Chapter 49. Otitis Media

Otitis media (OM) is a global health care problem most commonly seen in the pediatric population. Aside from upper respiratory infections, OM is the most commonly rendered diagnosis in the pediatric primary care setting. The majority of children will be diagnosed with at least one episode of acute otitis media (AOM) with rates of incidence peaking at age 2. Various retrospective studies demonstrate a wide berth of incidence, suggesting that 19–62% of children will experience at least one episode of AOM by age 1, and 50–84% of children by age 3.

While mainly considered a pediatric medical problem, OM does present in the adolescent and adult population, albeit at a lower rate. Approximately 3% to 15% of all-comers with OM presenting to otolaryngologists are adults.

Over the past decade, in particular, health care discussions have intently focused on cost and consequences of medical conditions and interventions. While the economic implications of OM are largely abstruse, estimates of a single episode of AOM range from $233 to $1330 USD. When considering these figures, OM (including medical and surgical interventions) in the United States costs $3 to 18 billion dollars annually.

Essentials of Diagnosis

• OM is stratified into two distinct categories: AOM and otitis media with effusion (OME).
• The most common bacterial pathogens that cause AOM are Streptococcus pneumoniae, Haemophilus influenzae, and Branhamella (moraxella) catarrhalis.
• OME is defined as the presence of a middle ear effusion for 3 months or more.

Classification of a disease process is paramount to optimal diagnosis and management. Historically, extensive efforts have been put forth to define OM and its manifestations. Generally, OM refers to an inflammatory process localized to the middle ear cleft. The term “otitis media” can be separated into two distinct categories: AOM and OME.

AOM is characterized by a rapid onset of signs and symptoms, such as pyrexia and otalgia, leading to inflammation of the middle ear. Traditionally, terms such as acute suppurative or purulent OM have been used interchangeably with AOM. Current recommendations state, however, that AOM is the most accurate term used to describe middle ear inflammation in absence of effusion. Recurrent AOM is defined as: three or more episodes in a 6 month period, or four or more episodes in a 12 month period with complete resolution of symptoms between episodes.

OME, as the name suggests, is characterized by an inflammation of the middle ear space with the presence of effusion. As in the case with AOM, myriad terms such as secretory, nonsuppurative, and serous OM have been used synonymously with OME. Because effusions localized to the middle ear space may be asymptomatic or sterile and/or contain bacteria or even purulence, it is a misnomer to describe all effusions as “secretory” or “serous” or “transudative.”

The middle ear cleft is a continuous space that begins at the Eustachian tube orifice in the nasopharynx and extends to include the mastoid air cells. The cleft comprises three different contiguous components: the Eustachian tube, the middle ear, and the mastoid air cells (including the petrosa). The middle ear cleft is lined with variable epithelium—ranging from thick, ciliated respiratory epithelium found in the Eustachian tube to the thin, nonglandular cuboidal epithelium in the mastoid cells.

The underlying pathogenesis of all forms of OM (with the exception of cholesteatoma-related OM) is Eustachian tube dysfunction. The main function of the Eustachian tube is to aerate the middle ear space, providing pressure equivalent to atmospheric pressure. Additionally, the Eustachian tube plays a role in mucociliary clearance of the middle ear space and furthermore, prevents nasopharyngeal contents from entering the middle ear. Obstruction of the Eustachian tube, whether it is functional (eg, failure of contraction of tensor veli palatini during swallowing) or anatomic (eg, adenoid hypertrophy), results in the development of OM. Also of note, in patients with OM, there is an increase in the number of goblet cells found in the respiratory epithelium lining the Eustachian tube. While most episodes of AOM are preceded by viral infections, the majority of AOM have a bacterial component. Table 49–1 provides a comparative evaluation of middle ear cultures from children worldwide.

Despite the environmental differences, the results are universal—the most common bacterial pathogens found in AOM are Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis.

OME has a similar pathogenesis to AOM in that Eustachian tube dysfunction is nearly universal in children with OME as well. OME develops following untreated or unresolved episodes of AOM. Teele et al. found persistent effusion (>30 days) in 40% of children after their first episode of AOM, and continued effusion (up to 3 months) in 10%. Risk factors for AOM and subsequent OME include parental smoking, absence of breast feeding, day care attendance, craniofacial anomalies, adenoid hypertrophy, and allergic rhinitis. All predisposing factors appear to have a deleterious impact on Eustachian tube function.

Essentials of Diagnosis

• Manifestations of AOM include: otalgia, pyrexia, thickened or bulging tympanic membrane, hearing loss, and otorrhea.
• Manifestations of OME include: persistent hearing loss, dull or immobile tympanic membrane, and flat tympanogram.

Accurate diagnosis of AOM versus OME is becoming increasingly important, especially in the present day challenge of antibiotic-resistant organisms. Diagnosis of AOM and OME can be made by direct visualization of the TM using an otoscope or pneumatic otoscope. The symptoms most often associated with AOM are otalgia, fevers, decreased appetite, upper respiratory infection, and fatigue. In children less than 2 years old, otalgia is evidenced by fussiness, insomnia, and generalized irritability. Since these symptoms are vague and may be attributable to a variety of conditions, symptomatology alone should not be used as sole criteria to render a diagnosis of AOM or OME.

Examination of the TM can be challenging and heavily clinician dependent. Description of otoscopic findings is variable and subjective. It is helpful to consider physical examination of the TM systematically—the use of a mnemonic, “COMPLETES” has been published as a teaching and clinical tool to ensure thorough and methodical examination (Table 49–2).

Otoscopy in AOM classically demonstrates a thickened, hyperemic, immobile TM. As diagnosis can often be made on history and physical exam alone, further studies are not indicated for AOM. OME, in contrast, is often asymptomatic. The most common complaint associated with OME is decreased hearing. Otoscopy classically demonstrates a dull gray- or yellow-tinged, immobile TM. If the TM is clear, bubbles or air fluid levels can be elucidated. Tympanometry and audiometry are complimentary diagnostic tools used in evaluating patients with OME.

Tympanometry is an objective and quantitative way to evaluate TM mobility and middle ear function. It is defined as “the measurement of the acoustic immittance of the ear as a function of ear canal air pressure”. The procedure involves placing a probe into the external auditory canal and measuring the amount of sound energy returned. Patients with OME demonstrate flattened tracings on tympanometry indicating fluid in the middle ear space. Table 49–3 depicts examples of different tympanometry tracings.

As mentioned, OME often presents with varying degrees of hearing loss. Therefore, serial audiometry is helpful in establishing a diagnosis of OME. Audiologic testing may include pure tone threshold, speech reception threshold, speech awareness testing, behavioral observation, and auditory brain-stem response (ABR). Conductive hearing loss is most often documented in children with OME.

Essentials of Diagnosis

• The basis for medical treatment of AOM is antibiotic therapy
• Amoxicillin remains the first line antibiotic treatment for AOM
• Observation for 48 hours for fever or progressive symptoms is an acceptable alternative to initiating antibiotics

Tympanostomy tubes and adenoidectomy are the surgical treatments of choice for OME.

Medical Management

Although most episodes of AOM will resolve spontaneously, the basis of medical treatment in clinical practice in the United States is antibiotic therapy. Several randomized control trials (RCTs) have been conducted comparing antimicrobial therapy versus placebo or no drug as initial therapy for AOM. Antibiotics used in these studies were penicillin or aminopenicillin alone or in combination with sulfisoxazole or clavulanate given for 7 to 14 days. Although various meta-analyses demonstrate only marginal benefit with antibiotic use and earlier resolution of symptoms in some instances, amoxicillin remains as first-line antibiotic treatment for AOM. Specifically, studies found no benefit within the first 24 hours and small benefit at 2 to 7 days. Observation for 48 hours for fever or progressive symptoms prior to initiating antibiotic coverage has also been shown as a safe alternative.

As an adjunctive therapy, using decongestants, vasoconstrictors, or other forms of topical therapy to diminish nasal symptoms did not have an effect on shortening the course of AOM.

The treatment of OME varies from observation with close follow-up in asymptomatic patients to extended courses of antibiotics for symptomatic patients. Review of various RCTs demonstrates that antimicrobial therapy (including but not limited to ampicillin, amoxicillin, trimethoprim/ sulfisoxazole, erythromycin) is indicated in OME. The Agency for Health Care Policy and Research in 1994 recommended a course of antibiotics in children with symptomatic OME followed by a 1-month period observation. If symptoms fail to improve or effusions persist, surgical intervention is indicated. While steroids, decongestants, and antihistamines are all used as adjunctive treatment for OME in the general otolaryngology practice, RCTs do not demonstrate statistically significant benefit. Another topic of discussion in the management of OME is the use of antibiotic prophylaxis. Prophylactic doses typically administered are generally half of the therapeutic dose. Review of the literature showed only one study that demonstrated benefit using sulfisoxazole as antibiotic prophylaxis in a small sample size).

Surgical Management

Surgical management of AOM and OME is largely dependent on the impending development of complications as a result of the disease process. AOM is largely a medically managed disease, as discussed above, with antibiotic therapy and often times, spontaneous resolution. However, tympanocentesis and placement of tympanostomy tubes can play a role for refractory cases. Selection of appropriate antibiotic therapy can be enhanced by tympanocentesis (direct transtympanic membrane needle aspiration of middle ear fluid) in immunocompromised patients and patients who fail initial appropriate antibiotic therapy. Typically, tympanostomy tube placement is reserved in the acute setting for those patients who develop complications of AOM (discussed later in this chapter).

The mainstay of treatment for chronic OME is surgical intervention although a wide array of debate focuses on indications. The purpose of surgical intervention is to provide ventilation of the middle ear space and prevent onset of serious OME sequelae, including conductive hearing loss and speech development in the pediatric population. Surgery for OME is recommended for patients with hearing loss and persistent middle ear effusion for 4–6 months. Historically, myringotomy, insertion of tympanostomy tubes, adenoidectomy, and tonsillectomy have been offered as possible surgical treatments for OME. Once commonly practiced, tonsillectomy has been shown to demonstrate little to no benefit on resolution of middle ear effusions. Myringotomy alone, although commonly practiced, does not play a significant role in the modern treatment of OME when considering the cost-benefit ratio of myringotomy alone versus myringotomy with tube placement and risks of anesthesia.

Tympanostomy tubes were first introduced in 1954 by Armstrong and have been the therapeutic treatment of choice for OME. The goal of placement of tympanostomy tubes is to aerate the middle ear space and prevent accumulation of middle ear inflammation and effusion. In effect, ventilation of the middle ear enhances hearing thresholds. Once tympanostomy tubes extrude from the TM, there is no residual clinical benefit.

Adenoidectomy serves an increasingly important role in the effective surgical treatment of OME. Hypertrophic adenoid tissue causes nasal obstruction, mouth-breathing, and similarly, obstruction of the Eustachian tube orifices. Removing large adenoids enhances the patency of the nasopharyngeal airway, relieving the overall pressure in the nasopharynx, in turn allowing improved aeration of the middle ear cleft. Adenoidectomy also reduces distortion of the mucosal lining of the nasopharynx, making it a less hospitable environment for bacterial colonization or nidus of inflammation.

The sequelae and complications of OM are vast, boasting a significant impact on both the pediatric and adult populations. Different types of complications result from AOM and OME as seen in Table 49–4.

Complications of AOM

The spectrum of complications resultant from AOM ranges from the more common persistent TM perforation to the infrequent, but more severe intracranial complications. Critical complications of AOM arise in the modern antibiotic era generally due to poor access to medical care, poor compliance, or inappropriate diagnosis and management.

Tympanic Membrane Perforation

TM perforation can occur in the setting of AOM from accumulating inflammation and corresponding ischemia of the TM. The vast majority of perforations from AOM heal spontaneously within 48 to 72 hours. Non-healing perforations can lead to long-term sequelae such as conductive hearing loss or otorrhea.

Mastoiditis

Acute mastoiditis, the most common intratemporal complication of AOM, occurs due to direct extension of disease from the middle ear cleft to the mastoid air cells. Classically, acute mastoiditis refers to the coalescent type with mastoid bone destruction and possible subperiosteal abscess formation lateral to the mastoid cortex. The patient typically presents with fevers, post-auricular erythema, and tenderness, ear proptosis, and AOM on otoscopy. Computerized tomography (CT) imaging demonstrates loss of mastoid air cell trabeculations, local bone destruction, and presence of soft tissue within the mastoid cavity and middle ear cleft.

If infection escapes through the mastoid tip and tracks down the upper neck along the sheath of the sternocleidomastoid muscle (SCM), an abscess, known as Bezold's abscess, forms just deep to the SCM. Bezold's abscess occurs in older children with fully pneumatized mastoid tips, and in adults with mastoiditis or cholesteatoma. Similarly, when infection extends beyond the mastoid to penetrate the plane adjacent to the posterior belly of the digastric muscle, it is referred to as a Citelli's abscess.

The term “masked mastoiditis” is used to describe granulation tissue and bony erosion of the mastoid in the absence of otorrhea. On otoscopy, the TM appears normal however a focus of infection (not responsive to antibiotics) continues to persist in the mastoid cavity. Patients may experience chronic postauricular pain with only slight tenderness on palpation of the mastoid. Furthermore, CT scan demonstrates localized opacification with an otherwise normal appearing mastoid.

Patients with chronic mastoiditis classically present with purulent otorrhea, dull otalgia, often associated with multiple episodes of AOM, TM perforation, or cholesteatoma.

Petrositis

Although exceptionally rare, petrositis is a known complication of AOM. Petrositis occurs when infection spreads within the temporal bone into the petrous apex. The classic triad, or Gradenigo's syndrome, is rare and characterized by retroorbital pain, AOM, and ipsilateral abducens nerve paresis. In conjunction with the clinical triad, diagnosis is confirmed with radiographic findings of bony destruction of the petrous apex.

Facial Nerve Paresis

Facial nerve paresis can occur in the setting of AOM or OME, by two different mechanisms: (1) from the release of locally produced bacteria-mediated toxins or (2) from the direct effect of inflammatory tissue adjacent to the facial nerve as it transverses the mastoid cavity. Detecting the site of lesion can be a challenge especially in the setting of grossly inflammatory diseases such as AOM, cholesteatoma, or mastoiditis. The nerve excitability, maximum nerve excitability, electromyography, and electroneurography may be beneficial in identifying a neuro-destructive lesion. MRI with gadolinium can also provide additional information about inflammatory or neoplastic-mediated processes. In this context, the etiology of facial paresis differs when comparing the adult and pediatric populations. In adults, facial paresis most often occurs in the setting of cholesteatoma, whereas in children, AOM will precede the onset of facial paresis.

Labyrinthitis

Patients with labyrinthitis present with sudden sensorineural hearing loss, severe vertigo, and nystagmus accompanied by nausea and vomiting. In the setting of middle ear infection, bacterial infection can invade through the round window causing acute suppurative labyrinthitis. From the labyrinth, bacteria gain access to the cochlear aqueduct, forming a conduit between the perilymph and the cerebrospinal fluid (CSF) resulting in meningeal infiltration. It is important to diagnose and treat labyrinthitis early as to prevent the subsequent development of meningitis.

Intracranial Complications

Intracranial complications, including meningitis, encephalitis, otitic hydrocephalus, and abscess, are rare but serious, resulting from severe or neglected AOM (Figure 49–1). In children who develop fever, headache, photophobia, fluctuating mental status, and neck rigidity within hours of AOM, meningitis should be suspected. Furthermore, if patients also present with unilateral of bilateral congenital sensorineural hearing loss and vestibular symptoms, a Mondini malformation should be considered. Mondini malformations allow for communication between the CSF and the middle ear space through the stapes footplate or round window to the vestibule or cochlea. Meningitis secondary to AOM should be treated urgently with a myringotomy.

Otitic hydrocephalus typically presents as headaches and lethargy without evidence of meningeal signs or intracranial abscess. Often associated with papilledema, otitic hydrocephalus is defined as increased intracranial pressure secondary to AOM or OME.

Extradural, subdural, and brain abscesses are all severe, uncommon complications of untreated AOM. The most commonly cultured organisms from these abscesses include streptococci, Staphylococcus aureus, Streptococcus pneumoniae, Haemophilus influenzae, Pseudomonas aeruginosa, Bacteroides fragilis, and Proteus. Once diagnosed, both brain and subdural abscesses require urgent neurosurgical intervention for drainage. In contrast, extradural abscesses can be approached via mastoidectomy while addressing underlying middle ear disease.

The sigmoid (or lateral) sinus lies in close proximity to the mastoid cavity. If virulent AOM or mastoiditis penetrates the sigmoid sinus, sigmoid sinus thrombophlebitis may occur. Patients present classically with diurnal or “picket fence” fever curves, septicemia, and torticollis. Systemic signs and symptoms occur due to the showering of infected emboli both proximally and distally to the sigmoid sinus. MRI with gadolinium is considered to be the gold standard for diagnosis of sigmoid sinus thrombophlebitis.

Complications of Ome

As noted above, substantial overlap exists in terms of complications resulting from AOM and OME. In contrast to the acute process, OME exhibits disease chronicity, symptoms expressed over longer periods of time.

Conductive Hearing Loss & Speech Delay

Conductive hearing loss is a well-studied complication of OME. Hsu et al. report “average duration of effusion in patients with chronic OME as 5.5 months” and “duration of AOM prior to referral as 9.3 months.” While OME-associated hearing loss is temporary, it is not fleeting and can have a significant impact on development. Studies suggest that the intermittent, fluctuating hearing loss caused by OME can influence certain aspects of language including articulation, receptive vocabulary, and phonologic awareness.

Atelectasis

Atelectasis in the setting of OME refers to either a grossly retracted or collapsed TM. TM retraction occurs when the negative pressure in the middle ear space accumulates, most often as a result of chronic Eustachian tube dysfunction. Over time, a retracted TM may lead to ossicular erosion and conductive hearing loss, which may be salvageable only through surgical repair. In the event that the TM is partially ateletatic, a localized retraction pocket can form leading to an altered migration pattern of squamous epithelium. This disruption of migration patterns predisposes to accumulation of debris and finally, cholesteatoma formation.

Cholesteatoma

With long-term tympanic retraction, acquired cholesteatoma development may occur. Acquired cholesteatoma, a consequence of AOM, OME or both, can be further divided into two categories: primary or secondary. Primary acquired cholesteatomas classically arise in the epitympanum adjacent to the pars flaccida component of the ear drum. In comparison, secondary acquired cholesteatomas migrate through a TM perforation into the middle ear. In the setting of chronic Eustachian tube dysfunction, the normal migration pattern of squamous epithelium in the external auditory canal is agitated. Disruption of squamous epithelium can lead to accumulation of debris and cholesteatoma formation. Cholesteatoma will expand locally destroying local bone in its path including the scutum, ossicles, mastoid cavity, tegmen, or otic capsule. This destruction can lead to long-term serious complications including facial paralysis, labyrinthitis, meningitis, and hearing loss.

Otitis media is a complex, global health care problem impacting both the adult and pediatric population. The sequelae of AOM and OME are serious, functionally impairing, and potentially lethal if poorly followed or inadequately treated. Diagnosis and appropriate, timely therapy of AOM and OME are essential for reducing complications and improving overall patient quality of life.

We would like to acknowledge Philip D. Yates, MB ChB, FRCS, and Shahram Anari, MD, MRCS for their contribution to this chapter in the previous editions of CDT.