eMedicine Specialties > Otolaryngology and Facial Plastic Surgery > Middle Ear & Mastoid

Middle Ear, Mastoiditis

Author: PP Devan, MBBS, MS, Chief of ENT, A J Institute of Medical Sciences, India
Coauthor(s): John D Donaldson, MD, FRCS(C), FAAP, FACS, Chairman, Board of Directors, Lee Memorial Health System; Vice-President, Florida Pediatric Society
Contributor Information and Disclosures

Updated: Mar 19, 2008

Introduction

A purist's definition of mastoiditis includes all inflammatory processes of the mastoid air cells of the temporal bone. As the mastoid is contiguous to and an extension of the middle ear cleft, virtually every child or adult with acute otitis media (AOM) or chronic middle ear inflammatory disease has mastoiditis. In most cases, the symptomatology of the middle ear predominates (eg, fever, pain, conductive hearing loss), and the disease within the mastoid is not considered a separate entity.

In some patients, the infection spreads beyond the mucosa of the middle ear cleft, and they develop osteitis within the mastoid air-cell system or periosteitis of the mastoid process, either directly by bone erosion through the cortex or indirectly via the emissary vein of the mastoid. These patients have acute surgical mastoiditis (ASM), an intratemporal complication of otitis media. Chronic mastoiditis is most commonly associated with chronic suppurative otitis media and particularly with cholesteatoma formation.

History of the Procedure

In the preantimicrobial era, mastoidectomy was performed in as many as 20% of patients with AOM. By 1948, this figure had dropped to less than 3%, and it is presently thought to be performed in fewer than 5 cases per 100,000 persons with AOM.

Problem

• Posterior extension to the sigmoid sinus (causing thrombosis)
• Posterior extension to the occipital bone to create an osteomyelitis of calvaria or a Citelli abscess
• Superior extension to posterior cranial fossa, subdural space, and meninges
• Anterior extension to the zygomatic root
• Lateral extension to form a subperiosteal abscess
• Inferior extension to form a Bezold abscess
• Medial extension to the petrous apex
• Intratemporal involvement of facial nerve and/or labyrinth

Frequency

Frequency is unknown. Prevalence is most likely to rise with the emergence of multidrug-resistant streptococcal pneumonia (MDRSP), but it should decline with the availability and administration of the conjugated pneumococcal vaccine recently released for clinical use.

For all forms of mastoiditis, frequency parallels that of otitis media and varies with race. In some populations, such as the Inuit, descendants of an Indian tribe living in Alaska and the northwest United States, almost everyone has middle ear disease; the mastoiditis forms exhibited by these populations are invariably chronic.

No sex predilection exists.

Acute mastoiditis is a disease of the very young. Most patients present when younger than 2 years, with a median age of 12 months. However, it can occur in persons of any age.

The mean interval from onset of illness to mastoiditis is usually 4.5 days.

Etiology

ASM occurs as a result of chronic otitis media.

• Etiologic agents are discussed under Microbial factors. Invasive strains of the bacteria associated with AOM are most commonly recovered from ASM.
• Gram-negative organisms and Staphylococcus aureus are recovered more frequently from patients with chronic mastoiditis.
• Decreased or immature host resistance factors appear to cause predisposition to ASM.

Of late, ear cultures have most often grown Streptococcus pneumoniae and Pseudomonas aeruginosa.

A high white blood cell count on admission may serve as a predictive factor for complicated cases.

Half of children admitted with acute mastoiditis have no previous history of recurrent AOM. In those children, S pneumoniae was the leading pathogen, while P aeruginosa was more prevalent in children with recurrent AOM.

Pathophysiology

As with most infectious processes, consider host and microbial factors when evaluating surgical mastoiditis. Host factors include mucosal immunology, temporal bone anatomy, and systemic immunity. Microbial factors include protective coating, antimicrobial resistance, and ability to penetrate local tissue or vessels (ie, invasive strains).

Host factors

Most children presenting with ASM are younger than 2 years and have little history of otitis media. This is an age at which the immune system is relatively immature, particularly with regard to its ability to respond to challenges from polysaccharide antigens.

Host anatomical factors may have a role. The mastoid develops from a narrow outpouching of the posterior epitympanum (ie, the aditus ad antrum). Pneumatization occurs shortly after birth, once the middle ear becomes aerated, and this process is complete by age 10 years. Mastoid air cells are created by invasion of epithelia-lined sacs between spicules of new bone and by degeneration and redifferentiation of existing bone marrow spaces. Other areas of the temporal bone pneumatize similarly, including the petrous apex and the zygomatic root. The antrum, as with the mastoid air cells, is lined with respiratory epithelium that swells when infection is present. Blockage of the antrum by inflamed mucosa entraps infection within the air cells by inhibiting drainage and precluding reaeration from the middle ear side.

Persistent acute infection within the mastoid cavity may lead to a rarifying osteitis, which destroys the bony trabeculae that form the mastoid cells, hence the term coalescent mastoiditis. Essentially, coalescent mastoiditis is an empyema of the temporal bone that, unless its progress is arrested, drains either through the natural antrum to give spontaneous resolution or creates further complication by draining unnaturally to the mastoid surface, petrous apex, or intracranial spaces. Other temporal bone or nearby structures, such as the facial nerve, labyrinth, or venous sinuses, may become involved.

As AOM is the antecedent disease, the most common etiologic agent causing surgical mastoiditis is S pneumoniae followed by Haemophilus influenzae and group A Streptococcus pyogenes (GAS). Each of these bacteria has invasive forms and is recovered most often from children presenting with ASM. More than half of the S pneumoniae recovered are of serotype 19, followed by serotypes 23 and 3. The literature and the authors' experience indicate that a high frequency of MDRSP is now associated with ASM, and this may alter selection of antimicrobials (40-50% penicillin-resistant, approximately 25% ceftriaxone-resistant). Treatment of AOM with antimicrobials in the previous month increases the frequency of MDRSP. Cultures from chronic draining otitis media with mastoiditis can also yield coagulase-positive staphylococci and/or pseudomonal species. Microbiologic diagnosis is important to guide specific therapy.

Presentation

Terminology

• Otitis media: This term refers to an inflammation of the mucosal lining of the middle ear, which, in fact, is a mucoperiosteum.
• Osteitis: During otitis media, if the underlying bone becomes involved as a secondary development, this involvement is known as osteitis or, rarely, osteomyelitis.
• Mucositis: Inflammation confined to the middle ear cleft is known as tympanitis. When this mucositis spreads to the retrotympanic spaces, it is called mastoiditis. In clinical practice, mastoiditis is used to refer to a complication of otitis media with erosion of the pneumatized bone.
• Mastoidectomy: This term refers to complete and meticulous opening of the mastoid cells, either endaurally or by using a transcortical approach.

History

Persistent otorrhea beyond 3 weeks is the most consistent sign that a process involving the mastoid has evolved.

The patient’s fever may be high and unrelenting in acute mastoiditis, but this may be related to the associated AOM. Persistence of fever, particularly when the patient is receiving adequate and appropriate antimicrobial agents, is common in ASM.

Pain is localized deep in or behind the ear and is typically worse at night. Persistence of pain is a warning sign of mastoid disease. This may be difficult to evaluate in very young patients.

Hearing loss is common with all processes that involve the middle ear cleft. Most patients (>80%) have no history of recurrent otitis media.

Mastoiditis progresses in the following 5 stages and may be arrested at any point:

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

Tenderness and inflammation over the mastoid process is the most consistent sign of ASM. Periosteal thickening requires comparison to the other side, and some 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.

Acute mastoiditis is a serious bacterial infection of the temporal bone and is the most common complication of otitis media. Frequent symptoms include mastoid area erythema, proptosis of the auricle, and fever.

Although the diagnosis of acute mastoiditis can often be made on clinical basis alone, CT scanning should be performed for confirmation of the diagnosis, evaluation of potential complications, and surgical planning. Half of the children admitted with acute mastoiditis had no previous history of recurrent AOM. In those children, S pneumoniae was the leading pathogen, while P aeruginosa was more prevalent in children with recurrent AOM.

Otitis media is revealed on otoscopy, often with one of the following additional features:

• Sagging of the posterosuperior canal wall (possibly a sign of ASM)
• Nipplelike protrusion of the central tympanic membrane, usually oozing pus
• Findings consistent with a complication of extension beyond the mastoid process and its covering periosteum or another intratemporal complication such as facial palsy

In adults, the most common symptoms of mastoiditis are otalgia, otorrhea, and hearing loss, and the physical signs of mastoiditis (ie, swelling, erythema, tenderness of the retroauricular region) are usually present. Localization and enlargement of the pathological process within the middle ear spaces can be determined based on CT scan findings.

Differentials

Wegener Granulomatosis

Histiocytoses

Sarcoidosis

External otitis

Mastoid trauma

Suppuration of postauricular lymph node

Furuncle of meatus of the ear

Suppuration of the postauricular (mastoid) lymph node (This node collects drainage from the scalp and becomes inflamed with infections involving this region.)

Catscratch disease and atypical mycobacteria tend to have poor response to antimicrobials and a high frequency of nodal abscess formation. Differentiation from ASM is relatively easy with preservation of the skin crease and presence of a normal middle ear.

Lateral sinus thrombosis (LST) is now known to cause mastoid air sinus abnormalities; this is due to venous congestion as a consequence of LST. 

Indications

Indications for the simple mastoid operation include cases of acute suppurative otitis media that fail to respond to appropriate antibiotic therapy and progress to coalescent mastoiditis.

Mastoid conditions and management

• Acute mastoiditis without osteitis or periosteitis (the condition normally associated with AOM)
  • This is the only mastoid condition treated purely with medical management.
  • Standard antibiotic therapy is administered for AOM, and resolution is anticipated within 2 weeks.
  • If complications occur (pain and fever persist beyond 48 h or tenderness increases), obtain cultures via the middle ear, commence new antimicrobial therapy, and obtain imaging of the mastoid.
  • Consider mastoidectomy if symptoms persist or if the new antibiotics fail.
• Acute mastoiditis with osteitis
  • This is a surgically treated disease, although coverage with appropriate antibiotics is mandatory. Mastoidectomy with insertion of a tympanostomy tube is necessary to remove areas of coalescence within the temporal bone.
  • Antibiotic selection should provide good intracranial penetration and MDRSP coverage. With the high frequency of invasive resistant strains in mastoiditis, initial therapy of intravenous vancomycin and ceftriaxone is most appropriate until results of the culture and sensitivity (C&S) studies are available.
  • Postoperatively, antibiotic/steroid drops are used to keep the tube patent and to reduce middle ear swelling.
  • Patients with spread of empyema beyond the mastoid require drainage of the abscess and mastoidectomy.
  • Intracranial spread requires a combined neurosurgical and otolaryngological approach.
• Acute mastoiditis with periosteitis
  • Postauricular swelling and erythema without subperiosteal abscess or mastoid osteitis can be treated more conservatively using parenteral antibiotics, high-dose steroids, and tympanostomy tube insertion.
  • Vancomycin and ceftriaxone are recommended until cultures become available.
  • If substantial resolution of pain, fever, and erythema does not occur within 36-48 hours after institution of therapy, mastoidectomy is warranted.

Relevant Anatomy

See Intraoperative details.

Contraindications

When considering surgery, the risks of exposure to general anesthesia must be weighed against the risk of complications and progression of the infection. Contraindication to surgery include a low hemoglobin concentration and general systemic illness that must be controlled (eg, diabetes, hypertension, poor cardiac condition, bleeding disorders with prolonged bleeding and clotting time).

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