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Pediatric Mastoiditis

  • Author: Itzhak Brook, MD, MSc; Chief Editor: Russell W Steele, MD  more...
 
Updated: Feb 25, 2016
 

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 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.

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Anatomy

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.

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Pathophysiology

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).

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Etiology

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. {Int J Pediatr Otorhinolaryngol. 2015 Sep;79(9):1429-35. doi: 10.1016/j.ijporl.2015.06.019.}

Children hospitalized due to acute otitis media: how does this condition differ from acute mastoiditis?

Laulajainen-Hongisto ASaat RLempinen LAarnisalo AAJero J.} 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.[4] 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).[5, 6] 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.[7]  In contrast in a prospective study of 8 children's hospitals from 2011 to 2013, Kaplan et al. { Clin Infect Dis. 2015 May 1;60(9):1339-45. doi: 10.1093/cid/civ067. Multicenter surveillance of S. pneumoniae isolates from middle ear and mastoid cultures in the 13-valent pneumococcal conjugate vaccine era. Kaplan SL, Center KJ, Barson WJ, Ling-Lin P, Romero JR, Bradley JS, Tan TQ, Hoffman JA, Peters TR, Gurtman A, Scott DA, Trammel J, Gruber WC, Hulten KG, Mason EO} 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. 

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, 8] However, those strains were replaced by strains not included in the vaccine.[9, 10]

Staphylococcus aureus, especially methicillin-resistant S aureus (MRSA), has emerged as an important pathogen.[11] 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.[12] GAS was recovered more often from children older than 2 years.[13]

Although P aeruginosa has been recovered in some series,[14] higher rates of recovery may happen when samples are obtained from the external canal in patients with otorrhea.[15]

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),[11] 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.[16]  { Infection. 2015 Dec;43(6):663-70. doi: 10.1007/s15010-015-0782-x. Epub 2015 May 1.

Infections caused by Fusobacterium in children: a 14-year single-center experience.

Shamriz OEngelhard DTemper VRevel-Vilk SBenenson SBrooks RTenenbaum AStepensky PKoplewitz BKaufmann MAverbuch D} Recent studies suggest an increase in the incidence of F necrophorum mastoid infections in the last 2 decades.[17]

Over one half of anaerobic gram-negative bacilli and Fusobacterium species can produce the enzyme beta-lactamase.[18]

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,[19] M tuberculosis, nontuberculous mycobacteria, and Mycobacterium bovis are infrequent causes of mastoiditis.[20, 21]

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Epidemiology

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,[22, 23] 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..ref24} 

A recent study[25] illustrated a downward trend in otitis media-related healthcare use in the United States from 2001 to 2011. 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 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.[26]

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.

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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.

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
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Contributor Information and Disclosures
Author

Itzhak Brook, MD, MSc Professor, Department of Pediatrics, Georgetown University School of Medicine

Itzhak Brook, MD, MSc is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians-American Society of Internal Medicine, American Medical Association, American Society for Microbiology, Association of Military Surgeons of the US, Infectious Diseases Society of America, International Immunocompromised Host Society, International Society for Infectious Diseases, Medical Society of the District of Columbia, New York Academy of Sciences, Pediatric Infectious Diseases Society, Society for Experimental Biology and Medicine, Society for Pediatric Research, Southern Medical Association, Society for Ear, Nose and Throat Advances in Children, American Federation for Clinical Research, Surgical Infection Society, Armed Forces Infectious Diseases Society

Disclosure: Nothing to disclose.

Coauthor(s)

John D Donaldson, MD, FRCSC, FACS Pediatric Otolaryngologist, Chief of Surgery, Galisano Children's Hospital, Lee Memorial Health System

John D Donaldson, MD, FRCSC, FACS is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery, American Society of Pediatric Otolaryngology, American Academy of Pediatrics, American College of Surgeons

Disclosure: Nothing to disclose.

Chief Editor

Russell W Steele, MD Clinical Professor, Tulane University School of Medicine; Staff Physician, Ochsner Clinic Foundation

Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, Southern Medical Association

Disclosure: Nothing to disclose.

Acknowledgements

Joseph Domachowske, MD Professor of Pediatrics, Microbiology and Immunology, Department of Pediatrics, Division of Infectious Diseases, State University of New York Upstate Medical University

Joseph Domachowske, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American Society for Microbiology, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Gary J Noel, MD Professor, Department of Pediatrics, Weill Cornell Medical College; Attending Pediatrician, New York-Presbyterian Hospital

Gary J Noel, MD is a member of the following medical societies: Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

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