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eMedicine Specialties > Otolaryngology and Facial Plastic Surgery > Middle Ear & Mastoid

Middle Ear, Acute Otitis Media, Surgical Treatment

John D Donaldson, MD, FRCS(C), FAAP, FACS, Chairman, Board of Directors, Lee Memorial Health System; President-elect, Florida Pediatric Society

Updated: May 12, 2009

Introduction

In the United States, acute otitis media (AOM) is the most common affliction necessitating medical therapy for children younger than 5 years. The total annual cost to society of this disease and of otitis media with effusion (OME) runs into the billions of dollars. Yet, despite research into prevention and therapy, costs of this disease continue to rise, while incidence remains unabated. The emergence of antimicrobial-resistant bacteria requires reevaluation of the traditional management of this disease.

Surgical management of acute otitis media (AOM) can conveniently be divided into 3 related procedures: tympanocentesis, myringotomy, and myringotomy with insertion of a ventilating tube. This article examines the indications for each and appropriate selection of individual patients.

Tympanocentesis is the aspiration of the contents of the middle ear cleft by piercing the tympanic membrane (TM) with a needle and collecting that material for diagnostic examination. Normally the hole is small enough to permit healing within a day or two.

Myringotomy is the incision and drainage (I&D) procedure for acute otitis media (AOM). In this procedure, the TM is incised with a knife, which allows a fluid-filled middle ear to drain to the ear canal and the exterior. Depending upon the size of the hole and the method used to create it, the TM usually returns to normal within days to a few weeks.

Myringotomy with ventilation tube insertion is performed to maintain the opening to the middle ear to permit longer-term drainage, access for medication, or ventilation for acute otitis media (AOM) prophylaxis.

Drawing of a normal right tympanic membrane. Note...

Drawing of a normal right tympanic membrane. Note the outward curvature of the pars tens (*) of the eardrum. The tympanic annulus is indicated anteriorly (a), inferiorly (i), and posteriorly (P). M = long process of the malleus; I = incus; L = lateral (short) process of the malleus.


History of the Procedure

Mastoidectomy predates the extensive use of tympanic membrane incision, primarily because of the severity of the disease and the relatively frequent occurrence of spontaneous perforation in otitis-prone individuals. For example, in Eskimo communities of northern Canada, native Inuit are often found with large central perforations from chronic otitis.

Myringotomy, as a procedure, is a product of technology that allows the illumination of the TM with or without magnification.

Myringotomy and tube placement were attempted in the 19th century using red rubber tubes. This material caused granulation and cholesteatoma formation within the ear, and the procedure was abandoned until the mid 20th century. Tube placement was resurrected in the 1950s by Dr. Beverly Armstrong, who fashioned polyethylene tubes that were relatively nonreactive and were successfully placed. Since then, a host of tube designs and materials have been available to the otolaryngologist, each with its own weaknesses and strengths with respect retention, reactivity, and complications. Selection of any tympanostomy tube design is governed by the length of time the patient is estimated to need ventilation, by the quality of fibrous tissue of the tympanic membrane, and by the incidence any known long-term complication balanced against the benefit derived using that particular tube.

Problem

Acute otitis media (AOM) is defined by convention as the first 3 weeks of a process in which the middle ear experiences the signs and symptoms of acute inflammation. Otitis media with effusion (OME) is defined as the presence of fluid in the middle ear with accompanying conductive hearing loss and without concomitant symptoms or signs of acuity. Otitis media with effusion (OME) is classified as subacute when persisting from 3 weeks to 3 months after acute otitis media (AOM) onset and as chronic thereafter.

Frequency

In the United States
Approximately 70% of all children experience one or more attacks of acute otitis media (AOM) before their second birthday. A recent study in Pittsburgh prospectively monitored urban and rural children for the first 2 years of life. The study indicates that the incidence of middle ear effusion episodes is approximately 48% in infants aged 6 months, 79% in infants aged 1 year, and 91% in children aged 2 years. The peak incidence of acute otitis media (AOM) is in infants aged 3-18 months. Some infants may experience their first attack shortly after birth and are considered otitis prone, ie, at risk for recurrent OM. In the Pittsburgh study, the incidence was highest among the urban poor.1

Internationally
The differences in incidence between nations are influenced by racial, socioeconomic, and climatic factors.

Mortality/Morbidity
Death from acute otitis media (AOM) is rare in the era of modern medicine.

Race
Definite racial differences occur in the incidence of acute otitis media (AOM). Native Americans and Inuit have very high rates of acute and chronic ear infection, while African Americans appear to have a slightly lower rate than do white children living in the same communities.

Sex
The incidence is slightly higher in boys than in girls.

Age
Children aged 6-11 months appear to be particularly susceptible to acute otitis media (AOM), with frequency declining around age 18-20 months. A small percentage of children begin to experience acute otitis media (AOM) later in life, often in the fourth and early in the fifth year. After the eruption of permanent teeth, incidence drops dramatically, although some otitis-prone individuals continue to have acute episodes into adulthood. Occasionally, an adult with no previous history of ear disease but with an acute viral upper respiratory infection (URI) presents with acute otitis media (AOM).

Etiology

Viral Role in Acute Otitis Media

Viral infection in the nasopharynx with subsequent inflammation of the orifice and mucosa of the eustachian tube has been long understood as part of the pathogenesis of acute otitis media (AOM), although the complete role of the virus is not understood fully. Concurrent or antecedent URIs are identified in at least one quarter of all attacks of acute otitis media (AOM) in children, but the virus itself seldom appears as the pathogen in the middle ear.

Clements has shown that administration of trivalent influenza A vaccine decreases the frequency of acute otitis media (AOM) during the influenza season.2 Viruses have been recovered with increasing frequency as techniques to identify them by direct culture and by indirect means such as enzyme-linked immunosorbent assay (ELISA) testing have improved. On direct culture, the yield is less than 10%, with respiratory syncytial virus (RSV) recovered most frequently; the influenza virus is a distant second. When ELISA testing is performed on middle ear aspirates, the presence of viral antigens is detected in approximately one quarter of samples. RSV is the virus most frequently detected by this method.

The presence of viruses in the middle ear effusion may influence the outcome of therapy for otitis media (OM). Results of outcome studies have been mixed, ranging from no effect to evidence of prolongation of acuity and effusion when viruses are present in acute otitis media (AOM).

Due to RSV's high incidence of association with acute otitis media (AOM), the practitioner must be familiar with this pathogen. Most commonly, RSV is associated with bronchiolitis and pneumonia in the very young, but it may cause acute respiratory disease in persons of any age. In northern climates, RSV is normally identified during annual epidemics in the winter and early spring, but it should be suspected in any neonate with lethargy, irritability, or apnea, with or without otitis media (OM). In older infants and children, respiratory symptoms are usually more prominent, making diagnosis easier to establish.

A large ribonucleic acid (RNA) paramyxovirus, RSV was identified early as a pathogen that appeared to create long-term pulmonary complications, primarily asthma, in up to half of infants with bronchiolitis. RSV may be particularly lethal for children with congenital heart disease, cystic fibrosis, immunodeficiency, bronchopulmonary dysplasia, or prematurity of less than 37 weeks' gestational age. RSV-specific intravenous immunoglobulin prophylaxis is recommended only in children at high-risk for the condition.

When treating a child with concomitant pneumonia or other system disease and otitis media (OM), the practitioner must ensure appropriate diagnosis and management of all aspects of the child's illness. Drainage of the ear by tympanocentesis or myringotomy for culture and therapy may be necessary in some cases. Drainage is mandatory in neonates with sepsis or in children with immunosuppression.

Bacterial Pathogens in Acute Otitis Media

Pathogenic bacteria are recovered from the middle ear effusion in at least half of children with acute otitis media (AOM), and bacterial deoxyribonucleic acid (DNA) or cell wall debris is found in another quarter to third of specimens previously classified as sterile. Four species of bacteria (ie, Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, and Streptococcus pyogenes) are responsible for the preponderance of episodes of acute otitis media (AOM) in persons older than 6 weeks. Other bacteria recovered and implicated in acute otitis media (AOM) include Staphylococcus aureus, Streptococcus viridans, and Pseudomonas aeruginosa.

The emergence of resistance to antimicrobial agents is of increasing importance in the management of acute otitis media (AOM) and other bacterial illnesses. The various mechanisms used by bacteria to confer this resistance will be delineated as the common pathologic agents linked to acute otitis media (AOM) are described.

  • Streptococcus pneumoniae
    • This bacterium is the most common etiologic agent responsible for acute otitis media (AOM) and for invasive bacterial infections in children of all age groups. S pneumoniae is a gram-positive diplococcus with 90 identified serotypes (classified on the basis of the polysaccharide antigen), the frequency of which varies between age groups and geography. On direct culture, various studies have shown this bacteria to be responsible for 29-40% of isolates, but pneumococcal antigens are recovered from approximately one third of those cultures classified as sterile.
    • Pneumococcal infections are probably responsible for a minimum of one half of the acute otitis media (AOM) episodes. Serotypes 4, 6B, 9V, 14, 18C, 19F, and 23F are responsible for most invasive pneumococcal disease in America; in ear aspirates from patients with acute otitis media (AOM), serotypes 19 (23%), 23 (12.5%), 6 (12%), 14 (10%), 3 (8.5%), and 18 (6%) are most commonly isolated. Polyvalent pneumococcal vaccine confers immunity to approximately 85% of those serotypes responsible for acute otitis media (AOM).
    • Until recently, this bacterium was susceptible to almost all common antibiotics, including penicillin G, erythromycin, and even most sulfonamides. Alteration of the cell wall's penicillin binding protein has led to widespread resistance to beta-lactam compounds, macrolides, and sulfonamides by alteration of the antimicrobial target. These mutations are termed multiple drug resistant strains (MDRS). Resistance rates as high as 40% have been reported for these 3 therapeutic antimicrobial groups. Serotypes 6B, 9V, 14, 19A, 19F, and 23F have the highest frequency of resistance to penicillin. Ceftriaxone, cefotaxime, rifampin, and vancomycin still appear to have therapeutic efficacy, as does immunization with polyvalent pneumococcal vaccine for prevention.
    • Unfortunately, polysaccharide antigens are not immunogenic early in life. To overcome this problem "conjugated" antigens, in which the polysaccharide antigen is attached to a protein carrier, may be administered to induce production of antibodies to these bacterial capsular polysaccharides. Some conjugated antigens (eg, vaccinations to H influenzae type b [Hib]) are in widespread use. A heptavalent vaccine to S pneumoniae is now in widespread use and appears to confer long-term immunity to 7 of the most common and invasive strains.
  • Haemophilus influenzae
    • In middle ear aspirates from patients with acute otitis media (AOM), H influenzae is the second most frequently isolated bacterium and is responsible for approximately 20% of episodes in preschool children. The frequency may be higher in otitis-prone children, older children, and adults who have received pneumococcal vaccine. The bacterium is a small, pleomorphic, gram-negative coccobacillus. Those bacteria encapsulated with a polysaccharide coating are classified into 6 distinct types (a-f), while nonencapsulated types are termed nontypeable and are responsible for the great majority of acute otitis media (AOM) episodes. (The nonencapsulated strains have been subtyped biochemically and antigenically, but this classification has limited clinical application to date.)
    • Traditionally, Hib has been found responsible for most invasive illnesses attributed to these bacteria and for meningitis, epiglottitis, and septicemia. Hib accounts for only 10% of all episodes of acute otitis media (AOM) in which H influenzae is recovered.
    • In areas of the world where the aforementioned Hib-conjugated vaccine is administered early in life, risks from this potentially lethal strain have diminished greatly. Antimicrobial resistance by these bacteria almost exclusively (95%) is due to formation of a single enzyme, triethylenemelamine 1 (TEM1) lactamase, which is formed by as many as 40% of all nontypeable strains in some series. This resistance is overcome relatively easily by using blocking agents, extended-coverage cephalosporins, broad-spectrum macrolides, or sulfonamides.
  • Moraxella catarrhalis
    • In the mid 1970s, this common organism was classified as nonpathogenic in middle ear infections, although, when previously known as Neisseria catarrhalis, it had constituted approximately 10% of all isolates from middle ear aspirates. At that time, M catarrhalis was almost universally susceptible to ampicillin-type penicillins. Twenty years and 2 name changes later (ie, N catarrhalis to Branhamella catarrhalis to M catarrhalis), it is isolated in up to a quarter of children with acute otitis media (AOM), and resistance to the ampicillin-type beta-lactams is almost universal. M catarrhalis is a gram-negative diplococcus and is considered part of the normal flora of the human upper respiratory tract.
    • Resistance is conferred by the secretion of multiple isoenzymes of lactamase, which may be plasmid or chromosomal in origin and which may be inducible (ie, present only in low levels until a substrate is provided). More than 1 isoenzyme may be secreted by a single bacterium. To date, almost all forms are blocked by clavulanic acid, and most are still susceptible to sulfonamides, lactamase-stable cephalosporins, or broad-spectrum macrolides. M catarrhalis often is found to coexist with other airway pathogens. The lactamases (cephalosporinases) that M catarrhalis secretes may protect those other bacteria from antimicrobial agents to which the second target pathogen ordinarily might be susceptible.
  • Streptococcus pyogenes: This bacterium, group A streptococci (GAS), while still occupying the fourth spot in frequency of isolates from ears with acute otitis media (AOM), has shown a steady decline in frequency of recovery from the ear and in virulence over the past half-century. Similarly, a substantial decline in the major complications of streptococcal infection, rheumatic fever, glomerulonephritis, and scarlet fever, has occurred. GAS may be associated with streptococcal toxic shock syndrome, which may include coagulopathy, soft tissue necrosis or fasciitis, desquamating rash, and liver or renal involvement. GAS, a gram-positive coccus, primarily is a pathogen of the pharynx with more than 80 distinct M-protein strains identified. Now, with the improvement in primary care and the availability of rapid identification tests, early aggressive treatment normally is instituted against this bacterium, which has shown minimal ability to develop resistance to antimicrobial agents.
    • Acute necrotic otitis media
      • In the early 1900s, acute necrotic otitis commonly was associated with scarlet fever, although the condition also was associated with measles, pneumonia, and influenza. Generally, the patient was extremely ill with the systemic component of the disease and presented with a spontaneous perforation shortly after the onset of otalgia. Early inspection of the ear showed the perforation was already of moderate-to-large size; within days, significant evidence of tissue necrosis would be observed, perhaps including the entire tympanic membrane, ossicles, tympanic mucoperiosteum, or the bone of the mastoid air cells. The patient demonstrated a marked conductive hearing loss, although sensorineural loss was not uncommon.
      • Pathologically, the ear showed a marked paucity of the normal vascular proliferation associated with an inflammatory reaction. Instead, a complete loss of the vascularity normally associated with vasculitis or toxin exposure occurred. Healing was never normal; tissue was replaced by epithelial invasion or scar tissue formation. In industrialized societies, acute necrotic otitis media now is primarily of historic interest. The disease still is reported in aboriginal peoples living in areas where modern medicine has not yet penetrated. Thomas Edison appears to have suffered from the sequelae of this condition, according to historical research by Dr Robin Brown.
    • Acute coalescent mastoiditis: GAS also appeared to have been the most prominent organism recovered from patients with acute coalescent mastoiditis in the preantibiotic era. In the 1990s, GAS relinquished this distinction to S pneumoniae but remains a prominent pathogen when this disease is encountered in the very young.
  • Other aerobic pathogens:Except in neonates and children with chronic disease, few other pathogens have been demonstrated in aspirates from the middle ears of immunologically intact individuals. S aureus is recovered rarely, except in Japan, where studies indicate a somewhat higher incidence (up to 10%) may exist. Mycobacterium tuberculosis is associated most often with chronic otitis media (COM) but should be considered when a patient presents with painless otorrhea as an initial complaint. Consider any patient with a compromised immune system at risk for such an opportunistic infection. Chlamydia pneumoniae has been shown to be an uncommon but significant pathogen in acute otitis media (AOM) and responds only to macrolide therapy.
  • Anaerobic bacteria:Anaerobic bacteria have been recovered from the middle ears of children with acute otitis media (AOM), but the data do not support a prominent role for these microorganisms in otitis media (OM), at least in the acute form. When recovered from ears of children with acute otitis media (AOM), the anaerobic pathogen most often is not the sole pathogen cultured.
  • Acute otitis media in the neonatal period
    • In the perinatal period, the gram-negative bacteria Escherichia coli, enterococci, and group b S pyogenes are the most common etiological agents responsible for sepsis and meningitis. These agents are often recovered from the middle ear, although the total percentage probably is less than 10% of neonates with acute otitis media (AOM).
    • S pneumoniae remains the most common pathogen responsible for acute otitis media (AOM) in all age groups, including the neonate. The nonencapsulated H influenzae or nontypeable varieties may be invasive in these neonates and constitute the second-most common pathogen recovered from the ear. As bacteremia is common in all neonates with acute otitis media (AOM), tympanocentesis should be undertaken, for both diagnosis and therapy, in any infant with signs of acute otitis media (AOM) or generalized sepsis and any middle ear effusion.

Immunology in Acute Otitis Media

Immunological activity may play a significant role in the frequency of acute otitis media (AOM) and its outcome. While most research has focused on the immunological aspects of otitis media with effusion (OME), certain relationships between acute otitis media (AOM) and the patient's immune status have been demonstrated, as follows:

  • Production of antibodies may promote the clearance of middle ear effusion following an acute attack.
  • Previous exposure or immunization may have a preventative role by suppressing colonization of the nasopharynx by pathogens.
  • Formation of antibodies during an attack may prevent or modify future attacks. Unfortunately, antibodies to both S pneumoniae and H influenzae are of the polysaccharide type and develop late unless conjugated to proteins.
  • Minor and/or transient immunological defects may give rise to recurrent OM.

Much attention has been focused on the immunoglobulins and the patient's ability to form them. Immunoglobulin G2 (IgG2) and immunoglobulin G4 (IgG4) are responsible for immunity against polysaccharide antigens; deficiencies in formation of these antibodies invariably lead to OM. Research has demonstrated that many patients with Down syndrome have decreased function of immunoglobulin A (IgA), IgG2, and/or IgG4, partially explaining their increased risk for chronic rhinitis and OM.

The immunologic aspects of acute otitis media (AOM) are not confined to the middle ear. The nasopharynx plays an important role in the pathogenesis of acute otitis media (AOM), and immunologic modifications in this lymphoid tissue provide some protection from pathogens by preventing their adherence to mucosal surfaces. The presence of nasopharyngeal IgA antibodies to pneumolysin toxin released by pneumococcal autolysis appears to protect against invasion by healthy pneumococci. Conversely, not all immunoglobulins in the nasopharynx are protective. Bernstein describes effects of immunoglobulin E (IgE) hypersensitivity or hyperimmune effects on the eustachian tube mucosa.3 The allergic response in the nasopharyngeal end of the eustachian tube promotes stasis and subsequent formation of middle ear effusion.

Pathophysiology

Obstruction of the eustachian tube appears to be the most important antecedent event associated with acute otitis media (AOM). The vast majority of acute otitis media (AOM) episodes are triggered by an upper respiratory infection (URI) involving the nasopharynx, usually of viral origin, but allergic and other inflammatory conditions involving the eustachian tube may create a similar outcome. Inflammation in the nasopharynx extends to the medial end of the eustachian tube, creating stasis and inflammation, which, in turn, alters pressure within the middle ear. These changes may be either negative (most common) or positive, relative to ambient pressure.

Stasis also permits pathogenic bacteria to colonize the normally sterile middle ear space by direct extension from the nasopharynx by reflux, aspiration, or active insufflation. The response is the establishment of an acute inflammatory reaction characterized by typical vasodilatation, exudation, leukocyte invasion, phagocytosis, and local immunological responses within the middle ear cleft to give the clinical pattern of acute otitis media (AOM).

In a minority of otitis-prone children, the eustachian tube is patulous or hypotonic. Children with neuromuscular disorders or abnormalities of the first or second arch most likely are "too open" and are predisposed to reflux of nasopharyngeal contents into the middle ear cleft. To become pathogenic in hollow organs, such as the ear or sinus, most bacteria must adhere to the mucosal lining. Viral infections that attack and damage mucosal linings of respiratory tracts may facilitate the ability of the bacteria to become pathogenic in the nasopharynx, eustachian tube, and middle ear cleft. This postulate might explain the recovery of viral antigens from middle ear aspirates in children with acute otitis media (AOM), while only rarely is the actual virus isolated. Data also have been presented indicating that mucosal damage by endotoxins secreted by bacterial invaders similarly may enhance adhesion of pathogens to mucosal surfaces.

Presentation

History
Patient history of acute otitis media (AOM) varies with age, but a number of constant features manifest during the otitis-prone years. Irritability or feeding difficulties may be the only indication of a septic focus in the neonate. Older children begin to demonstrate a consistent presence of fever (with or without a coexistent URI) and otalgia or ear tugging. These latter symptoms are not entirely exclusive to acute otitis media (AOM), as teething pain or pharyngitis (particularly coxsackievirus infection) can mimic these symptoms.

In older children and adults, hearing loss becomes a constant feature of acute otitis media (AOM) and OME, with complaints of ear stuffiness noted even before the detection of middle ear fluid. Otalgia without hearing loss or fever is observed in adults with external otitis, dental abscess, or pain referred from the temporomandibular joint. Orthodontic appliances often elicit referred pain as the dental occlusion is altered.

Physical
A thorough clinical examination has no substitute. Pneumatic otoscopy is the standard of care in the diagnosis of acute otitis media (AOM) and COM. In acute disease, the tympanic membrane normally demonstrates signs of inflammation, beginning with reddening of the mucosa and progressing to the formation of purulent middle ear effusion and poor tympanic mobility. The tympanic membrane may bulge in the posterior quadrants, and the superficial epithelial layer may exhibit a scalded appearance. Perforation of the tympanic membrane is not unusual as the process advances, most frequently in posterior or inferior quadrants. Prior to or instead of a single perforation, an opaque serumlike exudate oozing through the entire tympanic membrane sometimes is seen.

With perforation and in the absence of a coexistent viral infection, the patient generally obtains rapid relief of pain and fever. The discharge initially is purulent, although it may be thin and watery or bloody; pulsation of the otorrhea is common. Otorrhea from acute perforation normally lasts 1-2 days before spontaneous healing occurs. Otorrhea may persist if the perforation is occupied with mucosal swelling or polypoid changes that can act as a ball valve.

Other considerations include the following:

  • Bullous myringitis
    • Pneumatic otoscopy is an important diagnostic tool when differentiating acute otitis media (AOM) from acute bullous myringitis. The latter, in its purest form, presents 10-14 days following a viral infection and gives severe localized otalgia without middle ear effusion.
    • The bullae or blebs may contain serous or hemorrhagic fluid and may extend onto the adjacent canal wall. Pain is relieved by puncturing the bleb. Similar blebs may occur in association with acute otitis media (AOM).
    • These patients demonstrate more systemic symptoms and continue to have pain associated with purulent middle ear effusion, which persists following rupture of the blebs.
  • Immunosuppressed patients
    • Remember that the descriptions above are for patients who are immunocompetent. Children who are immunosuppressed, particularly those undergoing chemotherapy, may not manifest the typical inflammatory responses described.
    • In these patients, the simultaneous appearance of systemic sepsis and a serous middle ear effusion might be the only indicators of acute otitis media (AOM).
  • Danger signs of possible impending complications
    • Sagging of the posterior canal wall
    • Puckering of the attic
    • Postauricular swelling with loss of the skin crease
  • Systemic examination
    • A finding of acute otitis media (AOM) does not relieve the practitioner of the responsibility to search for coexistent related or unrelated conditions. This responsibility is particularly important when antimicrobial agents are prescribed to ensure appropriate simultaneous coverage of coexistent infections such as acute otitis media (AOM) with streptococcal pharyngitis or mycoplasmal pneumonia.
    • Transtympanic measurements of temperature in children with middle ear effusions have been shown to be inconsistent. Accordingly, measure body temperature using oral, rectal, or axillary means.

Causes
The following are proven risk factors for OM:

  • Patient factors
    • Prematurity and low birth weight
    • Young age
    • Early onset
    • Family history
    • Race (Native American, Inuit, Australian Aborigine)
    • Altered immunity
    • Craniofacial abnormalities
    • Neuromuscular disease
    • Allergy
  • Environmental factors
    • Day care
    • Crowded living conditions
    • Low socioeconomic status
    • Tobacco and pollutant exposure
    • Use of pacifier
    • Prone sleeping position
    • Fall or winter season
    • Not breastfed, prolonged bottle use

Indications

Generally, indications for these 3 procedures can be divided into 3 categories: diagnostic, therapeutic, and prophylactic. More than one indication for selection of the appropriate procedure may need to be considered on a case-by-case basis.

Selection of the appropriate procedure results from evaluation of a number of considerations categorized into patient factors, surgeon factors, available resources, and urgency. Each of these aspects must be examined to select that procedure that gives the optimal predicted outcome.

With increasing antimicrobial resistance, surgical intervention in the form of tympanostomy tube placement can be expected to increase in the coming years, after having fallen into disfavor in the past two decades when resistance was less of a factor. In the author's practice, children younger than 15 months and those in day care centers are most likely to require surgery.

  • Diagnostic procedure - Tympanocentesis
    • Consider tympanocentesis in (1) children who are immunosuppressed or immunocompromised, (2) neonates with acute otitis media (AOM), because they are more likely to have an unusual or more invasive pathogen, (3) patients who have exhibited antimicrobial failure and continue to experience local or systemic signs of sepsis, and (4) patients who have had a complication of acute otitis media (AOM) in conjunction with attempts to recover the etiological agent from other sites such as cerebrospinal fluid (CSF) and/or blood.
    • Additionally, tympanocentesis remains a valuable research tool in the evaluation of new antimicrobial agents for efficacy in acute otitis media (AOM) and for identification of host defense mechanisms or flaws in the middle ear immunochemistry.
  • Therapeutic procedure - Myringotomy
    • A myringotomy may be an extension of a tympanocentesis or a separate incision of the tympanic membrane to provide drainage of the middle ear cleft to the ear canal.
    • Any number of instruments from knives to lasers are available to perform this task, but the basic principles remain constant. The hole design, established either by size, by the application of material to retard healing, or by the type of initial tissue damage, is the primary factor in controlling how long the perforation remains open, which, in turn, is determined by patient need.
  • Extended relief - Myringotomy with tube insertion
    • Some patients with acute otitis media (AOM) require ventilation and/or drainage of the middle ear cleft for an extended period of time (eg, patients with mastoiditis), while others may have a history of repetitive attacks. These patients benefit with the placement of a tympanostomy tube at the time of myringotomy.
    • The selection of the design of the tube is governed by the need to ventilate for varying lengths of time. Tube design permits tube placement for 6-9 months, 9-18 months or longer than 2 years, and selection is governed by patient need versus the increasing complication rates associated with prolonged ventilation.

Relevant Anatomy

Incision of the tympanic membrane (TM) is primarily governed by the relationship of the structures behind the tympanic membrane. We divide the TM into quadrants with an imaginary line drawn vertically along the long process of the malleus extending to the inferior annulus and a horizontal line at the umbo. Generally, the TM can safely be incised in all quadrants except the posterior superior section, behind which lie the incus and stapes, which might be injured inadvertently by incision in this area. Two other structures, the facial nerve and the round window, are generally protected from anyone but the clumsiest of surgeons, the former by its high position in the middle ear and the latter by the overhanging niche.

Tubes are generally placed anteriorly, either superiorly or inferiorly. Because the posterior segments are deeper and have more vibratory motion, posterior placement gives a greater dampening effect. Anteriorly, any incision should avoid exposure of the malleus, the malleolar ligament, and the annulus, as this creates a greater tendency for perforations to persist after extrusion of the tube.

Contraindications

Contraindications for incision of the tympanic membrane (TM) are relatively few in the presence of acute disease as discussed under indications. In 25 years of practice, the author has twice managed to tap through "thick TMs" to find himself aspirating CSF from low-hanging and exposed dura (one associated with a porencephalic cyst). Neither resulted in a prolonged complication, but CSF may be obtained with considerably less excitement via a spinal tap.

Patients with patulous eustachian tubes most frequently have persistent otorrhea after placement of tympanostomy tubes. Children with neuromuscular disease, unrepaired cleft palates, or Down syndrome are more prone to this outcome. Otorrhea may be the lesser evil when the child is septic, uncomfortable, or damage to the middle ear cleft is imminent. This contraindication is a relative one and the parent needs to be informed of the risk and participate in the decision to proceed.

Workup

Laboratory Studies

Culture and sensitivity from a fresh perforation or a tympanocentesis may be helpful in the ongoing management of the residual infection. Early indication of the etiologic agent may be obtained from a Gram stain of the aspirate; however, more than one species of bacteria may be present in the middle ear.

Imaging Studies

CT scanning may be necessary to determine if a complication such as coalescent mastoiditis has occurred, but in the absence of any such suggestion, imaging is unnecessary. MRI may be more appropriate when an intracranial complication is suspected.

Other Tests

  • Audiometry
    • All children with acute otitis media (AOM) have conductive hearing loss associated with the middle ear effusion; consequently, testing in the acute phase probably is unhelpful.
    • Tympanometry may assist in the diagnosis of middle ear effusion but, for the skilled pneumatic otoscopist, is seldom necessary.

Treatment

Medical Therapy

Acute otitis media (AOM) has been described as a self-limiting disease provided the patient does not succumb to a complication. This is an old description, but in the new millennium, practitioners will be forced to observe the lessons of history because these may serve as our models of life without effective antimicrobials. Presently, a chorus of advocates recommends withholding antibiotic therapy for patients with acute otitis media (AOM). Despite these advocates, the overwhelming consensus remains that antibiotics are the initial therapy of choice for acute otitis media (AOM) for 3 very valid reasons, as follows:

  • After institution of antibiotic therapy, a marked decline in the suppurative complications of acute otitis media (AOM) has occurred.
  • Practitioners cannot predict with certainty which patients will develop complications.
  • Studies have demonstrated that use of antibiotics improves patient outcome in both the early and late phases of acute otitis media (AOM).

Recently, some order has been brought to the discussions of antibiotic use under the auspices of the Centers for Disease Control and Prevention (CDC) and by the Agency for Health Care Policy and Research, both agencies of the US government. The CDC has published 6 principles of appropriate antibiotic use in an attempt to bring precepts of good public health and responsible therapy to the discussion, while minimizing selection of resistant strains of bacteria within the community. These principles are listed below.

Antibiotic therapy

Selection of an antibiotic, in the absence of cultures obtained from tympanocentesis, should have 2 objectives, as follows:

  • The antibiotic should cover most of the common bacterial pathogens (see Etiology).
  • The antibiotic must be individualized for the child with regard to allergy, tolerance, previous exposure to antibiotics, cost, and community resistance levels.

Duration of therapy also is somewhat empiric, and data indicate that significant numbers of children do not receive prescribed antibiotics beyond relief of acute symptoms. Ten to 14 days of therapy has been traditional and is convenient for office scheduling but may not necessarily be more efficacious than 5 days of therapy, or even 2 days.

Studies have demonstrated that short-duration therapy may not be appropriate in children younger than 2 years who appear prone to failure even after 14 days of therapy. Mandel has shown that 20 days of antibiotic therapy gives improved outcome versus 10 days of therapy or placebo, when an effusion-free ear is the prime objective. After 90 days, however, no difference in the groups existed and recurrence was not prevented by the additional therapy.

Administration of prescribed antimicrobials may differ from recommendations for the same antibiotic when used for soft tissue infections.

Pulse-dosing antibiotics, when administered for infections of hollow organs, such as the ear or sinuses, appear to have efficacy because of poorly understood antimicrobial mechanisms, increased compliance on the part of the patient or parent, and slower penetration into and removal from middle ear effusion.

Subminimal serum levels of antibiotics have been shown to disrupt adhesive bonds between bacteria and mucosal cell walls and to provide a postantibiotic effect, in which reproduction of bacteria is disrupted for a period of hours after exposure to antibiotics. Similarly, a leukocyte-enhancing action has been demonstrated at these low concentrations. When used in this manner, a marked variation exists in the effectiveness of individual antibiotics and susceptibility for the various etiologic agents.

Generally, beta-lactam antibiotics are most successful against gram-positive pathogens for both disruption of adhesion and postantibiotic effect.

Amoxicillin (erythromycin/sulfisoxazole in patients who are penicillin allergic) remains the initial treatment of choice in children with acute otitis media (AOM).

With the emergence of resistant strains, the practitioner may need to select an alternative antimicrobial therapy from either a broad-spectrum beta-lactamase-resistant cephalosporin or a combination drug such as amoxicillin/clavulanate or trimethoprim/sulfamethoxazole. Use of combination therapy may help prevent emergence of resistance by mutation, provided the pathogen is initially sensitive to both components. (Efficacy and dosages for selected antimicrobials are provided in the article, Middle Ear, Acute Otitis Media, Medical Treatment.)

With the emergence of multiple drug-resistant S pneumoniae, oral therapy consisting of amoxicillin and amoxicillin/clavulanate may have efficacy when the total amoxicillin dose reaches 80-100 mg/kg/d.

Failure of a child to respond to an antibiotic within 48 hours accompanied by local and systemic signs of toxicity may indicate resistance to the selected drug. Treatment options include an empirical change of antimicrobial agent or a drainage procedure with culture. Failure to improve with antibiotic therapy may indicate coexistent viral infection in children with prolonged acute symptoms.

  • Principles for judicious use of antimicrobials in the treatment of acute otitis media (AOM)
    • Episodes of OM should be classified as acute otitis media (AOM) or OME.
    • Antimicrobials are indicated for treatment of acute otitis media (AOM); however, diagnosis requires documented middle ear effusion and signs or symptoms of acute local or systemic illness.
    • Uncomplicated acute otitis media (AOM) may be treated with a 5- to 7-day course of antimicrobials in certain patients older than 2 years.
    • Antimicrobials are not indicated for initial treatment of OME; treatment may be indicated if effusions persist for longer than 3 months.
    • Persistent OME after therapy for acute otitis media (AOM) is expected and does not require re-treatment with antimicrobials.
    • Antimicrobial prophylaxis should be reserved for control of recurrent acute otitis media (AOM), defined by 3 or more distinct well-documented episodes in 6 months or 4 or more episodes in 12 months.
  • Other medical therapies
    • Analgesics and antipyretics have a definite role in the symptomatic management of acute otitis media (AOM).
    • Decongestants and antihistamines do not appear to have efficacy either early or late in the acute process, although they may relieve coexistent nasal symptoms.
    • Systemic steroids have no demonstrated role in the acute phase.

Surgical Therapy

Tympanocentesis and myringotomy are the procedures used to treat acute otitis media (AOM). Tympanocentesis, in its purest form, is a diagnostic procedure that gives the clinician access to acute or chronic middle ear effusion for culture and other evaluations. Generally, perform tympanocentesis without anesthesia, after sterilization of the ear canal with isopropyl alcohol or Betadine. Insert a needle through the anterior portion of the tympanic membrane, and aspirate the contents of the middle ear into a sterile trap for identification of microbes and their properties.

A tympanocentesis may be converted to a myringotomy and become therapeutic by enlargement of the hole in the tympanic membrane, often by spreading the edges with a microalligator forceps or suction tip. Instillation of antibiotic drops and suctioning of the middle ear may be performed through the myringotomy. Typically, the patient experiences prompt relief of local symptoms. Cultures must be obtained prior to extension of the incision.

The use of a carbon dioxide laser in myringotomy on children with acute otitis media (AOM) has been promoted widely and directly to the consumer by the manufacturers of these instruments; proponents claim to have ushered in a "new treatment" for acute otitis media (AOM) without the use of antimicrobials. While undoubtedly a boon to the otolaryngologist who is less technically adept, emerging studies demonstrate little or no change in efficacy over standard myringotomy.

If the patient has a suppurative complication of the temporal bone and requisite prolonged drainage seems likely, insertion of a tympanostomy tube may be needed. In most instances, general anesthesia or sedation is necessary in older children, as topical anesthesia is relatively ineffective in acutely inflamed tympanic membranes.

Complications

Complications of tympanocentesis and myringotomy are few and rare in appropriately performed procedures in children with otherwise normal anatomy. They include the following:

  • Immediate complications
    • Injury to skin of ear canal
    • Injury to ossicular chain
  • Intermediate complications
    • Persistent otorrhea
    • Persistent perforation
    • External otitis from persistent drainage
    • Implantation cholesteatoma
  • Long-term complications
    • Persistent perforation with or without otorrhea
    • Ear canal stenosis

The complications for myringotomy with tube placements are the same with the addition of those related to the tube and to longer perforation. Medialization of tubes of modern design is now quite rare. Some tube designs have a tendency to collect epithelial debris and inherently have a higher rate of cholesteatoma formation. As a rule, longer ventilation increases the likelihood of persistence of the perforation, the formation of aural polyps, and chronic otorrhea. Most are reversed by removal of the tube with or without repair of the hole with a small myringoplasty.

Multimedia

Drawing of a normal right tympanic membrane. Note...

Media file 1: Drawing of a normal right tympanic membrane. Note the outward curvature of the pars tens (*) of the eardrum. The tympanic annulus is indicated anteriorly (a), inferiorly (i), and posteriorly (P). M = long process of the malleus; I = incus; L = lateral (short) process of the malleus.

References

  1. Paradise JL, Rockette HE, Colborn DK, et al. Otitis media in 2253 Pittsburgh-area infants: prevalence and risk factors during the first two years of life. Pediatrics. Mar 1997;99(3):318-33. [Medline].

  2. Clements DA, Langdon L, Bland C, Walter E. Influenza A vaccine decreases the incidence of otitis media in 6- to 30-month-old children in day care. Arch Pediatr Adolesc Med. Oct 1995;149(10):1113-7. [Medline].

  3. Bernstein JM. The role of IgE-mediated hypersensitivity in the development of otitis media with effusion. Otolaryngol Clin North Am. Feb 1992;25(1):197-211. [Medline].

  4. American Academy of Pediatrics. Respiratory syncytial virus. In: Red Book: Report of the Committee on Infectious Diseases. 24th ed. 1997:443-447.

  5. American Academy of Pediatrics. Haemophilus influenzae infections. In: Red Book: Report of the Committee on Infectious Diseases. 24th ed. 1997:220-231.

  6. American Academy of Pediatrics. Pneumococcal infections. In: Red Book: Report of the Committee on Infectious Diseases. 24th ed. 1997:410-419.

  7. American Academy of Pediatrics. Group A streptococcal infections. In: Red Book: Report of the Committee on Infectious Diseases. 24th ed. 1997:483-494.

  8. Arola M, Ruuskanen O, Ziegler T, et al. Clinical role of respiratory virus infection in acute otitis media. Pediatrics. Dec 1990;86(6):848-55. [Medline].

  9. Arola M, Ziegler T, Ruuskanen O. Respiratory virus infection as a cause of prolonged symptoms in acute otitis media. J Pediatr. May 1990;116(5):697-701. [Medline].

  10. Barenkamp SJ, Shurin PA, Marchant CD, et al. Do children with recurrent Haemophilus influenzae otitis media become infected with a new organism or reacquire the original strain?. J Pediatr. Oct 1984;105(4):533-7. [Medline].

  11. Berman S, Roark R. Factors influencing outcome in children treated with antibiotics for acute otitis media. Pediatr Infect Dis J. Jan 1993;12(1):20-4. [Medline].

  12. Block SL. Causative pathogens, antibiotic resistance and therapeutic considerations in acute otitis media. Pediatr Infect Dis J. Apr 1997;16(4):449-56. [Medline].

  13. Bluestone CD. State of the art: definitions and classifications. In: Recent Advances in Otitis Media with Effusion. Decker Inc; 1984:1-4.

  14. Bluestone CD, Casselbrant M, Scheetz MD. Workshop on epidemiology of otitis media. Ann Otol Rhinol Laryngol Suppl. Jul 1990;149:1-60. [Medline].

  15. Bluestone CD, Klein JO. Epidemiology. In: Otitis Media in Infants and Children. WB Saunders; 1988:31-43.

  16. Bluestone CD, Klein JO. Otitis media, atelectasis, and eustachian tube dysfunction. In: Otitis Media in Infants and Children. 2nd ed. Philadelphia: WB Saunders; 1995:39-72.

  17. Bluestone CD, Klein JO. Otitis media, atelectasis, and eustachian tube dysfunction. In: Pediatric Otolaryngology. Philadelphia: WB Saunders; 1990:320-487.

  18. Byrns PJ, Bondy J, Glazner JE, Berman S. Utilization of services for otitis media by children enrolled in Medicaid. Arch Pediatr Adolesc Med. Apr 1997;151(4):407-13. [Medline].

  19. Chonmaitree T, Owen MJ, Patel JA, Hedgpeth D, Horlick D, Howie VM. Effect of viral respiratory tract infection on outcome of acute otitis media. J Pediatr. Jun 1992;120(6):856-62. [Medline].

  20. Culpepper L, Froom J. Routine antimicrobial treatment of acute otitis media: is it necessary?. JAMA. Nov 26 1997;278(20):1643-5. [Medline].

  21. Daigler GE, Markello SJ, Cummings KM. The effect of indoor air pollutants on otitis media and asthma in children. Laryngoscope. Mar 1991;101(3):293-6. [Medline].

  22. Doern GV. Trends in antimicrobial susceptibility of bacterial pathogens of the respiratory tract. Am J Med. Dec 29 1995;99(6B):3S-7S. [Medline].

  23. Donaldson JD, Martin GF, Maltby CC, Seywerd EB. The efficacy of pulse-dosed antibiotic therapy in the management of persistent otitis media with effusion. J Otolaryngol. Jun 1990;19(3):175-8. [Medline].

  24. Dowell SF, Marcy M, Phillips WR. Otitis Media-Principles of Judicious Use of Antimicrobial Agents. Pediatrics. 1998;101(1-2):165-171.

  25. Duncan B, Ey J, Holberg CJ, Wright AL, Martinez FD, Taussig LM. Exclusive breast-feeding for at least 4 months protects against otitis media. Pediatrics. May 1993;91(5):867-72. [Medline].

  26. Erramouspe J, Cady PS. What is optimal for antibiotic studies in acute otitis media?. Ann Pharmacother. Jan 2004;38(1):158-60. [Medline].

  27. Gaillat J. [Clinical manifestations of Chlamydia pneumoniae infections]. Rev Med Interne. 1996;17(12):987-91. [Medline].

  28. Gannon MM, Haggard MP, Golding J. Sleeping position: a new environmental risk for otitis media? [abstract]. Abstract of Sixth International Symposium on Recent Advances in Otitis. 1995.

  29. Gliklich RE, Eavey RD, Iannuzzi RA, Camacho AE. A contemporary analysis of acute mastoiditis. Arch Otolaryngol Head Neck Surg. Feb 1996;122(2):135-9. [Medline].

  30. Greenfield BJ, Selesnick SH, Fisher L, Ward RF, Kimmelman CP, Harrison WG. Aural tuberculosis. Am J Otol. Mar 1995;16(2):175-82. [Medline].

  31. Hando S, Nonomura N, Niijima H, Fujioka O, Nakano Y. Adherence of Haemophilus influenzae to middle ear mucosa injured by killed H. influenzae. Auris Nasus Larynx. 1992;19(2):69-74. [Medline].

  32. Koivunen P, Uhari M, Luotonen J, et al. Adenoidectomy versus chemoprophylaxis and placebo for recurrent acute otitis media in children aged under 2 years: randomised controlled trial. BMJ. Feb 28 2004;328(7438):487. [Medline].

  33. Loh RK, Harth SC, Thong YH, Ferrante A. Immunoglobulin G subclass deficiency and predisposition to infection in Down's syndrome. Pediatr Infect Dis J. Aug 1990;9(8):547-51. [Medline].

  34. Mandel EM, Casselbrant ML, Rockette HE, Bluestone CD, Kurs-Lasky M. Efficacy of 20- versus 10-day antimicrobial treatment for acute otitis media. Pediatrics. Jul 1995;96(1 Pt 1):5-13. [Medline].

  35. Marx J, Osguthorpe JD, Parsons G. Day care and the incidence of otitis media in young children. Otolaryngol Head Neck Surg. Jun 1995;112(6):695-9. [Medline].

  36. Niemelä M, Uhari M, Möttönen M. A pacifier increases the risk of recurrent acute otitis media in children in day care centers. Pediatrics. Nov 1995;96(5 Pt 1):884-8. [Medline].

  37. Palva T, Lehtinen T. Pneumococcal antigens and endotoxin in effusions from patients with secretory otitis media. Int J Pediatr Otorhinolaryngol. Dec 1987;14(2-3):123-8. [Medline].

  38. Paradise JL. Short-course antimicrobial treatment for acute otitis media: not best for infants and young children. JAMA. Nov 26 1997;278(20):1640-2. [Medline].

  39. Reed BD, Lutz LJ, Zazove P, Ratcliffe SD. Compliance with acute otitis media treatment. J Fam Pract. Nov 1984;19(5):627-32. [Medline].

  40. Roberton DM, Colgan T, Ferrante A. IgG subclass concentrations in absolute, partial and transient IgA deficiency in childhood. Pediatr Infect Dis J. Aug 1990;9(8 Suppl):S41-5.

  41. Rosenfeld RM. What to expect from medical treatment of otitis media. Pediatr Infect Dis J. Sep 1995;14(9):731-7; quiz 738. [Medline].

  42. Rovers MM, Schilder AG, Zielhuis GA, Rosenfeld RM. Otitis media. Lancet. Feb 7 2004;363(9407):465-73. [Medline].

  43. Sahm DF, Brown NP, Thornsberry C, Jones ME. Antimicrobial susceptibility profiles among common respiratory tract pathogens: a GLOBAL perspective. Postgrad Med. Sep 2008;120(3 Suppl 1):16-24. [Medline].

  44. Shambaugh GE, Glasscock ME. Pathology and clinical course of inflammatory diseases of the middle ear. In: Surgery of the Ear. 3rd ed. WB Saunders Company; 1980:191, 200-207.

  45. Shimamura K, Shigemi H, Kurono Y, Mogi G. The role of bacterial adherence in otitis media with effusion. Arch Otolaryngol Head Neck Surg. Oct 1990;116(10):1143-6. [Medline].

  46. Shurin PA, Howie VM, Pelton SI, Ploussard JH, Klein JO. Bacterial etiology of otitis media during the first six weeks of life. J Pediatr. Jun 1978;92(6):893-6. [Medline].

  47. Shurin PA, Rehmus JM, Johnson CE, et al. Bacterial polysaccharide immune globulin for prophylaxis of acute otitis media in high-risk children. J Pediatr. Nov 1993;123(5):801-10. [Medline].

  48. Stenstrom R, Bernard PA, Ben-Simhon H. Exposure to environmental tobacco smoke as a risk factor for recurrent acute otitis media in children under the age of five years. Int J Pediatr Otorhinolaryngol. Aug 1993;27(2):127-36. [Medline].

  49. Stool SE, Berg AO, Berman S. Otitis media with effusion in young children- Clinical practice guideline. Agency for Health Care Policy and Research Publication. 1994;94-0622.

  50. Sung BS, Chonmaitree T, Broemeling LD, et al. Association of rhinovirus infection with poor bacteriologic outcome of bacterial-viral otitis media. Clin Infect Dis. Jul 1993;17(1):38-42. [Medline].

  51. Teele DW, Klein JO, Rosner B. Epidemiology of otitis media during the first seven years of life in children in greater Boston: a prospective, cohort study. J Infect Dis. Jul 1989;160(1):83-94. [Medline].

  52. Thornsberry C, Brown NP, Draghi DC, Evangelista AT, Yee YC, Sahm DF. Antimicrobial activity among multidrug-resistant Streptococcus pneumoniae isolated in the United States, 2001-2005. Postgrad Med. Sep 2008;120(3 Suppl 1):32-8. [Medline].

  53. Virolainen A, Jero J, Kayhty H, Karma P, Eskola J, Leinonen M. Nasopharyngeal antibodies to pneumococcal pneumolysin in children with acute otitis media. Clin Diagn Lab Immunol. Nov 1995;2(6):704-7. [Medline].

  54. Wald ER. Anaerobes in otitis media and sinusitis. Ann Otol Rhinol Laryngol Suppl. Sep 1991;154:14-6. [Medline].

  55. Wald ER. Otitis media and sinusitis: a clinical update. Clin Updates Pediatr Infect Dis. 1995;1:1-4.

Keywords

otitis media, otitis media surgery, otitis media treatment, ear infection, ear infections, ear infection treatment, acute suppurative otitis media, acute otitis media, AOM, purulent otitis, otitis media with effusion, OME, tympanocentesis, myringotomy, myringotomy with ventilation, chronic otitis media, COM, ear infection, ear pain, ear ache

Contributor Information and Disclosures

Author

John D Donaldson, MD, FRCS(C), FAAP, FACS, Chairman, Board of Directors, Lee Memorial Health System; President-elect, Florida Pediatric Society
John D Donaldson, MD, FRCS(C), FAAP, FACS is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery, American Academy of Pediatrics, American College of Surgeons, and American Society of Pediatric Otolaryngology
Disclosure: Nothing to disclose.

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John C Li, MD, Private Practice in Otology and Neurotology; Medical Director, Balance 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
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