Pediatric Mastoiditis

Updated: Nov 24, 2021
Author: Itzhak Brook, MD, MSc; Chief Editor: Russell W Steele, MD 


Practice Essentials

Mastoiditis is an inflammatory process of the mastoid air cells in the temporal bone.[1]  Because the mastoid is contiguous to the middle ear cleft and an extension of it, virtually all children or adults with acute otitis media (AOM) and most individuals with chronic middle ear inflammatory disease have mastoiditis. In most cases, symptoms involving the middle ear (eg, fever, pain, conductive hearing loss) predominate, and the disease in the mastoid is not considered a separate entity.

In some patients, the infection spreads beyond the mucosa of the middle ear cleft, and osteitis in the mastoid air-cell system or periosteitis of the mastoid process develops, either directly by means of bone erosion through the cortex or indirectly via the emissary vein of the mastoid. These patients are considered to have acute mastoiditis (also called acute surgical mastoiditis [ASM]), which is an intratemporal complication of otitis media.

Mastoiditis can be acute, subacute or chronic.

Acute mastoiditis is divided into acute mastoiditis with periosteitis (incipient mastoiditis), characterized by purulence in the mastoid cavities; and coalescent mastoiditis (acute mastoid osteitis), characterized by effacement of the bony septae between the mastoid air cells. This can lead to abscess formation cavity and the dissection of pus into surrounding areas.

Subacute mastoiditis (masked mastoiditis) is persistent and low-grade ear and mastoid infection that causes bony septae destruction.

Chronic mastoiditis is a prolonged mastoid air cell suppurative infection lasting months to years. Chronic mastoiditis most commonly is associated with chronic suppurative otitis media (CSOM) and, in particular, with cholesteatoma formation.


The mastoid is a division of the temporal bone. It surrounded by the posterior cranial fossa, the middle cranial fossa, the canal of the facial nerve, the sigmoid and lateral sinuses, and the petrous tip of the temporal bone.

It develops from a narrow outpouching of the posterior epitympanum named the aditus ad antrum. The mastoid initially consists of a single cell, the antrum, that is linked to the middle ear by a narrow channel.

Pneumatization takes place shortly after birth, after the middle ear becomes aerated. This process is complete by the age of 10 years. Mastoid air cells are created by the invasion of epithelial lined sacs between spicules of new bone and by the degeneration and redifferentiation of existing bone marrow spaces.

Other areas of the temporal bone, including the petrous apex and zygomatic root, pneumatize similarly. The antrum, similar to the mastoid air cells, is lined with respiratory epithelium that swells in the presence of infection.

Because of their adjacency to the mastoid, infection can lead to complications involving the semicircular canals, sternocleidomastoid muscle, seventh nerve, internal carotid artery, jugular vein, meninges, sigmoid sinus, and brain.


Acute mastoiditis generally complicates acute otitis media (AOM). Because the middle ear and mastoid air cells are connected,[2] the middle ear mucosal inflammations can also ivolve the mastoid. Generally, the mastoid infection subsides as the middle ear infection resolves. However, when middle ear infection persists, purulence accumulates in the mastoids.[3]

Blockage of the antrum by inflamed mucosa entraps infection in the air cells by inhibiting drainage and by precluding re-aeration from the middle-ear side. Mastoiditis can erode through the antrum and extend to any of the surrounding structures mentioned above (see Anatomy), causing clinically significant morbidity and life-threatening disease.

Mastoiditis may be arrested at any point. It progresses in the following 5 stages

  • Stage 1 - Hyperemia of the mucosal lining of the mastoid air cells

  • Stage 2 - Transudation and exudation of fluid and/or pus within the cells

  • Stage 3 - Necrosis of bone caused by the loss of vascularity of the septa

  • Stage 4 - Cell wall loss with coalescence into abscess cavities

  • Stage 5 - Extension of the inflammatory process to contiguous areas

Persistent acute infection in the mastoid cavity can lead to a rarifying osteitis, which destroys the bony trabeculae that form the mastoid cells; hence, the term coalescent mastoiditis is used for this condition.

Coalescent mastoiditis is essentially an empyema of the temporal bone that, unless its progress is arrested, either drains through the natural antrum to cause spontaneous resolution or unnaturally drains to the mastoid surface, petrous apex, or intracranial spaces to create a further complication. Other temporal bone or nearby structures, such as the facial nerve, labyrinth, or venous sinuses, may become involved.

As with most infectious processes, both host and microbial factors are involved in the development of acute mastoiditis. Host factors include mucosal immunology, temporal bone anatomy, and systemic immunity, whereas microbial factors include the protective coating, antimicrobial resistance, and ability of the pathogen to penetrate local tissue or vessels (ie, invasive strains).


Acute mastoiditis

Because AOM is the antecedent disease, the most common etiologic agents for acute mastoiditis are similar and are Streptococcus pneumoniae, followed by Haemophilus influenzae and group A streptococci (GAS), called also Streptococcus pyogenes.[4] Each of these bacteria has invasive forms and is found most often in children with acute mastoiditis.

More than half of the S pneumoniae organisms recovered are of serotype 19, with serotypes 23 and 3 being the next most common.[5] The introduction of conjugated vaccine for S pneumoniae may affect the distribution of these serotypes. Pseudomonas aeruginosa and other gram-negative aerobic bacilli and anaerobes are infrequently recovered in acute infection. However, recent studies suggest an increase in the incidence of Fusobacterium necrophorum acute mastoiditis (8.5% of isolates).[6, 7] P aeruginosa should only be considered as a potential pathogen in acute mastoiditis in those who have a history of recurrent AOM and recent antibiotic therapy and perforated tympanic membrane. Mycobacterium tuberculosis is rarely the cause of mastoiditis in developed countries.

The incidence of multidrug-resistant S pneumoniae (MDRSP) associated with acute mastoiditis is currently high. This observation may alter the selection of antimicrobials, in that 35-40% of MDSRP are penicillin-resistant, 30-35% are macrolide-resistant, and approximately 15% are ceftriaxone-resistant. However, resistance may vary according to local resistance rate. 

A study by Koutouzis et al looked to determine whether serotype distribution and antibiotic resistance of Streptococcus pneumoniae acute mastoiditis in children have changed in the post pneumococcal conjugate vaccines (PCVs) era. The study found that after the introduction of PCV7, a significant increase of serotype 19A and replacement of PCVs serotypes was identified. After PCV13, the overall proportion of pneumococcal mastoiditis and the incidence of serotype 19A were not significantly declined. A significant proportion of resistant isolates to penicillin and erythromycin is attributed to serotype 19A.[8]  In contrast, in a prospective study of 8 children's hospitals from 2011 to 2013, Kaplan et al found that the number of pneumococcal isolates and the percentage of isolates with high-level penicillin resistance from cultures taken from children with otitis media or mastoiditis for clinical indications have decreased following PCV13 use, largely related to decreases in serotype 19A isolates.[9]

Recent treatment with antimicrobials, attendance at a daycare center, and the winter season are associated with an increased incidence of MDRSP. After the introduction of vaccination with the 7- and later 13 valent pneumococcal vaccines, a reduction of MDRSP occurred.[2, 10] However, those strains were replaced by strains not included in the vaccine.[11, 12]

Staphylococcus aureus, especially methicillin-resistant S aureus (MRSA), has emerged as an important pathogen.[13] A study from Israel noted an increase in the recovery of GAS (isolated in 20% of cases) in acute mastoiditis was observed between 1983-2007.[14] GAS was recovered more often from children older than 2 years.[15]

Although P aeruginosa has been recovered in some series,[16] higher rates of recovery may happen when samples are obtained from the external canal in patients with otorrhea.[17]

Obtaining cultures with samples from the infected site is important to guide specific therapy.

Chronic mastoiditis

Chronic mastoiditis is generally a result of CSOM; it is rarely a result of failure of treatment of acute mastoiditis. The most frequently recovered isolates from chronically inflamed mastoids are similar to the one isolated from CSOM and include P aeruginosa, Enterobacteriaceae, S aureus (including MRSA),[13] and anaerobic bacteria. The infection may be polymicrobial (aerobic and anaerobic) in over one half of patients.

The predominant anaerobic bacteria are Peptostreptococcus species, anaerobic gram-negative bacilli (eg, pigmented Prevotella, Porphyromonas, and Bacteroides species) and Fusobacterium species.[18, 19]  Recent studies suggest an increase in the incidence of F necrophorum mastoid infections in the last 2 decades.[20]

Over one half of anaerobic gram-negative bacilli and Fusobacterium species can produce the enzyme beta-lactamase.[21]

S pneumoniae and H influenzae are rarely isolated. The pathogenic role of P aeruginosa in many of these patients is often questionable because it colonizes the ear canal and can contaminate specimens obtained through the nonsterile canal. Blastomycosis,[22] M tuberculosis, nontuberculous mycobacteria, and Mycobacterium bovis are infrequent causes of mastoiditis.[23, 24]


United States statistics

The epidemiology of acute mastoiditis is similar to that of AOM, with the highest incidence in children younger than 2 years. In the preantimicrobial era, mastoidectomy was performed in as many as 20% of patients with AOM. Since the advent of antimicrobial agents, the incidence of mastoiditis has decreased. By 1948, this rate had fallen below 3%, and at present, it is thought to be lower than 5 cases per 100,000 persons in the United States or other developed countries. Although the incidence of the disease has substantially declined in the United States, it is still a clinically significant infection with the potential of life-threatening complications.

Of great concern was the sharp increase in the incidence of acute mastoiditis reported in several locations in the turn of the century. This increase may be due to a rising rate of infections caused by antibiotic-resistant organisms,[25, 26] increased virulence of the pathogens, and decreased use of antibiotics to treat AOM. However, the incidence significanly declined as the conjugated pneumococcal vaccine, which was licensed for clinical use in the United States in 2000 (7 valent) and 2010 (13 valent), became more widely available and more frequently administered.  Decrease in all  types of pneumocococcal disease including mastoidits was reported from multiple countries in which universal immunization was implemented.[25]  

A study illustrated a downward trend in otitis media-related healthcare use in the United States from 2001 to 2011.[27] The significant reduction in otitis media visit rates in 2010-2011 in children younger than 2 years coincided with the advent of pneumococcal conjugate vaccine 13. Although tympanic membrane perforation/otorrhea rates steadily increased during that period, mastoiditis and ventilating tube insertion rates decreased in the last years of the study.

A study by King et al found that in the United States, between 2000 and 2012, the estimated incidence of pediatric mastoiditis peaked in 2006, at 2.7 cases per 100,000 population, and fell to its lowest point in 2012, at 1.8 cases per 100,000 population.[28]

A study by Raveh et al that assessed the characteristics, treatment, and outcome of acute mastoiditis in children with a cochlear implant reported that of the 370 children who underwent cochlear implantation, 13 (3.5%) were treated for acute mastoiditis. In all of the 9 children who had unilateral cochlear implant, the acute mastoiditis episode occurred in the implanted ear.[29]

International statistics

Developing countries and countries where uncomplicated AOM is not managed with antibiotics have an increased incidence of mastoiditis, presumably resulting from untreated otitis media. For example, the incidence of acute mastoiditis in the Netherlands, which has a low antibiotic prescription rate for AOM, is reported as 3.8 cases per 100,000 person-years. In all other countries with high antibiotic prescription rates, the incidence is considerably lower than this, at 1.2-2 cases per 100,000 person-years.

Age-, sex-, and race-related demographics

Acute mastoiditis is a disease of the young. Most children with acute mastoiditis are younger than 2 years (median age, 12 months) and have little history of antecedent otitis media. At this age, the immune system is relatively immature, particularly with regard to its ability to respond to challenges from polysaccharide antigens.

No sex predilection is known. However, for all forms of mastoiditis, race affects the incidence of otitis media. Some populations, such as the Inuit, almost universally have middle-ear disease and, invariably, have chronic mastoiditis.


Expect patients with acute mastoiditis to recover completely if the facial nerve, vestibule, or intracranial structures are not involved.

In most cases, cosmetic deformity of the surgically treated ear can be prevented with judicious placement of the incision and the development of flaps to pull the ears posteriorly when replaced.

Conductive hearing loss should resolve, provided the ossicular chain remains intact. Conduct testing after otorrhea ceases and the ear has healed.

Mastoiditis, when it progresses beyond the first 2 stages (see Pathophysiology), is considered a complication of otitis media. Complications of mastoiditis result from further extensions of the process in or beyond the mastoid itself. Such extensions include the following:

  • Posterior extension to the sigmoid sinus, which causes thrombosis

  • Extension to the occipital bone, which creates an osteomyelitis of the calvaria or a Citelli abscess

  • Superior extension to the posterior cranial fossa, subdural space, and meninges

  • Anterior extension to the zygomatic root

  • Lateral extension to form subperiosteal abscess

  • Inferior extension to form a Bezold abscess

  • Medial extension to the petrous apex

  • Intratemporal involvement of facial nerve and/or labyrinth




Patients may have unique features of acute and chronic mastoiditis. Acute mastoiditis generally follows a recent or concurrent episode of acute otitis media (AOM) and often results in fever. Presentation varies according to age and the stage of the infection. Chronic disease, which can be subclinical, is often secondary to partial treatment of AOM with antibiotics. Otorrhea that persists longer than 3 weeks is the most consistent sign that a chronic process involving the mastoid has evolved.

Fever may be present (76% of patients).[30] The patient’s temperature may be high. The fever may be unrelenting in acute mastoiditis and may be related to the associated AOM. Persistence of fever, particularly when the patient is receiving adequate and appropriate antimicrobial agents, is common in acute mastoiditis. High fever spikes may be suggestive of sigmoid sinus thrombophlebitis.

Pain may be reported (67% of patients).[30] Pain is localized deep inside or behind the ear and typically worsens at night. Persistence of pain is a warning sign of mastoid disease. This finding may be difficult to evaluate in young patients. Other systemic symptoms and signs may include lethargy, malaise, irritability, poor feeding, or diarrhea.

Hearing loss may occur. This is common with all processes involving the middle-ear cleft. More than 80% of patients have no history of recurrent otitis media.

Nonspecific symptoms (most commonly observed in infants) include poor feeding and irritability.

The clinical findings of acute mastoiditis may differ according to the causative pathogen. S. pneumoniae, especially strains with reduced susceptibility, causes severe symptoms and leads to mastoidectomy more often than the other pathogens. S. pyogenes causes less otalgia than the other pathogens. P. aeruginosa particularly affects children with tympanostomy tubes and causes a less aggressive form of disease.[31]

Physical Examination

Signs of acute mastoiditis include the following[30] :

  • Bulging erythematous tympanic membrane

  • Tympanic membrane perforation (37%) and otorrhea (50%)

  • Erythema, tenderness, and edema over the mastoid area

  • Postauricular fluctuance

  • Protrusion of the auricle (generally downward and outward in children < 2 y and upward and outward in those >2 y)

  • Sagging of the posterosuperior canal wall (71% of patients)[30]

Chronic mastoiditis findings may be consistent with a complication of extension beyond the mastoid process and its overlying periosteum or with another intratemporal complication such as facial palsy. Signs include the following:

  • Infected or normal-appearing tympanic membrane

  • Absence of external signs of mastoid inflammation

Neurologic examination generally yields nonfocal findings. However, involvement of the cranial nerves can occur with advanced disease. Signs include the following:

  • Palsy of the abducens nerve (cranial nerve VI)

  • Palsy of the facial nerve (cranial nerve VII)

  • Pain from involvement of the ophthalmic branch of the trigeminal nerve

Findings observed in both acute and chronic mastoiditis include periosteal thickening, subperiosteal abscess, otitis media, and nipplelike protrusion of the central tympanic membrane.

Periosteal thickening requires comparison with the other side. Displacement of the auricle downward and outward (especially in children younger than 2 years) or upward and outward (in children younger than 2 years) may be present. Subperiosteal abscess (see the image below) displaces the auricle laterally and obliterates the postauricular skin crease. If the crease remains, the process is lateral to the periosteum.

Mastoiditis with subperiosteal abscess. Note the l Mastoiditis with subperiosteal abscess. Note the loss of the skin crease and the pointed abscess.

Otitis media is present at otoscopy, often with additional features. Nipplelike protrusion of the central tympanic membrane may be present; this usually oozes pus.

A persistent low-grade infection (masked mastoiditis) can occur in patients with recurrent otitis media or persistent ear effusion. This condition can cause fever, ear pain, and complications.[32]


Extracranial complications include the following[33] :

  • Facial nerve palsy

  • Conductive and sensorineural hearing loss

  • Subperiosteal abscess

  • Cranial osteomyelitis or bony erosion

  • Bezold abscess (a deep abscess in the soft tissues of the neck)

  • Labyrinthitis

  • Lemierre Syndrome [34]
  • Petrositis leading to Gradenigo syndrome (triad of abducens nerve palsy, deep facial pain from trigeminal nerve involvement, and suppurative otitis media)

Intracranial complications include the following[35] :

  • Intracranial spread (meningitis; epidural, temporal lobe or cerebral abscess, subdural empyema, subperiosteal abscess)

  • Dural sinus thrombosis



Diagnostic Considerations

Cat scratch disease and atypical mycobacteria tend to have a poor response to antimicrobials and a high incidence of nodal abscess formation. Differentiation of these conditions from acute mastoiditis is relatively easy with preservation of the skin crease and the presence of a healthy middle ear.

Besides the conditions listed in the differential diagnosis, other problems to be considered include the following:

  • Tumors

  • Auricular or mastoid trauma

  • Furuncle of meatus of the ear

  • Cervical or postauricular (mastoid) adenopathy

  • Parotitis

  • Basilar skull fracture

  • Cysts

  • Stroke

  • Fever of unknown origin

  • Sepsis

Differential Diagnoses



Laboratory Studies

Specimens from the mastoid cells obtained during surgery and myringotomy fluid, when obtained, should be sent for cultures for aerobic and anaerobic bacteria, fungi, and mycobacteria and Gram and acid-fast staining.

If the tympanic membrane is already perforated, the external canal can be cleaned, and a sample of the fresh drainage fluid taken. Care must be taken to obtain fluid from the middle ear and not the external canal.

Gram stains of the specimen can initially guide empiric antimicrobial therapy. Culture and susceptibility testing of the isolates can assist in modifying the initial empiric antibiotic therapy. The results of properly collected culture for both aerobic and anaerobic bacteria should guide the definite choice of therapy.

Blood cultures should be obtained. The baseline complete blood count (CBC) and erythrocyte sedimentation rate (ESR) are determined to permit subsequent assessment of the effectiveness of therapy.

Obtain cerebrospinal fluid (CSF) for evaluation if an intracranial extension of the process is suspected.

Computed Tomography

Computed tomography (CT) of the temporal bone is the standard in the evaluation of mastoiditis.[36] The sensitivity of CT scanning in acute mastoiditis is 87-100%. It may be overly sensitive because any acute otitis media (AOM) has a component of mastoid inflammation. Immediate CT scanning is warranted whenever intracranial extension or complications are suspected.

Evidence of mastoiditis is illustrated by appearance of haziness or destruction of the mastoid outline and cortex and a decrease or loss of the sharpness of the mastoid air cells bony septa (coalescent mastoiditis). In cases in which CT scanning reveals cloudiness of the air cells, a technetium-99 bone scan is helpful in detecting osteolytic changes.

Clouding of the middle ear and mastoid cells is a nonspecific finding that may be present early in the illness, and it is often observed in patients with AOM without mastoiditis.

Other findings include periosteal thickening, disruption of the periosteum, and subperiosteal abscess.

Plain radiographic findings of acute mastoiditis are similar to CT findings: clouding of the mastoid or coalescence of the mastoid air cells.[1, 2]


Plain radiography is unreliable in this setting, and the findings lag behind clinical symptoms. In areas of the world where CT scanning is not immediately available, plain radiography of the mastoids reveal clouding of the air cells with bone destruction in acute surgical mastoiditis (ASM). In the vast majority of cases, radiography is adequate to establish the diagnosis but lacks sensitivity in differentiating the stages of the disease and fails to reveal the petrous apex in any great detail.[37]

The following findings are used to differentiate AOM or acute mastoiditis without osteitis from chronic mastoiditis:

  • Clouding or haziness of the mastoid air cells and middle ear may be present. This is due to the inflammatory swelling of mucosa and the collected fluid.

  • Loss of sharpness or visibility of mastoid cell walls due to demineralization, atrophy, or necrosis of bony septa

  • Haziness or distortion of mastoid outline, possibly with visible defects of the tegmen or mastoid cortex

  • Enhancement of areas of abscess formation

  • Elevation of the periosteum of the mastoid process or posterior cranial fossa

  • Osteoblastic activity in chronic mastoiditis

Magnetic Resonance Imaging

Magnetic resonance imaging (MRI) is used more often in patients with clinical symptoms or CT findings suggestive of intracranial complications. However, MRI is not routinely used to evaluate the mastoid.

MRI is the standard for the evaluation of contiguous soft tissue, in particular, the intracranial structures, and for detecting extra-axial fluid collections and associated vascular problems. In addition, it is helpful in planning effective surgical treatment.

Tympanocentesis and Myringotomy

Tympanocentesis and myringotomy may be performed before the initiation of antibiotic therapy. Culturing middle-ear fluid before antimicrobial therapy is imperative. Although use of an operating microscope and specifically designed suction traps facilitate sampling from the middle ear, an otoscope, spinal needle, and syringe are equally helpful.

Sterilize the canal with an antiseptic. With the child restrained, aspirate fluid from the anterior half of the tympanic membrane.

Other Tests


Audiometry is seldom appropriate or useful in children with acute mastoiditis but must be performed after patients recover from the acute phase and in children with chronic mastoiditis. In the population at risk (ie, children younger than 2 years), thresholds for air and bone conduction under headphones are only rarely determined.

Lumbar puncture

Perform a lumbar puncture and spinal tap if intracranial extension of the infection is suspected.



Approach Considerations

The treatment of mastoiditis depends upon the stage of the infection and presence and type of complications if present. Antimicrobial therapy and surgical drainage of the middle ear and mastoid cells are the mainstay of therapy.

Medical care for mastoiditis includes intravenous (IV) antimicrobial therapy. The choice of antimicrobial should be based on findings from clinical specimens obtained from the middle ear by tympanocentesis or aspiration. Myringotomy and tympanocentesis are primarily used to obtain specimens and relieve discomfort from acute otitis media (AOM). The openings usually heal within a few days.

After obtaining cultures by means of tympanocentesis or at the time of tympanostomy tube placement with or without mastoidectomy, continue with the initial antibiotic until cultures are reported. If the patient becomes afebrile and if swelling decreases at 48-72 hours, oral medication may be selected on the basis of the culture reports.

Surgical therapy may include mastoidectomy, placement of tympanostomy tubes, and tympanoplasty, as indicated. Treatment of acute mastoiditis varies, depending on the presence or absence of osteitis and periosteitis. Patients with chronic otitis media should be referred to an otolaryngologist. Guidelines for medical management of AOM have been established.[38]

Antimicrobial Therapy

Treatment of mastoiditis mandates administration of parenteral antimicrobial therapy. However, this therapy may not necessarily be sufficient, especially in advanced stages the infection. Antimicrobial therapy may not prevent the emergence of complications, as was evident in a series of 223 patients, in whom 8.5% developed complications during antimicrobial treatment.[39]

Acute mastoiditis

The antimicrobials used to treat acute mastoiditis include vancomycin plus either ceftriaxone, cefepime (for Pseudomonas), or the combination of a penicillin with a beta-lactamase inhibitor (eg, ampicillin-sulbactam, piperacillin-tazobactam) or a carbapenem.

Aztreonam combined with vancomycin is administered to those with potential severe hypersensitivity (ie, anaphylaxis) to beta-lactam antibiotics.

Parenteral therapy should be given for at least for 7-10 days. Oral therapy can substitute for parenteral treatment (if improvement occurred) for a total of 4 weeks of treatment. Oral agents include clindamycin plus a third-generation cephalosporin or amoxicillin plus clavulanic acid.

Chronic mastoiditis

Treatment of chronic mastoiditis is similar to that of chronic suppurative otitis media (CSOM), which is treated with topical antimicrobial therapy. Thorough aural toilet and systemic antimicrobials are given if this approach fails. The empiric choice of systemic antimicrobials is directed at the eradication of both aerobic and anaerobic bacteria.

Over one half of all gram-negative anaerobic bacteria (eg, pigmented Prevotella, Porphyromonas, Bacteroides, and Fusobacterium) are resistant to penicillins because they produce beta-lactamase. Clindamycin, cefoxitin, metronidazole, chloramphenicol, amoxicillin-clavulanate, or piperacillin-tazobactam provides coverage for anaerobic bacteria.

Coverage for some aerobic bacteria is achieved by using several of these agents. Antimicrobials effective against S aureus and the aerobic gram-negative bacilli, including P aeruginosa, may also be needed. Whenever methicillin-resistant S aureus (MRSA) is present, vancomycin or linezolid should be administered.

An aminoglycoside, a third-generation cephalosporin (eg, ceftazidime, cefepime) or a quinolone (in adults) should be considered for coverage of aerobic gram-negative bacilli, including Pseudomonas. The carbapenems (eg, meropenem) provide single-agent therapy for most of the potential pathogens.

Oral therapy can substitute for parenteral therapy if improvement occurs; treatment should last a total of 6 weeks.

Mastoidectomy, Tympanoplasty, and Tympanostomy

With tympanostomy tube placement, a tube maintains the opening in the tympanic membrane and provides access to the middle ear and mastoid for the administration of antibiotic drops, steroid drops, or both and for drainage without concern about the patency of the eustachian tube. Place the tubes at the time of mastoidectomy, if performed.

Several different types of mastoidectomy procedures are available. Simple (or closed) mastoidectomy is performed through the ear or through an incision behind the ear. The surgeon opens the mastoid bone and removes the infected air cells. The tympanic membrane is incised to drain the middle ear. Topical antibiotics are then placed in the ear.

Radical mastoidectomy removes the most bone and is usually performed for extensive spread of infection. The tympanic membrane and middle ear structures may be completely removed. Usually, the stapes is spared, if possible, to preserve hearing.

In modified radical mastoidectomy, some middle-ear bones are left in place, and the tympanic membrane is reconstructed with tympanoplasty.

Iatrogenic injury during therapy is preventable with facial nerve monitoring, which is now available for use during mastoid surgery. Experienced otologists are unlikely to injure the ossicular chain during mastoid surgery. However, patients and their families should be warned about possible cosmetic deformity after mastoid surgery.

Children who have undergone mastoidectomy are released home after discharge from the surgically implanted drain has abated. The drain is typically removed 48-72 hours after surgery. Antibiotic or steroid drops are continued until the otorrhea ceases and the tympanostomy tube is noted to be open, with healing or healed mucosa behind it.

Special Considerations in Treating Acute Mastoiditis

Acute mastoiditis without osteitis or periosteitis

Consider mastoidectomy for the management of AOM if the patient had pain and fever persisting longer than 48 hours or increasing swelling or tenderness. Otherwise, acute mastoiditis without osteitis or periosteitis is typically associated with AOM and is the only condition of the mastoid that is treated solely with medical therapy.

Management includes the administration of parenteral antimicrobial therapy and myringotomy with or without the placement of a tympanostomy tube. The main goal of therapy is to prevent spread of the infection to the central nervous system (CNS) and to localize the infection. Successful therapy markedly shrinks the abscess, and the periosteal thickening and tenderness decreases within 48 hours.

If complications occur, obtain culture samples through the middle ear, commence new antimicrobial therapy, and image the mastoid. Culture results should guide antimicrobial therapy whenever possible.

Acute mastoiditis with osteitis

Acute mastoiditis with osteitis is a surgically managed disease, though coverage with appropriate antibiotics is mandatory. Mastoidectomy with insertion of a tympanostomy tube is necessary to remove the areas of coalescence in the temporal bone.

Antibiotics should be selected to provide good intracranial penetration and multidrug-resistant S pneumoniae (MDRSP) coverage. With the high incidence of invasive, resistant strains in mastoiditis, initial therapy of IV vancomycin and ceftriaxone or the combination of a penicillin plus a beta-lactamase inhibitor (eg, ampicillin-sulbactam) is most appropriate until the culture and sensitivity results are available.

After surgery, antibiotic drops, steroid drops, or both are used to keep the tube patent and reduce middle-ear swelling.

Patients in whom empyema spreads beyond the mastoid require drainage of the abscess and mastoidectomy. Intracranial spread necessitates a combined neurosurgical and otolaryngologic approach.

Acute mastoiditis with periosteitis

Postauricular swelling and erythema, without subperiosteal abscess or mastoid osteitis, can be treated conservatively by using parenteral antibiotics, high-dose steroids, and insertion of a tympanostomy tube. Vancomycin and ceftriaxone are recommended until culture results become available. If substantial resolution of pain, fever, and erythema does not occur 36-48 hours after the start of therapy, mastoidectomy is warranted.


Early recognition and appropriate treatment of AOM decreases the risk of mastoiditis but does not completely prevent it. The rate of mastoiditis was 1.8 versus 3.8 per 10,000 episodes of AOM in cases treated and not treated with antibiotics, respectively.[40]

The conjugated vaccine against invasive S pneumoniae should affect the incidence of pediatric mastoiditis. A study that examined immunization discomfort in children aged 4-6 years concluded that multifaceted distraction intervention significantly reduced pain and discomfort in childhood immunizations.[41]

Physicians should be aware of the signs and symptoms of mastoiditis and have a high index of suspicion.


Early consultation with an otolaryngologist is appropriate and necessary if the pediatrician is not comfortable performing tympanocentesis. After the culture results are available, the presence of resistant or unusual microbes may require consultation with an appropriate infectious disease specialist.

Consultation with an otolaryngologist is warranted for those with cervical fluctuance or postauricular fluctuance, mass or swelling, high-spiking fever, imaging studies showing mastoid air cell coalescence, rim-enhancing fluid collection, cortical bone erosion, or intracranial extension.[42]

Consultation with a neurologist is also warranted in those who exhibit neurologic signs (eg, meningeal signs, focal deficits, facial weakness, altered level of consciousness, and seizures).

Consultation with a neurosurgeon is appropriate if evidence of intracranial extension with abscess formation is present.

Transfer of the patient is invariably related to the availability of the relevant subspecialists. Available radiographs should be copied and sent with the patient, along with available laboratory data. The patient should take nothing by mouth until the receiving subspecialists can evaluate the condition.

Long-Term Monitoring

After the discontinuance of IV antibiotics, oral antibiotics should be continued to complete the treatment plan. PO antibiotics that offer the same coverage as the selected IV antibiotic for a given patient should be selected.

After discharge, patients should be followed up by an otolaryngologist. Audiography should be performed. Recurrences were seen in 5% of all patients with acute mastoiditis.[43]



Medication Summary

The principal medications used in the treatment of mastoiditis are antibiotics. Other medications include analgesics and antipyretics and topical antibiotic-steroid combinations. If open mastoid surgery is not undertaken, use of high-dose intravenous (IV) steroids is warranted to decrease mucosal swelling and promote natural drainage through the aditus ad antrum into the middle ear.

Antibiotics, Other

Class Summary

Culture and sensitivity results ultimately govern the selection of specific antibiotics. Until microbiologic information is available, the following principles guide selection:

- The antimicrobial must be appropriate to cover the most common invasive strains of bacteria in acute otitis media (AOM)

- The selected antibiotic should cross the blood-brain barrier

- The selected therapeutic spectrum should include consideration of multidrug-resistant S pneumoniae (MDRSP) organisms that are prevalent in the individual’s community

Coverage for anaerobic bacteria, as well as gram-negative aerobic bacteria and S aureus including methicillin-resistant S aureus (MRSA), are important in chronic mastoiditis. Specific microbiologic diagnoses should be treated with appropriate antibiotics.

Linezolid (Zyvox)

Linezolid prevents formation of functional 70S initiation complex, which is essential for the bacterial translation process. It is bacteriostatic against staphylococci.

Cefepime (Maxipime)

Cefepime is a fourth-generation cephalosporin. Its gram-negative coverage is comparable to that of ceftazidime, but it has better gram-positive coverage (comparable to that of ceftriaxone). Cefepime is a zwitterions and rapidly penetrates gram-negative cells. It is the best beta-lactam for intramuscular (IM) administration. Its poor capacity to cross the blood-brain barrier precludes its use for treatment of meningitis.


Because an increasing proportion of invasive strains of S pneumoniae are MDRSP and because MRSA is playing an increased role, beginning therapy with vancomycin is appropriate. After surgical or culture and sensitivity results confirm pathogenic sensitivity to other medications, medications that do not require the same degree of monitoring may be used instead. In patients with sensitivity to vancomycin, high-dose ceftriaxone or cefotaxime may be used. Rifampin is also effective in managing MDRSP.

The preferred method of administration is the individual analytic method. Adjust initial doses to provide peak levels of 25-40 µg/mL and trough levels below 10 µg/mL.

Ceftriaxone (Rocephin)

Ceftriaxone is a third-generation cephalosporin with broad-spectrum gram-negative activity. It arrests bacterial growth by binding to one or more penicillin-binding proteins. Initiate treatment with a high dose for adequate treatment of potential penicillin-resistant pneumococcal infection.

Meropenem (Merrem)

Meropenem is a bactericidal broad-spectrum carbapenem antibiotic that inhibits cell-wall synthesis. It is effective against most gram-positive and gram-negative aerobic and anaerobic bacteria. Compared with imipenem, meropenem possesses slightly increased activity against gram-negative organisms and slightly decreased activity against staphylococci and streptococci.

Clindamycin (Cleocin)

Because an increasing proportion of invasive strains of S pneumoniae are MDRSP and because MRSA is playing an increased role, beginning therapy with clindamycin is appropriate. This agent is a lincosamide that is effective against S aureus, aerobic streptococci (except enterococci) and anaerobic bacteria. It inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest.

Piperacillin and tazobactam sodium (Zosyn)

Piperacillin-tazobactam is a combination of an antipseudomonal penicillin with a beta-lactamase inhibitor. It inhibits biosynthesis of cell-wall mucopeptide and is effective during the stage of active multiplication. It is effective against aerobic and anaerobic gram-positive and gram-negative bacteria.

Antibiotics/Corticosteroids, Otic

Class Summary

After a tympanostomy tube is placed, with or without mastoidectomy, a pH-balanced solution or suspension of an antibiotic and a corticosteroid is useful to decrease mucosal swelling and to deliver topical antibiotics to the middle ear and mastoid. The drops should be continued until otorrhea has ceased and the view through the tube shows healing mucosa without swelling or obstruction. Several combinations are available; the best are those thin enough to apply through the tube into the middle ear.

Hydrocortisone/neomycin/polymyxin (Cortisporin, Cortomycin)

The combination of hydrocortisone with neomycin and polymyxin is an antibacterial and anti-inflammatory suspension for otic use. It is used to treat superficial bacterial infections in the external auditory canal.

Dexamethasone/tobramycin (TobraDex)

Tobramycin interferes with bacterial protein synthesis by binding to 30S and 50S ribosomal subunits, which results in a defective bacterial cell membrane. Dexamethasone decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reducing capillary permeability. This combination is available in sterile ophthalmic drops that are also commonly used for otic infections.

Gentamicin/betamethasone (Garasone)

The combination of gentamicin with betamethasone is supplied in a sterile ophthalmic solution available only in Canada. It is commonly used for otic infections. Gentamicin is an aminoglycoside antibiotic used for gram-negative bacterial coverage. Betamethasone decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reducing capillary permeability.

Antibiotic, Otic

Class Summary

Otic antibiotics may be considered after tympanostomy tube placement to treat acute or chronic otitis media.

Ofloxacin otic solution

Ofloxacin inhibits bacterial growth by inhibiting DNA gyrase.