Updated: Jun 14, 2007
Inflammatory diseases of the middle ear include a broad range of pathological conditions, including acute otitis media (AOM; suppurative or nonsuppurative), bullous myringitis, granular myringitis, eosinophilic otitis media, and chronic suppurative otitis media (CSOM), with or without cholesteatoma. The range and complexity of the problems that can arise pose a challenge to the clinician, who sometimes has only subtle clues that lead to the discovery of extensive disease.
AOM is characterized by a short-lived infection (<3 mo) that may be initially viral and then bacterial in origin. Patients generally experience pain and some hearing loss and often develop a fever. Discharge from the ear usually accompanies this infection in patients with acute suppurative otitis media.
CSOM has traditionally been classified into safe ear disease and unsafe ear disease. Safe ear disease, sometimes called tubotympanic disease, is characterized as a central perforation of the pars tensa with the inflammatory process affecting the mucosa of the middle ear cleft. Unsafe ear disease, sometimes called atticoantral disease, is typified by a marginal perforation of the posterosuperior pars tensa or pars flaccida. Cholesteatoma is frequently present in CSOM with posterosuperior perforations. Partially due to induced bony erosion and secondary infection, cholesteatomas can lead to potentially devastating sequelae. Admittedly, all cases of CSOM, including those described above as safe, can be associated with serious intracranial complications. Therefore, the term safe does not adequately categorize any cases of CSOM.
CSOM can be more simply divided into mucosal disease and cholesteatoma. Mucosal disease is typified by a bacterial infection of the middle ear cleft with the presence of pus, associated with discharge through a pars tensa perforation, for longer than 3 months. Acquired cholesteatoma, usually arising from the pars flaccida skin, typically involves the epitympanum and the mastoid antrum and, as stated above, can be erosive, causing serious complications.
Eosinophilic otitis media is an intractable middle ear disease associated with bronchial asthma and nasal allergy that sometimes induces deterioration of sensorineural hearing loss. How eosinophils accumulate in the middle ear has yet to be determined; active eosinophilic inflammation may occur in the entire respiratory tract, including the middle ear, in patients with this disease. EOM often produces a yellow and highly viscous middle ear effusion and can cause symptoms that range from prolonged hearing loss and otorrhea to sudden deafness. The middle ear symptoms are unresponsive to conventional treatments for otitis media and are instead treated with steroids.1
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:
One third of all antibiotics purchased for children are for the treatment of otitis media.2
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 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.
Over the last 20 years, the incidence of AOM increased by 68% in Finland, while that of repeat AOM increased by 39% in the United States. In developed countries, the current prevalence of secretory otitis media (SOM) is 20% in infants. In the United Kingdom, the incidence of active CSOM in the adult population was reported to be 0.6%. An Israeli study estimated the annual incidence of CSOM in children (birth to age 15 y) to be 39 cases per 100,000 population.
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.
The 2 most common complications of suppurative otitis include mastoiditis and facial paralysis. 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 3500.3
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. The most common complication was meningitis.
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.
In most studies on the incidence of acute suppurative otitis media, little difference exists between males and females.
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.
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.
External Ear, Inflammatory Diseases
Culturing of the discharge after a spontaneous perforation in patients with acute suppurative otitis media is reliable in only the first few hours because external ear canal flora contaminates the otorrhea.
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. 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 re-evaluating the patient at this time.
Recent guidelines from the AmericanAcademy of Pediatrics and AmericanAcademy of Otolaryngology-Head and Neck Surgery have helped 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.
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.
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.
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.
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.
250 mg PO q8h; doubled in severe infections
<10 years: 90 mg/kg PO divided bid
>10 years: Administer as in adults
Increased risk of rash; reduced excretion of methotrexate (increased risk of toxicity); excretion of penicillins reduced by probenecid
Documented hypersensitivity
B - Usually safe but benefits must outweigh the risks
History of allergy; renal impairment
Has an antibacterial spectrum similar but not identical to that of penicillin; alternative for patients who are allergic to penicillin.
250-500 mg PO q6h or 0.5-1 g PO q12h; in severe infections, not to exceed 4 g/d
<2 years: 125 mg PO q6h
2-8 years: 250 mg PO q6h; double dose for severe infections
>8 years: Administer as in adults
Coadministration may increase toxicity of theophylline, digoxin, carbamazepine, and cyclosporine; may potentiate anticoagulant effects of warfarin; coadministration with lovastatin and simvastatin increases risk of rhabdomyolysis; decreases metabolism of repaglinide, thus increasing serum levels and effects; avoid concomitant administration with pimozide; inhibits metabolism of methylprednisolone and possibly other corticosteroids; cimetidine increases plasma concentrations (increased risk of toxicity, including deafness)
Documented hypersensitivity
B - Usually safe but benefits must outweigh the risks
Caution in liver disease and renal impairment; estolate formulation may cause cholestatic jaundice; GI side effects are common (give doses pc); discontinue use if nausea, vomiting, malaise, abdominal colic, or fever occur; prolongation of QT interval may occur (ventricular tachycardia reported); porphyria may occur
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).
2.4-4.8 mg/d IV/IM divided qid; increase prn in more serious infections
Premature infants and neonates: 50 mg/kg/d IV/IM divided bid
Infants, 1-4 weeks: 75 mg/kg/d IV/IM divided tid
1 month to 12 years: 100 mg/kg/d IV/IM divided qid (may require higher doses)
>12 years: Administer as in adults
Increased risk of rash; reduced excretion of methotrexate (increased risk of toxicity); excretion of penicillins reduced by probenecid
Documented hypersensitivity
B - Usually safe but benefits must outweigh the risks
History of allergy; renal impairment
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.
2-3 gtt tid/qid
1 gtt qid
None reported
Documented hypersensitivity
C - Safety for use during pregnancy has not been established
Not to be used for prolonged periods (ie, >5 d)
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.
5 gtt bid for 10 d
Administer as in adults
Antacids, iron salts, and zinc salts may reduce serum levels; administer antacids 2-4 h before or after taking fluoroquinolones; cimetidine may interfere with metabolism of fluoroquinolones; ciprofloxacin reduces therapeutic effects of phenytoin; probenecid may increase ciprofloxacin serum concentrations; may increase toxicity of theophylline, caffeine, cyclosporine, and digoxin (monitor digoxin levels); may increase effects of anticoagulants (monitor PT)
Documented hypersensitivity
C - Safety for use during pregnancy has not been established.
In prolonged therapy, periodically evaluate organ system functions (eg, renal, hepatic, hematopoietic); adjust dose in renal function impairment; superinfections may occur with prolonged or repeated antibiotic therapy
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:
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.
Failure to identify intratemporal and intracranial complications of chronic otitis media that can cause significant permanent morbidity and are potentially lethal
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inflammatory diseases of the middle ear, acute suppurative otitis media, bullous myringitis, granular myringitis, chronic suppurative otitis media, CSOM, mucosal disease, cholesteatoma, otorrhea, myringotomy, adenoidectomy, transtympanic ventilation tubes, microscopic aural toilet, otitis media, acute otitis media, eosinophilic otitis media, safe ear disease, unsafe ear disease, tubotympanic disease, atticoantral disease, chronic otitis media, secretory otitis media, SOM, middle ear inflammatory diseases, mastoiditis, acute otomastoiditis
Nasir Aziz, MA, George Washington University School of Medicine
Disclosure: Nothing to disclose.
Diego Preciado, MD, PhD, Assistant Professor, George Washington University School of Medicine, Department of Otolaryngology, Division of Pediatric Otolaryngology, Children's National Medical Center
Diego Preciado, MD, PhD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Otolaryngology-Head and Neck Surgery, and Association for Research in Otolaryngology
Disclosure: Nothing to disclose.
Sanjeev Silva, MBBS, MRCS, DLO, Senior House Officer, Department of Otorhinolaryngology, Head and Neck, Facial Plastics, Great Ormond Street Hospital for Sick Children, London
Disclosure: Nothing to disclose.
John C Li, MD, Chairman, Section of Otolaryngology, Palm Beach Gardens Medical Center
John C Li, MD is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery, American College of Surgeons, American Medical Association, American Neurotology Society, American Tinnitus Association, Florida Medical Association, and North American Skull Base Society
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.
Gerard J Gianoli, MD, Clinical Associate Professor, Department of Otolaryngology-Head and Neck Surgery, Tulane University School of Medicine
Gerard J Gianoli, MD is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery, American College of Surgeons, American Neurotology Society, American Otological Society, Louisiana State Medical Society, and Triological Society
Disclosure: Nothing to disclose.
Christopher L Slack, MD, Otolaryngology-Facial Plastic Surgery, Private Practice, Associated Coastal ENT; Medical Director, Treasure Coast Sleep Disorders
Christopher L Slack, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, and American Medical Association
Disclosure: Nothing to disclose.
Arlen D Meyers, MD, MBA, Professor, Department of Otolaryngology-Head and Neck Surgery, University of Colorado School of Medicine
Arlen D Meyers, MD, MBA is a member of the following medical societies: American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, and American Head and Neck Society
Disclosure: UST Grant/research funds Consulting
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