Mastoiditis

Etiology

Mastoiditis can subdivide into three different categories based on the mechanism of infection, as detailed below:

• Incipient Mastoiditis: Infection of the mastoid air cells alone with no continuation with the middle ear cavity.
• Acute Coalescent Mastoiditis (most common presentation): Inflammation of the epithelial lining with erosion through the boney septations of the mastoid air cells. This erosion can progress to intracavity abscess formation, which can extend further to adjacent structures.
• Subacute Mastoiditis: Persistent middle ear infection or recurrent episodes of acute otitis media with inadequate antimicrobial therapy lead to persistent infection of the middle ear and mastoid air cells resulting in erosion of boney septations between mastoid air cells.[1]

Epidemiology

Although mastoiditis can occur at any age, the majority of patients are less than two years of age, with a median age of 12 months. In the pre-antibiotic era, 20% of cases of acute otitis media were complicated by acute mastoiditis and frequently associated with severe intracranial complications.

With the advent of antibiotics, mastoidectomy, and PCV-7 by 2008, the incidence has fallen drastically. Specifically, before the antibiotic era, 5 to 10% of children with acute otitis media developed coalescent mastoiditis with a mortality rate of 2/100000 population. After antibiotics and pneumococcal vaccination (PCV-7), 0.002% of children with acute otitis media progress too acute coalescent mastoiditis with a mortality rate of less than 0.01 per 100000 population.[2][3]

Pathophysiology

The majority of cases of mastoiditis result from the progression of acute otitis media. The ear subdivides into three cavities: the outer ear, middle ear, and inner ear. In particular, the middle ear cavity extends from the tympanic membrane to the cochlea and includes important structures such as the Malleus, Incus, Stapes, and Eustachian tube. The middle ear cavity is continuous with the lining of the mastoid air cells, which are a portion of the temporal bone.

The Eustachian tube is a connection from the middle ear to the oral cavity. It is responsible for draining fluid or air from the middle ear. If this tube becomes narrowed via inflammation or debris, it provides an opportunistic environment for pathogens to grow. This lining in the middle ear cavity, as mentioned above, is continuous with the lining of the mastoid air cells. In acute mastoiditis, the extension of the infection from the middle ear to the mastoid air cells can lead to bony septation erosion and coalescence of small air cells into larger ones full of pus referred to as acute coalescent mastoiditis. The pus filling this eroding cavity can extend via direct extension, thrombophlebitis, and bony pathways resulting in sequela that include subperiosteal abscess, sigmoid sinus thrombosis, meningitis, and intracranial abscess.

The most common pathogen in mastoiditis is streptococcal pneumonia. Other common pathogens include Group A beta-hemolytic streptococci, Staphylococcus aureus, Streptococcus pyogenes, and Haemophilus influenzae. Risk factors for mastoiditis include age less than two years old, immunocompromised state, recurrent acute otitis media, or incomplete pneumatization fo the mastoid process.[4]

History and Physical

Most commonly, the patient will be a child under the age of two years presenting with irritability, fussiness, lethargy, fever, ear pulling, ear pain. The adult patient will typically complain of severe ear pain, fever, and headache. Physical examination in both children and adults will reveal postauricular erythema, tenderness, warmth, and fluctuance with protrusion of the auricle.

The otoscopic examination will reveal a bulging of the posterosuperior wall of the external auditory canal and bulging of and pus behind the tympanic membrane. Often the tympanic membrane can be ruptured and draining pus. Some important considerations include the following. A normal tympanic membrane usually, but not always, excludes acute mastoiditis. Also, although a history of recent or concurrent otitis media is common, it is not required to make the diagnosis of acute mastoiditis as some cases may take place rapidly during the onset of acute otitis media.[5]

Evaluation

Mastoiditis is a clinical diagnosis. Laboratory and imaging are used as an adjunct when you are unsure of the diagnosis or considering a complication of acute mastoiditis. Laboratory studies to obtain include a CBC with differential, ESR, and CRP. Most commonly, one will see an elevated white blood cell count with a left shift, and elevated inflammatory markers ESR and CRP. Radiologic evaluation of acute mastoiditis uses CT imaging. CT imaging can reveal the disruption of the bony septation in the mastoid air cells and the potential extension of the infection. In particular, CT imaging in patients with mastoiditis reveals the following:

• Fluid and/or mucosal thickening in the middle ear and mastoid condensation.
• Loss of definition of the bony septae that define mastoid air cells
• Destruction of the irregularity of the mastoid cortex
• Periosteum thickening, disruption of periosteum, or subperiosteal abscess.[6][1]

Treatment / Management

Although antibiotics are the centerpiece of mastoiditis treatment, antibiotics alone have shown to result in an 8.5% complication rate. Additional measures, including myringotomy, tympanostomy tube placement, and mastoidectomy may be indicated depending on the severity of the infection. The majority of patients with acute mastoiditis are admitted to the hospital.

Uncomplicated patients with no significant medical history have had successful treatment as an outpatient with daily IV ceftriaxone with low complication rates—uncomplicated acute mastoiditis qualifies as patients with no significant past medical history and minimal physical examination findings. The patient case becomes complicated if the patient develops a large post auricular lesion, imaging studies showing bone erosion, high fevers, or neurological signs. Uncomplicated inpatient cases are manageable with IV antibiotics, high dose IV steroids, and myringotomy with placement of tympanostomy tube.

Serial physical examinations are necessary as the patient clinical status can deteriorate quickly. If mastoiditis does not improve in 48 hours, mastoidectomy is indicated. IV antibiotic of choice for patients without chronic otitis media is IV vancomycin alone to cover for the most common pathogens, including Streptococcus pneumoniae. Other common pathogens include Group A beta-hemolytic streptococci, Staphylococcus aureus, Streptococcus pyogenes, and Haemophilus influenza.

In patients with a chronic history of ear infections, an anti-pseudomonal agent is added to vancomycin. In a multicenter study, Streptococcus pyogenes correlated with the highest rate of complications at presentation, with n nearly 50% of cases, and Staphylococcus aureus correlated with the highest rate of complications during hospitalization.[6][7]

Differential Diagnosis

It is essential to have a thorough history and physical examination, as common mimics can be overlooked, resulting in missed diagnosis and delay in treatment. Common mimics of acute mastoiditis include cellulitis, otitis externa, lymphadenopathy, trauma, and tumor. In particular, there have been many case reports of confusing tumors or cancer for mastoiditis, including rhabdomyosarcoma, Ewing sarcoma, myofibroblastic tumor. Tumors were more likely to be bilateral, have cranial nerve involvement, and less likely to have a fever.[2][3][4] These differentials are an important consideration as the pediatric population is a common demographic for both mastoiditis and tumor.[8][9][10]

Prognosis

The majority of patients with uncomplicated acute mastoiditis have a resolution of symptoms with conservative measures, including antibiotics, steroids, and myringotomy, without the need for mastoidectomy. However, research in conservative versus invasive treatment for acute mastoiditis is lacking. Additionally, it is critical to monitor patients who are receiving treatment for acute mastoiditis, particularly in the first 48 hours. In cases where the patient's clinical status does not change or deteriorates from admission, mastoidectomy is then indicated.[6][11]

Complications

The progression of uncomplicated acute mastoiditis can result in devastating consequences. Based on the location of the mastoid process, opportunistic infections can spread inward towards the brain or outward toward the periphery. Extracranial complications of acute mastoiditis include the following:

• Subperiosteal abscess referring to an abscess at the periphery of the skull near the mastoid process
• Facial nerve palsy via compression of the facial nerve.
• Labyrinthitis is due to the spread of infection within the middle ear cavity resulting in tinnitus.
• Petrous apicitis, referring to osteomyelitis of other portions of the skull. Often can present with a constellation of symptoms including otorrhea, retro-orbital pain, ipsilateral abducens palsy, and additional cranial nerve deficits referred to as Gradenigo syndrome.
• Bezold abscess is an abscess in the sheath of the sternocleidomastoid muscle.

Intracranial manifestations of acute mastoiditis occurred in 6 to 23% of cases. These patients will often present with physical exam findings concerning intracranial involvement, including seizures, nuchal rigidity, headaches, and altered mental status. They include:

• Temporal lobe or cerebellar abscess
• Epidural or subdural abscess
• Venous sinus thrombosis, which is the least common of all intracranial complications.[12][1][13]