Otitis Media Clinical Presentation
- Author: Muhammad Waseem, MD, MS; Chief Editor: Ravindhra G Elluru, MD, PhD more...
Acute otitis media (AOM), with or without effusion, should be suspected in children with a history of characteristic head-neck and general symptoms.
Common head and neck symptoms of AOM include the following:
Otalgia - Young children may exhibit signs of otalgia by pulling on the affected ear or ears or pulling on the hair; otalgia apparently occurs more often when the child is lying down (eg, during the night, during nap time), which may be due to increased eustachian tube dysfunction (ETD) when the child is in a recumbent position
Otorrhea - Discharge may come from the middle ear through a recently perforated tympanic membrane (TM), through a preexisting tympanostomy tube (TT), or through another perforation; for trauma patients, excluding a basilar skull fracture with associated cerebrospinal fluid (CSF) otorrhea is important
Concurrent or recent symptoms of upper respiratory infection (URI), such as cough, rhinorrhea, or sinus congestion
Common general symptoms include the following:
Two thirds of children with AOM have a history of fever, although fevers greater than 40°C are uncommon and may represent bacteremia or other complications
Irritability may be the sole early symptom in a young infant or toddler
A history of lethargy, although nonspecific, is a sensitive marker for sick children and should not be dismissed
Gastrointestinal (GI) tract symptoms may include the following:
Otitis media (OM) with effusion (OME) often follows an episode of AOM. Consider OME in patients with recent AOM in whom the history includes any of the following symptoms:
Hearing loss - Most young children cannot provide an accurate history; parents, caregivers, or teachers may suspect a hearing loss or describe the child as inattentive
Tinnitus - This is possible, though it is an unusual complaint from a child
Vertigo - Although true vertigo (ie, room-spinning dizziness) is a rare complaint in uncomplicated AOM or OME, parents may report some unsteadiness or clumsiness in a young child with AOM
Otalgia - Intermittent otalgia tends to worsen at night
OM treatment varies widely, depending on the duration of symptoms, past therapeutic failures, and severity of current symptoms.
Exposure to environmental risk factors is another important aspect of the history and includes the following:
Passive (ie, secondhand) exposure to tobacco smoke
Group daycare attendance
Seasonality - AOM prevalence is much higher in winter and early spring than in summer and early fall
Supine bottle feeding (ie, bottle propping)
Pneumatic otoscopy remains the standard examination technique for patients with suspected OM. When performed correctly, it is 90% sensitive and 80% specific for diagnosis of AOM, and its findings are more accurate than those of myringotomy.
Proper pneumatic otoscopy technique is crucial to distinguish AOM from OME because recommended therapies for these entities are significantly different. Studies show that most practitioners improperly perform otoscopic examinations. Almost one half of physicians never use pneumatic compression of the TM during routine otoscopic examination, and almost 30% use otoscopes with inadequate light sources.
Tympanometry, acoustic reflectometry, and audiometry are important adjunctive techniques with which to evaluate patients with middle ear effusion (MEE).
In addition to a carefully documented examination of the external ear and TM, examining the entire head and neck region of patients with suspected OM is important. Several congenital syndromes, craniofacial anomalies, and systemic diseases have increased incidence associated with OM, including cleft palate, Down syndrome, Treacher Collins syndrome (ie, mandibulofacial dysotosis), hemifacial microsomia, diabetes mellitus, human immunodeficiency virus (HIV) infection, and many types of mucopolysaccharidosis.
Under direct visualization, first remove any cerumen, which causes a limited and sometimes inaccurate view of the TM and inaccurate and confusing results on tympanometry and audiometry.
To move the TM, the ear speculum must create an air seal against the external auditory canal (EAC), which is seldom possible with a standard disposable speculum. All otoscope manufacturers sell inexpensive cuffed ear speculums to perform insufflation. A rubber sleeve over the speculum may reduce patient discomfort during the examination.
Usually, the TM is in the neutral position (ie, neither retracted nor bulging), pearly gray, translucent, and unperforated. It responds briskly to positive and negative pressure, indicating an air-filled space. Many older texts emphasize a TM "light reflex" in an otherwise normal ear. Because this reflex may be absent in entirely normal ears and present in ears with MEE, the light reflex does not help confirm or exclude an OM diagnosis.
Every examination should include an evaluation and description of the following four TM characteristics:
A normal TM is a translucent pale gray. An opaque yellow or blue TM is consistent with MEE. Dark red indicates a recent trauma or blood behind the TM. A dark pink or lighter red TM is consistent with AOM or hyperemia of the TM caused by crying, coughing, or nose blowing.
The color of the eardrum is less important diagnostically than its position and mobility. Redness of the TM alone does not necessarily suggest AOM because crying, removal of cerumen with associated irritation of the auditory canal, coughing, nose blowing, and fever can all cause redness of the eardrum without a middle ear infection. Note that most children cry when their ears are examined.
A study of 85 infants showed that the otoscopic finding most predictive of AOM was a poorly mobile, bulging, yellow, and opacified TM. However, this appearance was noted in only 19% of patients. In another analysis, a slightly red TM in a normal position and with normal mobility had a predictive value of only 7% for AOM.
The position of the TM (ie, bulging, retracted, neutral, full) is key to differentiating AOM from OME. In AOM, the TM is usually bulging. In OME, the TM is typically retracted or in the neutral position.
Abnormal movement of the TM during pneumatic otoscopy can suggest various conditions or disorders. Movement during negative pressure only suggests ETD. A TM that moves only slightly with both positive and negative pressure applied indicates the probable presence of middle ear fluid. No movement occurs with a TM perforation or a TT.
Studies show that the most consistent physical finding in patients with OME is impaired mobility of the TM during pneumatic otoscopy. Pay special attention to movement of retracted segments of the TM because immobility of these sections may indicate middle ear cholesteatoma in the retraction pockets.
Single perforations are most common, but some patients may have multiple perforations.
Note the location and cause of the perforation. Perforations in the posterosuperior quadrant, which are the most difficult to detect, are important because they occasionally are associated with cholesteatoma. Pus or other fluid may drain through a perforation. Multiple perforations and otorrhea that does not yield pathogens on culture may indicate tuberculosis.
Adjunctive screening techniques
Adjunctive techniques help identify patients with asymptomatic OME, which may account for 10% of cases.
Tympanometry (ie, impedance audiometry), the most commonly used adjunctive technique, measures changes in acoustic impedance of the TM/middle ear system with air pressure changes in the EAC.
Current recommendations call for screening tympanometry at the beginning of school and 1 year later to identify children aged 4-6 years with asymptomatic OME. Tympanometry screening has a high degree of sensitivity (>90%) but is not specific for OME. The test may yield false-positive results in children with a retracted TM or a thickened TM without effusion. Screening tests may also yield invalid results in children who have cerumen obstructing the external canal or who are crying during the examination.
Middle ear pressure more than –200 daPa or a flat tympanometric curve is classified as a failure.
Further physician evaluation is indicated in a child in whom tympanometry screening fails in both ears and who has at least a 20-dB hearing loss at 1, 2, or 4 kHz.
After 2 months, retest any child in whom tympanometry screening fails in one ear and hearing loss occurs (>20 dB). Also retest children in whom tympanometry screening fails in both ears, even without marked hearing loss (ie, <20 dB). A second screening failure should lead to physician evaluation. Assess the child's hearing, speech, and language and immediately start therapy to correct deficits.
Acoustic reflectometry uses an acoustic otoscope to measure reflected sound from the TM; the louder the reflected sound, the greater the likelihood of an MEE. The breakpoint is defined as the level of sound reflectivity that correlates with the presence of MEE.
Acoustic reflectometry is rapid and easy to perform. Among its advantages over tympanometry is that an airtight seal of the EAC is unnecessary and that the test is unaffected by a crying patient or the presence of cerumen in the EAC. Despite these advantages, acoustic reflectometry has not been widely accepted by otolaryngologists because of the difficulty in setting standards to interpret test results.
Because no accepted breakpoint standards have been established, reported sensitivity and specificity vary according to the breakpoints set for each study. A low breakpoint leads to high sensitivity but low specificity. A high breakpoint leads to higher specificity but lower sensitivity.
Mastoid infections have two forms: acute coalescent mastoiditis and chronic mastoiditis with osteitis. Treatment for both types consists of a mastoidectomy.
Acute coalescent mastoiditis occurs when obstruction of the aditus (the small opening between the epitympanum and the mastoid antrum) creates a sealed space in the mastoid antrum (the air space in the mastoid portion of the temporal bone that communicates with the tympanic cavity and mastoid air cells). Acute infection of the fluid in this space usually occurs as an extension of middle ear infection. Diagnosis is confirmed with a computed tomography (CT) scan of the head that reveals loss of septation between mastoid air cells.
Chronic mastoiditis occurs when acute mastoiditis remains undetected, with subsequent changes in the mucosal lining of the mastoid air cells. Granulation tissue filled with inflammatory cells replaces the air spaces of the mastoid and middle ear, and bone necrosis with erosion may result, leading to an extracranial Bezold abscess (see the image below) or intracranial complication. Chronic mastoiditis may not be depicted on CT. Magnetic resonance imaging (MRI) reveals regions of nonspecific bright signal, consistent with inflammation.
Cholesteatomas are cystlike expanding lesions of the temporal bone, lined by stratified squamous epithelium and containing desquamated keratin and purulent material. Their etiology is controversial. Although cholesteatoma development is complicated and incompletely understood, contributing factors include ETD, increased negative pressures in the middle ear, repeated infection, chronic MEE, loss of collagen fibers and structural support of the TM, collapse of the TM, and formation of chronic retraction pockets.
Diagnosis is difficult but can be made by an experienced clinician using a pneumatic otoscopic examination in patients with chronic middle ear disease and progressive conductive hearing loss.
Treatment is surgical excision or exteriorization. In very rare cases (eg, when the patient is not a surgical candidate because the cholesteatoma is secondary to a comorbid disease), repeated cleansing under a surgical microscope may temporarily control the cholesteatoma.
Inflammation of the labyrinth produces vestibular and auditory symptoms. In patients with chronic OM (COM), bacteria may infiltrate the bony labyrinth and produce a condition of suppurative labyrinthitis. Acute symptoms include hearing loss and vertigo, which usually improve after the body goes through a phase of central compensation for the damaged vestibular organs. Prolonged labyrinth infection leads to vestibular end-organ damage and permanent hearing loss.
Diagnosis of labyrinthitis in patients with COM is most often retrospectively confirmed. Vertigo and sensorineural hearing loss in these patients is presumptive evidence for labyrinthitis.
In patients in whom hearing or vestibular function recovers, labyrinthitis is classified as serous rather than suppurative; recovery indicates that the bacteria never truly invaded the labyrinth and that the symptoms were caused by severe inflammation of the vestibular organs without bacterial invasion.
Labyrinthitis treatment includes intravenous (IV) antibiotics directed against the common pathogens in COM to limit damage to vestibular organs. Vestibular suppressants are used in the acute period to relieve dizziness and nausea.
In patients with invasive OM (especially OM with cholesteatoma), infection and inflammation of the facial nerve leads to edema and nerve fiber compression that causes facial paralysis. The facial nerve courses through the temporal bone in the fallopian canal, protected by bone and epineurium. Naturally occurring bony dehiscences of the fallopian canal and reactive osteitis (often due to cholesteatoma) place the facial nerve at risk in invasive OM.
The combination of OM with concurrent ipsilateral facial paralysis suggests an obvious diagnosis, but other entities in the differential diagnosis for acute facial paralysis should be considered. Treatment is immediate administration of IV antibiotics and/or surgical treatment of the cholesteatoma involving the facial nerve.
Meningitis is among the most common intracranial complications of OM, occurring in children with either AOM or COM. Fever accompanied by neck stiffness should immediately prompt a search for an intracranial complication. As with all intracranial complications, perform contrast-enhanced CT or MRI.
Lumbar puncture and examination of the cerebrospinal fluid (CSF) is mandatory in patients in whom meningitis is suspected. CSF leukocytosis, with low glucose and high protein and lactate levels, is characteristic of meningitis. Studies of the CSF should include Gram staining, culturing, and testing for bacterial antigens.
The treatment of choice is immediate administration of broad-spectrum IV antibiotics, followed by directed therapy based on CSF culture results. Some experts have reduced neurologic and auditory sequelae resulting from meningitis by administering dexamethasone early in the treatment course.
Epidural abscesses secondary to OM occur near the temporal bone. Infection extends to the epidural space through venous channels in the bone or by bone erosion. The most common routes for extension are through the thin bone of the tegmen to the middle cranial fossa or through the bone adjacent to the sigmoid sinus and posterior cranial fossa. Most intracranial complications are accompanied by a concomitant epidural abscess because of the pathways involved in OM spread.
Diagnosis relies on high clinical suspicion and is confirmed using contrast-enhanced CT or MRI. Treatment requires surgical exploration, with a cortical mastoidectomy and thinning of the bone overlying the tegmen tympani, sigmoid sinus, and posterior fossa to allow the epidural space to be seen. If granulation tissue or purulent fluid is discovered in the epidural space, continue removing bone until noninflamed dura is encountered.
Lateral sinus thrombophlebitis
Lateral and sigmoid sinuses are relatively unprotected from direct extension of infections from the middle ear and mastoid. Direct extension occurs secondary to bone erosion from osteitis or necrosis. Indirect extension occurs via retrograde thrombophlebitis of the mastoid emissary veins.
Obstruction of venous drainage by thrombosis can produce elevated intracranial pressure (ICP) and headache. Otitic hydrocephalous can complicate the course of lateral sinus thrombosis, leading to vision changes and sixth cranial nerve (CN VI) palsy. Septic emboli can disseminate the infection to distant body sites, and the constant bacteremia produces febrile episodes.
The classic clinical picture of high spiking fevers, headache, and active ear disease is rare.
Diagnosis of this complication relies on high clinical suspicion and is confirmed by MRI or contrast-enhanced CT demonstrating the thrombosis. Early administration of IV antibiotics and surgical exploration are the mainstays of therapy. After exposing the sigmoid sinus, a needle may be used to aspirate the sinus. If free-flowing blood returns, no further surgery is needed. If no blood returns, open and drain the sinus.
Brain abscess is the first or second most common intracranial complication of COM. Most abscesses form in the temporal lobe or cerebellum, supporting the theory that brain abscesses associated with OM are probably caused by direct extension of infection and not hematogenous spread of bacteria.
In addition to fever from the infectious process, symptoms and signs of brain abscess relate to abscess location and the overall mass effect of the abscess. Headache, vomiting, and lethargy may indicate increased ICP. Significant localizing signs include seizures, hemiparesis, cranial nerve palsies, and aphasia. Abscesses in the temporal lobe or cerebellum can exist with relatively few early localizing symptoms.
Contrast-enhanced CT or MRI is the diagnostic study of choice. The initial therapy of choice is administration of broad-spectrum antibiotics. Consult with a neurosurgeon for decisions about abscess drainage. In some patients, mastoid surgery can be performed with a neurosurgical procedure. Otologic surgery can be delayed in patients who are less stable until neurologic stability is established.
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