Updated: Sep 28, 2009
Mastoiditis is any inflammatory process of the mastoid air cells or posterior process of the temporal bone.
Acute mastoiditis, also known as classic mastoiditis, is a rare complication of acute otitis media (AOM). Antibiotic treatment of acute otitis media is believed to have decreased the incidence of acute mastoiditis. Chronic mastoiditis, a more latent and sometimes clinically silent version of mastoiditis, is most commonly associated with chronic suppurative otitis media or with cholesteatoma formations. Cholesteatomas are benign tumors of squamous epithelium that can grow and alter normal structure and function of surrounding soft tissue and bone.
The mastoid bone develops from an out-pouching of the posterior epitympanum, a part of the temporal bone behind the ear. Pneumatization of the mastoid bone begins shortly after birth and is complete by approximately age 10 years. These air cells are lined with respiratory epithelium. When infection spreads to this area, a blockage of the antrum by inflamed mucosa prevents drainage of fluid. Mucopurulent build up increases air cell pressure, initiates demineralization of cell walls, and potentiates abscess formation and the possibility of extension to surrounding structures: posterior cranial fossa, middle ear fossa, canal of the facial nerve, sigmoid sinus, lateral sinus, petrous tip of the temporal bone.
The incidence of mastoiditis from acute otitis media (AOM) is 0.004%. Prior to the 1980s, the reported incidence was 0.4%. Although the incidence of acute mastoiditis decreased dramatically with the introduction of antibiotic treatment, due to contradictory publications, whether the recent incidence is increasing or decreasing is unclear.
Incidence of mastoiditis from acute otitis media is reported as 0.004% in the United States.1 Some fear that untreated otitis media increases the risk of acute mastoiditis and is the cause of higher incidences in developing countries. Rates of antibiotic treatment for otitis in the Netherlands, Norway, and Denmark were 31%, 67%, and 76%, respectively. The incidence of mastoiditis was approximately 4 cases per 100,000 children per year over 5 years. In Canada and the United States, prescription of antibiotics for otitis is greater than 96%, and the incidence was 2 cases of mastoiditis per 100,000 children per year.2
Mastoiditis is a clinically significant infection with the potential of life-threatening complications. Common complications include hearing loss and extension of the infectious process beyond the mastoid system. If the spread of suppuration is anterior to the middle ear via the aditus ad antrum, often spontaneous resolution occurs. However, if the spread of infection is to the intracranial region, deadly and devastating consequences develop.
The Inuit population has a high predilection for middle-ear disease and, as a likely consequence, mastoiditis.
Mastoiditis occurs equally in females and males.
Acute mastoiditis affects mostly young children and peaks in those aged 6-13 months.
Although mastoiditis is a clinical diagnosis, it is possible to have disease with no history of otitis media, normal external anatomy, no tenderness, and no external signs of infection.
In advanced disease, various symptoms and physical findings will be consistent with the area of extension.
The distribution of causative organisms in acute mastoiditis differs from that in acute otitis media. For example, Haemophilus influenzae, a common cause of otitis media, is isolated much less often in mastoiditis. Gram-negative organisms are found to be the cause of many aggressive cases of mastoiditis. Pseudomonas and Staphylococcus aureus are more commonly isolated in cases of chronic mastoiditis. In general, the prevalence of organisms causing mastoiditis varies greatly between studies, among countries, and according to the age of the patient.
One recent study out of Houston found that, since the introduction of the 7 valent pneumococcal conjugate vaccine in 2000, the predominant serotype of pneumococcal mastoiditis was the 19A serotype. They also found that this serotype was associated with a more complicated disease course including the increased need for surgical intervention and a greater resistance to antibiotics.3
Reported pathogens are as follows:
| Basilar Skull Fracture | Otitis Externa |
| Bell Palsy | Otitis Media |
| Cellulitis | Parotitis |
| Cysts | Stroke |
| Deep Neck Infections | Trauma |
| Lymphadenopathy | Tumors |
Laboratory studies for mastoiditis include the following:
The goals of pharmacotherapy are to eradicate the infection, reduce morbidity, and prevent complications.
These agents should cover the empiric organisms that cause mastoiditis. A third-generation cephalosporin or the combination of a penicillinase-resistant penicillin and an aminoglycoside is recommended. If a patient is allergic to penicillin (history of anaphylaxis), clindamycin can be considered instead of penicillins. If Pseudomonas species is suspected, an antipseudomonal penicillin should be used.
After identification of the organism, antibiotic coverage can be narrowed. Patients should be afebrile for 48 hours before intravenous antibiotics are discontinued. Oral antibiotics should then be administered for an additional 14 days.
Effective against organisms implicated in mastoiditis. Third-generation cephalosporin that has broad gram-negative spectrum, lower efficacy against gram-positive organisms, and higher efficacy against resistant organisms.
1-2 g IV q12-24h
50-75 mg/kg IV q24h
Probenecid may increase ceftriaxone levels; coadministration with ethacrynic acid, furosemide, and aminoglycosides may increase nephrotoxicity
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Adjust dose in renal impairment; caution in breastfeeding women and those allergic to penicillin; not to be given in conjunction with calcium-containing products
Bactericidal antibiotic that inhibits cell wall synthesis, used in the treatment of infections caused by penicillinase-producing staphylococci. May be used to initiate therapy when a staphylococcal infection is suspected. Should be used in combination with an aminoglycoside.
1-2 g IV q4h
200 mg/kg/24h IV divided q6h
Decreases effects of contraceptives and tetracycline; administered concomitantly with disulfiram and probenecid, may increase oxacillin levels; effects of anticoagulants increase when large IV doses of oxacillin administered
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in impaired renal function
Aminoglycoside antibiotic used for gram-negative bacterial coverage. Commonly used in combination with both an agent against gram-positive organisms and one that covers anaerobes. Should be used in conjunction with a penicillinase-resistant penicillin.
5-7.5 mg/kg/24 h IV divided q8h; adjust dosage in renal impairment
Administer as in adults
Coadministration with other aminoglycosides, cephalosporins, penicillins, and amphotericin B may increase nephrotoxicity; aminoglycosides enhance effects of neuromuscular blocking agents, thus prolonged respiratory depression may occur; coadministration with loop diuretics may increase auditory toxicity of aminoglycosides; possible irreversible hearing loss of varying degrees may occur (monitor regularly)
Documented hypersensitivity; non–dialysis-dependent renal insufficiency
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Narrow therapeutic index (not intended for long-term therapy); caution in renal failure (not on dialysis), myasthenia gravis, hypocalcemia, and conditions that depress neuromuscular transmission; adjust dose in renal impairment
Lincosamide for treatment of serious skin and soft tissue staphylococcal infections. Also effective against aerobic and anaerobic streptococci (except enterococci). Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest.
150-450 mg/dose PO q6-8h; not to exceed 1.8 g/d
600-1200 mg/d IV/IM divided q6-8h depending on degree of infection
8-20 mg/kg/d PO as hydrochloride or 8-25 mg/kg/d as palmitate divided tid/qid
20-40 mg/kg/d IV/IM divided tid/qid
Increases duration of neuromuscular blockade induced by tubocurarine and pancuronium; erythromycin may antagonize effects of clindamycin; antidiarrheals may delay absorption of clindamycin
Documented hypersensitivity; regional enteritis; ulcerative colitis; hepatic impairment; antibiotic-associated colitis
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Adjust dose in severe hepatic dysfunction; no adjustment necessary in renal insufficiency; associated with severe and possibly fatal colitis by allowing overgrowth of Clostridium difficile
Antipseudomonal penicillin plus beta-lactamase inhibitor. Inhibits biosynthesis of cell wall mucopeptide and is effective during stage of active multiplication.
3/0.375 g (piperacillin 3 g and tazobactam 0.375 g) IV q6h
<12 years: Not established
>12 years: Administer as in adults
Tetracyclines may decrease effects of piperacillin; high concentrations of piperacillin may physically inactivate aminoglycosides if administered in same IV line; effects when administered concurrently with aminoglycosides are synergistic; probenecid may increase penicillin levels; high-dose parenteral penicillins may result in increased risk of bleeding
Documented hypersensitivity; severe pneumonia, bacteremia, pericarditis, emphysema, meningitis, and purulent or septic arthritis should not be treated with an oral penicillin during the acute stage
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Perform CBCs prior to initiation of therapy and at least weekly during therapy; monitor for liver function abnormalities by measuring AST and ALT levels during therapy; caution in patients with hepatic insufficiencies; perform urinalysis and BUN and creatinine determinations during therapy, and adjust dose if values become elevated; monitor blood levels to avoid possible neurotoxic reactions
These agents are used for patient comfort.
DOC for treatment of pain in patients with documented hypersensitivity to aspirin or NSAIDs and in patients diagnosed with upper GI disease or who are taking oral anticoagulants.
Reduces fever by direct action on hypothalamic heat-regulating centers, which increases dissipation of body heat via vasodilation and sweating.
500-1000 mg PO q4-6h; not to exceed 4 g/d
15 mg/kg PO q4h; not to exceed 2.6 g/d
Rifampin can reduce analgesic effects of acetaminophen; coadministration with barbiturates, carbamazepine, hydantoins, and isoniazid may increase hepatotoxicity
Documented hypersensitivity; known G-6-PD deficiency
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Hepatotoxicity possible in individuals with chronic alcoholism following various dose levels; severe or recurrent pain or high or continued fever may indicate a serious illness; acetaminophen is contained in many OTC products, and combined use with these products may result in cumulative acetaminophen doses exceeding recommended maximum dose
Complications of mastoiditis include the following:
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Ongkasuwan J, Valdez TA, Hulten KG, Mason EO Jr, Kaplan SL. Pneumococcal mastoiditis in children and the emergence of multidrug-resistant serotype 19A isolates. Pediatrics. Jul 2008;122(1):34-9. [Medline].
Casula S, Castro JG, Espinoza LA. An unusual cause of mastoiditis that evolved into multiple ring-enhancing intracerebral lesions in a person with HIV infection. AIDS Read. Aug 2007;17(8):402-4. [Medline].
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Gliklich RE, Eavey RD, Iannuzzi RA, et al. A contemporary analysis of acute mastoiditis. Arch Otolaryngol Head Neck Surg. Feb 1996;122(2):135-9. [Medline].
Katz A, Leibovitz E, Greenberg D, et al. Acute mastoiditis in Southern Israel: a twelve year retrospective study (1990 through 2001). Pediatr Infect Dis J. Oct 2003;22(10):878-82. [Medline].
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mastoiditis, acute otitis media, chronic mastoiditis, classic mastoiditis, latent mastoiditis, cholesteatoma
Karin S Chase, MD, Assistant Clinical Instructor and Resident Physician, Department of Emergency Medicine, State University of New York Downstate Medical Center/Kings County Hospital
Karin S Chase, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, and Emergency Medicine Residents Association
Disclosure: Nothing to disclose.
Christopher I Doty, MD, FACEP, FAAEM, Assistant Professor of Emergency Medicine, Residency Program Director, Department of Emergency Medicine, Kings County Hospital Center, State University of New York Downstate Medical Center
Christopher I Doty, MD, FACEP, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, Council of Emergency Medicine Residency Directors, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Eric M Kardon, MD, FACEP, Attending Emergency Physician, Georgia Emergency Medicine Specialists; Physician, Division of Emergency Medicine, Athens Regional Medical Center
Eric M Kardon, MD, FACEP is a member of the following medical societies: American College of Emergency Physicians
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment
Jeter (Jay) Pritchard Taylor III, MD, Compliance Officer, Attending Physician, Emergency Medicine Residency, Department of Emergency Medicine, Palmetto Health Richland, University of South Carolina; Medical Director, Department of Emergency Medicine, Palmetto Health Baptist
Jeter (Jay) Pritchard Taylor III, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Rick Kulkarni, MD, Assistant Professor of Surgery, Section of Emergency Medicine, Yale-New Haven Hospital
Rick Kulkarni, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: WebMD Salary Employment
The authors and editors of eMedicine gratefully acknowledge the contributions of previous authors, Dominique C Fontenette, MD, Ewen N Wang, MD, and Alyssa K Hamman, MD, to the development and writing of this article.
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