AUTHOR AND EDITOR INFORMATION

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INTRODUCTION

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• Introduction
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• Follow-up
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Background

Mastoiditis is an inflammatory process of the mastoid air cells in the temporal bone. Because the mastoid is contiguous to the middle ear cleft and an extension of it, virtually every child or adult 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. Chronic mastoiditis most commonly is associated with chronic suppurative otitis media (CSOM) and particularly, with cholesteatoma formation. (This is not discussed in detail in this article.)

Pathophysiology

As with most infectious processes, consider host and microbial factors in the evaluation 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).

Host factors

Most children with acute mastoiditis are younger than 2 years 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.

Anatomy

The mastoid develops from a narrow outpouching of the posterior epitympanum named the aditus ad antrum. Pneumatization takes place shortly after birth, after the middle ear becomes aerated. This process is complete by the time an individual is aged 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.

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. Surrounding the mastoid are 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. Mastoiditis can erode through the antrum and extend to any of the above contiguous sites, causing clinically significant morbidity and life-threatening disease. 

Coalescence

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

1. Stage 1 - Hyperemia of the mucosal lining of the mastoid air cells
2. Stage 2 - Transudation and exudation of fluid and/or pus within the cells
3. Stage 3 - Necrosis of bone caused by the loss of vascularity of the septa
4. Stage 4 - Cell wall loss with coalescence into abscess cavities
5. Stage 5 - Extension of the inflammatory process to contiguous areas

Frequency

United States

In the pre-antimicrobial era, mastoidectomy was performed in as many as 20% of patients with AOM. The incidence of mastoiditis has decreased since the advent of antimicrobial agents and has become rare. By 1948, this rate decreased to <3%, and it presently is thought to be <5 cases per 100,000 persons in the United States or other developed countries. The incidence of mastoiditis is higher in developing countries than elsewhere, mostly as a consequence of untreated otitis media.

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 is the sharp increase in the incidence of acute mastoiditis in the last decade reported in several locations. This increase may be due to a rising rate of infections caused by antibiotic-resistant organisms, increased virulence of the pathogens, and decreased use of antibiotics to treat AOM. The incidence is most likely to decline with the availability and administration of the conjugated pneumococcal vaccine, which became licensed for clinical use in 2000.

International

Developing countries and countries where uncomplicated AOM is not 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.

Mortality/Morbidity

Mastoiditis, when it progresses beyond the first 2 stages (see Coalescence) is considered a complication of otitis media. Complications of mastoiditis are further extensions of the process in or beyond the mastoid itself.

Common complications include hearing loss and extension of the infectious process beyond the mastoid system, resulting in intracranial complications or extracranial complications. Other complications are the following (see also Complications):

• 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

Race

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 they invariably have chronic mastoiditis.

Sex

No sex predilection exists.

Age

Acute mastoiditis is a disease of the young. Most patients seek care before they are aged 2 years (median, 12 mo).

CLINICAL

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History

Patients may have unique features of acute and chronic mastoiditis. Acute mastoiditis generally follows recent or concurrent episode of AOM and often results in fever.

• 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. The patient's temperature may be high.
• • The fever may be unrelenting in acute mastoiditis, but it 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.
• Pain may be reported.
• • Pain is localized deep inside or behind the ear and typically worse at night.
  • Persistence of pain is a warning sign of mastoid disease. This finding may be difficult to evaluate in young patients.
• 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.

Physical

Findings in 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, and lateral displacement of the auricle may be present. Subperiosteal abscess displaces the auricle laterally and obliterates the postauricular skin crease. If the crease remains, the process is lateral to the periosteum. Otitis media is present at otoscopy, often with additional features. Nipplelike protrusion of the central tympanic membrane may be present; this usually oozes pus.

• Signs of acute mastoiditis include the following:
• • Bulging erythematous tympanic membrane
  • Erythema, tenderness, and edema over the mastoid area
  • Postauricular fluctuance
  • Protrusion of the auricle
  • Sagging of the posterosuperior canal wall
  • Fever
• Signs of chronic mastoiditis include the following:
• • Infected or normal-appearing tympanic membrane
  • Recurrent or persistent fever
  • Absence of external signs of mastoid inflammation
  • 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.
• Neurologic examination generally yields nonfocal findings. However, involvement of the cranial nerves can occur with advanced disease.
• • 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

Causes

• Acute mastoiditis
• • Because AOM is the antecedent disease, the most common etiologic agent for acute mastoiditis is Streptococcus pneumoniae, followed by Haemophilus influenzae and group A streptococci (GAS), called also Streptococcus pyogenes. Each of these bacteria has invasive forms and is found most often in children with acute mastoiditis.
  • More than half of the S pneumoniae recovered are of serotype 19, followed by serotypes 23 and 3.The introduction of conjugated vaccine for S pneumoniae may effect the distribution of these serotypes.
  • Pseudomonas aeruginosa and other gram-negative aerobic bacilli and anaerobes are infrequently recovered in acute infection.
  • Mycobacterium tuberculosis is rarely the caused 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, as 35-40% are penicillin resistant, 30-35% are macrolide resistant, and approximately 15% are ceftriaxone resistant.
  • Recent treatment with antimicrobials, attendance at a daycare center, and the winter season are associated with an increased incidence of MDRSP.
  • 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, Staphylococcus aureus 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. Over one half of anaerobic gram-negative bacilli and Fusobacterium species can produce the enzyme beta-lactamase.
  • 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.

DIFFERENTIALS

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Other Problems to be Considered

In both acute and chronic mastoiditis
Otitis media
otitis externa
Tumors
Catscratch disease
Atypical mycobacteria

In acute mastoiditis
Auricular or mastoid trauma
Furuncle of meatus of the ear
Cervical or postauricular (mastoid) adenopathy
Parotitis
Basilar skull fracture
Cysts
Stroke

In chronic mastoiditis
Fever of unknown origin
Sepsis

WORKUP

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Lab Studies

• Specimens from the mastoid cells obtained during surgery and myringotomy fluid, when obtained, should be sent for cultures for both aerobic and anaerobic bacteria, Gram staining, 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.
  • 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.
  • Gram stains of the specimen can initially guide empirical antimicrobial therapy.
• Blood cultures should be obtained.
• The baseline CBC and sedimentation rate are determined to later evaluate the effectiveness of therapy.
• Obtain spinal fluid for evaluation if an intracranial extension of the process is suspected.

Imaging Studies

• CT scanning of the temporal bone is the standard in the evaluation of mastoiditis. The sensitivity of CT in acute mastoiditis is 87-100%. It may be overly sensitive since any AOM has a component of mastoid inflammation. Immediate CT scanning is warranted whenever intracranial extension or complications are suspected.
• • Plain radiographs are unreliable, and the findings lag behind clinical symptoms.
  • In areas of the world where CT scanning is not immediately available, plain radiographs of the mastoids demonstrate clouding of the air cells with bone destruction in ASM. In the vast majority of cases, radiographs are adequate to establish the diagnosis, but they lack sensitivity in differentiating the stages of the disease, and they fail to show the petrous apex in any great detail.
  • The following findings are used to differentiate AOM and/or AOM/acute mastoiditis without osteitis, and 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
• 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.
  • MRI is helpful in planning effective surgical treatment.

Other Tests

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

Procedures

• Tympanocentesis and/or myringotomy: Myringotomy may be performed initially, followed by 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.
• Perform a lumbar puncture and spinal tap if intracranial extension of the infection is suspected.

TREATMENT

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Medical Care

Medical care includes antimicrobial treatment.

• Acute mastoiditis
• • The antimicrobials used are vancomycin plus either ceftriaxone or the combination of a penicillin plus a beta-lactamase inhibitor (eg, ampicillin plus sulbactam).
  • Parenteral therapy should be given for at least for 7-10 days.
  • Oral (PO) therapy can substitute parenteral treatment (if improvement occurred) for a total of 4 weeks of treatment.
  • PO agents include clindamycin plus a third-generation cephalosporin or amoxicillin plus clavulanic acid.
• Chronic mastoiditis
• • Treatment of chronic mastoiditis is similar to that of CSOM, which is treated with topical antimicrobial therapy. Thorough aural toilet and system antimicrobials are given if this approach fails.
  • The empirical 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 produced beta-lactamase.
  • Clindamycin, cefoxitin, metronidazole, chloramphenicol, or the combination of amoxicillin and clavulanic acid 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 be also needed.
  • Whenever methicillin-resistant S aureus is present, vancomycin or linezolid should be administered instead of beta-lactam resistant penicillin (eg, oxacillin).
  • An aminoglycoside, a third-generation cephalosporin (eg, ceftazidime, cefepime) or a quinolone (in adults) should be considered for coverage of aerobic gram-negative bacilli.
  • The carbapenems (eg, meropenem) provide single-agent therapy for most of the potential pathogens.
  • PO therapy can substitute parenteral agents if improvement occurs; treatment should last a total of 6 weeks.

Surgical Care

• General surgical therapy of the ear
• • Myringotomy and/or tympanocentesis primarily are used to obtain specimens and relieve discomfort from AOM. The openings usually heal within a few days.
  • 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 and/or steroid drops 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.
• Therapy for 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, this condition is typically associated with AOM, and it is the only condition of the mastoid that is treated only with medical management.
    • The management includes the administration of parenteral antimicrobial therapy and myringotomy with or without the placement of tympanostomy tube. The main goal of therapy is to prevent spread of the infection to the 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.
• Therapy for acute mastoiditis with osteitis
• • This 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 MDRSP coverage. With the high incidence of invasive, resistant strains in mastoiditis, initial therapy of intravenous (IV) vancomycin and ceftriaxone or the combination of a penicillin plus a beta-lactamase inhibitor (eg, ampicillin plus sulbactam) is most appropriate until the culture and sensitivity results are available.
  • After surgery, antibiotic and/or steroid drops 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 requires a combined neurosurgical and otolaryngologic approach.
• Therapy for 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.

Consultations

• 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 a neurosurgeon is appropriate if evidence of intracranial extension with abscess formation exists.

MEDICATION

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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 single, high-dose IV steroids is warranted to decrease mucosal swelling and promote natural drainage through the aditus ad antrum into the middle ear.

Drug Category: Antibiotics

Culture and sensitivity results ultimately govern the selection specific antibiotic agents. Until microbiologic information is available, the following principles guide the selection: The antimicrobial must be appropriate to cover the most common invasive strains of bacteria in AOM, the selected antibiotic should cross the blood-brain barrier, and the selected therapeutic spectrum should include consideration of MDRSP organisms that are prevalent in the individual's community. Coverage for anaerobic bacteria, as well as gram-negative aerobic bacteria and S aureus, are important in chronic mastoiditis.

Specific microbiologic diagnoses should be treated with appropriate antibiotics.

Drug Category: Topical antibiotic and corticosteroid combinations

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.

FOLLOW-UP

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Further Inpatient Care

• 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, PO medication may be selected on the basis of the culture reports.
• 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 and/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.

Further Outpatient Care

• Continue PO antibiotics to complete the treatment plan after the discontinuation of IV antibiotics. PO antibiotics that offer the same coverage as the selected IV antibiotic for a given patient should be selected
• Patients should follow up with an otolaryngologist (ENT specialist) after discharge. Audiography should be done.

Transfer

• Transfer of patient is invariably related to the availability of subspecialists, most notably a pediatric otolaryngologist or otologist, pediatric neurosurgeon, or pediatric critical care specialist.
• Available radiographs should be copied and sent with the patient, along with available laboratory data.
• Instruct patient to take nothing by mouth (NPO) until the receiving subspecialists can evaluate the condition.

Deterrence/Prevention

• Regarding immunization, the recently released conjugated vaccine against invasive S pneumoniae should affect the incidence of this disease.
• Physicians should be aware of the signs and symptoms of mastoiditis and have a high index of suspicion
• Refer patients with chronic otitis media to an ENT specialist.

Complications

• See also Mortality/Morbidity.
• • Facial nerve palsy
  • Conductive and sensorineural hearing loss
  • Subperiosteal abscess
  • Osteomyelitis or bony erosion
  • Bezold abscess (a deep abscess in the soft tissues of the neck)
  • Labyrinthitis
  • Petrositis leading to Gradenigo syndrome (triad of abducens nerve palsy, deep facial pain from trigeminal nerve involvement, and suppurative otitis media)
  • Intracranial spread (meningitis; epidural, temporal lobe or cerebral abscess, subdural empyema)
• Dural sinus thrombosis

Prognosis

• 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.

MISCELLANEOUS

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Medical/Legal Pitfalls

• Medical legal pitfalls are almost entirely related to either a delay in diagnosis, or iatrogenic injury during therapy. Both are 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.
• Legal pitfalls include the failure to diagnose, failure to treat, and failure to detect complications.
• Warn patients and their families about possible cosmetic deformity after mastoid surgery.

Special Concerns

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

MULTIMEDIA

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Media file 1:  Mastoiditis with subperiosteal abscess. Note the loss of the skin crease and the pointed abscess.
	View Full Size Image
Media type:  Photo

REFERENCES

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• Antonelli PJ, Dhanani N, Giannoni CM, Kubilis PS. Impact of resistant pneumococcus on rates of acute mastoiditis. Otolaryngol Head Neck Surg. Sep 1999;121(3):190-4. [Medline].
• Bluestone CD, Klein JO. Intratemporal complications and sequelae of otitis media. In: Pediatric Otolaryngology. Vol 1. 2nd ed. Philadelphia, Pa: WB Saunders;. 1990: 521-6.
• Brook I. The role of anaerobic bacteria in acute and chronic mastoiditis. Anaerobe. Oct 2005;11(5):252-7. [Medline].
• 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].
• Kaplan SL, Mason EO, Wald ER, et al. Pneumococcal mastoiditis in children. Pediatrics. Oct 2000;106(4):695-9. [Medline].
• Katz A, Leibovitz E, Greenberg D, et al. Acute mastoiditis in Southern Israel: a twelve year retrospective study (1990 through 2001). Pediatr Infect Dis J. Oct 2003;22(10):878-82. [Medline].
• Kvestad E, Kvaerner KJ, Mair IW. Acute mastoiditis: predictors for surgery. Int J Pediatr Otorhinolaryngol. Apr 15 2000;52(2):149-55. [Medline].
• Oestreicher-Kedem Y, Raveh E, Kornreich L, et al. Complications of mastoiditis in children at the onset of a new millennium. Ann Otol Rhinol Laryngol. Feb 2005;114(2):147-52. [Medline].
• Shambaugh GE, Glasscock ME. Pathology and clinical course of inflammatory diseases of the middle ear. In: Surgery of the Ear. 1967: 186-220.
• Taylor MF, Berkowitz RG. Indications for mastoidectomy in acute mastoiditis in children. Ann Otol Rhinol Laryngol. Jan 2004;113(1):69-72. [Medline].
• Van Zuijlen DA, Schilder AG, Van Balen FA, Hoes AW. National differences in incidence of acute mastoiditis: relationship to prescribing patterns of antibiotics for acute otitis media?. Pediatr Infect Dis J. Feb 2001;20(2):140-4. [Medline].
• Vazquez E, Castellote A, Piqueras J, et al. Imaging of complications of acute mastoiditis in children. Radiographics. Mar-Apr 2003;23(2):359-72. [Medline].
• Wald E. Mastoiditis. In: Long SS, Pickering LK, Prober CG. Principles and Practice of Pediatric Infectious Diseases. 2nd ed. New York; Churchill Livingstone;. 2003;2nd ed:2003: 200-5.

Article Last Updated: Aug 21, 2006