Inflammatory Diseases of the Middle Ear

The ciliated, pseudostratified columnar epithelium of the respiratory tract extends up the eustachian tube as far as the anterior part of the middle ear cavity. Because of the presence of goblet cells and mucus-secreting glands, this epithelium is capable of mucus production. More posteriorly, the mucosa changes patchily into a simple cuboidal or stratified epithelium with no secretory elements. The medial aspect of the tympanic membrane and the mastoid air cells are lined by a single layer of cells that range in shape from cuboidal to flat.

In the early stages of inflammation, regardless of cause, vasodilatation of the submucosal tissues occurs. Glandular secretion is stimulated with the production of a thin mucoid fluid. Some epithelial cells die, and bacteria that are usually in the area multiply in the denuded areas and aggravate the condition. The neutrophils in the blood cause a polymorphonuclear reaction, resulting in a mucopurulent discharge. This discharge may remain stagnant within the middle ear and the mastoid air cell system because of immobility or loss of the cilia, including those in the eustachian tube.

Resolution frequently occurs, but, if the condition is prolonged for some reason, such as the inability of the secretions to drain down the eustachian tube, the number of glands and goblet cells increases, and the areas formerly covered by a cuboidal or flat epithelium change into areas of a similar but perhaps less well-differentiated pseudostratified columnar epithelium. Differentiation into squamous epithelium, most frequently nonkeratinized, can also occur.

Granulation tissue results from the nonresolution of an inflammatory process. Localized areas of the mucosa become hyperplastic with invasion of fibroblasts, capillaries, macrophages, plasma cells, and lymphocytes. Granulation tissue can be covered by all the mucosal types described above, but, because the tissue is frequently ulcerated, it does not have a mucosal covering.

Anatomical considerations also contribute to the pathophysiology of middle ear diseases. The eustachian tube is important in pressure regulation of the middle ear, protection from nasopharyngeal sound pressure and secretions, and clearance (into the nasopharynx) of secretions produced within the middle ear. The eustachian tube has been found to be highly compliant in infants and young children, providing the eustachian tube with an abnormal patency. Greater patency of the eustachian tube allows not only gas to readily flow from the nasopharynx into the middle ear but also easier access for unwanted secretions from the nasopharynx. This increases the likelihood of infection.

The length of the eustachian tube is another key anatomical consideration in the pathogenesis of middle ear inflammatory disorders. The shorter the tube, the more likely secretions can reflux into the middle ear. For instance, young children with a cleft palate and those with Down syndrome have eustachian tubes that are statistically shorter than those of age-matched controls younger than 6 years, which may explain the frequent occurrence of troublesome otorrhea in these populations.

Various chemical mediators of inflammation have been described and categorized into the following groups:

• Histamine

• Lipid mediators

• Plasma enzyme systems

• Kinins

• Cytotoxins

• Neurogenic substances

Various interleukins are of particular importance in otitis media. An example of the recent ongoing work in this field is the discovery that the bone-resorbing activity of cholesteatoma with chronic otitis media may be attributed to interleukin-1 α (IL-1 α).

Frequency

United States

One third of all antibiotics purchased for children are for the treatment of otitis media.[13]

The Center for Disease Control (CDC) showed that otitis media was the principal diagnosis for 12% of ambulatory-care visits provided to children younger than 15 years.

AOM accounts for 24 million pediatric office visits and $5 billion in costs annually. A study by Tong et al indicated that in the United States between 2008 and 2014, healthcare use associated with AOM reached a mean annual incidence of 60.5 AOM cases per 1000 person-years, with this rate varying little over the investigation period. The greatest share of this utilization involved office/outpatients visits (55.7 cases per 1000 person-years). The study estimated that AOM affects 19.5 million patients each year in the United States.[14]

A study of cholesteatoma in the United States revealed an incidence of 6 cases per 100,000 population. Within this population, cholesteatoma was most common in children aged 10-19 years, with an incidence of 9.2 cases per 100,000 population.

International

A study by Hullegie et al found that during the coronavirus disease 2019 (COVID-19) pandemic, the incidence of otitis media among children aged 0-12 years declined in the Netherlands. In this pediatric population, before the pandemic, the incidence rate for AOM per 1000 child-years was 73.7, versus 27.1 during the pandemic, while the incidence rates per 1000 child-years for otitis media with effusion (OME) were 9.6 versus 4.1, respectively.[15]

Mortality/Morbidity

Since the advent of the antimicrobial era, the mortality rate associated with complications of middle ear inflammatory disorders has dramatically decreased. The mortality rates associated with otitis media and mastoiditis decreased from about 2 per 100,000 persons in 1936 to less than 0.01 per 100,000 persons in 1976.

Between 2000 and 2012, a period marked by the rise in the use of pneumococcal conjugate vaccines, pediatric mastoiditis in the United States reached its highest incidence in 2006 (2.7 per 100,000 population), while the lowest incidence was seen in 2012 (1.8 per 100,000 population).[16]

The 2 most common complications of suppurative otitis include mastoiditis and facial paralysis.[17] In developing nations, these complications remain relatively common because of the lack of adequate primary care. According to studies in developing countries, the rate in some communities was as high as 33% for perforation of the tympanic membrane, 6% for otorrhea, and 5% for mastoiditis.

Cholesteatoma, atticoantral mucosal disease, and acute suppurative otitis media cause complications by spread of infection.

Complications of CSOM are associated with high morbidity and may be life threatening. In a retrospective study, Browning calculated that the risk of a patient with CSOM developing an intracerebral abscess is 1 in 3500.[18]

Extracranial complications include chronic otitis externa and meatal stenosis, ossicular discontinuity due to ossicular erosion, middle ear adhesions, tympanosclerosis, otosclerosis, mastoid tip (Bezold) abscess, lower motor neuron facial nerve palsy, serous or purulent labyrinthitis, petrositis, Gradenigo syndrome, and labyrinthine fistula. All of these represent significant morbidity to the patient.

Intracranial complications include lateral (transverse and sigmoid) sinus thrombosis; meningitis; extradural, subdural, or intracerebral (cerebellar and temporal lobe) abscess; and otitic hydrocephalus. In a study of patients with chronic middle ear disease and cholesteatoma, 7.5% developed intracranial complications. A 2009 study by Dubey et al revealed that the most common complication was meningitis.[19]

Race

American Indians and Canadian Inuits have a strikingly high incidence of acute suppurative otitis media. In children of African and Australian Aboriginal origin, middle ear infections are more commonly severe. African American children seem to have fewer episodes of middle ear infections than American white children.

CSOM suppurative otitis media without cholesteatoma is extremely common in certain racial groups, including American Indians, Canadian Inuits, Alaskan Inuits, Australian Aborigines, and New Zealand Maoris.

In racial groups with a high incidence of central tympanic membrane perforations, such as North American Inuits and Australian Aborigines, cholesteatoma is relatively uncommon.

Sex

In most studies on the incidence of acute suppurative otitis media, little difference exists between males and females.

Age

See the list below:

• AOM falls into 2 distinct age groups; it is more common in the younger group (0-5 y) than in the older group (5-11 y). By age 6 months, about 25% of all children have had 1 or more episodes of AOM. At age 1 year, this figure rises to 62%; by age 3 years, to 81%; and by age 5 years, to 91%. After age 7 years, the incidence declines.

• The combined results of selected published studies on CSOM showed a bimodal prevalence curve with peaks of 20% at age 2 years and 15% at age 5 years.

The earliest clinical manifestation of acute suppurative otitis media is a sense of fullness in the ear with some conductive hearing loss. An earache may be present but is not severe.

In the exudative stage, the middle ear fills with an exudate, which is under pressure. Marked otalgia and fever are also present. In smaller children, anorexia, vomiting, and diarrhea may occur. Conductive hearing loss is noticeable. If the infection progresses, the tympanic membrane may perforate, initially producing hemorrhagic discharge and then mucopurulent discharge. The otalgia usually reduces after perforation.

The 2 classic symptoms of chronic suppurative otitis media (CSOM; mucosal disease) include otorrhea and hearing loss, which can affect one or both ears. The discharge varies in character, from serous or mucoid to frankly purulent, and the discharge may be intermittent or continuous. Blood-stained discharge is found in association with florid granulation tissue and aural polyps, and it is a common indicator of underlying cholesteatoma.

The predominant form of hearing loss associated with chronic middle ear disease is conductive in nature. More recently, the occurrence of sensorineural hearing loss in the ears with chronic discharge has been recognized. This hearing loss, which mainly involves high frequencies, is thought to result from the passage of bacterial toxins across the round window membrane to the cochlea.

The main symptom of CSOM with cholesteatoma is purulent otorrhea, with or without associated conductive hearing loss, similar to that of mucosal disease alone. Signs found during physical examination coupled with radiologic imaging findings are critical for the diagnosis of cholesteatoma because history symptoms are largely unreliable for determining the presence of cholesteatoma.

A study by McCormick et al indicated that during an infant’s first year, symptom severity in upper respiratory tract infection helps to predict whether concurrent AOM exists. Other factors that aid in the prediction include whether the child attends day care and whether earache and cough are present.[20]

Otoscopic examination in patients with AOM reveals a hyperemic, opaque, bulging tympanic membrane. Pneumatic otoscopy demonstrates reduced mobility. Mucopurulent otorrhea is a reliable sign.

When the diagnosis of otitis media with effusion (OME) is questionable, tympanometry can be beneficial in the examination of infants older than 4 months. Alternatively, acoustic reflectometry with spectral gradient analysis may also be used because it costs less and does not require an airtight seal in the ear canal.

Examination with an operating microscope and adequate suction equipment is required for CSOM diagnosis. In young children, a short-acting, general anesthetic is sometimes required, especially when suction is needed.

In ears without cholesteatoma, the perforation is usually of the central type. Perforations vary in size, and the activity of the disease relates to the degree of discharge. The discharge may be mucoid or purulent. Microbiological swabs should be obtained to identify aerobic and anaerobic pathogens. Pulsatile purulent discharge occurs in heavily infected cases with capillary engorgement of the middle ear mucosa.

If the size of the perforation permits, various middle ear structures can be visualized. The middle ear mucosa is either normal or edematous, and aural polyps may be present, arising from the middle ear mucosa or the margins of the perforation. The most common ossicular abnormalities include disruption of the incudostapedial joint, necrosis of the incus long process, and medial retraction and shortening of the malleus handle. Other features include secondary otitis externa in ears with profuse discharge and scars in patients who have previously undergone otologic surgery.

The hearing loss should be assessed clinically using Rinne and Weber tuning fork tests.

In patients with CSOM with cholesteatoma, the site and the extent of the tympanic membrane defect and the presence and the extent of squamous epithelium and keratin debris should be noted. The involvement of the ossicular chain and the presence of inflammatory polyps, granulation tissue, or osteitis should also be noted.

Rigid lens otoscopy is particularly useful in assessing the extent of cholesteatoma.

The use of angled endoscopes permits examination of the facial recess and the sinus tympani, which is often involved in pars tensa cholesteatoma.

Postnasal space masses can block the orifices of the eustachian tube and cause otitis media. Therefore, an examination of an adult with unilateral otitis media must include a postnasal evaluation with flexible fiberoptic nasopharyngoscopy.

Acute otitis media (AOM) prevalence varies by season, with an increased incidence in the colder months.

Day care is a major risk factor in the incidence of middle ear infections. Upper airway hygiene in children who attend day care is poor, and coughing, sneezing, and nasal dripping contaminate the environment with bacteria and viruses.

Anatomical variants, such as of the overt and submucous cleft palate, may cause recurrent episodes, often with subsequent complications.

Immunologic deficiencies and functional changes (eg, barotrauma, patulous eustachian tube) have an important influence on the incidence of middle ear infections.

Adenoid hypertrophy may be an important factor in the etiology of recurrent attacks, possibly because of its close relationship to the eustachian tube.

Passive smoking has been shown to be associated with the occurrence of otitis media, especially in preschool-aged children whose parents smoke.

Allergic rhinitis in children has been shown to be associated with higher prevalence of otitis media with effusion (OME). Inflammatory obstruction of the nasopharynx may lead to inflammatory swelling of the eustachian tube with resultant obstruction. This facilitates a reflux of bacteria-laden allergic nasopharyngeal secretions that can then enter the middle ear cavity to cause repeated bouts of otitis media.

Gastroesophageal reflux disease has also been recently implicated in the pathogenesis of OME. A recent study revealed higher concentrations (up to 1000-fold greater than serum levels) of pepsin/pepsinogen in children with OME. Although direct mechanistic causation has not been shown, the authors concluded that reflux of gastric juice into the middle ear may be the primary factor in the initiation of OME in children.

A study by Miura et al suggested that the presence of epithelium-derived thymic stromal lymphopoietin (TSLP) in the eustachian tube is essential to the development of eosinophilic otitis media. In patients with the condition, middle ear mucosa around the tympanic ostium of the eustachian tube showed immunoreactivity for TSLP, a cytokine that is key to the etiology of T-helper 2–type allergic disease. An animal model also showed immunoreactivity for TSLP, in the eustachian tube epithelium.[21]

Several studies have attempted to determine a genetic link to recurrent otitis media. A recent study examined the frequency of otitis media in infants hospitalized with respiratory syncytial virus (RSV) infection and found that a certain interferon gamma (IFN-γ) polymorphism may represent one member of a family of genes that contributes to the measured heritability of otitis media. Rates of otitis media are significantly concordant in monozygotic twins.

Culturing of the discharge after a spontaneous perforation in patients with acute suppurative otitis media is reliable only in the first few hours because external ear canal flora contaminates the otorrhea.

See the list below:

• Cholesteatoma is usually treated surgically. Bearing this in mind, radiologic evaluation serves to demonstrate any underlying anatomical variation and to assist in diagnosing both the extent and the nature of pathological change. The extent of mastoid pneumatization influences the surgical approach taken.

  • CT scanning is generally the imaging modality of choice in the assessment of cholesteatoma.

    • High-resolution CT scans can demonstrate bony erosion of the tegmen, the lateral semicircular, and the bony covering of the facial nerve. Ossicular erosion of the malleus and the incus is often visible on CT scans, although stapes erosion is frequently not demonstrated.

    • MRIs are inferior to CT scans in demonstrating bony abnormalities associated with cholesteatoma. However, MRIs help distinguish between the different pathological processes that cause soft tissue accumulation in the mastoid and the middle ear spaces.

    • MRIs are particularly useful in distinguishing among cholesteatoma, cholesterol granuloma, and inflammatory granulation tissue.

  • Radiologic documentation of ears with chronic cholesteatoma, which usually require surgery, reveals underlying anatomical variations and assists in diagnosis of the extent and the nature of the disease.

  • Plain radiographs may depict the height of the middle fossa dura and the site of the sigmoid sinus, but they usually reveal little information on the extent of disease.

    • Both CT scans and MRIs can reveal the disease and its extent.

    • CT scans reveal a nonenhancing mass eroding the bone, including the ossicles, with sharply defined smooth margins, isodense with CSF; likewise, MRI depicts a mass with a low-intensity T1-weighted signal and a high T2 signal. In practice, distinguishing between cholesteatoma and pure mucosal disease is often difficult on imaging.

  • A high-definition CT scan of the petrous temporal bone depicts the extent of the mastoid disease, although it may not assist in distinguishing cholesteatoma from mucosal disease.

• High-resolution CT scanning has allowed better detection of acute otomastoiditis. The mastoid air cells appear opacified because of mucosal swelling and the presence of mucus or mucopurulent secretions. With effective therapy, the inflammatory process can be arrested, and the mastoid air cells resume a normal radiographic appearance.

• A gadolinium-enhanced magnetic resonance scan is currently the imaging modality of choice to aid in the diagnosis of intracranial venous thrombosis and intracranial abscess.

  • With intracranial venous thrombosis, simple thrombus shows an intermediate signal; vascularized thrombus, granulation tissue, and slow-flowing blood show a high signal; and fast-flowing blood shows no signal.

  • Intracranial abscess shows a center of low attenuation with an outer rim of a high signal.

See the list below:

• Audiometry is not diagnostic, but it allows an examiner to assess the severity of the patient's condition.

  • Audiometry may also be used to monitor the progress of the patient's condition.

  • According to observations made in a prospective cohort study of 3-year-old children, dry ears have a mean hearing threshold of 17 dB, while ears with mild chronic secretory otitis media (SOM) and moderate chronic SOM have thresholds of 23 dB and 29 dB, respectively.

The degree of inflammation in chronic suppurative otitis media (CSOM) without cholesteatoma is related to clinical activity, with the most intense changes seen in ears with continuous otorrhea. First, chronic inflammatory infiltrate (eg, lymphocytes, plasma cells, histiocytes) develops with increased capillary permeability of the lamina propria of the middle ear mucosa and resultant mucosal edema. The middle ear epithelium transforms as counts of goblet cells and ciliated cells increase, with the epithelium generally becoming more glandular and secretory.

Inflammatory granulation tissue develops during the early stages of healing after the destruction of the tissue. Sometimes, polyps covered with ciliated columnar epithelium form when the granulation tissue is florid. Later, the disease is characterized by decreased vascularity, fibrosis with sclerosis, and new bone formation in the mastoid air cells.

Ossicular changes are mainly due to osteoclastic bone resorption in granulation tissue or avascular necrosis. New bone formation may occur with fixation of the heads of the malleus and the incus in the attic. A foreign body granulomatous response to cholesterol crystals can result after hemorrhage into the middle ear, with crystals surrounded by foreign body giant cells and other chronic inflammatory cells. Tympanosclerosis is associated with CSOM with hyalinization of collagen and calcium deposition and may result from a specific autoimmune reaction.

Cholesteatomatous CSOM appears macroscopically as a crystallike structure with pale debris in the middle ear cleft. Light microscopy reveals a matrix of fully differentiated stratified squamous epithelium resting on connective tissue. The central core of cholesteatoma consists of anucleate keratin squames. Other inflammatory changes are similar to noncholesteatomatous CSOM, including aural polyps. Histologically, aural polyps that consist of granulation tissue with keratin as masses or flakes suggest that cholesteatoma is a likely diagnosis. Conversely, polyps without this feature but with lymphoid aggregates, a connective tissue core with glands, and a covering epithelium make cholesteatoma a much less likely diagnosis. Epidermal Langerhans cells are found in high numbers in cholesteatoma and are thought to be epidermal macrophages.

Acute otitis media (AOM) is the most common cause of severe pain in young children. Many infections are viral in origin, especially those that accompany coryza. The most common viruses isolated include respiratory syncytial virus (RSV), influenza viruses, adenovirus, and parainfluenza. Treatment is purely symptomatic and supportive.

The role of antibiotics in the treatment of AOM remains ill defined because studies have shown that antibiotics do not affect the outcome. For instance, studies of children with persistent symptoms of AOM have shown that resistant bacteria account for only approximately 20% of these cases. This has given credence to the theory that the middle ear mucosa is infected with both bacteria and viruses simultaneously, and eradication of the bacteria with antibiotics may not be sufficient to stop the inflammatory cascades in the middle ear.

Therefore, some physician groups advocate observation and withholding antibiotics in children with uncomplicated AOM and no comorbid factors.[12] The withholding of antibiotics is based on diagnostic certainty, age, severity of the illness, and means for adequate follow-up. Observation involves monitoring the child for resolution of symptoms within 48-72 hours and reevaluating the patient at this time.

Guidelines from the American Academy of Pediatrics and American Academy of Otolaryngology-Head and Neck Surgery have helped to clarify whom to definitely treat with antibiotics. For infants younger than 6 months, prescribing antibiotics is still recommended because of the increased risk of complications in this age group, even if the diagnosis of AOM is uncertain. If the child is aged 6 months to 2 years and is severely ill (fever ≥ 39°C or moderate-to-severe otalgia) and the diagnosis of AOM is uncertain, antibiotics should be considered.

However, most doctors still universally prescribe antibiotics. Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis cause most episodes of acute suppurative otitis media. First-line antimicrobial drugs include beta-lactamase–resistant medications, such as amoxicillin with or without clavulanate and cefuroxime. Adjunctive treatment includes analgesics and antipyretics.

High doses of amoxicillin (90 mg/kg) are recommended by the guidelines; these doses result in middle ear fluid levels that exceed the minimum inhibitory concentration of all S pneumoniae, including those that have intermediate resistance to penicillin and many that are highly resistant. The recommended length of treatment is 10 days for children younger than 6 years and for children with severe symptoms; children older than 6 years can be treated for 5-7 days.

If no clinical response occurs after the first 48-72 hours of therapy, the patient should be reassessed, and further therapy should be chosen based on the most likely pathogens. H influenzae should be suspected as a causative agent in a child who has been immunized with the pneumococcal vaccine and who does not respond to first-line antibiotic therapy. Tympanocentesis should be reserved for patients in whom multiple courses of antibiotics fail in order to determine bacterial etiology.

Pain control is essential to treatment, especially in the first 24 hours after diagnosis, regardless of whether the patient is receiving antibiotics. This is an important recommendation because the pediatric population is often undertreated for pain. In addition to ibuprofen and acetaminophen, topical benzocaine can also be given for pain control. The guidelines also include the use of narcotic analgesia with codeine for severe pain.

The aim of medical treatment in uncomplicated cases of chronic suppurative otitis media (CSOM) is to eliminate infection and to control otorrhea. Treating an ear with chronic discharge requires regular otologic surveillance with microscopic aural toilet. Such treatment is particularly important when a topical medication is used to allow it to reach the middle ear in sufficient concentration.

Topical liquid agents used in the treatment of chronic middle ear disease include a combination of antibiotics, antifungals, antiseptics, solvents, and steroids. The most commonly used topical antibiotics for CSOM include quinolone derivatives, such as ciprofloxacin and ofloxacin (eg, Cipro HC Otic, Floxin), and aminoglycosides. Theoretically, topical aminoglycosides can gain access through a perforated tympanic membrane to the inner ear through the round window membrane and cause cochleovestibular toxicity.

The scientific literature contains sporadic reports of sensorineural hearing loss associated with the use of topical agents; however, clinical studies in humans fail to show significant sensorineural hearing loss attributable to their use. In severe resistant cases of CSOM that involve diffuse mucosal disease, systemic antibiotics have been used in conjunction with topical agents.

Antibiotic prophylaxis at one half of the daily therapeutic dose for an acute attack may be used and can be given for up to 6 months. Adverse effects are low. The development of increased drug resistance in upper respiratory tract organisms remains a possibility.

Preventive measures for otitis media are integral in reducing its incidence and complications. This can be accomplished by educating parents about reducing known risk factors for otitis media, including exposure to passive smoke, bottle propping, and pacifier use.

Because S pneumoniae is the most commonly reported bacterial cause of AOM, accounting for 28-55% of cases, counseling parents to the use of pneumococcal vaccines in their children can significantly reduce the incidence of AOM. Multiple studies demonstrate significant population reductions in AOM rates and antibiotic usage after universal introduction of pneumococcal vaccination.

Viral vaccines have also been associated with reducing the incidence of AOM related to viral etiologies. Encouraging children to receive the influenza vaccine can protect against episodes of otitis media during influenza outbreaks. Their exact role in reducing rates of AOM, however, remains to be epidemiologically demonstrated.

Updated guidelines for the evaluation and management of otitis media with effusion were released in 2016 by the American Academy of Otolaryngology-Head and Neck Surgery Foundation and include the following[22, 23] :

• A recommendation that children at high risk for developing otitis media with effusion—ie, those with an increased likelihood due to developmental issues or a syndrome or condition—be screened for it when the risk factor is diagnosed and again between age 12 and 18 months

• A strengthened recommendation that medical therapy for otitis media with effusion—including systemic antibiotics, systemic steroids, intranasal steroids, antihistamines, and decongestants—be employed only in exceptional circumstances

• A recommendation against using adenoidectomy to treat otitis media with effusion in children under age 4 years unless an indication for adenoid removal, such as nasal obstruction or chronic adenoiditis, is present

When correctly indicated, the surgical procedure on a diseased middle ear and mastoid must be performed meticulously and precisely; such a procedure is often demanding. The aim of surgery is to achieve a dry, pain-free ear, with possible improvement in hearing, freedom from vertigo, and reversal of a facial palsy.

Myringotomy

Myringotomy is a technique in which an incision is made in the tympanic membrane to adequately drain the middle ear.

Myringotomy is reserved for acute otitis media (AOM) associated with severe otalgia or high fever in patients who have had a poor response to antibiotics. Myringotomy is also indicated when a suppurative complication is present, in children who are acutely ill, in cases of AOM that occur during antibiotic treatment, in newborns, and in patients with primary or secondary immunodeficiency in whom an unusual organism may be present. When a myringotomy is performed, the effusion may be cultured, although it is not mandatory.

Myringotomy is performed with a myringotomy knife. The incision is made in the anterior-inferior quadrant of the tympanic membrane in a radial fashion. The incision may be placed in the posteroinferior quadrant but never in the posterosuperior quadrant because the incudostapedial joint could be damaged. Unlike in secretory otitis media (SOM), local anesthesia is inadequate for AOM.

In a retrospective study of 248 pediatric patients who received tympanostomy tubes and postoperative otic drop therapy, Conrad et al found the highest rate of tube occlusion in patients with middle ear fluid and in those with longer time to postsurgical follow-up. The investigators determined that at first follow-up, one or both tubes were occluded in 10.6% of patients. The likelihood of having unobstructed tubes was three times higher in children with no serous fluid than in children with fluid. It was also found that the chance of occlusion increased in relation to the amount of time that existed between surgery and follow-up.[24, 25]

Other procedures

Recurrent AOM in children may be due to chronic sinus infections, nasopharyngeal obstruction (enlarged and chronically infected adenoids), or cleft palate. Surgically treating these conditions (eg, with adenoidectomy) may decrease the number of ear infections.

Transtympanic ventilation tubes may be used to prevent recurrent AOM, even in the absence of a middle ear effusion, although the reason for this remains unclear.

The removal of discharge from an ear with active CSOM is essential for successful treatment. Regular surveillance and microscopic aural toilet with suction are performed until resolution of discharge. Aural toilet is particularly important when a topical medication is used to allow sufficient application.

If a patient's fitness for general anesthesia permits, cholesteatoma should be surgically treated, regardless of its association with CSOM.

Italian Society of Pediatrics

In 2019, the Italian Society of Pediatrics published updated recommendations regarding the management of acute otitis media (AOM) in children. They include the following.[6]

The assessment and treatment of otalgia should be prioritized in AOM management.

The administration of adequate doses of ibuprofen or paracetamol should be the mainstay of otalgia therapy.

All children with otorrhea, intracranial complications and/or a history of recurrence, as well as AOM patients under age 6 months, should receive prompt antibiotic treatment. Children aged 6 months to 2 years should undergo prompt antibiotic treatment for all forms of unilateral and bilateral AOM, whether mild or severe. Children over age 2 years with severe bilateral AOM should also receive prompt antibiotic therapy.

Children over age 2 years with mild or severe unilateral AOM or mild bilateral AOM can be managed with watchful waiting.

It is necessary to assess watchful waiting on a case-by-case basis and discuss it with the patient’s parents; the watchful waiting approach is appropriate only when follow-up is possible within 48-72 hours.

In children with no risk factors for bacterial resistance and no history of recurrence, uncomplicated AOM with mild signs and symptoms should be treated with amoxicillin at a dose of 80-90 mg/kg/day.

Treatment of AOM with amoxicillin-clavulanic acid 80-90 mg/kg/day (dose of amoxicillin) is recommended for children who have taken antibiotics in the last 30 days, have severe symptoms and/or purulent conjunctivitis, have a history of recurrent AOM that is unresponsive to amoxicillin, have otorrhea from a spontaneous perforation, or are at high risk of bacterial resistance (ie, those attending day care, who are not vaccinated against pneumococcus, or who reside in area with a high prevalence of resistant isolates).

Only children with a documented history of recent and/or severe allergy to penicillin should receive macrolides (clarithromycin 15 mg/kg/day). In children who are not severely allergic to penicillin, class II or III cephalosporins are recommended, since molecular cross-reaction is rare.

Treatment with amoxicillin or amoxicillin-clavulanic acid should last 10 days in children at greater risk for unfavorable evolution (ie, those under age 2 years and/or with spontaneous otorrhea).

Quinolone use should be avoided subsequent to AOM treatment failure.

Aside from pain relief therapy, it is not recommended that treatments be combined with antibiotic therapy.

Avoid systemic and topical decongestant and steroid use.

Ototopical antibiotic treatment, whether or not associated with steroid therapy, is recommended only for patients with tympanostomy tubes.

The aim of medical treatment in uncomplicated cases of AOM and CSOM is to eliminate infection and to control otorrhea. The main medical therapies include various antibiotics and topical medications. Topical agents include a combination of antibiotics, antiseptics, solvents, and steroids.

Class Summary

S pneumoniae, H influenzae, and M catarrhalis cause most episodes of AOM. These organisms are known to be sensitive to amoxicillin and ampicillin. Although a short course of topical aminoglycoside through a perforated eardrum and an infected middle ear can be used, these are not FDA approved for middle ear usage, and prolonged use is certainly not recommended because of possible ototoxic effects. Only fluoroquinolones, specifically ofloxacin, are approved for middle ear usage in draining AOM.

Amoxicillin (Amoxil)

Derivative of ampicillin and has similar antibacterial spectrum, namely certain gram-positive and gram-negative organisms. Better absorbed than ampicillin when given orally, producing higher plasma and tissue concentrations.

Erythromycin (E-Mycin, Ery-Tab)

Has an antibacterial spectrum similar but not identical to that of penicillin; alternative for patients who are allergic to penicillin.

Penicillin G benzathine (Bicillin L-A)

Remains an important and useful antibiotic but is inactivated by bacterial beta-lactamases. Parenteral therapy with benzylpenicillin is used initially in severe infections, followed by 3-7 days of oral phenoxymethylpenicillin (penicillin V).

Gentamicin with hydrocortisone (Jenamicin, Garamycin)

Aminoglycosides although commonly used topical antibiotics, controversy surrounds topical therapy because of its potential for ototoxicity. Literature contains sporadic reports of sensorineural hearing loss associated with their use. Medication must be compounded at pharmacy.

Ciprofloxacin otic (Ciloxan)

Quinolone derivatives, such as ciprofloxacin and ofloxacin, have excellent antipseudomonal activity. Fluoroquinolone with activity against Pseudomonas and Streptococcus species, methicillin-resistant Staphylococcus aureus, Staphylococcus epidermidis, and most gram-negative organisms; no activity against anaerobes. Inhibits bacterial DNA synthesis and, consequently, growth. Also available as ototopical preparations, with little demonstrable systemic effects. Approved for ophthalmic use but used ototopically off-label.

Treatment of an ear with chronic discharge requires close otologic supervision, preferably by the same clinician. Regular microscopic aural toilet using an operating microscope and a suction apparatus is needed until resolution of discharge.

Patients who have undergone mastoidectomy, particularly those with an open mastoid cavity, need regular follow-up visits. Debris, desquamated epithelium, and wax tend to collect in the cavity. Without regular cleaning of the mastoid, this debris becomes infected with persistent and recurrent aural discharge.

Many studies show that breastfeeding influences the occurrence of acute suppurative otitis media (SOM), with a lower incidence of infection in breastfed children. Many hypotheses have been suggested for this effect: the presence of immunologic (immunoglobulin A [IgA]) and nonimmunologic antiviral and antibacterial factors in breast milk; a difference in the development of facial musculature between children who are breastfed and those who are bottle-fed; an allergy to cow milk, formula milk, or both, with resultant changes in the upper respiratory tract mucous membrane; and a difference in the positioning of children during breastfeeding and bottle feeding.

Complications of SOM occur when infection spreads outside the bony walls of the middle ear and the mastoid spaces. Infection can spread to the intracranial structures or involve structures within the temporal bone. The following are intracranial complications:

• Extradural abscesses are the most common intracranial complication and occur after bone demineralization or erosion to the middle or posterior fossa dura. Spread of infection from the petrous apex can cause a middle fossa extradural abscess with resultant irritation of the trigeminal ganglion and the abducens nerve. The triad of otorrhea, facial pain, and diplopia is known as Gradenigo syndrome.

• A subdural abscess forms when infection spreads into the subdural space with the formation of granulation tissue. Neurologic deterioration rapidly occurs, with headache and drowsiness being followed (within hours) by coma and death. The treatment of an otogenic subdural abscess involves high doses of antibiotics and neurosurgical drainage. Postoperative anticonvulsants may be required. Surgical exploration of the middle ear is delayed until the patient's general condition has improved.

• Before antibiotics were developed, sigmoid and transverse sinuses, together forming the lateral sinus, could thrombose, and this condition was a common complication of acute ear infections. Today, this is much less common with acute disease and is more common following chronic suppurative otitis media (CSOM).

  • Thrombophlebitis of the lateral sinus is often associated with perisinus extradural abscess. Infected clots can cause bacteremia, septicemia, and septic embolization. Cranial extension of the thrombus may lead to thrombosis in other sinuses.

  • Untreated, the clinical picture constitutes a wasting illness, with a fluctuating picket-fence fever pattern, rigors, and headache that develops over several weeks, as well as signs of papilledema in a patient with CSOM. These clinical signs are often masked when a patient is partially treated with antibiotics.

• Meningitis remains the most common complication of SOM and is potentially lethal. Infection to the meninges usually spreads directly through necrotic bone from the middle ear. Early symptoms and signs include headache, neck stiffness, and photophobia; monitor for progression to neck stiffness and a positive Kernig sign with vomiting and high pyrexia.

• Otogenic brain abscess is a complication of CSOM, although its incidence has fallen. Even with modern diagnostic imaging and expert neurosurgical management, the mortality rates are 10-20%. Temporal lobe abscesses follow direct spread of infection through the tegmen tympani, whereas cerebellar abscesses are usually found in association with lateral sinus thrombosis. Treatment involves high doses of antibiotics and neurosurgical intervention.

• Otitic hydrocephalus is a rare complication of otitis media and refers to the finding of increased intracranial pressure in association with a middle ear infection. The cause of this condition remains obscure, but it may be due to impaired CSF resorption after lateral sinus thrombosis. Common symptoms include headache, decreased visual acuity, drowsiness, nausea, and vomiting. CT scans of the brain show normal ventricular size. Treatment to reduce intracranial pressure includes steroids and mannitol.

The following are intratemporal complications:

• Facial nerve paralysis may occur as a complication of acute or chronic suppuration within the temporal bone. In acute disease, infection spreads from the middle ear into the fallopian canal, presumably via congenital dehiscences in the canal. Prognosis of nerve recovery with antibiotics is excellent. In chronic disease, facial nerve involvement is more common with cholesteatomatous disease and is thought to be due to osteitis, bony erosion, and compression due to edema and direct infection of the nerve. In cases that do not involve cholesteatoma, a dehiscent fallopian canal is common.

• Suppurative labyrinthitis and labyrinthine fistula are due to an acute infection from the middle ear into the labyrinth via the round window. Symptoms associated with labyrinthine fistula include vertigo, otorrhea, hearing loss, headache and facial palsy. In chronic infection, these complications are due to bony erosion of the otic capsule. The bone that covers the lateral semicircular canal is the most common site affected.

• Because of the close proximity of the mastoid system, most cases of SOM have a degree of mastoid air cell inflammation. Today, clinical mastoid involvement is uncommon because of antibiotics.

• Subperiosteal abscess and postauricular fistula are complications of both acute SOM and CSOM. They are due to the spread of infection through the mastoid air cells into the soft tissue around the ear. Although these complications are now rare in the postantibiotic era, they still remain common in areas where access to health care is poor. Swelling and erythema develop behind the ear with protrusion of the pinna and loss of the postauricular crease. In chronic disease, if left untreated, a subperiosteal abscess may spontaneously rupture and lead to a postauricular fistula between the mastoid and the exterior. Treatment involves surgical excision of the fistulous tract with mastoidectomy for the underlying CSOM.

• Petrositis due to the spread of infection to the petrous apex can occur as a complication of both acute SOM and CSOM. Because of the close proximity of the petrous apex to the trigeminal ganglion and the abducent nerve, corresponding nerve palsies can occur.

• A cholesterol granuloma, an uncommon inflammatory lesion of the temporal bone associated with a giant cell reaction, can be a complication of otitis media. Bony erosion is rare.

The following are developmental complications:

• Impaired hearing and delayed speech development are the most common long-term effects of recurrent episodes of otitis.

• One study showed that children aged 8-10 years who underwent myringotomy and ventilation tube insertion to treat SOM had performance results (articulation of words, discrimination of sounds, auditory attention) that were significantly worse than those of healthy controls. Another study suggested that children with otitis media during the first 3 years of life continued to have difficulties with the comprehension of visual language, the articulation of words, attention, and reading capacity until they were aged 11 years.[26]

Surgical management of chronic inflammatory conditions of the middle ear and the associated complications pose risks to the patient. Preoperative counseling of the patient is imperative. The patient must understand the nature of these risks.

In obtaining consent, the surgeon must explain to the patient, in layman's terms, the nature, the purpose, and the material risk of the proposed procedure. Such risks include hearing loss, facial nerve paralysis, bleeding, infection, vertigo, and disease recurrence.

If necessary, the surgeon should supplement a verbal explanation with drawings or diagrams to ensure that the patient has sufficient knowledge of the proposed procedure to make an informed decision.

Preventive measures for otitis media are integral in reducing its incidence and complications. This can be accomplished by educating parents about reducing known risk factors for otitis media, including exposure to passive smoke, bottle propping, and pacifier use.

Because S pneumoniae is the most commonly reported bacterial cause of AOM, accounting for 28-55% of cases, counseling parents to the use of pneumococcal vaccines in their children can significantly reduce the incidence of AOM. Multiple studies demonstrate significant population reductions in AOM rates and antibiotic usage after universal introduction of pneumococcal vaccination.

Viral vaccines have also been associated with reducing the incidence of AOM related to viral etiologies. Encouraging children to receive the influenza vaccine can protect against episodes of otitis media during influenza outbreaks. Their exact role in reducing rates of AOM, however, remains to be epidemiologically demonstrated.