eMedicine Specialties > Pediatrics: General Medicine > Infectious Disease

Mastoiditis

Author: Itzhak Brook, MD, MSc, Professor, Department of Pediatrics, Georgetown University School of Medicine
Coauthor(s): John D Donaldson, MD, FRCS(C), FAAP, FACS, Chairman, Board of Directors, Lee Memorial Health System; President-elect, Florida Pediatric Society
Contributor Information and Disclosures

Updated: Feb 24, 2010

Introduction

Background

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 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 (see Cholesteatoma).

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. The mastoid is 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. 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:

• 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

Frequency

United States

In the preantimicrobial 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 less than 3% and is presently thought to be less than 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,^2,3 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 2000.⁴

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 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 include the following (also see 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, invariably, have chronic mastoiditis.

Sex

No sex predilection is known.

Age

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

Clinical

History

Patients may have unique features of acute and chronic mastoiditis. Acute mastoiditis generally follows 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. 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.
• 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. Displacement of the auricle downward and outward (especially in children <2 y) or upward and outward (in children <2 y) 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.

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.⁵

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 (especially in children <2 y)
• Otalgia and retroauricular pain (especially in children <2 y)
• 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
  • Recurrent or persistent fever
  • 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

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 3.⁶ 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.
  • After the introduction of vaccination with the 7-valent pneumococcal vaccine, a reduction of MDRSP occured.^7,8 However, those strains were replaced by strains not included in the vaccine. Staphylococcus aureus, especially methicillin-resistant S aureus  (MRSA), has emerged as an important pathogen.
  • 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 chronic suppurative otitis media (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),⁹ 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.¹⁰ Over one half of anaerobic gram-negative bacilli and Fusobacterium species can produce the enzyme beta-lactamase.¹¹
  • 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.
  • M tuberculosis, nontuberculous mycobacteria, and Mycobacterium bovis are infrequent causes of mastoiditis.¹²

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