Otitis Media

Otitis media is inflammation of the middle ear, the cavity between the eardrum and the inner ear. 


This condition is due to a viral or bacterial infection that has usually travelled up the eustachian tube, the passage that runs from the back of the nose to the middle ear. The tube may become blocked by inflammation or enlarged adenoids, causing fluid and/or pus to accumulate in the middle ear rather than draining away through the tube.

Children, particularly those under seven years, are especially susceptible to otitis media because of the shortness of their eustachian tubes; some children have recurrent attacks.


Acute otitis media can cause sudden severe earache, a feeling of fullness in the ear, deafness, tinnitus (ringing or buzzing in the ear) and fever. The eardrum may burst, discharging pus and relieving pain, in which case healing usually occurs within a few weeks.

Diagnosis and treatment

The condition is diagnosed by examination of the middle ear with an otoscope; the eardrum appears red and may bulge outwards. Treatment is with analgesic drugs (painkillers). Antibiotic drugs may be prescribed if the infection is thought to be bacterial.


A complication of otitis media is glue ear, in which a thick fluid builds up in the ear and affects hearing. Glue ear may follow severe or recurrent otitis media, which occurs mainly in children. In rare cases, the infection spreads inwards to cause mastoiditis (inflammation of the mastoid bone in the skull).

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Acute Otitis Media in detail - technical

Otitis media and middle ear effusions in detail - technical 


Otitis media represents an inflammatory condition of the middle ear space, without reference to cause or pathogenesis. Middle ear effusion is the liquid resulting from OM. An effusion may be either serous (thin, watery), mucoid (viscid, thick), or purulent (pus). The process may be acute (0 to 3 weeks in duration), subacute (3 to 12 weeks in duration), or chronic (greater than 12 weeks in duration).

Otitis media may occur with or without effusion. In those cases without effusion, inflammation of the middle ear mucous membrane and tympanic membrane may be the only physical finding. Occasionally, infection may involve only the tympanic membrane (myringitis), without involving the mucosa of the middle ear space.

Acute otitis media (AOM) represents the rapid onset of an inflammatory process of the middle ear space associated with one or more symptoms or local or systemic signs. These usually include otalgia, fever, irritability, anorexia, vomiting, diarrhea, or otorrhea.

Physical examination usually reveals a thickened, erythematous, or bulging tympanic membrane with limited or no mobility to pneumatic otoscopy. Erythema of the tympanic membrane may be an inconsistent finding and may be absent in certain systemic illnesses such as immune deficiency, when the patient cannot mount a sufficient inflammatory response to present this more classic finding.

The acute onset of fever, otalgia, and, on occasion, a purulent discharge is usually evidence of AOM. Following such an episode, the patient may move into a subacute or even chronic phase during which fluid is present in the middle ear space, although active infection may be absent.

Chronic otitis media with effusion (COME) indicates the presence of asymptomatic middle ear fluid, usually resulting in conductive hearing loss. The tympanic membrane may present numerous physical findings including thickening, opacification, and impaired mobility. An air-fluid level and/or bubbles may be observed through a translucent tympanic membrane.

This entity is distinguished from AOM in that the signs and symptoms of acute infection are lacking (eg, otalgia, fever, otorrhoea).


Eustachian tube (ET) dysfunction is considered the major aetiologic factor in the development of middle ear disease. There are essentially two types of ET obstruction resulting in middle ear effusion: mechanical and functional.

Mechanical obstruction may be either intrinsic or extrinsic.

Intrinsic mechanical obstruction is usually caused by inflammation of the mucous membrane of the ET or an allergic diathesis causing edema of the tubal mucosa.

Extrinsic mechanical obstruction is caused by obstructing masses such as adenoid tissue or nasopharyngeal neoplasms.

Some observers believe that infants and younger children may suffer from functional ET obstructionas a result of either decreased tubal stiffness or an inefficient active opening mechanism. Proponents of this theory believe that either form of obstruction results in inadequate ventilation of the middle ear with resulting negative middle ear pressure.

The eustachia tube has three functions:

  1. Ventilation of the middle ear associated with equalization of air pressure in the middle ear with atmospheric pressure
  2. Protection of the middle ear from sound and secretions
  3. Drainage of middle ear secretions into the nasopharynx with the assistance of the mucociliary system of the ET and middle ear mucous membrane

The role of allergy in otitis media with effusion (OME) has been extensively investigated. Inhalant allergies are felt to play a greater role than food allergies. Most studies, however, have been unable to demonstrate an increase in serum globulin E (IgE) in children with OME.

Allergy is felt to affect ET function in several ways. Nasal obstruction can occur secondary to mast cell degranulation with increased vascular permeability, increased mucosal blood flow, and increased mucus production.

Retrograde extension of inflammatory mediators from the anterior nose to the nasopharynx as well as allergen contact with the nasopharynx can cause ET edema and obstruction with a secondary increase in the pressure gradient through nitrogen gas exchange and subsequent transudation of fluid.

Otitis media–prone children have been shown to have higher levels of IgG antibody and IgG-antigen immune complexes in their serum and middle ears versus a non-OM-prone cohort. Immunoglobulin G may be the predominant immune mechanism in the middle ear. It is felt that bacteria may actually cause immunosuppression of cell-mediated immunity. Immunoglobulin A is thought to be a late defense mechanism and may actually prevent bacteriolysis by IgG and its complement, acting as a blocking antibody. Others have proposed an IgE-mediated hypersensitivity reaction to viral antigens.


The most common bacterial pathogens responsible for acute infection include Streptococcus pneumoniae and nontypable Haemophilis influenzae. These two microorganisms account for approximately 60% of the cases associated with bacterial infection. Group A Streptococcus, Branhamella catarrhalis, Staphylococcus aureus, and gram-negative enteric bacteria are less frequent causes of OM.

Because of the difficulty in obtaining viral cultures, less specific data are available regarding their occurrence in patients with OM. However,respiratory syncytial virus accounts for a majority of the viral infections of the middle ear space. Otitis media may accompany exanthematous viral infections such as infectious mononucleosis and measles. 

Over the years, chronic effusions have been thought to be sterile. However, more recent studies have confirmed the presence of bacteria in middle ear fluid, and studies show that the bacterial spectrum closely resembles that found in acute otitis media.


In most cases, a careful history and physical examination will lead to the accurate diagnosis of otitis media. A careful history should elicit classic symptoms of OM. In the patient with the acute form of the disease, otalgia, fever, irritability, vomiting, and diarrhea may be present. Less frequently, otorrhea, vertigo, and facial paralysis may be associated with an acute infection of the middle ear space.

In those patients in whom infection has spread into the mastoid air cell system and beyond, swelling of the postauricular area may be present.

In COME, hearing loss may be the only symptom.

The most definitive part of the diagnosis is an appropriate physical examination to confirm the presence or absence of middle ear pathology. A complete examination of the head and neck should be undertaken first to identify the possibility of any predisposing condition such as craniofacial anomaly, nasal obstruction, palatal defect, or adenoid hypertrophy.

In patients with unilateral otitis media, the nasopharynx should be visualized to rule out the possibility of neoplasm. Otoscopy represents the most critical part of the examination to establish the diagnosis of OM. Use of the pneumatic otoscope is essential.

The existence of chronic middle ear effusion is most easily confirmed when there is a definite air-fluid level or when bubbles are clearly visible within the middle ear space. However,findings commonly associated with OME include a severely retracted tympanic membrane with apparent foreshortening of the handle of the malleus and a reduction in tympanic membrane mobility. Occasionally, the tympanic membrane may be dull or thickened and have an amber hue.

In severe cases, middle ear fluid may become purplish or blue, indicating hemorrhage within the tympanic cavity. The color of the tympanic membrane is important but is not conclusive in making a diagnosis. An erythematous tympanic membrane alone may not be indicative of a pathologic condition because the vasculature of the tympanic membrane may be engorged as a result of the patient’s crying or the presence of fever.

Acute otitis media usually presents with a hyperemic tympanic membrane that is frequently bulging and has poor mobility. Occasionally, perforation may be present, and purulent otorrhea is visible. The use of tympanometry confirms the findings of pneumatic otoscopy. This modality provides an objective assessment of the mobility of the tympanic membrane as well as the ossicular chain.

By measuring tympanic membrane impedance, one can accurately predict conditions of the middle ear space. The ultimate diagnostic test to confirm the presence of OM involves aspiration of middle ear contents. In acute situations, myringotomy or tympanocentesis may be undertaken to confirm the diagnosis, obtain material for culture, and relieve pus under pressure in an effort to avoid further complications. This may be necessary in patients who are unusually ill or toxic secondary to OM or in patients with severe suppurative complications. It may also be necessary in those patients who are having an unsatisfactory response to antibiotic therapy, in toxic newborns, or in patients who are significantly immune deficient.

With the rise in bacteria resistant to initial antibiotic therapy, tympanocentesis has been examined for its role in more specific antibiotic therapy.

Tympanocentesis has several indications:

  1. Otitis media in patients with severe otalgia or toxic patients;
  2. unsatisfactory response to antimicrobial therapy;
  3. onset of otitis media in a patient already receiving antibiotics;
  4. OM associated with a confirmed or potential suppurative complication; and
  5. OM in a newborn, sick neonate, or immunosuppressed patient.

This procedure does have significant risks, including conductive and sensorineural hearing losses if not done properly. Otolaryngologists and pediatricians must be well trained in the technique to prevent these serious complications.

The hearing loss associated with otits media should be documented whenever possible, especially in patients in whom chronic effusion is present. Although the presence of a conductive hearing loss does not confirm the diagnosis of COME, its presence does contribute to the confirmation of middle ear fluid. It is also important in documenting response to therapy.


Acute Otitis Media

Acute otitis media represents one point in a continuum of the disease process known as “otitis media.”The current standard of care strongly indicates that patients diagnosed as having an acute middle ear process should receive antimicrobial therapy for at least 10 to 14 days. In light of the fact that culture material is usually not readily available, therapy is begun on an empiric basis, with treatment being aimed at the more common microorganisms found in the acute process.

Some have recommended withholding antimicrobial agents in certain cases. However, in light of the fact that suppurative complications have markedly declined during the antibiotic era, antibiotic therapy is still strongly recommended in the acute process.

The standard initial treatment for AOM is amoxicillin, 40 mg/kg/24 h in three divided doses, or ampicillin, 50 to 100 mg/kg/24 h in four divided doses, for 10 days. In children allergic to penicillin, a combination of erythromycin, 40 mg/kg/24 h, and sulfisoxazole, 120 mg/kg/24 h, in four divided doses may be substituted. If β-lactamase-producing H. influenzaeor B. catarrhalisis suspected, either amoxicillin-clavulanate 40 mg/kg/24 h in three divided doses or trimethoprim-sulfamethoxazole, 8 mg of trimethoprim and 40 mg of sulfamethoxazole/kg/24 h, may be used in two divided doses.

Cefixime (Suprax, Lederle Laboratories, Wayne, NJ), 8 mg/kg in one dose, or cefprozil (Cefzil, Bristol-Myer-Squibb, Princeton, NJ), 15 mg/kg/24 h in two divided doses, may also be used effectively. A single intra-muscular injection of ceftriaxone (Rocephin, Hoffman-Roche, Nutley, NJ), 50 to 100 mg/kg mixed with 1% lidocaine, not to exceed 1.5 mL, may be used in patients with vomiting.

Newer treatment for β-lactamase-producing microorganisms include high-dose amoxicillin at 80 mg/kg/24 h. Most patients who are receiving antibiotic therapy for AOM have significant improvement within 48 hours. If the child has not improved or the condition has worsened, tympanocentesis for culture and possibly myringotomy for drainage may be indicated.

The patient may be re-examined some time during the course of therapy to ensure that the treatment has been effective. Most children will have an effusion present at the completion of a 10- to 14-day course of antibiotic therapy. Such effusions may last up to 12 weeks before spontaneous clearance can be expected.

Additional therapy such as analgesics, antipyretics, and oral decongestants (antihistamines and sympathomimetic amines) may be useful. Oral decongestants may relieve nasal congestion, providing some aeration of the ET. Their efficacy has not been proven, however.

Repeated episodes of AOM plague many children, especially during the first 3 to 4 years of life. Several issues should be considered and evaluated in the management of such patients. A search should be made for a concomitant source of infection in the upper respiratory tract such as chronic adenoiditis or chronic sinusitis.

Mild immune immaturity, especially in the IgG subclass group, may be responsible for this relentless process. Testing of immunoglobulins should be considered in relentless cases. Prevention A heptavalent pneumococcal conjugate vaccine, PCV7 (Prevanar, Wyeth-Lederle Vaccines), has become available. PCV7 and other pneumococcal vaccines may prove to be an important step in the prevention of AOM. This vaccine is recommended for universal use in children 23 months and younger.

The American Academy of Pediatrics recommends that if immunization is initiated in infants younger than 7 months, four doses of PCV7 should be given concurrently with other recommended childhood immunizations at 2, 4, 7, and 12 to 15 months. If immunization is initiated in infants who are between 7 and 23 months of age, who have not received their prior doses of PCV7, fewer doses are recommended.

Children with congenital immune deficiency, chronic cardiac disease, infection with human immunodeficiency virus, chronic pulmonary disease, and other serious chronic conditions are especially vulnerable to pneumoccocal infection.

Chronic Otitis Media with Effusion

Medical Therapy

Chronic otitis media with effusion may occur as a sequela to AOM or in patients who have had no documented recent episodes of acute suppurative disease. Numerous associated factors must be considered; thus, a careful history should be taken for the possibility of underlying allergy, sinus disease, or nasopharyngeal obstruction, which may be secondary to hypertrophic adenoids or even neoplasm. Numerous methods of management have been advocated over the years for the persistent form of the disease. Antihistamine-sympathomimetic amine preparations were used frequently to clear the effusion.

However, controlled clinical trials have demonstrated a lack of efficacy.

The use of corticosteroids, either applied topically in the nose or given systemically, has been reported to be advantageous in clearing middle ear fluid. The proposed therapeutic mechanisms of corticosteroids include stabilization of phospholipids to prevent arachidonic acid formation and subsequent inflammatory mediator formation, possible decrease in peritubal lymphoid tissue size, enhanced secretion of ET surfactant, and reduced middle ear fluid viscosity by action on muco-proteins. Unfortunately, there is a paucity of data to demonstrate efficacy; therefore, their use cannot be strongly recommended at this time.

The most effective medical therapy used to this point has been antibiotic administration. Numerous trials have concluded that some patients may respond to a 21- to 30-day course of full-dose antibiotic therapy. The demonstration of viable bacteria in the middle ear effusions of chronically diseased ears has led to this recommendation. In light of the similarity of the bacterial spectrum, the same antibiotics recommended for AOM may be used in this disease. This form of therapy is strongly recommended in any child who has not received antibiotic treatment before consideration is given to myringotomy and ventilation tube insertion and/or adenoidectomy.

In children with concomitant disease of the upper respiratory tract such as chronic sinusitis or adenoiditis, consideration must be given to the simultaneous control of these diseases. In addition, systemic problems such as allergy or immunodeficiency must also be addressed if long-term reversal of the middle ear abnormality is to be achieved.


The use of ventilation tubes with or without adenoidectomy has become the ultimate treatment of COME. This surgical intervention immediately corrects the conductive hearing loss associated with the middle ear process and diminishes the patient’s tendency toward recurrent infection.

It should be strongly considered in the following situations:

1. Recurrent AOM a. Unresponsive to antibiotic therapy b. Significant antibiotic allergy or intolerance

2. Negative middle ear pressure with impending cholesteatoma

3. Chronic effusion of the middle ear space with a duration of greater than 3 months

a. Conductive hearing loss of greater than 15 dB

b.Nasopharyngeal neoplasm for which treatment such as radiation therapy may be necessary

Although some controversy exists over the use of ventilation tubes, they do provide a safe method for normalizing middle ear pressure and, in most cases, restoring hearing to normal. They are usually associated with minimal morbidity, although tympanosclerosis or persistent perforation may be seen in a few instances. In most circumstances, it is difficult to determine whether these findings are a result of the underlying middle ear pathology with middle ear atelectasis or secondary to the ventilation tube itself.

Numerous types of tubes are available for ventilation of the middle ear space, but basically they are all designed to provide equalization of pressure across the tympanic membrane. Some designs favor intubation of greater duration but also carry a slight risk of an increased incidence of persistent perforation on extrusion.

Depending on the age of the patient, tube insertion may be carried out under local or general anesthesia. It is usually advisable to allow spontaneous extrusion of the tubes to occur. Most tympanostomy tubes remain in the tympanic membrane for approximately 6 to 12 months, with some extruding earlier and some later.

Adenoidectomy may be useful as an adjunct to myringotomy in the treatment of middle ear effusion. Removal of adenoid tissue improves the ventilatory function of the ET, thus allowing for appropriate equalization of pressure. The adenoid has been felt to play a role in OM in two ways: when hypertrophic, by causing mechanical obstruction of the ET, and when small, as a bacterial reservoir.

There is greater long-term efficacy in the treatment of otitis media in children 4 to 6 years of age when adenoidectomy was added to tympanostomy tube placement or myringotomies even if this was the first surgical intervention in a child. Some recommmend adenoidectomy only if a child fails initial tympanostomy tube placement. Studies have also shown that the recurrence rate of acute otits media may be reduced by adenoidectomy. In addition, other confounding factors may warrant adenoidectomy such as evidence of chronic adenoiditis, nasal obstruction, or recurrent or chronic sinusitis secondary to nasal obstruction.