfamethoxazole and macrolides traditionally have been second-line agents, but resistance is increasing—40% for trimethoprim-sulfamethoxazole and 30% for macrolides.^[4] In addition, there is substantial cross-resistance between these drugs and the β-lactams, resulting in further treatment failures in children finishing a course of amoxicillin. ^{[57] [58]} Fluoroquinolines may be effective, but their use in children is not approved.^[57]

Response to antibiotics is only one of a number of factors that affect clinical outcome. Other factors include impairment of endothelin [ET](B) function, co-infection with nonbacterial pathogens, and host immune response. ^{[58] [59]} Local practice patterns and antimicrobial sensitivities may also play a role in the types of treatment given. Other antibiotics available for treatment include erythromycin-sulfisoxazole, azithromycin, clarithromycin, cephalexin, cefaclor, cefprozil, loracarbef, cefdinir, cefixime, cefpodoxime, and ceftibuten. These were not included in the Centers for Disease Control and Prevention guidelines primarily because there was a lack of data on their efficacy.

Treatment historically involved a 10-day course. Numerous studies have compared traditional treatment courses with shorter therapy, which is most appropriate for uncomplicated AOM. ^{[60] [62]} Patients with TM perforations and patients at high risk for treatment failure or those with chronic or recurrent OM probably are more appropriately treated with a longer course.^[58] Shorter courses also are not appropriate for children younger than 2 years old. ^{[60] [62]} The antibiotic treatment of AOM in adults is the same as in older children. There is no indication for the use of antihistamines, decongestants, steroids, or tympanostomy tubes for an acute episode of AOM.

AOM can cause substantial pain and should be appropriately addressed. Acetaminophen, ibuprofen, and benzocaine-antipyrine, a local anesthetic, may be helpful in some patients with an intact TM. Recurrent AOM occurs primarily in the winter months, often in conjunction with upper respiratory infections. Individuals at risk include children younger than 2 years old, children in day care, and Native American children.^[60] These children may benefit from prophylaxis with amoxicillin (20 mg/kg).^[63]

After a 10-day treatment with antibiotics, 50% of children may exhibit OME, but 90% of cases resolve within 3 months.^[64] However, about 30 to 40% of children have recurrent OME and 5 to 10% of cases last 12 months or longer.^[65] The treatment of OME is controversial, but OME may interfere with hearing and subsequent development of speech and language. OME is, by definition, asymptomatic, and the effusion may be sterile or contain infectious agents. Clinical guidelines developed by the Agency for Health Care Policy recommend observation or the use of antibiotics in patients with acute or subacute OME, although some experts recommend observation alone, given increasing antibiotic resistance. ^{[1] [60]} Antihistamines, decongestants, steroids, or surgical procedures are not beneficial in patients with acute or subacute OME.^[65] Myringotomy and tympanostomy tubes may be beneficial in children for whom medical treatment has failed, those who have had OME for 4 to 6 months, and those with a greater than 20-dB hearing loss.^[1] Tonsillectomy is not beneficial, but adenoidectomy may be helpful in older children. Tympanostomy tubes have also been used in recurrent AOM unresponsive to prophylactic antibiotics; complications of AOM, and complications of eustachian tube dysfunction, including TM retraction with hearing loss, ossicular erosions, or retraction pocket formation.^[64]

Children normally are seen in 10 to 14 days for follow-up. This follow-up appointment may not be necessary in children older than 2 years in whom symptoms have resolved and who have no recurrent risk factors.^[66] Infants younger than 2 months old with OM should be evaluated with blood, cerebrospinal fluid, and urine cultures.^[8] Patients with complications need ear, nose, and throat (ENT) referral. Adults who have persistent OME need ENT referral to rule out nasopharyngeal carcinoma.