Clinical experiences with acute mastoiditis--1988 through 1998.
The incidence of acute mastoiditis has declined dramatically during the postantibiotic era. Even so, antibiotic-resistant or unusual pathogens can still cause this disease entity. At our hospital, we documented an increase in antibiotic-resistant and atypical pathogens such as Actinomyces spp. and Mycobacterium tuberculosis. In this paper, we discuss the optimal diagnosis and treatment strategy for acute mastoiditis, and we describe our retrospective review of 13 patients with mastoiditis who were treated at our hospital from 1988 through 1998. Eight of these patients recovered following treatment with intravenous antibiotics, with or without myringotomy, and five who had complications, of disease were managed surgically. Among these five, one developed chronic otitis media and one developed cholesteatoma 3 years later. For patients with acute mastoiditis, we emphasize the need to be aware of any unusual pathogens that do not respond to empiric antibiotic therapy.
Acute mastoiditis is an inflammation of the mastoid process that occurs with acute or subacute otitis media. Its distinct characteristics are erythematous swelling in the postauricular area or mastoid region and an anterior displacement of the auricle. When acute mastoiditis causes a subperiosteal abscess, a fluctuation of the postauricular area can occur.  Simple mastoid imaging series of the lesion side have shown a cloudiness in the mastoid air cell. If the mastoiditis is left untreated or if it is treated inappropriately, it can cause severe complications, such as subperiosteal abscess, Bezold's abscess, meningitis, brain abscess, sigmoid sinus thrombophlebitis, and Gradenigo's syndrome.
The widespread use of broad-spectrum antibiotics has led to a significant decline in the incidence of acute mastoiditis.  When it does occur, it requires an accurate diagnosis and appropriate treatment during the initial stages because of the possibility of serious complications. At our hospital, we observed an increase in the incidence of acute mastoiditis that was brought on by atypical and antibiotic-resistant organisms. In one of these cases, serious complications occurred because the mastoiditis was not diagnosed and treated properly.
Patients and methods
We retrospectively reviewed data on 13 patients (7 males), aged 7 months to 19 years, with acute mastoiditis who were treated at our hospital from 1988 through 1998. We used three diagnostic criteria to identify acute mastoiditis: the persistence of acute otitis media and otorrhea despite antibiotic therapy, the presence of complications (e.g., erythema, tenderness, swelling, or subperiosteal abscess in the mastoid region), and radiologic images that demonstrated haziness or bone destruction in the mastoid air cell.
Ordinary culture of purulent discharge and antibiotic sensitivity tests were conducted on nine patients, and they were treated with appropriate antibiotics via intravenous or intramuscular injection. When culture results were not confirmed or when the organism was not detected, cephalosporin and aminoglycoside antibiotics were prescribed empirically.
Myringotomy was performed in cases when fever and swelling of the tympanic membrane worsened despite the use of antibiotics because of the concern over further complications. Mastoidectomy was performed if there was no sign of improvement 48 to 72 hours after the initiation of antibiotic therapy and if temporal bone computed tomography (CT) showed absorption of mastoid air cells and common cavity formation (coalescent mastoiditis). As a general rule, the initial procedure involved only a simple cortical mastoidectomy to drain purulent discharge from the mastoid cavity. However, when there was mucosal disease caused by severe osteitis of the mastoid air cell, a canal-wall-up mastoidectomy was performed. A canal-wall-down mastoidectomy was performed if a posterior canal-wall bone defect was found during surgery.
Case 1. An 8-year-old boy with Down's syndrome was brought to our hospital for treatment of otorrhea that had persisted for 7 days. He had no history of tooth extraction or trauma, other than an operation to correct a cataract 6 years earlier. Three days prior to his arrival at our hospital, he had been taken to a local clinic, where he underwent a myringotomy with ventilation tube insertion and was prescribed antibiotic treatment.
The physical examination revealed a perforation and purulent otorrhea in the tympanic membrane, polypoid tissue in the posterosuperior wall of the external auditory canal, and a marked swelling of the postauricular region with pus drainage. The patient was admitted and started on cephalosporin and aminoglycoside injections for 3 days. During that time, CT revealed destruction of the mastoid cortical bone and that the postauricular swelling had worsened (figure lA). At that point, the decision was made to perform a mastoidectomy.
Surgical exploration revealed a severe inflammation of the mastoid air cells. The mastoid antrum was filled with bumpy, yellowish tissue that resembled a cholesterol granuloma. A biopsy was performed, and culture identified the presence of Actinomyces pathogens with sulfa granules (figure 1B). In order to confirm their origin, cultures were obtained from the oral cavity, pharynx, and tonsils by swab smear; no Actinomyces spp. were present.
The boy was discharged 7 days after surgery and was prescribed a 3-month course of low-dose amoxicillin. During followup, he experienced two episodes of febrile convulsion and acute tonsillitis. A tonsillectomy was performed, and histologic examination of the extracted tissue revealed no Actinomyces. The patient recovered uneventfully.
Case 2. A 4-year-old boy had undergone a simple mastoidectomy at another hospital. He had been diagnosed with acute mastoiditis because of the presence of postauricular pain and swelling. Three weeks later, he was transferred to our hospital. The boy had a high fever and headache that did not resolve with treatment.
CT of the brain revealed an extradural abscess (figure 2A). During revision surgery, it was noted that severely inflamed tissue and purulent discharge had filled the mastoid cavity. A marked swelling was observed in the epithelium of the auditory canal, but there was no perforation of the tympanic membrane. Part of the posterior canal wall was necrotic, while Korner' s septum was preserved. The extradural abscess had originated in the posterosuperior portion of the sigmoid sinus and had spread to the jugular bulb. The abscess was filled with caseation substance and was encapsulated by the surrounding structures. The
abscess wall was adherent to the sinus wall, so we carefully separated the abscess wall from the sinus. We then punctured the sinus with a fine needle, but we found no thrombosis.
Biopsy of the mastoid mucosa revealed a tuberculous granuloma (figure 2B). A subsequent tuberculosis culture and polymerase chain reaction assay could not confirm tuberculous species, nor could dot-blot hybridization. The patient was transferred to the pediatric department 5 days after surgery. He underwent a spinal tap, but his cerebrospinal fluid was normal. The boy was placed on an antituberculous drug regimen for 9 weeks. Followup magnetic resonance imaging of the brain showed no peculiar findings.
Among our group of 13 patients with acute mastoiditis, the most common abnormal finding on physical examination was an abnormal tympanic membrane, which was observed in 12 (table 1). Eight of the 12 also had otorrhea, and the other four had only erythema. The second most common finding was swelling and erythema in the postauricular or mastoid area, which was seen in 10 patients. Four patients had a fever of more than 38[degrees] C on hospital admission; a blood culture was performed on all four, but no organisms were detected. Blood test results also identified five cases of elevated erythrocyte sedimentation rate and four cases of leukocytosis (table 1).
In four of the 13 patients, radiologic examination showed a normal pneumatization of the mastoid. Among the other nine patients, a clouding of the mastoid air cell was seen in six and a common cavity was observed in three (table 1).
Bacterial culture was performed on specimens from nine patients who had otorrhea and abscess, and no organism was detected in six (table 2). Methicillin-resistant Staphylococcus aureus (MRSA) was isolated in two patients. They were administered intravenous vancomycin for 1 week, and both responded to it. Staphylococcus epidermidis was found in one patient; pathologic examination revealed a tuberculous granuloma. Actinomyces was found in the mastoid mucosa of one patient.
Eight of the 13 patients were cured within 2 weeks by intravenous antibiotics; two of them also underwent a myringotomy. These eight patients had erythema and swelling in the postauricular and mastoid area, but no subperiosteal abscess. One patient had a subperiosteal abscess, but no fluctuation of the swollen area was found.
Surgery was performed on the five patients who did not respond to medical treatment (table 3). Two of the three patients who underwent a simple cortical mastoidectomy experienced no complications. The other patient developed chronic otitis media and required a canal-wall-up mastoidectomy and tympanoplasty 1 year later. However, this patient developed a cholesteatoma 3 years after surgery and required a canal-wall-down mastoidectomy. The remaining patients who underwent surgery had good results.
The diagnosis of acute mastoiditis is, for the most part, based on clinical findings. Myer found that patients with acute mastoiditis always have signs and symptoms of acute otitis media along with pain, erythema, and auricular displacement in the mastoid area.  The onset of acute otitis media usually occurs approximately 30 days before the manifestation of acute mastoiditis.
Acute mastoiditis is easy to overlook in children younger than 1 year of age.  Because their mastoid is not fully developed, purulent discharge in the cavity can drain through the tympanomastoid fissure. This can displace the superior portion of the auricle posteroinferiorly.
Simple radiologic examination of the mastoid is often used as an adjuvant diagnostic tool. While some studies have shown that it takes 14 days for acute otitis media to develop into mastoiditis, Rosen et al found that this took an average of only 5.8 days in their cases.  They argued, then, that simple radiologic examination is not an adequate diagnostic tool because it is not able to detect such a rapid progression. Also, we should not overlook the possibility of masked mastoiditis, which occurs without the signs or symptoms of acute otitis media. Therefore, when an infant has a fever of unknown origin, it is sometimes necessary to perform a radiologic examination even though there is no sign of acute otitis media. 
Distinct clinical findings were evident in four of our 13 patients. But because radiologic examination of the mastoid showed a relatively well-formed mastoid pneumatization, we cannot conclude that radiologic findings are necessarily important in making the diagnosis. Although temporal bone CT cannot differentiate between a discharge in the mastoid cavity and a lesion, it can easily diagnose coalescent mastoiditis. It can also be an effective diagnostic tool in situations similar to those presented in case 2, where two or more intracranial complications are present. Shanley and Murphy reported that temporal bone CT is an essential tool in diagnosing serious complications of acute mastoiditis--especially Bezold' s abscess, meningitis, brain abscess, thrombophlebitis, extradural abscess, and osteitis--and in determining their anatomic relationship to surrounding structures. 
Although Streptococcus pneumoniae, S aureus, and Hemophilus influenzae are generally the most common pathogenic causes of acute mastoiditis, there have been reports of a change in the type of causative organisms as a consequence of antibiotic use. For example, Prellner and Rydell reported that organisms were not isolated in bacterial culture even when antibiotics were used for only a short time.  Hawkins et al found that the most common organism in acute mastoiditis was Streptococcus pyogenes.  Maharaj et al reported an increase of acute mastoiditis caused by anaerobes.  In their study, they found aerobic bacteria in only 11.4% of cultures, while anaerobic bacteria were present in 62.8%. Therefore, they suggested that detailed tests are necessary, especially testing of purulent discharge in the external auditory canal, because of the possibility of secondary or superficial infection. Holt and Young advised that ordinary cultures for causative organisms should be performed on the postauricular absces s in order to obtain better results.  In our study, bacteria were not identified in six of nine specimens and MRSA was found in two. Therefore, we thought that those pathogens that were not identified were susceptible to antibiotics. The S epidermidis cultured from tuberculous mastoiditis was thought to be most likely caused by a secondary infection.
There is no set way of treating acute mastoiditis that physicians agree on. But according to many authors, it is best to first try medical treatment and reserve surgery for those patients who do not respond. Rosen et al,  Hawkins et al,  and Ogle and Lauer  all reported that they were able to cure acute mastoiditis without complications with medical treatment alone in 64, 57, and 63% of their cases, respectively. Harley et al found that surgical treatment was not necessarily more effective than medical treatment for patients who had no intratemporal or intracranial complications.  On the other hand, Hawkins and Dru have suggested that when the boundaries are demarcated and the inflammation has progressed to subperiosteal abscess, surgery will shorten the length of hospital stay. 
Even though simple mastoidectomy is an effective surgical treatment for acute mastoiditis, [5,8,11-13] a careful and detailed observation is necessary for school-age children because acute mastoiditis in these patients is often accompanied by cholesteatoma. 
In our experience, we were able to achieve good results with antibiotic therapy alone in patients who did not have a subperiosteal abscess. But in cases where severe osteitis has developed and pathologic changes have occurred in the mastoid mucosa, it is better to completely remove the pathologic tissue rather than merely draining it during mastoidectomy. In the patient in our study who developed a cholesteatoma 3 years following simple mastoidectomy, we observed that a canal epithelium had invaded the posterior canal wall through its damaged parts. Based on this finding, the decision to perform either a canal-wall-up or a canal-wall-down mastoidectomy after a careful study of the necrosis in the posterior canal wall is an important one. Holt and Gates advised exposing the dura to look for intracranial complications when tegmen tympani osteitis or granulation tissue is found during mastoidectomy. 
Actinomycosis rarely causes otomastoiditis. Actinomycosis is thought to develop primarily in an unhygienic oral cavity. The triggering mechanisms that cause oral actinomycosis to progress to a middle ear infection have been reported to be trauma, tooth extraction, and surgery.  The patient described in case 1 had poor oral hygiene and a history of myringotomy and ventilation tube insertion. We were unable to determine the exact route of organism invasion. It has been reported that administering oral penicillin for 6 months following the surgical removal of the lesion effectively cures the patient without recurrence.  In our patient, we accomplished this with low-dose amoxicillin for 3 months.
It is prudent to suspect tuberculous mastoiditis when polypoid tissue is observed in the external auditory canal.  Compared with bacterial mastoiditis, tuberculous mastoiditis is more often preceded by pulmonary tuberculosis and accompanied by complications.  Also, because secondary infection is common,  tuberculous mastoiditis is difficult to diagnose by ordinary culture alone. A biopsy is essential when suspicious tissues are found during surgery. We were able to accurately diagnose the two patients described in the case studies because we had performed a biopsy after discovering a general infection and a mucosal lesion.
Our experience suggests that an accurate early diagnosis and appropriate antibiotic therapy are usually sufficient to cure acute mastoiditis. However, when the inflammation does not respond to medical treatment, the physician should suspect that the infection might be caused by antibiotic-tolerant organisms, anaerobes, or atypical pathogens. If complications ensue, we believe it is best to carry out surgical treatment as soon as possible.
From the Department of Otolaryngology-Head and Neck Surgery, College of Medicine, Korea University, Seoul.
Reprint requests: Han-Kyu Suh, MD, Department of Otolaryngology-Head and Neck Surgery, Ansan Hospital, College of Medicine, Korea University, #516, Kojan-dong, Ansan-shi, Kyunggi-do, 425-020, Korea. Phone: +82-31-412-5170; fax: +82-31-401-4365; e-mail: firstname.lastname@example.org
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|Comment:||Clinical experiences with acute mastoiditis--1988 through 1998.|
|Publication:||Ear, Nose and Throat Journal|
|Article Type:||Brief Article|
|Date:||Nov 1, 2000|
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