Mastoid and Mastoiditis

The mastoid process is an inferior extension of the petrous temporal bone of the skull and serves a structural function as an anchor point for the large muscles of the neck. It contains multiple air cells that develop from a single main cavity (the antrum), after the age of about two. In cross section it has a vacuolated or honeycomb appearance.

The tympanic cavity of the middle ear is in communication with the mastoid antrum via a small canal that runs through the petrous temporal bone. The mastoid air cells are related superiorly to the middle cranial fossa, and posteriorly to the posterior cranial fossa. This means that suppuration in the mastoid may, rarely, spread to cause meningitis or a cerebral abscess. Other surrounding structures include the facial nerve canal, the sigmoid sinus and the lateral sinus.

Mastoiditis occurs when suppurative infection extends from a middle ear affected by otitis media to the mastoid air cells. The infective process causes inflammation of the mastoid and surrounding tissues and may lead to bony destruction.

• Classic, or acute, mastoiditis is a rare complication of acute otitis media.
• Chronic, latent, or masked, mastoiditis presents in a chronic, or subclinical, fashion. It is usually associated with chronic suppurative otitis media or cholesteatoma.

• Mastoiditis in acute or chronic form is now quite rare.
• Before the advent of antibiotics, mastoiditis was relatively common. It developed in 5–10% of children with acute otitis media (AOM), with a mortality rate of 2 per 100,000 children. The mortality rate is now < 0.01 per 100,000 children.²
• The rates of mastoiditis seem to be higher in countries where antibiotic prescribing rates for AOM are lower but this in itself does not prove a causal relationship.³ If a causal link is assumed, it is estimated that the numbers needed to treat with antibiotics are 50,000 children to avoid one child developing mastoiditis.⁴
• As serious complications are rare, guidance is that the routine use of antibiotics in AOM is not thought to be justified by the potential reduction in risk of these complications.^3,5,6,7,8 See separate article on Acute Otitis Media.
• A BMJ review looked at trends in antibiotic prescribing rates in UK general practice between 1993 and 2003 and admissions for peritonsillar abscess, mastoiditis and rheumatic fever in children between 1993 and 2002. Antibiotic prescribing rates halved during this time but hospital admission rates for mastoiditis had increased by 19% over the preceding 10 years.⁵ The authors suggested that the apparent increase could reflect coding error and that the reduction in general practice events could reflect the fact that sick children are increasingly being taken straight to hospital.

Risk factors

• Much more common in young children, with peak incidence at age 6–13 months.¹
• Patients with immunocompromise may be more prone to mastoiditis.
• Children or adults with intellectual impairment or communication difficulties are thought to be susceptible to the condition, possibly as a result of not being able to communicate their symptoms.
• Pre-existence of cholesteatoma is a risk factor for subsequent mastoiditis.

• S. pneumoniae (most frequently isolated)
• S. pyogenes
• Staphylococcus species
• H. influenzae
• Ps. aeruginosa (becoming increasingly common)¹
• Moraxella (Branhamella) catarrhalis
• Other Gram negative organisms (occur more frequently in chronic form)
• Mycobacteria (rare)
• Aspergillus and other fungi (rare)

Acute (classic) mastoiditis

• History of acute or recurrent episode of otitis media
• Otalgia and pain behind the ear
• Fever
• Infants may present with irritability, intractable crying and feeding problems
• Swelling, redness or a boggy, tender mass behind the ear
• The external ear may protrude forwards; fluctuance can sometimes be demonstrated behind the ear (examine from behind)
• Ear discharge may be present and the eardrum may be perforated
• Tympanic membrane bulges and is erythematous
• Patient is unwell

Chronic mastoiditis

• Presents in a subtle or subclinical fashion after an episode of acute otitis media or with history of chronic suppurative otitis media
• Recurrent bouts of otalgia and retro-aural pain
• Recurrent headache
• Episodes of fever
• Infants may present with irritability, intractable crying and feeding problems
• Tympanic membrane may appear infected or may be normal
• May be no external evidence of peri-mastoid inflammation

Other points on examination

• Examine for evidence of local neurological involvement. There may be an ipsilateral VIth or VIIth cranial nerve palsy, or pain over the distribution of the ophthalmic division of the Vth cranial nerve.
• Patient may complain of deafness and there may be signs of conductive deafness (Rinne negative; Weber test - sound localised/loudest in affected ear).
• There may be no history of otitis media, no mastoid area tenderness and no external signs of infection.¹

• Otitis media or externa
• Trauma to ear/mastoid
• Cervical lymph node enlargement
• Meningitis
• Cellulitis
• Parotid swelling
• Bone cysts or tumours
• Basal skull fracture
• Other source of intracranial or localised sepsis
• Pyrexia of unknown origin

• Full blood count may show leucocytosis.
• ESR may be elevated.
• Blood cultures should be taken.
• Fluid can be extracted from the middle ear through perforated drums or by intervention (tympanocentesis) and should be sent for Gram staining, culture and acid-fast stain.¹
• Skull X-ray of the mastoid area is not usually helpful but may show clouding of mastoid air cells.
• CT and/or MRI scanning can be used for to aid diagnosis and look for intracranial complications. Some say that CT scanning should be used in all suspected cases of mastoiditis.¹
• Lumbar puncture should be carried out if intracranial spread is suspected.
• Audiograms during and after mastoiditis help to quantify and monitor any associated hearing loss.

• Patients with suspected mastoiditis should be managed in a hospital setting.
• Appropriate clinical suspicion and prompt diagnosis are important to reduce the likelihood of complications.
• Usual initial therapy is high-dose, broad spectrum intravenous antibiotics, given for at least 1–2 days (e.g. with a third generation cephalosporin).¹
• Oral antibiotics are usually used after this, starting after 48 hours without fever on IV treatment, and continuing for at least 1–2 weeks.
• Paracetamol, ibuprofen and other agents may be given as antipyretics and/or painkillers.
• Myringotomy ± tympanostomy tube insertion may be performed in some cases as a therapeutic procedure, or to collect middle ear fluid for culture.
• Surgical intervention, usually in the form of mastoidectomy ± tympanoplasty, is suggested if there is:¹
  • Mastoid osteitis
  • Intracranial extension
  • Abscess formation
  • Co-existing cholesteatoma
  • Limited improvement after IV antibiotics
• Mastoidectomy can be:¹
  • Simple: infected mastoid air cells are removed
  • Radical: the tympanic membrane and most middle ear structures are removed and the Eustachian tube is closed
  • Modified: the ossicles and part of the tympanic membrane is preserved
• Incision and drainage of a subperiosteal abscess in another procedure that may be required.
• Patients with intracranial spread may also need neurosurgical intervention.
• In cases with unusual infecting organisms, specialist infectious disease input may be helpful.

• Conductive and/or sensorineural hearing loss
• Osteomyelitis or bone erosion
• Extension to the zygoma (zygomatic mastoiditis)
• Subperiosteal abscess (abscess between the periosteum and mastoid bone; gives appearance of protruding ear)
• Cranial nerve palsies (especially V, VI and VII)
• Intracranial spread leading to extradural abscess, cerebral abscess, subdural empyema and meningitis
• Intracranial venous sinus thrombosis (e.g. lateral sinus thrombosis)
• Bezold's abscess (spread of pus from mastoid process along the digastric muscle to other neck muscles)⁹
• Petrositis causing Gradenigro syndrome (VIth cranial nerve palsy + deep trigeminal facial pain + suppurative otitis media)
• Carotid artery spasm, arteritis, occlusion, rupture or metastatic septic emboli leading to intracerebral infection (all very rare and associated with the most severe cases)

Nowadays the prognosis for the vast majority of cases that are diagnosed early is excellent with a low chance of complications or severe hearing loss. A recent review reported that most who had suffered an episode of acute mastoiditis had no long term otological sequelae.¹⁰ However, complicated cases may still lead to significant morbidity or even death.

The disease itself is difficult to prevent, except possibly by electing to treat some severe cases of acute otitis media with adequate doses and duration of appropriate antibiotics. The sequelae of the condition can be prevented by having an appropriate index of suspicion for the condition and admitting patients suspected of having mastoiditis for early hospital assessment.

Failure to diagnose mastoiditis leading to life-threatening complications or death, is a recurrent, if relatively rare, cause of legal claims made against general practitioners in the UK. It should be borne in mind that the symptoms and signs can be quite subtle in chronic or latent mastoiditis.