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 2 or so.¹ 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, so suppuration in the mastoid may rarely spread to cause meningitis or cerebral abscess.

Mastoiditis occurs when suppurative infection extends from the 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. Acute mastoiditis was formerly a common complication of acute otitis media, affecting up to about 50% of cases.² Since the advent of effective antibiotics to treat otitis media, this has dropped to about 0.4% of cases of acute otitis media.²

Mastoiditis in acute or chronic form is now quite rare. UK hospital admission rates in 2002 for mastoiditis were 8.2 per 100,000 population. This had increased by 19% over the preceding 10 years.³ However, the apparent increase in incidence was not reflected in primary care cases and was thought to be due to increased admission rates for young children, the principal sufferers of acute otitis media, rather than any increase brought about by a change in antibiotic prescribing habits. The routine use of antibiotics for acute otitis media in children is not thought to be justified by any potential reduction in risk of its more serious complications, although the low incidence of mastoiditis makes it difficult to be certain.^3,4 In the US the incidence of mastoiditis from acute otitis media is estimated at 0.004%.¹

Risk factors

Much commoner 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.

Symptoms

• Acute (classical) otitis media occurs after an acute or recurrent episode of acute otitis media, and causes otalgia and pain behind the ear, perhaps with a noting of swelling or a boggy, tender mass. Fever usually accompanies these symptoms.
• Chronic or latent mastoiditis may present in a subtle or subclinical fashion after an episode or series of recurrences of acute otitis media. It tends to cause recurrent bouts of otalgia, retro-aural pain or headache and may be accompanied by episodes of fever.
• Irritability, intractable crying and feeding problems can be the mode of presentation of both forms in infants.

Signs

• In acute cases the tympanic membrane bulges and is erythematous and there may be sagging of the posterosuperior meatal wall. The patient may be febrile and unwell. There will be swelling, tenderness and redness over the mastoid area. The external ear may protrude forward and fluctuance can sometimes be demonstrated behind the ear.
• In chronic form there may be no external evidence of peri-mastoid inflammation. Pyrexia may occur recurrently or chronically. The tympanic membrane appears infected in some cases, but may be normal.
• Patients with suspected mastoiditis should be examined 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.

• Acute mastoiditis
  • Otitis media or externa
  • Trauma to ear/mastoid
  • Cervical lymph node enlargement
  • Meningitis
  • Parotid swelling
  • Bone cysts or tumours
  • Basal skull fracture

• Chronic mastoiditis
  • Other source of intracranial or localised sepsis
  • Meningitis
  • Pyrexia of unknown origin

• FBC 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 (myringotomy) and may be sent for Gram staining and culture.
• Skull XR not usually helpful but may show clouding of mastoid air cells.
• CT scanning is sensitive but not very specific in picking up changes in the mastoid, since such changes may occur with some cases of uncomplicated otitis media.
• MRI is more specific and useful for making surgical management decisions.
• CT and MRI may be used to detect intracranial spread of infection from mastoiditis.
• 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 severe or complicated cases.
• Usual initial therapy is high dose broad spectrum intravenous antibiotics, given for at least 1–2 days.
• 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.
• If there is no clinical improvement within 48 hours, or there is evidence of mastoid osteitis, subperisoteal abscess, intracranial spread, cholesteatoma or other complications, then surgical intervention in the form of mastoidectomy is carried out .⁵
• In cases with unusual infecting organisms, specialist infectious disease input may be helpful.
• Cases with intracranial spread may require neurosurgical intervention, dependent on severity.

• Conductive and/or sensorineural hearing loss
• Osteomyelitis or bone erosion
• Subperiosteal abscess
• Cranial nerve palsies (esp. V, VI and VII)
• Intracranial spread leading to epidural abscess, cerebral abscess, subdural empyema and meningitis
• Intracranial venous sinus thrombosis
• Bezold's abscess (deep abscess in soft tissues of neck)
• Petrositis causing Gradenigro syndrome (VIth CN 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 severest 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. Complicated cases may lead to significant morbidity or even death.

The disease itself is not usually preventable, 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 it 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.