A purist's definition of mastoiditis includes all inflammatory processes of the mastoid air cells of the temporal bone. As the mastoid is contiguous to and an extension of the middle ear cleft, virtually every child or adult with acute otitis media (AOM) or chronic middle ear inflammatory disease has mastoiditis. In most cases, the symptomatology of the middle ear predominates (eg, fever, pain, conductive hearing loss), and the disease within the mastoid is not considered a separate entity (see the image below).[1] (See Etiology and Presentation.)
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Mastoiditis with subperiosteal abscess. Note the loss of the skin crease and the pointed abscess.
Acute mastoiditis is associated with AOM. In some patients, the infection spreads beyond the mucosa of the middle ear cleft, and they develop osteitis within the mastoid air-cell system or periosteitis of the mastoid process, either directly by bone erosion through the cortex or indirectly via the emissary vein of the mastoid. These patients have acute surgical mastoiditis (ASM), an intratemporal complication of otitis media. (See Etiology.)
Chronic mastoiditis is most commonly associated with chronic suppurative otitis media and particularly with cholesteatoma formation. Cholesteatomas are benign aggregates of squamous epithelium that can grow and alter normal structure and function of surrounding soft tissue and bone. This destructive process is accelerated in the presence of active infection by the secretion of osteolytic enzymes by the epithelial tissue. (See Etiology.)
Progression of mastoiditis
Mastoiditis progresses in the following 5 stages and may be arrested at any point (see Presentation and Workup):
Hyperemia of the mucosal lining of the mastoid air cells
Transudation and exudation of fluid and/or pus within the cells
Necrosis of bone by loss of vascularity of the septa
Cell wall loss with coalescence into abscess cavities
Extension of the inflammatory process to contiguous areas
Patient education
Warn patients and their families of possible cosmetic deformity following mastoid surgery.
Workup and management
Despite the use of antibiotics, acute mastoiditis still remains a threat for patients with acute otitis media (AOM), especially for children younger than age 5 years. Great care is required on the part of clinicians to make an early diagnosis in order to promote adequate treatment and to prevent complications.[2]
Material for culture and sensitivity should be obtained from the ear (via tympanocentesis or myringotomy), blood, any abscess, and mastoid tissue (if it becomes available). Obtain and evaluate spinal fluid if any suggestion exists of intracranial extension of the process.
Workup also includes the following:
Complete blood count (CBC)
Audiometry
Tympanocentesis/myringotomy
Computed tomography (CT) scanning - CT scanning of the temporal bone is the standard for evaluation of mastoiditis, with published sensitivities ranging from 87-100%
Surgical therapy confined to the ear includes myringotomy/tympanocentesis, tympanostomy tube placement, and mastoidectomy.
Antibiotics are the principal medications used in acute surgical mastoiditis (ASM). Culture results and the sensitivity of the organism ultimately govern selection of medications.
As with most infectious processes, consider host and microbial factors when evaluating surgical mastoiditis. Host factors include mucosal immunology, temporal bone anatomy, and systemic immunity. Microbial factors include protective coating, antimicrobial resistance, and ability to penetrate local tissue or vessels (ie, invasive strains). As the clearance of the mastoid is dependent upon a patent antrum, resolution is unlikely unless this anatomical isthmus opens by control of mucosal swelling, which otherwise creates a reservoir for infection.
Host factors
Most children presenting with acute surgical mastoiditis (ASM) are younger than age 2 years and have little history of otitis media. This is an age at which the immune system is relatively immature, particularly with regard to its ability to respond to challenges from polysaccharide antigens.
Host anatomical factors may have a role. The mastoid develops from a narrow outpouching of the posterior epitympanum (ie, the aditus ad antrum). Pneumatization occurs shortly after birth, once the middle ear becomes aerated, and this process is complete by age 10 years. Mastoid air cells are created by invasion of epithelium-lined sacs between spicules of new bone and by degeneration and redifferentiation of existing bone marrow spaces.
Other areas of the temporal bone pneumatize similarly, including the petrous apex and the zygomatic root. The antrum, as with the mastoid air cells, is lined with respiratory epithelium that swells when infection is present. Blockage of the antrum by inflamed mucosa entraps infection within the air cells by inhibiting drainage and precluding reaeration from the middle-ear side.
Persistent acute infection within the mastoid cavity may lead to a rarifying osteitis, which destroys the bony trabeculae that form the mastoid cells (hence the term coalescent mastoiditis). Essentially, coalescent mastoiditis is an empyema of the temporal bone that, unless its progress is arrested, drains either through the natural antrum to give spontaneous resolution or creates further complication by draining unnaturally to the mastoid surface, petrous apex, or intracranial spaces. Other temporal bone structures or nearby structures, such as the facial nerve, labyrinth, and venous sinuses, may become involved.
A retrospective study by Adams et al indicated that children with autism spectrum disorder have an increased likelihood of developing middle ear infections and otitis-related complications, including a more than two-fold greater chance of developing mastoiditis.[3]
Microbial factors
Reported pathogens in mastoiditis include the following:
Streptococcus pneumoniae – Most frequently isolated pathogen in acute mastoiditis, prevalence of approximately 25%
Group A beta-hemolytic streptococci
Staphylococcus aureus
Streptococcus pyogenes
Moraxella catarrhalis
Haemophilus influenzae
Pseudomonas aeruginosa
Mycobacterium species
Aspergillus fumigatus and other fungi
Nocardia asteroides - Case report[4]
Because acute otitis media (AOM) is the antecedent disease, the most common etiologic agent causing surgical mastoiditis is Streptococcus pneumoniae, followed by Haemophilus influenzae and group A Streptococcus pyogenes (GAS). Each of these bacteria has invasive forms and is recovered most often from children presenting with ASM. More than half of the Streptococcus pneumoniae recovered are of serotype 19, followed by serotypes 23 and 3.
The literature and the authors' experience indicate that a high frequency of multidrug-resistant Streptococcus pneumoniae (MDRSP) is now associated with ASM, and this may alter selection of antimicrobials (40-50% penicillin resistant, approximately 25% ceftriaxone resistant). Treatment of AOM with antimicrobials in the previous month increases the frequency of MDRSP.[5]
Gram-negative organisms and Staphylococcus aureus are recovered more frequently from patients with chronic mastoiditis.
Half of children admitted with acute mastoiditis have no previous history of recurrent AOM. In those children, Streptococcus pneumoniae has been the leading pathogen, while Pseudomonas aeruginosa has been more prevalent in children with recurrent AOM.
Incidence of surgical mastoiditis from acute otitis media is reported as 0.004% in the United States.[6] Some fear that untreated otitis media increases the risk of acute mastoiditis and is the cause of higher incidences in developing countries and very young children.[7, 8]
The Inuit population has a high predilection for middle-ear disease and, as a likely consequence, mastoiditis.
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.
Acute mastoiditis is a disease of the very young. Most patients present when younger than age 2 years, with a median age of 12 months. However, it can occur in persons of any age.
A retrospective review of pediatric patients in Colorado found that despite an initial drop in the incidence of acute mastoiditis in children under age 2 years following the introduction of heptavalent pneumococcal conjugate vaccine (PCV7), the incidence rose again to pre-PCV7 levels within a few years. The study, by Halgrimson et al, examined pediatric inpatient data from 1999-2008 for documented cases of acute mastoiditis or patients who had undergone mastoidectomy.[9]
The investigators found that the annual incidence of acute mastoiditis in children under age 2 years dropped from 11.0 per 100,000 population in 2001, a year after PCV7 was introduced, to 4.5 per 100,000 population in 2003. By 2008, however, the incidence had again risen, to 12.0 per 100,000 population. An increase in the prevalence of S pneumoniae isolates nonsusceptible to penicillin also occurred in Colorado, from 0% between 1999 and 2004 to 38% between 2005 and 2008. Halgrimson and colleagues suggested that the presence of non-PCV7 pneumococcal serotypes and a rise in pneumococcal antibiotic resistance may have caused the incidence of acute mastoiditis to increase.[9]
Another study, however, found that the introduction of pneumococcal conjugate vaccines may have led to a national reduction in pediatric mastoiditis rates. The study, by Marom et al, looked at insurance claims from a nationwide managed health care plan to analyze health care visits associated with otitis media in children aged 6 years or younger. The investigators found that between 2008 and 2011, mastoiditis rates decreased from 61 per 100,000 child-years to 37 per 100,000 child-years.[10]
Noting a reduction in US hospitalization rates for acute mastoiditis in children aged 0-2 years between 2009 and 2012, a study by Tawfik et al suggested that use of the 13-valent pneumococcal vaccine (PCV13) may have had a protective benefit against mastoiditis for youngsters in this age group. However, the study, which looked at annual incidences of hospitalization for pediatric acute mastoiditis after the introduction of PCV7 and PCV13, did not find an overall decline in hospitalization rates for acute mastoiditis between 2000 and 2012 in persons below age 21 years.[11]
Expect patients with acute surgical mastoiditis (ASM) to recover completely provided that the facial nerve, vestibule, and intracranial structures are not involved. Cosmetic deformity of the operated ear can usually be prevented with judicious placement of the incision and the development of flaps to pull the ears posteriorly when replaced.
Conductive hearing loss should resolve provided that the ossicular chain remains intact. Conduct testing after otorrhea has ended and the ear has healed.
Extension of the infectious process of mastoiditis can include the following:
Posterior extension to the sigmoid sinus (causing thrombosis)
Posterior extension to the occipital bone to create an osteomyelitis of calvaria or a Citelli abscess
Superior extension to the posterior cranial fossa, subdural space, and meninges
Anterior extension to the zygomatic root
Lateral extension to form a subperiosteal abscess
Inferior extension to form a Bezold abscess
Medial extension to the petrous apex
Intratemporal involvement of the facial nerve and/or labyrinth
Complications
Complications of mastoiditis include the following:
Hearing loss
Facial nerve palsy
Cranial nerve involvement
Osteomyelitis
Petrositis
Labyrinthitis
Gradenigo syndrome - Otitis media, retro-orbital pain, and abducens palsy
Abscess formation - Citelli abscess (extension to occipital bone, calvaria), subperiosteal abscess (abscess between the periosteum and mastoid bone, resulting in the typical appearance of a protruding ear; see the image below), and Bezold's abscess (abscess of soft tissues that track along the sternomastoid sheath; Bezold abscesses are very rare complications and are usually found only in adults with a well-pneumatized mastoid tip)
See the image below.
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Mastoiditis with subperiosteal abscess. Note the loss of the skin crease and the pointed abscess.
Meningitis and facial nerve paralysis are possible in mastoiditis. Approximately 7% of patients may develop intracranial complications related to acute mastoiditis. These complications can include sigmoid sinus thrombosis, epidural abscess, and meningitis. Persistent otalgia or otorrhea with associated neurologic symptoms in a patient taking oral antibiotics are ominous signs that suggest a complication.
Otogenic meningitis is the most common intracranial complication of neglected otitis media. In the Western world, such complications seldom occur in children and adolescents and are extremely rare in adults. The current use of antibiotics and of more sophisticated surgery has greatly diminished the incidence of otogenic meningitis; however, this has resulted in physicians having less experience with diagnosis and treatment of this complication. Emergency surgical treatment is mandatory.
In a study done by Luntz et al of 223 consecutive cases of acute mastoiditis, 16 patients presented with complications, including cerebellar abscess, perisinus empyema, subdural abscess or empyema, extradural abscess, cavernous sinus thrombosis, lateral sinus thrombosis, bacterial meningitis, labyrinthitis, petrositis, and facial nerve palsy.[12]
A study by Garcia et al indicated that in children with acute mastoiditis, the risk of complications is greater in those under age 24 months who have a high leukocyte count or a high C-reactive protein (CRP) level. The investigators suggested that 7.21 mg/dL CRP is a good cutoff value for monitoring children for complications.[13]
In a retrospective study of children admitted to the hospital with acute mastoiditis, Carmel et al found that patients who received preadmission antibiotic therapy had a higher complication rate than did those who were not treated prior to admission (52% vs 27%, respectively).[14]
Most patients (>80%) have no history of recurrent otitis media. Persistent otorrhea beyond 3 weeks is the most consistent sign that a process involving the mastoid has evolved.
The patient’s fever may be high and unrelenting in acute mastoiditis, but this may be related to the associated acute otitis media (AOM). Persistence of fever, particularly when the patient is receiving adequate and appropriate antimicrobial agents, is common in acute surgical mastoiditis (ASM).
Pain is localized deep in or behind the ear and is typically worse at night. Persistence of pain is a warning sign of mastoid disease. This may be difficult to evaluate in very young patients. Hearing loss is common with all processes that involve the middle ear cleft.
For infants, be attentive to any nonspecific history consistent with infection, such as poor feeding, fever, irritability, or diarrhea.
In a study by Oestreicher-Kedem et al, the mean interval from onset of illness to mastoiditis was found to be 4.5 days.[15] Ear cultures most often grew S pneumoniae and P aeruginosa (23.7% each). Complications occurred in 15.8% of cases. The only factor differentiating children with and without complications was the white blood cell count (high in children with complications).
The findings in this study indicate that acute mastoiditis is not only a complication of prolonged infection of the middle ear but also may present as an acute infection of the mastoid bone that can progress within 48 hours. The complication rate remains high, and antibiotic treatment at the onset of symptoms does not prevent complications. A high white blood cell count on admission may serve as a predictive factor for complicated cases.
In a study by Niv et al of 113 patients with acute mastoiditis (128 episodes) treated between 1990 and 2002, the authors concluded that (1) a significant increase in the incidence of acute mastoiditis in infants had been recorded, although the reason for the trend was uncertain; (2) in most infants with acute mastoiditis, the disease arose after the infant's initial AOM episode, and most of the infants had not received prior antibiotic therapy; (3) infants showed more severe clinical signs and symptoms of acute mastoiditis than did older patients; (4) S pneumonia was the most common pathogen isolated in middle ear fluid cultures, but there was a greater involvement of S pyogenes in the cases of acute mastoiditis than had been reported for AOM.[16]
Acute mastoiditis is a serious bacterial infection of the temporal bone and is the most common complication of otitis media. Frequent symptoms include mastoid area erythema, proptosis of the auricle, and fever.[2]
Tenderness and inflammation over the mastoid process is the most consistent sign of acute surgical mastoiditis (ASM). Periosteal thickening requires comparison to the other side, and some lateral displacement of the auricle may be present. Subperiosteal abscess displaces the auricle laterally and obliterates the postauricular skin crease. If the crease remains, the process is lateral to the periosteum.
Although the diagnosis of acute surgical mastoiditis can often be made on a clinical basis alone, computed tomography (CT) scanning may be performed for confirmation of the diagnosis, evaluation of potential complications, and surgical planning. Also keep in mind that it is possible to have mastoiditis with no history of otitis media, normal external anatomy, no tenderness, and no external signs of infection.
Otitis media is revealed on otoscopy, often with 1 of the following additional features:
Sagging of the posterosuperior canal wall (possibly a sign of ASM, although not as reliable in infants)
Nipplelike protrusion of the central tympanic membrane, usually oozing pus
Findings consistent with a complication of extension beyond the mastoid process and its covering periosteum or another intratemporal complication, such as facial palsy
In adults, the most common symptoms of mastoiditis are otalgia, otorrhea, and hearing loss, and the physical signs of mastoiditis (ie, swelling, erythema, tenderness of the retroauricular region) are usually present. Localization and enlargement of the pathological process within the middle ear spaces can be determined based on CT scan findings.
Despite the use of antibiotics, acute mastoiditis still remains a threat for patients with acute otitis media (AOM), especially for children younger than age 5 years. Great care is required on the part of clinicians to make an early diagnosis in order to promote adequate treatment and to prevent complications.[2]
Material for culture and sensitivity should be obtained from the ear (via tympanocentesis or myringotomy), blood, any abscess, and mastoid tissue (if it becomes available). Obtain and evaluate spinal fluid if any suggestion exists of intracranial extension of the process.
Complete blood count
A complete blood count (CBC) and sedimentation rate are obtained for baseline studies used to evaluate the efficacy of therapy. A high white blood cell count on admission may serve as a predictive factor for complicated cases.
Audiometry
In the light of the prevailing medicolegal climate, an audiometric evaluation must be obtained. Audiometry is seldom appropriate or useful for children with ASM, but it must be performed after convalescence from the acute phase and with children who have chronic mastoiditis. In the at-risk population (children < 2 y), thresholds for air and bone conduction under headphones are only rarely obtained.
Tympanocentesis/myringotomy
Tympanocentesis is a puncture of the tympanic membrane for aspiration of middle ear fluid. The tympanic membrane typically heals within several days. Send fluid for cultures, Gram stain, and acid-fast stain. It is often possible in an acute infection to convert a tympanocentesis into a myringotomy without undue discomfort by widening the needle hole with alligator forceps.
Myringotomy is a small incision of the tympanum to express fluid from the middle ear in chronic or recurrent otitis media; it often relieves discomfort associated with pressure from acute otitis media (AOM). Tympanostomy tube insertion is also performed in most cases to allow for continued drainage and so that administered therapeutic otic drops reach the middle ear.
CT scanning of the temporal bone is the standard for evaluation of mastoiditis, with published sensitivities ranging from 87-100%. Some argue that all suspected cases of mastoiditis warrant CT scan evaluation.[17]
The following findings are used to differentiate acute otitis media (AOM)/acute mastoiditis without osteitis, acute surgical mastoiditis (ASM), and chronic mastoiditis:
Opacification of the mastoid air cells and middle ear by inflammatory swelling of mucosa and by collection of fluid
Loss of sharpness or visibility of mastoid cell walls due to demineralization, atrophy, or necrosis of bony septa
Haziness or distortion of the mastoid outline, possibly with visible defects of the tegmen or mastoid cortex
Enhancement of areas of abscess formation
Elevation of the periosteum of the mastoid process or posterior cranial fossa
Osteoblastic activity in chronic mastoiditis
It is this author’s belief that in the presence of clear clinical indications of acute surgical mastoiditis, CT scanning may be omitted prior to surgical intervention, avoiding unnecessary radiation exposure as recommended by the US National Institutes of Health.[18]
MRI
Magnetic resonance imaging (MRI) is not typically the radiographic study of choice; however, it is helpful in showing inflammatory processes and differentiating certain tumors. Do not use MRI as a method of evaluating the mastoid, although it is the standard for evaluation of contiguous soft tissue, particularly the intracranial structures. However, MRI is the preferred imaging modality for the potential complications of ASM (ie, abscess formation, sinus thrombosis).
A retrospective study by Saat et al found differences in the MRI characteristics of acute mastoiditis in children, compared with adults. The study, which included 10 children and 21 adults with acute mastoiditis, reported that in the pediatric patients, the prevalences of total opacification of the tympanic cavity and mastoid air cells, intense intramastoid enhancement, destruction of outer cortical bone, subperiosteal abscess, and enhancement of perimastoid meninges were significantly higher than in adults.[19]
A study by Singh et al, however, found that incidental opacification of the mastoid is frequently seen in children, indicating that the diagnosis of pediatric mastoiditis should not hinge on radiologic reports of fluid or mucosal thickening in the mastoid air cells. The study included 515 children who underwent brain MRI for indications not involving mastoiditis or otitis media, with mastoid opacification found in 110 (21.4%) of these patients. Opacification rates in children younger than 1 year and those between ages 1 and 2 years reached 41.7% and 47.5%, respectively.[20]
Plain radiography
In areas of the world where CT scanning is not immediately available, plain radiographs of the mastoids demonstrate clouding of the air cells with bone destruction in ASM. In the vast majority of cases, radiographs suffice to establish the diagnosis but lack the sensitivity to differentiate the stages of the disease and fail to show the petrous apex in any great detail.
A literature review by Loh et al indicated in uncomplicated acute mastoiditis, conservative therapy is a highly successful first-line treatment. In terms of medical treatment, conservative surgery, and mastoidectomy, cure rates for the disease were found to be 95.9%, 96.3%, and 89.1%, respectively.[21]
Surgical therapy confined to the ear includes myringotomy/tympanocentesis, tympanostomy tube placement, and mastoidectomy. In the preantimicrobial era, mastoidectomy was performed in as many as 20% of patients with acute otitis media (AOM). By 1948, this figure had dropped to less than 3%, and it is presently thought to be performed in fewer than 5 cases per 100,000 persons with AOM. (See the images below.)
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Extent of cortical mastoidectomy in a well-pneumatized mastoid.
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Cortical mastoidectomy in a densely sclerosed mastoid.
Indications for the simple mastoid operation include cases of acute suppurative otitis media that fail to respond to appropriate antibiotic therapy and progress to coalescent mastoiditis. Incidence of mastoiditis and, thus, mastoidectomy should decline further with the availability and administration of conjugated pneumococcal vaccine.
A study at a tertiary care hospital, by Stern Shavit et al, found that of 570 children admitted with acute mastoiditis from 2008-2017, the most common pathogen in patients who underwent surgical treatment (cortical mastoidectomy) was Fusobacterium necrophorum (50%). The most common pathogen in those who did not require surgery was group A streptococcus (22%). The investigators also determined that the preadmission rate of acute otitis media was higher in the surgical group, as was the rate, at admission, of prolonged fever, otorrhea, and subperiosteal abscess.[22]
When considering surgery, the risks of exposure to general anesthesia must be weighed against the risk of complications and progression of the infection. Contraindications to surgery include a low hemoglobin concentration and general systemic illness that must be controlled (eg, diabetes, hypertension, poor cardiac condition, bleeding disorders with prolonged bleeding and clotting time).
Acute mastoiditis without osteitis or periosteitis
This is the only mastoid condition treated purely with medical management. Standard antibiotic therapy is administered for AOM, and resolution is anticipated within 2 weeks.
If complications occur (pain and fever persist beyond 48 h or tenderness increases), obtain cultures via the middle ear, commence new antimicrobial therapy, and obtain imaging of the mastoid. Consider mastoidectomy if symptoms persist or if the new antibiotics fail.
Acute mastoiditis with osteitis
This is a surgically treated disease, although coverage with appropriate antibiotics is mandatory. Mastoidectomy with insertion of a tympanostomy tube is required to remove areas of coalescence within the temporal bone.
This author uses single-, high-dose systemic steroids preoperatively or intraoperatively to control swelling, nausea, and inflammation without negatively impacting the child’s immunological response.
Antibiotic selection should provide good intracranial penetration and MDRSP coverage. With the high frequency of invasive resistant strains in mastoiditis, initial therapy of intravenous vancomycin and ceftriaxone is most appropriate until results of the culture and sensitivity studies are available.
Postoperatively, antibiotic/steroid drops are used to keep the tube patent and to reduce middle ear swelling.
Patients with spread of empyema beyond the mastoid require drainage of the abscess and mastoidectomy. Intracranial spread requires a combined neurosurgical and otolaryngological approach.
Acute mastoiditis with periosteitis
Postauricular swelling and erythema without subperiosteal abscess or mastoid osteitis can be treated more conservatively, using parenteral antibiotics, high-dose steroids, and tympanostomy tube insertion. Vancomycin and ceftriaxone are recommended until cultures become available. Again, systemic steroids slow the inflammation and promote drainage.
If substantial resolution of pain, fever, and erythema does not occur within 36-48 hours after institution of therapy, mastoidectomy is warranted.
Transfer
If transfer is required, it invariably relates to the availability of subspecialists, most notably pediatric otolaryngologists or otologists, pediatric neurosurgeons, or pediatric critical care specialists. Available radiographs should be copied and should accompany the patient, along with any available laboratory data. Instruct patients to take nothing by mouth until the receiving subspecialists evaluate their conditions.
When transfer is not possible, occasional operators (particularly in children) should be aware that it is more important to establish wide communication between mastoid cavity and middle ear than to open all the air cells of the mastoid. Almost always, opening the antrum and leaving an external drain will suffice.
Consultations
Early consultation with an otolaryngologist is appropriate and necessary if the pediatrician is not comfortable performing tympanocentesis. If cultures indicate the presence of resistant or unusual microbes, consultation with appropriate infectious-disease specialists may be required. Consultation with a neurosurgeon is appropriate if evidence of intracranial extension with abscess formation exists.
Monitoring
Monitor the patient's temperature; it usually falls dramatically within the first 24 hours, after which the patient can be allowed up. After obtaining cultures (either by tympanocentesis or during tympanostomy tube placement, with or without mastoidectomy), continue initial antibiotic selection until cultures are reported. If the patient becomes afebrile and if swelling decreases at 48-72 hours, oral medication may be selected based on culture reports.
Children who have had a mastoidectomy are released from the hospital after the discharge from the surgically implanted drain abates. The drain is normally removed 48-72 hours postoperatively.
Antibiotic/steroid drops are continued until the otorrhea ceases and the tympanostomy tube is noted to be open with healing or healed mucosa behind.
Antibiotics are the principal medications used in acute surgical mastoiditis (ASM). Culture results and the sensitivity of the organism ultimately govern selection of medications. Until microbiology information is available, the following principles guide the selection: (1) the antimicrobial must be appropriate to cover the invasive strains of bacteria most common for AOM, (2) the selected antibiotic should cross the blood-brain barrier, and (3) the selected therapeutic spectrum should include consideration of MDRSP organisms that are prevalent in the individual’s community. Specific microbiologic diagnoses should be treated with appropriate antibiotics.
If open mastoid surgery is not undertaken, use of single, high-dose, intravenous steroids is warranted to decrease mucosal swelling and to promote natural drainage through the aditus ad antrum into the middle ear.
Other medications used include analgesics, antipyretics, and topical antibiotic/steroid combinations. After placement of a tympanostomy tube, with or without mastoidectomy, a pH-balanced solution or suspension of an antibiotic and steroid is useful to decrease mucosal swelling and to deliver topical antibiotics to the middle ear and mastoid. Continue the drops until otorrhea ceases and the view through the tube shows healing mucosa without swelling or obstruction. Multiple combinations are available, the best being those thin enough to rub through the tube into the middle ear.
Myringotomy/Tympanocentesis and Tympanostomy Tube Placement
Myringotomy/tympanocentesis is primarily used to obtain specimens and to relieve discomfort from acute otitis media (AOM). These openings usually heal within a few days.
A tympanostomy tube allows for drainage of entrapped pus and aeration of the middle ear and mastoid. It may sometimes allow topical antimicrobials to enter the middle ear space. Because it is used as a drain, a tympanostomy tube is usually placed during mastoidectomy.
A tube maintains the opening in the tympanic membrane and provides access to the middle ear and mastoid for antibiotic/steroid drops and for drainage without concern for patency of the Eustachian tube. Ear drops containing only antibiotics are less effective than those containing a steroid to control swelling.
A retrospective study by Enoksson et al indicated that in pediatric patients with subperiosteal abscess caused by acute mastoiditis, retroauricular needle aspiration and/or incision, used in combination with intravenous antibiotics and myringotomy, is an effective first-line treatment for the abscess. The study compared outcomes in 33 children who underwent this therapy with those of 67 children who underwent mastoidectomy, with few significant differences found between the two groups (although members of the mastoidectomy group tended to have longer hospital stays).[23]
Mastoidectomy is surgical removal of infected mastoid air cells. This procedure involves opening the mastoid air cells by making a postauricular incision and entering the mastoid by removing the mastoid cortex using a drill. Often, children will have thinned out cortex with pus coming through the residual bone and the mastoid can be entered easily and safely using a mastoid curette rather than a drill. Any subperiosteal abscess is opened during this time. Upon entering the mastoid, the surgeon most often encounters granulation tissue and swollen polypoid mucosa that block the aditus ad antrum. Most of the diseased air cells are opened, and access to the middle ear is gained by removing the blockage at the antrum. After irrigating the ear, a drain is inserted through the wound, where it is left for at least 2 days.
With a simple (or closed) mastoidectomy, the surgeon either makes an incision behind the ear to access the mastoid region or removes the infected air cells by approaching through the ear. Radical mastoidectomy, involves removal of the tympanic membrane, most middle ear structures, and closing the eustachian tube opening. Modified radical mastoidectomy preserves the ossicles and tympanic membrane remnants.
Mastoidectomy is indicated in cases of advanced disease, such as mastoid osteitis, intracranial extension, abscess formation, when cholesteatoma is involved, or if little improvement occurs after 24-48 hours of intravenous antibiotics.
Preoperative details
Preoperative preparation entails shaving the area behind the involved side (in the postaural area) a width of 3 fingers to avoid wound contamination. (See the images below.)
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Preoperative preparation of the patient.
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Draping the surgical area.
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Injection of the area with 2% Xylocaine and 1:100,000 adrenaline to reduce bleeding.
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Marking the incision site.
Intraoperative details
A postaural incision is placed a few millimeters from the postaural sulcus. In infants, the incision is placed higher and more horizontally because the mastoid process is not developed and the facial nerve is more superficial. (See the image below.)
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Placement of the incision, a few mm behind the postauricular sulcus.
The incision is deepened through the periosteum to the bone. At this stage, a subperiosteal abscess will discharge pus. Care must be taken in the upper half of the incision. The lower border of the temporalis muscle should be identified and conserved. If incising it to obtain adequate exposure is necessary, the vessels running at its lower border are first ligated or diathermied. (See the image below.)
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Deepening the incision down to the bone.
The periosteum is lifted from the underlying bone with periosteal elevators to expose the spine of Henle, the Macewen triangle, and the posterior bony margin of the meatus. In older children and adults, the tendon of the sternomastoid muscle has a wide attachment to the superficial aspect of the mastoid process; the fibers are scraped off with a periosteal elevator. (See the image below.)
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Elevation of the periosteum to expose the mastoid cortex to the mastoid tip.
The periosteum is elevated forward as far as the lateral end of the posterior bony meatal wall, backward for a few millimeters, and upward (simultaneously pushing up the temporalis muscle) to the level of the upper attachment of the pinna. A Mollison self-retaining hemostatic mastoid retractor is inserted to hold the soft tissues away from the underlying exposed bone.
The surgeon should use known visible landmarks to find the deeper landmarks. Drilling is commenced posterior to the posterior canal wall in a vertical direction. A triangle-shaped excavation is created, with the superior limit bounded by the extension of the linea temporalis (which becomes the floor of the middle fossa as one drills deeper), the posterior margin bounded by the sigmoid sinus, and the anterior margin bounded by the thinned wall of the posterior external ear canal. (See the images below.)
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Mastoid drilling in progress with simultaneous saline irrigation.
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Creation of the initial groove and the vertical line.
The mastoid cortex is now removed over the Macewen triangle (which is a rough guide to the position of the underlying mastoid antrum) using a drill fitted with a large cutting burr (5-6 mm). In adults, the antrum is encountered at a depth of 15-17 mm. If there is a deviation in the direction of drilling, the approach to the antrum can be seriously misaligned.
An ideal method to gauge the antrum is to insert an angled cell seeker beyond the posterosuperior bony meatal wall (which will be the site of the antrum) and then to drill toward it.
The antrum is usually apparent when opened by the drill. It can be confirmed by gentle anterior probing with a Dundas-Grant probe, which will slip into the aditus. Exercise care to avoid dislodging the short process of the incus. Simultaneously, the size of the aditus should be judged. If it is very small, it may be enlarged slightly with a fine bone curette to ensure adequate drainage of the middle ear.
The antral exposure is enlarged, opening adjacent cells until the lateral semicircular canal (the important landmark at this stage) can be identified. The position of middle and posterior fossa dura and the sigmoid sinus plate must be judged from the lateral oblique radiograph of the mastoid. Next, all cells in all directions are opened by drilling gently through their separating trabecula. Clearing all cells from the sinodural angle is particularly important. The smooth plate of bone covering the middle fossa dura above and lateral sinus posteriorly is recognized easily. (See the images below.)
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Exposure of the antrum and exenteration of the mastoid air cells.
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Curetting the aditus to enlarge it.
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Further exposure.
If the region is filled with necrotic mucosa, it may be safer to scoop out the material with a curette, always sweeping from the vertical position of the facial nerve as it descends just below the back of the lateral semicircular canal. Cells along the vertical portion of the facial nerve are best removed under microscope visualization with a diamond burr.
In a well-pneumatized skull, cells may extend anteriorly into the root of the zygoma and posteriorly into the occipital bone. These must also be followed as far as practicable. Consequent to mastoid clearance, a cavity is created with the antrum at the deepest point. The cavity is bounded above by the bony tegmen separating the region from the dura of the middle cranial fossa, behind by the bony plate over the sigmoid sinus, and in front by the posterior meatal wall and the aditus ad antrum.
In front of the bulge of the sigmoid sinus plate, cell removal uncovers the bone of the Trautman triangular space, protecting the dura of the posterior canal fossa and leading to the solid angle where the dense bone of the otic capsule protects the posterior semicircular canal. Anteriorly and much more superficially, cells should be opened as far as they extend into the root of the zygoma. Inferiorly, cell pursuit leads to the bone covering the digastric muscle as it passes forward, deep to the inferior part of the facial nerve at the stylomastoid foramen.
When cortical mastoidectomy is performed for proved suppurative mastoiditis, the bone over the sigmoid sinus should be sufficiently removed to allow insertion of a fine needle into that vessel to confirm that no thrombophlebitis exists within.
Closure of the wound is with interrupted sutures, and most otologists leave a soft drain in the lower part of the cavity for 1-2 days. A firm pressure dressing controls the bleeding. (See the image below.)
View Image
Healed postaural scar.
Although facial nerve monitoring is a useful adjunct, nothing substitutes for experience and attention to detail when preserving the facial nerve. Experienced otologists are unlikely to injure the ossicular chain during mastoid surgery.
Care must be taken to avoid damage to the ossicular chain. Persistent conductive hearing loss caused by tympanosclerotic plaques formed from residual bone dust can be avoided with copious irrigation at the end of the surgery.
Complications associated with mastoidectomy
Although mastoidectomy is a common surgical procedure in otology, postoperative complications of various degrees of severity may occur. Such complications include the following:
Injury to the facial nerve
Dislocation of the incus
Penetration of the middle or posterior fossa
Rupture of the sigmoid sinus
Labyrinthine transgression and destruction
Persistent deafness may be due to incus dislocation or removal. The ear dries, and the tympanic membrane heals; however, conductive deafness persists. Impedance audiometry indicates disruption of the ossicular chain. Anterior tympanotomy and reconstruction of the ossicular chain may be performed.
Persistent deafness may also be caused by persistent infection due to residual cells. Infection should resolve with proper medical treatment and good drainage. If infection persists, reopening of the mastoid and exenteration of the remaining cells is required.
If complete facial nerve paralysis is present immediately postoperatively, the facial nerve has been damaged intraoperatively. The mastoid must be reopened, and the vertical part of the nerve must be explored and, if necessary, grafted.
Meatal stenosis may ensue if the bony meatal wall has been taken down and if the skin has been dissected off the bony wall. Meatal stenosis requires excision of the stenosed area and firm packing of the canal until reepithelization occurs.
Complications reported have included brain abscess 1 week after mastoidectomy in a child and, in another child, seizures 5 days after the initial mastoidectomy and a subdural empyema that was drained during the revision surgery. Large bone defects with exposed middle cranial fossa dura were found during revision surgery in both patients, and Proteus vulgaris and methicillin-resistant S aureus were isolated from the mastoid and abscess cavities in these children.
A small epidural collection was diagnosed 2 days after initial mastoid surgery and was managed with intravenous antibiotics only.
In another reported case, sigmoid sinus thrombosis developed the day after mastoidectomy was performed for nonresponsive acute mastoiditis. This child received both intravenous antibiotics and anticoagulants. Timely revision surgery, combinations of third- or fourth-generation cephalosporins with vancomycin or metronidazole, and the addition of anticoagulants in cases of sinus thrombosis can lead to full recovery.
The principal medications used in the treatment of mastoiditis are antibiotics. Other medications include analgesics, antipyretics, and topical antibiotic-steroid combinations.
If open mastoid surgery is not undertaken, use of single, high-dose intravenous (IV) steroids is warranted to decrease mucosal swelling and promote natural drainage through the aditus ad antrum into the middle ear.
A study done by Roddy et al showed that in the post-pneumococcal vaccine era, ceftriaxone nonsusceptibility was seen in 30% of post-pneumococcal conjugate vaccine S pneumoniae isolates, compared with 7% of pre-pneumococcal conjugate vaccine isolates.[24] We can conclude that ceftriaxone alone is insufficient for empiric antimicrobial therapy in the post-pneumococcal conjugate vaccine era.
Clinical Context:
Culture and sensitivity results ultimately govern the selection of specific antibiotic agents. 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. If a Pseudomonas species is suspected, an antipseudomonal penicillin should be used.
Until microbiologic information is available, the following principles should guide antibiotic selection: (1) the antimicrobial must be appropriate to cover the most common invasive strains of bacteria in acute otitis media (AOM), (2) the selected antibiotic should cross the blood-brain barrier, and (3) the selected therapeutic spectrum should include consideration of MDRSP organisms that are prevalent in the individual's community. Coverage for anaerobic bacteria, as well as gram-negative aerobic bacteria and S aureus including methicillin-resistant S aureus, are important in chronic mastoiditis.
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.
Clinical Context:
Cefepime is a fourth-generation cephalosporin. It has gram-negative coverage comparable to that of ceftazidime but has better gram-positive coverage (comparable to that of ceftriaxone). Cefepime is a zwitter ion; it rapidly penetrates gram-negative cells. This agent is the best beta-lactam for intramuscular administration. Cefepime's poor capacity to cross the blood-brain barrier precludes the drug's use for the treatment of meningitis.
Clinical Context:
Because an increasing proportion of invasive strains of S pneumoniae are multidrug-resistant and owing to the increased role of methicillin-resistant S aureus, beginning therapy with vancomycin is appropriate. After surgical or culture and sensitivity results confirm pathogenic sensitivity to other medications, medications that do not require the same degree of monitoring may be used instead. In patients with sensitivity to vancomycin, high-dose ceftriaxone or cefotaxime may be used. Rifampin is also effective in managing MDRSP.
Clinical Context:
Ceftriaxone is a third-generation cephalosporin; it arrests bacterial growth by binding to 1 or more penicillin-binding proteins. Initiate ceftriaxone treatment with a high dose to adequately treat potential penicillin-resistant pneumococcal infection. Ceftriaxone has a broad gram-negative spectrum, lower efficacy against gram-positive organisms, and higher efficacy against resistant organisms.
Clinical Context:
Meropenem is a bactericidal, broad-spectrum carbapenem antibiotic that inhibits cell-wall synthesis. It is effective against most gram-positive and gram-negative aerobic and anaerobic bacteria. Meropenem has slightly increased activity against gram-negative organisms and slightly decreased activity against staphylococci and streptococci, compared with imipenem.
Clinical Context:
Because an increasing proportion of invasive strains of S pneumoniae are multidrug-resistant and because of the increased role of methicillin-resistant S aureus, beginning therapy with clindamycin is appropriate. This agent is a lincosamide that is effective against S aureus, aerobic streptococci (except enterococci), and anaerobic bacteria. It inhibits bacterial growth, possibly by blocking dissociation of peptidyl transfer ribonucleic acid (tRNA) from ribosomes, causing RNA-dependent protein synthesis to arrest.
Clinical Context:
This drug combination consists of an antipseudomonal penicillin plus a beta-lactamase inhibitor and is effective against aerobic and anaerobic gram-positive and gram-negative bacteria. It inhibits biosynthesis of cell-wall mucopeptide and is effective during the stage of active multiplication.
Clinical Context:
Oxacillin is a bactericidal antibiotic that inhibits cell-wall synthesis; it is used in the treatment of infections caused by penicillinase-producing staphylococci. Oxacillin may be used to initiate therapy when a staphylococcal infection is suspected. It should be employed in combination with an aminoglycoside.
Culture and sensitivity results ultimately govern the selection of specific antibiotic agents. 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. If a Pseudomonas species is suspected, an antipseudomonal penicillin should be used.
Until microbiologic information is available, the following principles should guide antibiotic selection: (1) the antimicrobial must be appropriate to cover the most common invasive strains of bacteria in acute otitis media (AOM), (2) the selected antibiotic should cross the blood-brain barrier, and (3) the selected therapeutic spectrum should include consideration of MDRSP organisms that are prevalent in the individual's community. Coverage for anaerobic bacteria, as well as gram-negative aerobic bacteria and S aureus including methicillin-resistant S aureus, are important in chronic mastoiditis.
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.
Clinical Context:
This is an antibacterial and anti-inflammatory suspension for otic use. It is used to treat superficial bacterial infections in the external auditory canal.
Clinical Context:
Tobramycin interferes with bacterial protein synthesis by binding to 30S and 50S ribosomal subunits, which results in a defective bacterial cell membrane. Dexamethasone decreases inflammation by suppressing the migration of polymorphonuclear leukocytes and reducing capillary permeability. Sterile ophthalmic drops are also commonly used for otic infections.
Clinical Context:
This is a sterile ophthalmic solution available only in Canada. It is commonly used for otic infections. Gentamicin is an aminoglycoside antibiotic used for gram-negative bacterial coverage. Betamethasone decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reducing capillary permeability.
After a tympanostomy tube is placed, with or without mastoidectomy, a pH-balanced solution or suspension of an antibiotic and a corticosteroid is useful to decrease mucosal swelling and to deliver topical antibiotics to the middle ear and mastoid. The drops should be continued until otorrhea has ceased and the view through the tube shows healing mucosa without swelling or obstruction. Several combinations are available; the best are those thin enough to apply through the tube into the middle ear.
Clinical Context:
Acetaminophen is the drug of choice for treatment of pain in patients with documented hypersensitivity to aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs) and in patients diagnosed with upper GI disease or who are taking oral anticoagulants. It reduces fever by direct action on hypothalamic heat-regulating centers, which increases dissipation of body heat via vasodilation and sweating.
What is mastoiditis?What is the pathophysiology of acute mastoiditis?What is the pathophysiology of chronic mastoiditis?What are the stages of mastoiditis disease progression?What is a possible complication of mastoiditis surgery?What is the relationship between acute otitis media (AOM) and mastoiditis?How is culture performed for the diagnosis of mastoiditis?Which lab tests are used in the workup of suspected mastoiditis?What are surgical options for the treatment of mastoiditis?What is the role of antibiotics in the treatment of acute surgical mastoiditis (ASM)?Which host factors may contribute to the etiology of mastoiditis?What age group is at highest risk for mastoiditis?Which anatomical factors increase the risk of mastoiditis?What is the role of autism in the etiology of mastoiditis?Which pathogens may increase the risk for mastoiditis?What is the most common cause of surgical mastoiditis?What is the role of Streptococcus pneumoniae in the etiology of mastoiditis?What is the incidence of surgical mastoiditis in the US?Which population is at increased risk for mastoiditis?What is the incidence of mastoiditis in European nations?How does the prevalence of acute mastoiditis vary by age?What are the possible complications of mastoiditis?What is the prognosis of acute surgical mastoiditis (ASM)?What is the likelihood of permanent conductive hearing loss in mastoiditis?Where might the infectious process of mastoiditis extend?What are intracranial complications of mastoiditis?What has reduced the incidence of otogenic meningitis in mastoiditis?What are the common complications of acute mastoiditis?How does age affect the risk of complications in acute mastoiditis?How does fever present in mastoiditis?What is the history characteristic of mastoiditis?How does pain present in mastoiditis?What should be the focus of history in infants with suspected mastoiditis?What is the mean interval from onset of illness to mastoiditis?What has caused an increase in the incidence of acute mastoiditis in infants?What is acute mastoiditis?What is the most consistent sign of acute surgical mastoiditis (ASM)?What is the role of CT scanning in the diagnosis of mastoiditis?Which findings on otoscopy are characteristic of mastoiditis?What are the symptoms of mastoiditis in adults?How is mastoiditis diagnosed?Which conditions should be included in the differential diagnoses of mastoiditis?How are catscratch disease and atypical mycobacteria differentiated from acute surgical mastoiditis (ASM)?How is lateral sinus thrombosis identified in mastoiditis?What are the differential diagnoses for Mastoiditis?How does early diagnosis of acute mastoiditis improve outcomes?What is the role of culture in the diagnosis of mastoiditis?What is the role of complete blood count (CBC) in the diagnosis of mastoiditis?What is the role of audiometry in the diagnosis of mastoiditis?What is the role of tympanocentesis in the diagnosis of mastoiditis?What is the role of myringotomy in the diagnosis of mastoiditis?What is the role of imaging in the diagnosis of mastoiditis?Which findings on CT scan are used to differentiate the type of mastoiditis?When is CT unnecessary in the diagnosis of mastoiditis?What is the role of MRI in the diagnosis of mastoiditis?What is the role of radiography in the diagnosis of mastoiditis?How effective is treatment for acute mastoiditis?Which surgical therapies are used for the treatment of mastoiditis?What are the indications for the simple mastoid operation in the treatment of mastoiditis, and what characteristics do children with acute mastoiditis who undergo surgery have in common?What are contraindications for the treatment for mastoiditis?When are antibiotics used in the treatment of mastoiditis?How are complications of acute mastoiditis without osteitis or periostitis managed?What are the treatment options for mastoiditis with osteitis?How are antibiotics selected in the treatment of acute mastoiditis with osteitis?What are the treatment options for mastoiditis that has spread?What are the treatment options for acute mastoiditis with periostitis?What are the transfer indications during treatment for mastoiditis?What is the treatment approach to mastoiditis when transfer for specialized care is not possible?Which specialist consultations are needed for the management of mastoiditis?What is included in the monitoring of mastoiditis?What is the role of antibiotics in the treatment of acute surgical mastoiditis (ASM)?What is the role of steroids in the treatment of mastoiditis?What are indications for medications in the treatment of mastoiditis?What is the role of myringotomy and tympanocentesis in the treatment of mastoiditis?How is a tympanostomy tube used in surgery for mastoiditis?What is first-line surgery for abscesses in mastoiditis?How is mastoidectomy performed for the treatment of mastoiditis?When is mastoidectomy indicated for the treatment of mastoiditis?What are the preoperative details for mastoidectomy to treat mastoiditis?Where is the incision site for mastoidectomy to treat mastoiditis?How is the mastoidectomy incision made for the treatment of mastoiditis?What is the purpose of elevating the periosteum in mastoidectomy for the treatment of mastoiditis?How is mastoidectomy drilling performed for the treatment of mastoiditis?How is the mastoid cortex removed during mastoidectomy for mastoiditis?How is the antrum gauged during mastoidectomy for the treatment of mastoiditis?What is the importance of enlarging the antral exposure during mastoidectomy for the treatment of mastoiditis?How is mastoid clearance performed during mastoidectomy for the treatment of mastoiditis?How is the absence of thrombophlebitis confirmed during mastoidectomy for the treatment of mastoiditis?How is the wound closed following mastoidectomy for mastoiditis?How is facial nerve preserved during surgery for mastoiditis?Which steps reduce the risk of conductive hearing loss following surgery for mastoiditis?What are possible complications of mastoidectomy for mastoiditis?What causes persistent deafness following mastoidectomy for mastoiditis?What are signs of facial nerve damage following mastoidectomy for mastoiditis?How is meatal stenosis managed during mastoidectomy for mastoiditis?Which are less common complications of mastoidectomy for mastoiditis have been reported in children?Which medications are used in the treatment of mastoiditis?What are the alternative treatments to mastoid surgery for mastoiditis?Which medications in the drug class Antipyretics are used in the treatment of Mastoiditis?Which medications in the drug class Antibiotics, Otic are used in the treatment of Mastoiditis?Which medications in the drug class Antibiotics/Corticosteroids, Otic are used in the treatment of Mastoiditis?Which medications in the drug class Antibiotics, Other are used in the treatment of Mastoiditis?
PP Devan, MBBS, MS, Professor and Head, Dept of ENT, A J Institute of Medical Sciences, Mangalore, India
Disclosure: Nothing to disclose.
Coauthor(s)
John D Donaldson, MD, FRCSC, FACS, Pediatric Otolaryngologist, Chief of Surgery, Galisano Children's Hospital, Lee Memorial Health System
Disclosure: Nothing to disclose.
Chief Editor
Arlen D Meyers, MD, MBA, Professor of Otolaryngology, Dentistry, and Engineering, University of Colorado School of Medicine
Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Cerescan;RxRevu;Cliexa;The Physicians Edge;Sync-n-Scale;mCharts<br/>Received income in an amount equal to or greater than $250 from: The Physicians Edge, Cliexa;Proforma;Neosoma<br/> Received stock from RxRevu; Received ownership interest from Cerescan for consulting; .
Acknowledgements
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.
Gerard J Gianoli, MD Clinical Associate Professor, Department of Otolaryngology-Head and Neck Surgery, Tulane University School of Medicine; Vice President, The Ear and Balance Institute; Chief Executive Officer, Ponchartrain Surgery Center
Gerard J Gianoli, MD is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery, American College of Surgeons, American Neurotology Society, American Otological Society, Society of University Otolaryngologists-Head and Neck Surgeons, and Triological Society
Disclosure: Vesticon, Inc. None Board membership
Alyssa K Hamman, MD Research Assistant, Division of Emergency Medicine, Stanford University
Alyssa K Hamman, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists, American Medical Association, and Colorado Medical Society
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.
John C Li, MD Private Practice in Otology and Neurotology; Medical Director, Balance Center
John C Li, MD is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery, American College of Surgeons, American Medical Association, American Neurotology Society, American Tinnitus Association, Florida Medical Association, and North American Skull Base Society
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 School of Medicine; 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.
N Ewen Wang, MD Consulting Staff, Department of Surgery, Division of Emergency Medicine, Stanford University Hospital
National Cancer Institute. Radiation Risks and Pediatric Computed Tomography (CT): A Guide for Health Care Providers. National Institutes of Health. Available at http://www.cancer.gov/cancertopics/causes/radiation/radiation-risks-pediatric-CT. Accessed: October 2, 2011.
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