Case Based Pediatrics For Medical Students and Residents
Department of Pediatrics, University of Hawaii John A. Burns School of Medicine
Chapter VI.8. Mastoiditis
Kathleen A. Morimoto, MD
January 2002

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A 7 year old male presents to the ER with a two day history of worsening ear pain and drainage. On the day prior to presentation, his parents noted redness behind his right ear, and that his right ear appeared to be sticking out. He had been well until 10 days ago when he started complaining of a cough and runny nose that progressed to include right ear pain and fever. He was evaluated in the clinic 5 days ago and diagnosed with an acute right otitis media. He was placed on amoxicillin and he initially appeared to improve until two days ago when his ear pain recurred and this is now accompanied by ear drainage, redness behind his right ear, and a prominent right pinna which is pointing up and out.

Exam: VS T 38.5, P 110, R 20, BP 100/60. He is non toxic, alert and responsive. His head is normocephalic. His eyes are normal. His left TM and ear are normal. His right pinna is upward and outwardly displaced with erythema and tenderness to the right mastoid. There is purulent drainage from his right ear which is obstructing visualization of tympanic membrane. His throat and neck are normal. Heart regular without murmurs. Lungs are clear. He has good strength (5/5) in all four extremities. His DTRs are 2+ in all four extremities. He ambulates well without ataxia

A CT scan of the mastoids is performed which demonstrates haziness and early bony destruction of the mastoid. No coalescence of air cells, empyema or subperiosteal abscess is noted. The patient is hospitalized for parenteral antibiotics. An ENT consult is obtained. The patient defervesces by 48 hours and he is then taken to the OR for myringotomy and tympanostomy tube placement. Long term IV access is placed and he receives 4 weeks of parenteral antibiotics. Following completion of therapy the patient does well without sequelae.

Mastoiditis is a suppurative infection of the mastoid air cells, and a potential complication of otitis media. Mastoiditis can basically be broken down into two types, acute and chronic. The acute form is defined as symptoms lasting less than one month and chronic for symptoms greater than one month. Within acute mastoiditis there are two pathologic forms, acute mastoiditis with periostitis, and acute mastoiditis with osteitis (with or without subperiosteal abscess). This section will be focusing on acute mastoiditis, as chronic mastoiditis is a unique entity in itself.

Prior to the antibiotic era, mastoiditis was a common complication of acute otitis media and frequently resulted in death. In 1938, the frequency of mastoidectomy for acute mastoiditis was 20%. With the advent of antibiotics, the frequency of mastoidectomy for acute mastoiditis had declined to 2.8% by 1948 with an almost 90% reduction in mortality rate (5).

The mastoid process is the posterior part of the temporal bone. At birth, the mastoid consists of a single cell called the antrum, which is connected to the middle ear by a narrow channel called the aditus ad antrum. Soon after birth, the mastoid undergoes pneumatization and by 2 years of age, is well pneumatized. Anatomically, the mastoid is surrounded by numerous vital structures, so if it become infected, this can lead to devastating results. Anterior to the mastoid lies the middle ear and ossicles, the facial nerve, the jugular vein, and the internal carotid artery. Posteriorly, lies the posterior cranial fossa and sigmoid sinus. Superior to the mastoid is the middle cranial fossa and medially the mastoid encases the cochlea and semicircular canals. Inferior to the mastoid are extensive soft tissue planes and muscles that are also potential areas for the spread of infection.

In acute otitis media, a certain amount of mastoid inflammation is observed because the mastoid air spaces and middle ear cavity are contiguous and they share the same modified respiratory epithelium. With appropriate antibiotic therapy, the inflammation within the middle ear and mastoid resolves. However, if the acute otitis media is not treated or inadequately treated, the inflammation within the mastoid persists. In acute mastoiditis, this persistence of inflammation results in accumulation of serous then suppurative material within the mastoid. Accumulation of the purulent exudate leads to increased middle ear pressure resulting in possible tympanic membrane perforation. The increased pressure in the mastoid causes destruction of the bony septa between the air cells leading to formation of large cavities. Subsequently, osteomyelitis of adjacent bone may develop as well as abscess formation and bony erosion with extension of infection into surrounding structures.

The clinical manifestations of acute mastoiditis are largely dependent on the age of the patient and the stage of the disease. The classic presentation however, is a febrile child with otalgia, mastoid swelling and tenderness, and a history of acute otitis media days to weeks ago. The patient may have received antibiotics with some temporary improvement before becoming ill again. Other signs and symptoms of mastoiditis include mastoid erythema, displaced auricle either up and out in an older child or down and out in an infant, otorrhea, and a bulging immobile tympanic membrane.

The diagnosis of acute mastoiditis can be made on clinical findings alone. However, if radiographic imaging is indicated, CT scan is the test of choice over plain radiographs. CT scans done early in the course of mastoiditis reveal clouding of the mastoid, however this is not diagnostic as 50% of patients with uncomplicated acute otitis media will have similar findings. True CT evidence of mastoiditis is destruction of the mastoid outline, loss of bony septa within the air cells, "coalescence" of mastoid air cells (loss of bony septa between air cells), and hypoaeration of the mastoid (1,2). Additionally, CT scans with contrast are helpful in delineating possible intracranial complications.

Cultures of middle ear aspirates, ear drainage in the case of a perforated TM, and/or actual mastoid cultures may be helpful in optimal management of mastoiditis. If the TM is intact, cultures obtained from middle ear aspirates have been shown to correlate with actual mastoid cultures. However, if the TM is perforated, cultures obtained are often contaminated by ear canal flora. Consequently, in these cases, cultures should be obtained as close to the perforation site as possible. Optimally cultures should be obtained prior to the initiation of antibiotics. Unfortunately this is not always feasible particularly if the patient is not stable for surgery.

Although intuitively one would expect the same organisms that cause acute otitis media to also cause acute mastoiditis, the actual microbiology differs. The most common bacteria isolated in acute mastoiditis are Streptococcus pneumonia, Streptococcus pyogenes, and Staphylococcus aureus. Pseudomonas, enteric gram negative rods, and Staphylococcus aureus are the three most common organisms isolated in patients with chronic mastoiditis (2).

Initial antibiotic therapy in acute mastoiditis is empiric. Based on the most likely organisms, oxacillin and cefotaxime have been recommended (1). Vancomycin may be preferable since the frequency of oxacillin and cephalosporin resistant Staph aureus (MRSA) exceeds 25% in most areas. Additionally, emerging pneumococcal resistance may also benefit from vancomycin treatment. Ceftazidime or other anti-pseudomonas therapy may be indicated if pseudomonas is suspected. Duration of therapy is similar to that of osteomyelitis, and depends on the organism, extent of disease, and clinical response. However, a minimum of three weeks is recommended (1).

Surgical treatment of acute mastoiditis depends on the severity of the disease. In cases of simple uncomplicated mastoiditis (acute mastoiditis with periostitis), IV antibiotics and myringotomy and tympanostomy tube placement are recommended (5). If the patient fails to respond to the above therapy, or the mastoiditis is complicated by osteitis with or without subperiosteal abscess, the addition of a simple mastoidectomy is indicated (2,5). In a simple mastoidectomy, the mastoid air cell system is eviscerated although the canal walls are left intact. In severe cases refractory to simple mastoidectomy, a modified radical or radical mastoidectomy may be indicated. These surgical procedures involve complete removal of the mastoid air system including the posterior ear canal wall thereby creating a single cavity between the mastoid, middle ear, and external auditory canal. In addition, the radical mastoidectomy removes the tympanic membrane, malleus, and incus thereby leaving just the stapes or portion of the stapes intact.

The associated complications of acute mastoiditis are dependent on how and where the infection spreads. Pus that erodes through the lateral aspect of the mastoid produces a subperiosteal abscess. Clinically this child will present with redness, swelling, or pain behind the ear over the mastoid process. Pus can also spread medially to the petrous air cells resulting in petrositis or spread to the occipital bone posteriorly leading to osteomyelitis of the calvarium (Citelli abscess). Infection could also spread and involve the facial nerve, and central nervous system leading to meningitis, epidural and cerebellar abscesses, subdural empyema, or venous sinus thrombosis. The middle ear ossicles can also be destroyed resulting in conductive hearing loss. Rarely, mastoiditis is associated with abscess formation beneath the sternocleidomastoid and digastric muscles (Bezold abscess) (2,5).

The prognosis of mastoiditis depends on the extent of the infection. Fortunately, if detected early prior to intracranial involvement, the prognosis is very good. Even sensorineural and conductive hearing deficits associated with mastoiditis may be reversible if treated early. Therefore, prevention with early and adequate treatment for acute otitis media and early recognition of mastoiditis are key in decreasing the risk of serious suppurative complications.


1. What are the three most common organisms in acute otitis media?

2. What are the three most common organisms in acute mastoiditis?

3. Name a few intracranial complications of acute mastoiditis.

4. Name a few extracranial complications of acute mastoiditis.

5. Classically what is the difference in ear position in acute mastoiditis between the older child and young infant?

6. True/False: A CT scan image demonstrating clouding of the mastoid air cells is diagnostic of mastoiditis (acute or chronic)?

7. True/False: Plain film radiographs of the mastoid air cells often show mastoid clouding in acute otitis media without true mastoiditis.


1. Lewis K, Newman A, Cherry JD. Chapter 20-Mastoiditis. In: Feigin RD, Cherry JD (eds). Principles of Pediatric Infectious Diseases, 4th edition. 1998, Philadelphia: W.B. Saunders Co., pp. 212-217.

2. Wald ER. Chapter 29-Mastoiditis. In: Long SS, Pickering LK, Prober CG (eds). Principles and Practice of Pediatric Infectious Disease. 1997, New York: Churchill Livingstone, Inc., pp. 229-234.

3. Wetmore RF. Complications of otitis media. Pediatr Ann 2000:29(10):637-645.

4. Carrasco VN, Pillsbury HC, Workman JR. Chapter 34. In: Johnson JT, Yu VL (eds). Infectious Diseases and Antimicrobial Therapy of the Ears, Nose, and Throat. 1997, Philadelphia: WB Saunders Co., pp. 292-299.

5. Bluestone CD, Klein JO. Intratemporal Complications and Sequelae of Otitis Media. In: Bluestone CD, Stool SE, Kenna MA. Pediatric Otolaryngology, 3rd edition. 1996, Philadelphia: WB Saunders Co., pp. 611-627.

Answers to questions

1. S. pneumonia, H. influenzae (non-typable), and M. catarrhalis.

2. S. pneumonia, S. pyogenes, and S. aureus.

3. Meningitis, epidural empyema, subdural empyema, venous sinus thrombosis.

4. Facial nerve paralysis, deafness, labyrinthitis, petrositis, Bezold abscess.

5. In the older child the ear is up and out and in the infant it is down and out.

6. False

7. True

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