Disclaimer: The information contained within the Grand Rounds Archive is intended for use by doctors and other health care professionals. These documents were prepared by resident physicians for presentation and discussion at a conference held at Baylor College of Medicine in Houston, Texas. No guarantees are made with respect to accuracy or timeliness of this material. This material should not be used as a basis for treatment decisions, and is not a substitute for professional consultation and/or peer-reviewed medical literature.

Acute mastoiditis is rarely seen today. Prior to the discovery of antibiotics, acute mastoiditis was the most common complication of acute otitis media and often resulted in death. The incidence has dropped significantly with the advent of antibiotics. Likewise, the frequency of mastoidectomy for this condition has decreased ten fold, down from 20% in 1938 to 2.8% in 1948 with a 90% decrease in mortality rate. Acute mastoiditis is a natural extension of acute otitis media. At the onset of infection, acute inflammation of the middle ear also involves inflammation of the mastoid air cells, which is not associated with bony resorption and must be differentiated from clinically significant mastoiditis.

Temporal bone development is integral in the ability to develop this disease. The degree of pneumatization varies greatly in temporal bones. Infection, heredity, ventilation, environment, and nutrition all play a role in the pneumatization process. Inflammation that develops is easily passed through these contiguous pneumatized regions. Not only can inflammation spread to these pneumatized regions, but it can spread to adjacent areas.

The evolution of acute mastoiditis begins when the mucosal lining of the pneumatized cells become inflamed and produce an exudate. Serosanguinous fluid eventually becomes mucopurulent. Spontaneous perforation of the tympanic membrane or myringotomy would halt the process at this point. However, 1-5% of these cases go on to the next phase. The cellular walls of the pneumatized cells then become demineralized due to: increased osteoclastic activity, pressure of the purulent exudate on the thin bony septae, and ischemia of the septae secondary to reduced blood flow. As the bony septae breakdown small abscess cavities form leading to coalescence. Finally the coalescent cells form an empyema, or pus under pressure, which then escapes to surrounding areas. Treatment of acute mastoiditis depends on the pathologic stage at which it is encountered.

The bacteriology of acute mastoiditis surprisingly differs from that of acute otitis media. The causative organism in acute otitis media are usually S Pneumo or H Flu. However, acute mastoiditis is more commonly due to Group A Beta-Hemolytic Strep and S Pneumo with rare involvement by H. Flu. Subacute and chronic disease is usually attributed to S. Aureus and gram negative rods such as E. Coli, Proteus and Pseudomonas.

The signs and symptoms of acute mastoiditis mimic severe acute suppurative otitis media; the disease entities are distinguished by the duration of symptoms. When the symptoms persist or recur after several weeks of acute otitis media, they point toward development of a coalescent process within the mastoid. The most common symptoms are otorrhea and otalgia. Subperiosteal abscess is noted by a fluctuant mass with overlying edema and erythema. This process produces displacement of the ear downward, outward, and forward. Sagging of the posterosuperior meatal wall occurs secondary to thickening of the periosteum overlying the bone in the area of the antrum. The tympanic membrane can simply appear normal, thickened or can demonstrate a small central perforation. Neurologic changes may be seen with intracranial complications. Perforation of the mastoid tip along the medial aspect of the SCM through the incisura mastoidea produces a deep abscess in the neck known as a Bezold's abscess.

Acute mastoiditis is one of the 10 basic complications of acute otitis media. Some worth noting are listed here. Petrositis is indicated by Gradenigo triad -- acute or subacute otitis media, retro-orbital pain and abducens palsy. Labyrinthitis due to suppurative ear disease is potentially fatal with spread to the cerebrospinal fluid producing meningitis. Presence of an extradural abscess is best evaluated by CT scan but must be excluded intraoperatively by visualizing normal dura through thin intact bone. Sigmoid sinus thrombosis may be asymptomatic or associated with toxemia or septic emboli. Griesinger's sign may be encountered and is noted by the presence of edema erythema of the posterior aspect of the mastoid process associated with mastoid emissary vein thrombosis. The Tobey - Ayer or Queckenstedt test is usually of historic significance and shows a rise in CSF pressure with occlusion of the normal IJ and NO change in CSF pressure with occlusion of the thrombosed vein. Brain abscess formation begins with cerebritis and should be closely monitored if suspected with CT scan every 1-2 weeks.

Evaluation of the patient with acute mastoiditis begins with the history and physical examination. The majority of the diagnosis is based on clinical judgment. Laboratory evaluation reveals a leukocytosis and elevated erythrocyte sedimentation rate. Mastoid radiographs are characteristic and will show cloudiness of the mastoid air cells associated with fuzziness of the bony partitions. Although helpful in the diagnosis, most agree that mastoid x-rays are not helpful in determining whether mastoid surgery is necessary. CT scan of the temporal bones is helpful in evaluation of concomitant intracranial complications as well as discerning any anatomical variations preoperatively. Chest x-ray is useful to rule out infiltrates in patients with septicemia and possible embolic phenomena secondary to lateral sinus thrombosis. Tympanocentesis is performed for guidance of antibiotic therapy.

Acute mastoiditis may be associated with periostitis, osteitis, or may be masked. This differentiation is key in the management of the patient. Acute mastoiditis with periostitis can be described as infection in the mastoid air cells which spreads to cause inflammation of the overlying periosteum. The route of infection may be through direct spread through a defect in the mastoid cortex or more commonly through venous channels, a.k.a. mastoid emissary veins. Periostitis should not be confused with subperiosteal abscess which requires surgical intervention.

Acute mastoiditis with osteitis is also known as coalescent mastoiditis. Less than 15% of patients with periostitis will progress to coalescence. This coalescence may spread in several directions. The spread of the pus anteriorly to the middle ear via the aditus ad antrum producing spontaneous resolution. If the pus spreads to the soft tissues lying anteromedially a Bezold's abscess may form. The infection may also spread lateral to produce a subperiosteal abscess. The spread of pus medially to the petrous air cells causes petrositis. Posterior spread to the occipital bone may result in osteomyelitis of the calvarium a.k.a. Citelli abscess.

Masked mastoiditis has an insidious course, owing to the use of broad spectrum antibiotics to treat middle ear disease. The apparent resolution of symptoms of acute otitis media "masks" the development of mastoiditis and leads to the presentation with intracranial complications. The presence of pathology may only be apparent on careful neurologic examination. Diagnosis is usually made on CT of the temporal bones which demonstrates temporal bone pathology in conjunction with the accompanying intracranial complication.

Acute mastoiditis can also occur in conjunction with chronic ear disease. It has been the teaching in the past that acute mastoiditis only occurred in well pneumatized mastoids in which the thin bony trabeculae are easily broken down. Chronic ear disease has long been associated with a sclerotic "cue - ball" like mastoid which is less susceptible to demineralization. However, several studies note the presence of cholesteatoma in patients with acute mastoiditis.

Antibiotic therapy is guided by the patients history. If the history is otherwise uncomplicated by ear disease or protracted episode of otitis media, the infecting organism is probably S. pneumo or S. pyogenes which is best treated by ampicillin. If the patient has a protracted course of otitis media then coverage for S. Aureus and gram negative organisms is necessary with a penicillinase resistant penicillin and an aminoglycoside or single antibiotic coverage with a cephalosporin. Anaerobic coverage should be added to the above therapy when suspected.

There exists controversy over the management of this disease. All studies on acute mastoiditis are retrospective and conclusions drawn regarding therapy are limited. There have been no prospective or controlled studies on the surgical and medical management of the disease. This is limited by the relative rarity of the disease in the current day. Options for treatment are antibiotics alone, antibiotics plus myringotomy, Incision and drainage of abscess, and mastoidectomy. If periostitis is present tympanocentesis followed by myringotomy should be performed with placement on intravenous antibiotics directed toward gram stain results. It is preferable to insert pressure equalization tubes for drainage over a longer period of time. This periosteal involvement usually resolves within 24 to 48 hours after initiation of therapy. If clinical deterioration occurs, manifest by persistent fever and otalgia, or development of subperiosteal abscess, then further surgical intervention is indicated. Analysis of the literature reveals approximately 57% of cases are able to be treated in this manner.

Indications for surgery include acute mastoiditis with subperiosteal abscess, acute mastoiditis not responsive after 24 to 48 hours of intravenous antibiotics and myringotomy, and intracranial complications with evidence of mastoid coalescence. These indications were derived from the current literature.

Some have managed the disease with simple I & D of the abscess which does not afford decompression and drainage of the underlying mastoid. There have been no studies to evaluate the efficacy of this mode of therapy versus mastoidectomy. Most reported cases of simple I & D have been anecdotal. 60% of the cases reported in the literature have come to mastoidectomy after I & D.

The procedure of choice is a complete simple mastoidectomy. Simple mastoidectomy is an emergency procedure and should be performed on a clinically stable patient with control of sepsis before undergoing anesthesia. Mastoidectomy may be performed at a later date if the patient is unstable after drainage of intracranial process. The goal of surgery is to effect drainage. Establishment of good communication between the middle ear and mastoid is achieved by removing the edema and granulation in the aditus ad antrum. External drainage is necessary with a drain in the mastoid cavity to drain the antrum, and a pressure equalization tube inserted to ventilate the middle ear space.

In conclusion, acute mastoiditis is a diagnosis based on clinical acumen. When acute mastoiditis is suspected a careful history and physical examination should be ascertained to evaluate for intratemporal or intracranial complications. The presence of acute mastoiditis does not exclude the presence of underlying chronic ear disease, and should be taken into account in the evaluation and treatment of the patient. The presence of subperiosteal abscess or progression of symptoms on the above therapy warrants surgical intervention. Simple mastoidectomy is the surgery of choice. Prospective controlled studies are necessary to firmly identify indications for medical versus surgical therapy.

An 11-year-old boy with a history of chronic otitis media with effusion presented with a 10-day history of fever, right otalgia, and a right, dull occipital headache. The headache was not associated with photophobia. A CT scan of the head revealed a right parieto-occipital epidural abscess.. Physical examination revealed a young, alert boy with a temperature of 102øF. Examination of his right ear revealed a thickened, but intact tympanic membrane and middle ear effusion. Postauricular edema, erythema, tenderness, and fluctuance was evident. The remainder of the physical examination, including a neurological exam, was normal. White blood cell count was 18.7 cells/mm3 with a left shift. CT scan of the temporal bones revealed soft tissue changes within the middle ear and mastoid and an overlying subperiosteal abscess and possible lateral sinus thrombosis.

The patient was taken to the operating room and underwent bur hole drainage and irrigation of a right parieto-occipital epidural abscess by the neurosurgical team followed by a right simple mastoidectomy, exploration of the lateral sinus, insertion of a pressure equalization tube, and Penrose drainage of the mastoid cavity. Findings included coalescent mastoiditis and no evidence of lateral sinus thrombus. Intraoperative cultures grew microaerophilic streptococcus; the antibiotic regimen was changed to Cefotaxime and Penicillin G. The right temporoparietal cerebritis showed no progression to brain abscess and no neurologic sequelae. Drains were discontinued when drainage decreased. The patient was discharged on the thirteenth postoperative day in good condition to continue intravenous antibiotics for a total course of 6 weeks. Weekly CT scan of the head demonstrated slow resolve of the cerebritis. The patient has had no further episodes of otitis media and is currently doing well in the sixth grade.

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