Wednesday, August 6, 2008

Otitis Media

Otitis Media

Philip D. Yates, MB ChB, FRCS, & Shahram Anari, MD, MRCS from Current Diagnosis & Treatment in Otolaryngology - Head & Neck Surgery.McGrawHill.2008.

The term otitis media (OM) refers to an inflammatory process within the middle ear cleft. Otitis media can be either acute or chronic. There is no absolute time period, but, in general, disease that persists for more than 3 months should be considered as chronic.

A subclassification of acute and chronic OM is summa­rized in Table 1. Otitis media associated with cholesteatoma is considered separately in other Chapter, Cholesteatoma. The eustachian tube appears to be central to the pathogenesis of all forms of OM (with the possible excep­tion of cholesteatoma). The normal physiologic functions of the eustachian tube are to (1) maintain the gaseous pres­sure within the middle ear cleft at a level that approximates atmospheric pressure; (2) prevent reflux of the contents of the nasopharynx into the middle ear; and (3) clear secre­tions from the middle ear by both mucociliary transport and a “pump action” of the eustachian tube. The failure of any or all of these normal functions of the eustachian tube can result in OM. Both anatomic and functional obstruction of the eustachian tube results in the failure of normal regulation of the middle ear pressure. Anatomic obstruction is most commonly caused by inflammation of the eustachian tube mucosa or extrinsic compression by tumor or large adenoids. Functional obstruction usually occurs as a result of either the failure of the normal muscular mechanism of eustachian tube opening, as seen in cleft palate, or insufficient stiffness of the cartilaginous portion of the eustachian tube, often seen in infants and young children. The more acute angle of the eustachian tube seen in children, compared with adults, may also result in the impaired function of the eustachian tube opening. If the eustachian tube is abnormally patent or short, its normal protective function against the reflux of nasopharyngeal contents is lost. These abnormalities are often seen in patients with Down syndrome, which may account for the high rate of OM in this particular patient population. Normal function of the eustachian tube is also dependent on ciliary function; therefore, any condition that affects mucociliary clearance, such as viral infection, bacterial toxins, or inherited abnormalities of ciliary struc­ture, can predispose to OM.


ACUTE OTITIS MEDIA

ESSENTIALS OF DIAGNOSIS

- Otalgia.

- Pyrexia.

- Thickened, bulging, hyperemic tympanic mem­brane.

- Hearing loss.

- Otorrhea.

General Considerations

Acute otitis media (AOM) is one of the most common infectious diseases seen in children, with its peak inci­dence in the first 2 years of life. Most of the population will suffer at least one episode of AOM at some point in their childhood. It can occur in suppurative, nonsuppurative, and recurrent forms. In nonsuppurative AOM, inflammation of the middle ear cleft mucosa occurs either without formation of an effusion or with a sterile effusion. This type of AOM is often seen prior to, or in the resolution stage of, the acute suppurative OM; however, resolution may occur before frank suppura­tion. Recurrent AOM is defined as ≥ 3 episodes of acute suppurative OM in a 6-month period, or ≥ 4 epi­sodes in a 12-month period, with complete resolution of symptoms and signs between the episodes.

The epidemiology of AOM and otitis media with effusion (OME) overlaps to such an extent that the risk factors apply to both conditions. Both environmental and host factors play a role in the epidemiology of OM Table 2). Attendance at day-care facilities is one of the major risk factors for OM. Child care results in many children being in close contact, which increases the exposure to respiratory tract pathogens responsible for OM. The risks associated with child care attendance are variable and are related to the number of children in a facility, the hours spent in child care, the child’s age at entry, and whether siblings are in child care. Breast­feeding appears to have a protective effect against OM, particularly when breast-feeding is used exclusively for at least the first 3–6 months of life. The protective mechanism of breast-feeding has not been clearly dem­onstrated, but is likely to be related to antibacterial and immunologic benefits conferred by breast milk.

Table 1. Classification of otitis media.

Acute Otitis Media

Chronic Otitis Media

Suppurative

Suppurative :

a. Tubotympanic

b. Cholesteatoma

Nonsuppurative

Non Suppurative :

a. Otitis media with effusion

Recurrent

Exposure to cigarette smoke has been implicated in the etiology of OM. Passive smoking results in inflammation of the mucosa of the middle ear cleft as well as impaired mucociliary clearance, which lead to an increased suscepti­bility to infection. There is a seasonal variation in the inci­dence of OM; it is more common in winter months, which mirrors the incidence of upper respiratory tract infections.

Genetics play an important role in the etiology of OM. Males have a higher incidence of OM than females, a fact that is true of most infections of infancy and childhood. The sibling, maternal, and paternal histories of OM are all independently related to a child’s risk of developing OM.

Table 2. Factors relevant to the epidemiology of otitis media.

Environmental Factors

Host Factors

Day-care attendance

Genetics

Not being breast-fed

Immunodeficiency

Exposure to tobacco smoke

Birth defects :

Cleft palate, Down syndrome

Seasonal variation in respiratory infections

Although OM is largely a uniform worldwide condition, some racial variations in the rates of OM exist; this condi­tion is more prevalent in Native Americans, Alaskan and Canadian Eskimos, and Australian Aboriginals. These genetic variations may be related to anatomic and physio­logic variations in the eustachian tube.

Otitis media is seen almost universally in children with cleft palate. Because the tensor veli palatini muscle lacks its normal insertion into the soft palate, it is unable to open the eustachian tube properly on swallowing. A small number of patients suffering from OM have an abnormal host defense owing to various conditions such as immunoglobulin deficiency, malig­nant neoplasms, immunosuppressive therapy, and AIDS.

Pathogenesis

In most cases of AOM, an antecedent viral upper respi­ratory tract infection leads to disruption of eustachian tube function. Inflammation of the middle ear mucosa results in an effusion, which cannot be cleared via the obstructed eustachian tube. This effusion provides a favorable medium for proliferation of bacterial patho­gens, which reach the middle ear via the eustachian tube, resulting in suppuration.

Although viral infection is important in the pathogenesis of AOM, the majority of patients develop subse­quent bacterial colonization, and therefore AOM should be considered a predominantly bacterial infection. Many studies, using tympanocentesis, have identified Strepto­coccus pneumoniae (up to 40%), Haemophilus influenzae (25–30%), and Moraxella catarrhalis (10–20%) as the organisms most commonly responsible for AOM. Less frequently identified pathogens include group A strepto­cocci, Staphylococcus aureus, and gram-negative organ­isms such as Pseudomonas aeruginosa. In all studies of the microbiology of AOM, a significant number of cultures prove negative. This finding may occur for a variety of reasons, including (1) antibiotic therapy before tympanocentesis; (2) nonbacterial pathogens (eg, viruses, chlamydia, and mycoplasma); and (3) pathogens that do not proliferate in classic culture conditions (eg, mycobacteria and anaerobic bacteria). Recent studies on bacte­riology of AOM show that the polymerase chain reac­tion (PCR) methods produce positive results in patients in whom cultures have been negative by the conven­tional methods.

The role of the adenoids (ie, the pharyngeal tonsils) in the pathogenesis of AOM and OME remains unproven. There are two mechanisms by which the adenoids may influence OM: (1) physical obstruction of the eustachian tube when the adenoids are enlarged and (2) a reservoir of pathogenic bacteria harbored in the adenoid tissue, which predisposes the patient to repeated episodes of AOM.

Prevention

Strategies for the prevention of AOM include prophy­lactic antibiotics, vaccines, and surgery. The most com­monly recommended regimen for antibiotic prophy­laxis of recurrent AOM is once-daily oral amoxicillin at 20 mg/kg/d. Although antibiotic prophylaxis has been demonstrated to significantly reduce the number of epi­sodes of AOM, this effect has to be considered along with the increased incidence of antibiotic-resistant organisms emerging as a direct result of the widespread prescription of antibiotics.

A pneumococcal vaccine has been introduced for use in infants and children younger than 2 years as well as in children older than 2 years who are at a high risk of recurrent AOM. However, until vaccines for other bac­teria and viruses commonly responsible for AOM are available, the effect of vaccination will be limited. The prophylactic use of tympanostomy tubes (not myringotomy alone) has been demonstrated to reduce the num­ber of episodes of AOM and hence the need for antibi­otics. Adenoidectomy also has a demonstrable effect, though more modest than that seen with tympanostomy tubes.

Clinical Findings

A.Symptoms and Signs

Before the onset of symptoms of AOM, the patient fre­quently has symptoms of an upper respiratory tract infection. Older children usually complain of earache, whereas infants become irritable and pull at the affected ear. A high fever is often present and may be associated with systemic symptoms of infection, such as anorexia, vomiting, and diarrhea. Otoscopy classically shows a thickened hyperemic tympanic membrane, which is immobile on pneumatic otoscopy.

Further progression of the infective process may lead to the spontaneous rupture of the tympanic membrane, resulting in otorrhea. If this occurs, the otalgia and fever often subside. At this stage, it is often not possible to visualize the tympanic membrane because of the dis­charge in the ear canal.

B.Special Tests

In most cases of AOM, no further investigations are neces­sary since the diagnosis is clinical. If symptoms are severe, a blood count often reveals a leukocytosis, and blood cultures may detect bacteremia during episodes of high fever. A cul­ture of the ear discharge is helpful in guiding antibiotic therapy in patients in whom the first-line treatment is unsuccessful. If recurrent AOM occurs along with recurrent infections in other systems, then an underlying immune deficiency (commonly IgA and IgG deficiency) should be considered and appropriate investigations requested. Ciliary motility disorders need to be considered if recurrent AOMis associated with recurrent/chronic respiratory or sinus infections. Radiologic investigation is not recommended unless complications are suspected.

Differential Diagnosis

In any patient who has otorrhea, particularly if it is recurrent, a diagnosis of chronic suppurative otitis media (CSOM), either tubotympanic or with cholesteatoma, should be considered. Otitis externa also pre­sents with otalgia and otorrhea and may be the primary diagnosis, or it may be secondary to the infected dis­charge from the middle ear.

If otalgia is the primary complaint, then referred pain should be considered, particularly when otoscopy reveals a normal tympanic membrane. The common sites of origin of referred otalgia are the teeth and temporomandibular joints. In adults, malignant neoplasms of the pharynx and larynx may present with otalgia as the only symptom.

In neonates and infants with a high fever and systemic upset, the possibility of meningitis should be considered.

Treatment

A.Nonsurgical Measures

Watchful waiting—The current practice guidelines advise on an initial watchful waiting without antibiotic therapy for healthy 2-year-olds or older children with nonsevere illness (mild otalgia and fever <>

Antibiotic therapy—If AOM does not settle after the watchful waiting period, then antibiotic therapy should begin. The use of antibiotics is probably benefi­cial, but there is a trade-off between benefits and side effects. There is no difference demonstrated in recur­rence rates or the development of complications among different antibiotics. Amoxicillin (80 mg/kg/d given in three divided doses for 10 days) remains the first-line therapy for AOM, although with increasing numbers of resistant strains of bacteria, it may be necessary to use more broad-spectrum antibiotics in the future. In resis­tant cases, amoxicillin should be given in combination with clavulanate.

Adjunctive therapy—The adjunctive therapy for AOM should include analgesics and antipyretics. There is no role for oral decongestants or antihistamines in the treatment of AOM.

B. Surgical Measures

A minority of patients with AOM fail to respond to medical therapy or develop a complication. Myringotomy is then indicated to allow the drainage of pus from the middle ear space. Randomized trials have shown myringotomy to be ineffective in uncomplicated AOM.

Prognosis

The vast majority of uncomplicated episodes of AOM resolves without any adverse outcome. In some cases, sup­puration resolves, but a sterile middle ear effusion persists. If this effusion persists for more than 3 months, then a diagnosis of OME should be made. Of patients who develop a perforation of the tympanic membrane with otorrhea, a small proportion go on to develop CSOM because of the failure of the tympanic membrane to heal.

OTITIS MEDIA WITH EFFUSION

ESSENTIALS OF DIAGNOSIS

- Persistent hearing loss.

- Dull, immobile tympanic membrane.

- “Flat” tympanogram.

General Considerations

Otitis media with effusion is defined as the persistence of a serous or mucoid middle ear effusion for 3 months or more. Various terms, such as chronic secretory otitis media, chronic serous otitis media, and “glue ear,” have been used to describe the same condition. It is the most common cause of hearing loss in children in the developed world and has peaks in incidence at 2 and 5 years of age. The risk factors for OME are closely interrelated with those associated with AOM and have already been described in the previous sec­tion. In fact, the formation of a middle ear effusion fre­quently occurs after an episode of AOM, and children with OME are far more likely to suffer from recurrent AOM.

Pathogenesis

Under normal conditions, the middle ear mucosa con­stantly secretes mucus, which is removed by mucociliary transport into the nasopharynx via the eustachian tube. As a consequence, factors resulting in an overproduction of mucus, an impaired clearance of mucus, or both can result in the formation of a middle ear effusion.

Both viral and bacterial infection can lead to the increased production and viscosity of secretions from the middle ear mucosa. Infection also leads to inflam­matory edema of the mucosa, which may obstruct the eustachian tube. Temporary paralysis of cilia by bacte­rial exotoxins further impedes the clearance of an effu­sion. Bacteriologic studies have demonstrated that the bacteria commonly responsible for AOM are cultured from about half of chronic effusions. The fact that not all patients with OME have a history of infection sug­gests that other mechanisms are involved in the forma­tion of a middle ear effusion. Experimental studies have confirmed that the failure of eustachian tube opening can result in a middle ear effusion. Because gas is con­stantly being absorbed into the microcirculation of the middle ear mucosa, a negative pressure develops in the middle ear cleft if the eustachian tube is blocked. This negative pressure results in the transudation of fluid into the middle ear cleft. The fact that a middle ear effusion can develop as a result of barotrauma (eg, scuba diving) supports this theory for the pathogenesis of middle ear effusions. Allergy has also been implicated in the pathogenesis of OME; however, evidence to sup­port this theory is lacking.

Exposure to passive smoking is also likely to contribute to ciliary dysfunction and hence to OME. There is an optimum viscosity of mucus at which effective mucociliary transport occurs. If the mucus formed in a middle ear effu­sion is either too serous or too mucoid, then the cilia will be unable to clear it efficiently. Recently, the concept of biofilms in the pathogenesis of otitis media has been raised, but the evidence is not conclusive. Biofilms are the struc­tured community of bacterial cells adherent to the mucosa and have antibacterial resistance property.

Prevention

Since OME often occurs as a direct result of AOM, the measures for preventing AOM previously described should also reduce the incidence of OME. Avoidance of risk factors (see Table 2) could also reduce the chance of a child developing OME, but its effectiveness remains unproven.

Clinical Findings

A. Symptoms and Signs

Otitis media with effusion may be completely asymp­tomatic and detected only on routine audiologic screen­ing. The most common symptom of OME is hearing loss. Although older children may complain of reduced hearing, in many cases the hearing loss is noticed by parents, nursery nurses, or teachers. In younger chil­dren, the only symptom may be delayed speech devel­opment or behavioral problems. Another common symptom is a “blocked” feeling in the ear, which may cause infants and young children to pull at their ears. More rarely, symptoms of earache, tinnitus, or balance disorder may be present.

Otoscopy classically reveals a dull gray- or yellow-colored tympanic membrane that has reduced mobility on pneumatic otoscopy. If the tympanic membrane is translucent, an air-fluid level or small air bubbles within the middle ear effusion may be seen.

Table 3. Types of tympanogram.

B. Special Tests

Tympanometry—Tympanometry is a valuable tool for the investigation of OME. It is easy to use, provides reproducible results, is inexpensive, and is widely toler­ated by patients—even young children. By measuring the compliance of the middle ear transformer mecha­nism, it provides an objective assessment of the status of the middle ear. Tympanometry produces a peak (ie, maximal compliance) when the pressure in the external ear canal equals that of the middle ear. By varying the pressure in the external ear, the tympanometer is able to provide information on the status of the middle ear (Table 3). If there is an effusion in the middle ear, then compliance does not vary with changes in canal pressure, and a flat (Type B) tympanogram is produced. If the air in the middle ear is at or near atmospheric pressure, then a normal (Type A) tympanogram is pro­duced. Negative middle ear pressure results in a Type C tympanogram, with the compliance peak being at less than –99 daPa (deca Pascal).

Audiometry—Patients who have OME usually have a moderate conductive hearing loss. Audiometry pro­vides an assessment of the severity of hearing loss and is therefore important in both monitoring the progress of the condition and providing information useful for management decisions. For example, in patients with hearing thresholds of 20 dB or better, it is unlikely that surgical intervention is indicated, despite the presence of OME.

Differential Diagnosis

There is considerable overlap between AOM and OME, and it may be difficult to distinguish between the two on first presentation unless otalgia and fever are prominent. Other causes of conductive hearing loss in childhood are much less common than OME, and congenital abnor­malities of the ossicular chain are frequently associated with abnormalities of the external ear or present as part of a syndrome.

In adults presenting with a unilateral middle ear effusion, the possibility of a nasopharyngeal carcinoma should be considered.

Treatment

A. Observation

A large number of patients with OME require no treat­ment, particularly if the hearing impairment is mild. Spontaneous resolution occurs in a significant proportion of patients. A period of watchful waiting of 3 months from the onset (if known) or from the diagnosis (if onset unknown) before considering intervention is therefore advisable. Ideally, early treatment should be initiated in patients in whom spontaneous resolution is unlikely. A multicenter randomized controlled trial identified both the season of attendance (ie, July to December) and a bilateral hearing impairment of > 30 dB as factors that make spontaneous resolution less likely. Early interven­tion should be considered if there is a significant delay in speech and language development or if OME is present in an only hearing ear.

B. Nonsurgical Measures

The medical treatment of OME is controversial and there is a wide geographic variability in practice. Autoinflation with purpose-built nasal balloon has been shown to be beneficial, although compliance is generally poor. Medical treatments include antibiotics, steroids, decongestants, and antihistamines. The use of antibiotics in OME has been shown to be effective in a small proportion of patients, but the effect is likely to be short-lived. The small chance of benefit from antibiotic therapy needs to be considered along with the fact that a number of patients treated with antibiotics develop significant side effects, such as gastroen­teritis and atopic reaction. A meta-analysis of the use of topical and systemic steroids for the treatment of OME found a short-term improvement in hearing, but no lasting benefit. Steroids are therefore not recommended in the treatment of OME. There is no evidence to support the use of decongestants, antihistamines, or mucolytics for the treatment of OME.

C. Surgical Measures

The surgical options for OME are tympanostomy tubes and adenoidectomy. Myringotomy and aspiration of middle ear effusion without ventilation tube insertion has a short-lived benefit and is not recommended.

Insertion of tympanostomy tubes—The aim of tympanostomy tube insertion is to allow ventilation of the mid­dle ear space—hence to improve hearing thresholds. The prolonged ventilation of the middle ear may also allow reso­lution of chronic inflammation of the middle ear mucosa. Complications include myringosclerosis, purulent otorrhea, and residual perforation after extrusion. There are two main types of tympanostomy tubes: short-term tubes (eg, grom-mets), which remain in the tympanic membrane for an average of 12 months, and long-term tubes (eg, T-tubes), which can remain for several years. The high incidence of residual perforation following the use of long-term ventila­tion tubes indicates that they should not be used in uncom­plicated cases.

Adenoidectomy—Controversy still exists over the role of adenoidectomy in the treatment of OME. The rationale for adenoidectomy is that it relieves nasal obstruction, improves eustachian tube function, and elimi­nates a potential reservoir of bacteria. Evidence does sug­gest that adenoidectomy is effective in reducing the mor­bidity of OME. However, because of the potential risks associated with adenoidectomy (primarily hemorrhage and, rarely, velopharyngeal insufficiency), many surgeons use tympanostomy tubes alone as a first-line treatment and consider adenoidectomy when repeated tympanostomy tube insertion is required for recurrent OME.

Prognosis

There is a sharp decline in the prevalence of OME in chil­dren over 7 years of age, which reflects improved eustachian tube function and maturation of the immune system.

CHRONIC SUPPURATIVE OTITIS MEDIA (TUBOTYMPANIC)

ESSENTIALS OF DIAGNOSIS

- Chronic or recurrent otorrhea or both.

- Hearing loss.

- Tympanic membrane perforation.

- General Considerations

Chronic suppurative otitis media is defined as a persis­tent or intermittent infected discharge through a non-intact tympanic membrane (ie, perforation or tympanostomy tube). Chronic perforation of the tympanic membrane can occur without suppuration and is often referred to as “inactive” CSOM.

Chronic suppurative otitis media is particularly preva­lent in developing countries and is more common in lower socioeconomic groups in the developed world. Many of the epidemiologic factors discussed in the section on AOM equally apply to the development of CSOM.

Pathogenesis

There are a number of mechanisms by which a persis­tent tympanic membrane perforation may develop. In most cases, CSOM occurs as a consequence of an epi­sode of AOM with perforation, with subsequent failure of the perforation to heal. There is also an association between OME and chronic perforation. The continued presence of a middle ear effusion leads, in some cases, to degeneration of the fibrous layer of the tympanic membrane. This weakness of the tympanic membrane both predisposes to perforation and reduces the likeli­hood of spontaneous healing. Although most tympanic membranes heal spontaneously after the extrusion of ventilation tubes, a small percentage do not. Traumatic perforations, particularly if large, may fail to heal.

There are two main mechanisms by which a chronic perforation can lead to continuous or repeated middle ear infections: (1) Bacteria can contaminate the middle ear cleft directly from the external ear because the protec­tive physical barrier of the tympanic membrane is lost. (2) The intact tympanic membrane normally results in a middle ear “gas cushion,” which helps to prevent the reflux of nasopharyngeal secretions into the middle ear via the eustachian tube. The loss of this protective mech­anism results in the increased exposure of the middle ear to pathogenic bacteria from the nasopharynx.

The most commonly isolated bacteria responsible for CSOM are P aeruginosa, S aureus, and the Proteus species.

Clinical Findings

A.Symptoms and Signs

Typically, a patient with CSOM presents with a history of otorrhea, which may be either intermittent or continu­ous, and hearing loss. The discharge is usually mucopurulent, although chronic infection of the middle ear may lead to polyp or granulation tissue formation, which can result in bloodstained otorrhea. Pain is not a usual fea­ture of CSOM and its presence should alert the physician to the possibility of a more invasive pathology.

Inspection may reveal scars from previous surgery for chronic ear disease. To properly visualize the tympanic membrane, it is necessary to suction the discharge from the external auditory canal with an operating microscope. The middle ear mucosa, seen through the perforation, is edematous, sometimes to the point of polyp formation. If the perforation is of sufficient size, it may be possible to identify the presence of ossicular discontinuity due to necrosis of the long process of the incus.

B.Special Tests

A swab of the discharge should be sent for culture and sensitivity, preferably before beginning antimicrobial therapy. An audiologic evaluation is necessary, because the majority of patients have an associated conductive hearing loss.

Since the diagnosis of CSOM can be made clinically, radiologic investigation is not usually indicated. Com­puted tomographic (CT) scans are useful in demonstrat­ing bony anatomy and are essential if an intracranial extension of the infection is suspected. However, CT scanning is poor in differentiating between the soft tissue opacity caused by CSOM and cholesteatoma.

Differential Diagnosis

The primary differential diagnosis is the presence of a cholesteatoma. Both pathologies present with a very sim­ilar clinical course, and the presence of severe inflamma­tion or granulation tissue can cause difficulty with the diagnosis. Reexamination after a course of medical treat­ment usually provides an accurate diagnosis.

If granulations are severe and unresponsive to anti­microbial therapy, then chronic granulomatous condi­tions such as Wegener granulomatosis, mycobacterial infection, histiocytosis X, and sarcoidosis should be considered. Biopsy of the granulation or polyp in these circumstances is recommended.

Pain is not usually a prominent feature of CSOM, and its presence should raise the possibility of necrotizing otitis externa (particularly in the immunocompromised, eg, AIDS patients or elderly diabetics) or a malignant neo­plasm of the eternal canal or middle ear.

Treatment

The treatment goals of uncomplicated CSOM are to eliminate infection, prevent further infection, and restore normal functioning to the middle ear. Both medical and surgical interventions play a role in achieving these aims (Table 4).

A. Nonsurgical Measures

Aural toilet—Aural toilet is important for the suc­cessful treatment of CSOM, particularly when topical medication is used. Clearing the discharge from the external auditory canal allows the topical agent to reach the middle ear in an adequate concentration.

Topical antibiotics—Although topical antibiotics are more effective than systemic antibiotics in the treat­ment of CSOM, many contain aminoglycosides, which are potentially ototoxic. Ototoxicity has been demon­strated in animal models, and the use of gentamicin for vestibular ablation in Meniere disease is well docu­mented. However, sensorineural hearing loss as a result of the use of topical aminoglycosides in CSOM is rarely reported. This circumstance is probably due to a combi­nation of the relatively low concentration of aminoglycoside reaching the middle ear and edema of the middle ear mucosa, which prevents the direct absorption of the drug through the round window. Despite the risk of ototoxicity, topical aminoglycosides are widely prescribed by otolaryngologists for the treatment of CSOM because the benefits of effective treatment outweigh the risks. The recent availability of topical ofloxacin preparations may prove to be as effective as topical aminoglycosides with­out the ototoxic potential.

Systemic antibiotics—Systemic antibiotics tend to have a poor penetration of the middle ear and are therefore less effective than topical antibiotics. Because P aeruginosa is the primary pathogen responsible for CSOM, the choice of oral systemic antibiotics is limited. Both ciprofloxacin and ofloxacin have good antipseudomonal activity. Unfor­tunately, these quinolone antibiotics are not recommended in children owing to the possibility of causing arthropathies. This circumstance limits the choice of systemic anti­biotics in children to broad-spectrum penicillins, such as piperacillin and cephalosporins, which must be adminis­tered parenterally.

B. Surgical Measures

Some cases of CSOM resolve with medical treatment, and if the patient is asymptomatic, then no further intervention is required. However, if otorrhea recurs or persists despite medical treatment or if the patient feels handicapped by a residual conductive hearing loss, sur­gical therapy should be considered.

Tympanoplasty—Ideally, surgery should be car­ried out when the infection has been adequately treated and the middle ear mucosa is healthy, since the chance of a successful outcome is increased. In this situation, a tympanoplasty, with repair of the tympanic membrane and ossicular chain (if required), is recommended.

Tympanomastoid surgery—In cases that are refrac­tory to medical treatment, it is necessary to perform tympanomastoid surgery (tympanoplasty combined with a cortical mastoidectomy). The aims of this procedure are to aerate the middle ear and mastoid, remove chronically inflamed tissue, repair the tympanic defect, and recon­struct the ossicular chain. The achievement of all of these goals often requires more than one procedure.

Table 4. Treatment summary for otitis media.


SEQUELAE & COMPLICATIONS OF OTITIS MEDIA

The sequelae and complications of otitis media can be found in Table 5.

1.Sequelae

Tympanosclerosis

Tympanosclerosis is characterized by hyalinization and the deposition of calcium in the tympanic membrane, middle ear, or both. It often occurs as a result of inflammation or trauma and is therefore commonly seen after recurrent epi­sodes of AOM and OME and after ventilation tube inser­tion. The typical clinical appearance is of white plaques in the tympanic membrane. If the process is limited to the tympanic membrane (ie, myringosclerosis), then hearing is usually unaffected. However, if the middle ear is involved, then the ossicular chain can become immobilized, result­ing in a conductive hearing loss. Attempts at surgical cor­rection by tympanoplasty may initially be successful, but refixation of the ossicles is not uncommon.

Atelectasis

Atelectasis refers to the presence of a grossly retracted or collapsed tympanic membrane. It probably occurs as a result of prolonged negative middle ear pressure secon­dary to chronic eustachian tube dysfunction. The whole of the tympanic membrane can be affected, but if col­lapse is only partial, then a localized retraction pocket is formed. The presence of an atelectatic tympanic mem brane may not produce any symptoms, but more com­monly results in a mild conductive hearing loss. Pro­longed contact between the tympanic membrane and the ossicles can result in ossicular erosion, particularly of the long process of the incus; consequently, a more signifi­cant hearing loss results. Another consequence of persis­tent atelectasis is that the normal migration pattern of squamous epithelium from the tympanic membrane may be disrupted, leading to the accumulation of squamous debris and cholesteatoma formation. This situation is a particular risk if the retraction pocket is located in the pars flaccida or the posterosuperior pars tensa.

The management of atelectasis is controversial. If eustachian tube dysfunction is still considered to be present, the insertion of ventilation tubes could poten­tially reverse the changes in the tympanic membrane by normalizing the pressure in the middle ear space. If no improvement is observed and the location of the retrac­tion raises the concern of subsequent cholesteatoma for­mation, then excision and grafting of the affected por­tion of the tympanic membrane are recommended. The recurrence of tympanic membrane retraction after this procedure is not uncommon; therefore, prolonged observation is advised.

Table 5. Sequelae and complications of otitis media.

Sequelae

Tympanosclerosis

Atelectasis

Intratemporal Complications

Mastoditis

Acute

Subacute (“masked”)

Petrositis

Facial nerve paralysis

Suppurative labyrinthitis

Intracranial Complications

Meningitis

Intracranial abscess

Brain abscess

Extradural

Subdural

Lateral sinus thrombosis

Otic hydrocephalus

2. Intratemporal Complications

Mastoiditis

The fact that the mastoid air cell system is part of the mid­dle ear cleft means that some degree of mastoid inflamma­tion occurs whenever there is infection in the middle ear. In most cases, this infection does not progress to clinically apparent acute mastoiditis. However, if pus collects in the mastoid air cells under pressure, necrosis of the bony trabeculae occurs, resulting in the formation of an abscess cavity. The infection may then progress to periostitis and subperiosteal abscess, or to a more serious intracranial infection.

A. Acute Mastoiditis

Typically, acute mastoiditis presents as a complication of AOM in a child. Pain and tenderness over the mastoid process are the initial indicators of mastoiditis. As the infection progresses, edema and erythema of the postauricular soft tissues with loss of the postauricular crease develop. These changes result in anteroinferior displacement of the pinna. Fullness of the posterior wall of the external auditory canal is frequently seen on otoscopy as a result of the underlying osteitis. If a subperiosteal abscess has developed, fluctuance may be elicited in the postauricular area. Rarely, a mastoid abscess can extend into the neck (Bezold’s abscess) or the occipital bone (Citelli abscess). Once the diagnosis of acute mastoiditis is suspected, the radiologic investigation of choice is a CT scan, which provides information about the extent of the opacification of the mastoid air cells, the formation of subperiosteal abscess, and the presence of intracranial complications.

In some cases, acute mastoiditis can be successfully managed by antibiotic therapy alone, but some patients require surgical intervention. When there is no clinical or radiologic indication of a subperiosteal abscess or an intracranial extension of disease, then high-dose broad-spectrum intravenous antibiotics should be commenced. If, after 24 hours of treatment, there is no evidence of resolution or if symptoms progress, a cortical mastoidectomy should be performed, along with myringotomy if spontaneous perforation of the tympanic membrane has not occurred. If a subperiosteal abscess or an intracranial extension of disease is suspected, surgery in combination with high-dose intravenous antibiotics should be the first-line therapy.

B. Subacute Mastoiditis

Subacute or “masked” mastoiditis may occur when inad­equate treatment of AOM results in a low-grade infec­tion of the mastoid air cells. The symptoms and signs are equivalent to those of acute mastoiditis, but are less severe and more persistent. Most cases resolve with venti­lation of the middle ear combined with appropriate anti­biotic therapy. If this treatment fails to resolve the infec­tion, cortical mastoidectomy is indicated.

Petrositis

This rare complication of suppurative OM occurs in both acute and chronic forms. In the acute form, there is extension of acute mastoiditis into a pneumatized petrous apex. The chronic form of petrositis usually occurs as a result of mucosal or cholesteatomatous CSOM; pneumatization of the petrous apex is not a prerequisite as the infection spreads by thrombophlebi­tis, hematogenous dissemination, or direct extension. Because of the close relationship of the ophthalmic division of the trigeminal nerve and the abducens nerve to the petrous apex, the classic features of petrositis are otorrhea associated with retroorbital pain and lateral rectus palsy (Gradenigo syndrome).

Because of the high incidence of an intracranial extension of infection from petrositis, a combination of antibiotics and surgical drainage of the petrous apex is the management of choice.

Facial Nerve Paralysis

Facial nerve palsy can occur as a result of either acute or chronic OM. There are two mechanisms by which OM can result in facial nerve paralysis: (1) as a result of the locally produced bacterial toxins or (2) from direct pres­sure applied to the nerve by cholesteatoma or granula­tion tissue. If there is a congenital dehiscence of the bony canal of the facial nerve in the middle ear, then an episode of AOM can lead to inflammatory edema of the nerve and a subsequent paresis. This situation should be managed by myringotomy with aspiration of pus from the middle ear along with antibiotic therapy, which will mostly result in the rapid resolution of paralysis. Further surgical exploration of the facial nerve is not indicated unless the paralysis fails to resolve. If facial nerve paralysis occurs as a result CSOM, urgent sur­gical exploration, with decompression of the facial nerve, is indicated.

Suppurative Labyrinthitis

Infection of the middle ear can lead to direct bacterial invasion of the inner ear, usually via the round window, resulting in acute suppurative labyrinthitis. Erosion of the bony capsule of the inner ear by a cholesteatoma (most commonly the lateral semicircular canal) pro­vides an alternative route of entry to the inner ear. Suppurative labyrinthitis presents with sudden sensorineural hearing loss, severe vertigo, nystagmus, and nausea and vomiting. The cochlear aqueduct provides a direct communication between the perilymph and the cerebrospinal fluid; therefore, there is a significant risk of developing meningitis.

The aim of treatment is to eradicate infection, thereby preventing meningitis. Surgical intervention is often required for underlying chronic middle ear dis­ease, although the timing of surgery is controversial. Cochlear and vestibular functions are invariably perma­nently lost and, as healing occurs, obliterative osteitis of the inner ear commonly develops.

3. Intracranial Complications

The incidence of intracranial complications has been considerably reduced since the introduction of antibi­otics. Despite this fact, once an intracranial complica­tion develops, it carries a significant risk to life. There­fore, early recognition and treatment are vital to improve the prognosis. It is not uncommon for more than one intracranial complication to occur simulta­neously. The most common early symptoms of intra-cranial extension of infection are persistent headache and fever. Other features include lethargy, irritability, and neck stiffness. A decreasing level of consciousness and seizures are late signs associated with a poor prog­nosis. Once suspicion of an intracranial infection is raised, an MRI of the brain is the investigation of choice, along with lumbar puncture if meningitis is sus­pected. The causative organism depends on whether the complication has developed as a consequence of acute or chronic OM; the initial antibiotic therapy should be prescribed accordingly until the results of bacterial cul­tures and sensitivity are available.

Meningitis

Acute otitis media is the most common cause of bacte­rial meningitis. It can occur as a result of hematogenous spread, of direct extension from the middle ear through a bony dehiscence, or through the cochlear aqueduct via the inner ear. The most common organisms respon­sible for otic meningitis are S pneumoniae and H influenzae type B. The classic presentation is with head­aches, photophobia, neck stiffness, and fluctuating levels of consciousness. The evaluation should include an MRI of the brain to rule out other intracranial com­plications as well as a lumbar puncture. If meningitis is secondary to AOM, then a myringotomy should be performed once antibiotic therapy has been initiated. In the case of CSOM resulting in meningitis, the patient should be fully stabilized before considering surgical management of the chronic ear disease.

Intracranial Abscess

Brain, subdural, and extradural abscesses can all arise as a complication of middle ear infections (commonly associated with chronic disease). Intracranial abscesses are usually caused by multiple aerobic and anaerobic bacteria. Commonly cultured organisms include strep­tococci, S aureus, S pneumoniae, H influenzae, P aeruginosa, Bacteroides fragilis, and Proteus species.

A. Brain Abscess

Most otogenic brain abscesses develop within the tem­poral lobe or cerebellum. The progression of symptoms from a brain abscess can be gradual, occurring over days or even weeks. In addition to the generalized symp­toms, focal neurologic signs can develop depending on the anatomic location of the abscess within the brain. As the abscess enlarges, features typical of raised intra-cranial pressure develop. Once a brain abscess has been diagnosed, urgent neurosurgical intervention is indi­cated to drain the abscess. Surgery for the associated ear disease is less urgent and should be planned when the patient’s condition is more stable.

B. Subdural Abscess

A subdural abscess forms between the dura mater and the arachnoid mater. Symptoms and signs tend to progress much more rapidly than those seen with a brain abscess. Drainage of the abscess is the mainstay of treatment.

C. Extradural Abscess

Extradural abscesses are typically formed in the middle fossa between the dura mater and the thin bony plate of the tegmen. They can also occur in the posterior fossa, where they are commonly associated with lateral sinus thrombosis. The clinical features are often nonspecific and may fluctuate if a dehiscence in the tegmen is present, allowing the abscess to partially drain into the mastoid cavity. As with other intracranial complica­tions, headache and fever are the most common fea­tures. Because of its location, an extradural abscess can usually be drained through a mastoidectomy approach while treating the underlying middle ear disease.

Lateral Sinus Thrombosis

Because of its close proximity to the mastoid air cells, the lateral, or sigmoid, sinus is prone to involvement in middle ear infections, which may lead to thrombosis. Once an infected thrombus has formed in the lateral sinus, it may propagate both distally and proximally and may give rise to infected emboli. Typically, there are intermittent episodes of high pyrexia associated with rigors. If the thrombus propagates into the neck, there will be neck tenderness along the internal jugular vein and neck stiffness or torticollis. Proximal extension of the thrombus to the sagittal sinus can result in symp­toms and signs of raised intracranial pressure. MRI most reliably makes the diagnosis of lateral sinus throm­bosis. The management of lateral sinus thrombosis requires broad-spectrum antibiotics and surgery. A com­plete mastoidectomy should be performed, with expo­sure of the lateral sinus. Once the diagnosis has been confirmed by needle aspiration, the sinus is opened and the infected thrombus evacuated. If symptoms persist after this procedure, consideration should be given to ligation of the ipsilateral internal jugular vein, once the possibility of other intracranial complications has been excluded.

Otic Hydrocephalus

Otic hydrocephalus is a rare complication in which raised intracranial pressure develops as a result of a mid­dle ear infection, but its pathophysiology is poorly understood. The usual features are headache, vomiting, disturbed mental state, visual disturbance, and papilledema associated with a middle ear infection. Imaging of the brain reveals the ventricular size to be normal, but lumbar puncture confirms raised cerebrospinal fluid pressure. Management is aimed at resolving the middle ear infection while normalizing intracranial pressure with the use of steroids, diuretics (eg, mannitol), and, if required, intermittent drainage of cerebrospinal fluid.

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