In the era of medicine prior to the development of antibiotics, acute otitis media (AOM) frequently led to both intratemporal and intracranial complications. In a series spanning the years 1928 to 1933, just prior to the introduction of antibiotic therapy, 1 in 40 deaths in a general hospital was the result of otitic intracranial complications.1 In other series, the incidence of intracranial complications during the pre-antibiotic era ranged from 2.3% to 6.4%, with a mortality rate of 76.4% in affected patients in the latter series.2-3
The introduction of antibiotic therapy and surgical procedures to prevent and treat intracranial complications of AOM has resulted in a decrease in the complication rate to 0.04% to 0.15%.4 Although this complication rate has dropped dramatically, mortality rates, when complications do occur, have remained high (10% to 31%}.5 In a review of 24,321 patients from 1978 to 1990, the incidence of intracranial complications was 0.36% with an associated mortality rate of 18.4%.6
It has been suggested that the emergence of multidrug-resistant strains of Streptococcus pneumoniae in the past few years could initiate an increase in suppurative complications of otitis media. A recent study at the Children's Hospital of Pittsburgh, however, found that rates of resistant S. pneumoniae from patients with acute mastoiditis did not exceed the rate of such organisms in the hospital, in general, suggesting that complications, such as acute mastoiditis, were not occurring as a result of resistant organisms.7 Of particular interest is that treatment failures of other otitic pathogens such as β;-lactamase-positive Haemophilus influenzae and Moraxella catarrhalis have been rarely associated with systemic infection and complications.8
Children are more likely to have complications from AOM, whereas adults are more likely to have these complications as the result of chronic ear disease, especially cholesteatoma.9 The risk of suppurative complications of AOM in cases in which antibiotics are withheld remains unknown.10
The development of intratemporal and intracranial complications of otitis media is thought to occur by one of three mechanisms: (1) direct extension of infection through bone weakened by osteomyelitis or cholesteatoma; (2) retrograde spread of infection by thrombophlebitis; or (3) extension of infection along preformed pathways, such as the round or oval windows or through dehiscentes that are the result of congenital malformations.
EVALUATION OF THE PATIENT
Important symptoms suggesting an intratemporal or intracranial complication include otorrhea, otalgia, hearing loss, vertigo, emesis, nuchal rigidity, or other specific neurologic symptoms such as facial paralysis. Although some of these symptoms (eg, vertigo, nuchal rigidity, or facial paralysis) are found in AOM rarely, their appearance should make one highly suspicious of a potential complication. Albers has suggested that the most common early symptoms of an impending complication include headache and fever.9 In the Children's Hospital of Pittsburgh study, 37% of patients who had intratemporal complications had symptoms lasting 5 days or longer. Of interest, 86.5% of these had recently been treated with oral antibiotics.7
Physical examination of the child with a suspected complication begins with inspection of the external ear to exclude erythema or swelling of the postauricular region from mastoiditis. Examination of the external canal and the tympanic membrane (TM) should be performed with an otoscope or operating microscope.
Many complications are associated with evidence of acute middle ear infection. With coalescent mastoiditis, there may be a small TM perforation that is not readily visible due to the large amount of mucopurulent drainage in the external canal. Patients with complications from chronic otitis media with cholesteatoma may have sagging of the posterior external canal. A deep retraction pocket in the TM also suggests a cholesteatoma. A child with a perforation of the TM accompanied by chronic drainage should generally be referred to an otolaryngologist for otomicroscopy to exclude a cholesteatoma. There, drainage should be suctioned and the middle ear examined through the perforation, looking for squamous debris. Of interest is that results of the examination of the TM were normal in 26% of complication cases in one series, so a normal TM does not exclude a complication.9
Although an audiologic assessment should be a part of the evaluation of any child with hearing loss, a history of frequent otitis media, or a suspected complication, the evaluation may not be possible in a patient with a severe intracranial complication. Depending on the child's age and the complication, more sophisticated testing such as brainstem audiometry or electronystagmography may be necessary.
Radiography is essential in any child with a suspected intratemporal or intracranial complication. For many years, plain radiography was the examination of choice for acute and chronic ear disease. Plain films have long since been replaced by computed tomography of the temporal bone and brain in these complications. Axial and coronal 1-mm sections of the temporal bone demonstrate details of the mesotympanum, the attic and the antrum of the mastoid, the facial canal, and the cochleovestibular apparatus. Computed tomography examination of the brain with contrast is mandatory for suspected intracranial complications.
Magnetic resonance imaging is not helpful in evaluating the fine bony detail of the middle ear and the mastoid, but it may reveal abnormalities in the soft tissue detail of the brain. When combined with contrast, magnetic resonance imaging may also be useful in determining flow within the vascular structures of the head and the neck (eg, the sigmoid sinus).
INTRATEMPORAL COMPLICATIONS OF OTITIS MEDIA
Conductive, sensorineural, or mixed hearing loss may be seen in patients with otitis media. Conductive hearing loss that results from otitis media ranges from 15 to 40 dB. The magnitude of this hearing loss appears to be the result of the quantity, rather than the quality, of the fluid11 and it typically disappears when the middle ear effusion (MEE) has resolved. High negative middle ear pressure from eustachian tube dysfunction can also cause a mild conductive hearing loss. Fluid of long-standing duration may lead to permanent conductive hearing loss due to adhesive otitis media with or without erosion of the ossicular chain.
Infectious or inflammatory mediators in the middle ear may enter the cochlea through either the round window or other bony defect and also cause a sensorineural hearing loss. Direct spread of infection into tine labyrinth with resultant suppurative Iabyrinthitis may cause a severe to profound sensorineural hearing loss of greater than 40 dB.
Effects of Otitis Media on Development
Several studies have demonstrated a conductive hearing loss of at least 15 dB in 30% to 40% of patients and of at least 30 dB in 25% of cases during either AOM or otitis media with effusion (OME).12-13 The long-term effects of such conductive hearing losses remain unknown. Bluestone and Klein have summarized multiple studies that suggest a correlation between recurrent episodes of otitis media at an early age and lower test results in speech and language.11 Other studies have failed to confirm such correlation.14,15
The effects of a severe or profound hearing loss on speech development are well documented. Less is known about the impact of mild or fluctuating hearing.11-16 Children with the greatest risk for expressive speech delays early in life, and perhaps behavioral or academic problems later in life, are those with chronic otitis media combined with other risk factors/ such as a low sodoeconomic status, day care attendance, bottle feeding, and passive exposure to smoke.17
TM perforation may occur from (1) an episode of AOM, (2) extrusion of a tympanostomy tube, (3) an acute traumatic perforation, or (4) long-standing atelectasis of the TM. A perforation is diagnosed by pneumatic otoscopy or otomicroscopy. In equivocal cases, it may be confirmed with tympanometry: excessive static compliance indicates a large volume that confirms the presence of a perforation. Of interest is that otorrhea may or may not be present with a perforation. Depending on the size and location of the perforation, audiologic assessment will show a hearing loss ranging from O to 40 to 50 dB.
The issue is not whether to dose the perforation, but when. Tympanoplasty in children has good results in experienced hands.18 The status of the other ear with an intact TM may or may not be helpful in determining when to close a perforation.19 A chronic perforation does provide middle ear ventilation, and some experts feel that a perforation should not be closed if the other ear has evidence of otitis media. On the other hand, some advocate closure of the perforation in children with a history of recurrent drainage through the perforation. Establishing the air cushion provided by the mastoid air-cell system may prevent the reflux of nasopharyngeal secretions into the middle ear.11 There is no evidence that an adenoidectomy with or without a tonsillectomy is useful in the management of a chronic perforation.11
Chronic Suppurative Otitis Media
Chronic suppurative otitis media is defined as chronic drainage from the middle ear and the mastoid through either a perforation or a tympanostomy tube. This otorrhea is the result of chronic inflammation and infection of the middle ear and mastoid that may be due to reflux of secretions from the nasopharynx or the direct contamination of the middle ear through a chronic perforation. Patients with this diagnosis have no evidence of cholesteatoma, although a cholesteatoma should always be suspected if an ear has chronic drainage.
The diagnosis of chronic suppurative otitis media is made by a history of purulent, mucoid, or serous otorrhea through a central perforation or a tube for 2 to 3 months or longer.11 Patients usually do not complain of pain, fever, or vertigo. If they do, another complication should be suspected. Physical examination should include otomicroscopic examination. Suctioning of secretions should be done to allow a more thorough evaluation of the TM and to collect specimens for culture. Audiologic assessment typically demonstrates a conductive hearing loss of 20 to 40 dB, although this depends on the amount of drainage and the size of the perforation. Computed tomography is essential to delineate the condition of the mastoid air-cell system and to exclude cholesteatoma.
Children suspected of having chronic suppurative otitis media should be referred to an otolaryngologist. The management begins with oral antibiotics and topical otomicrobials. If there is no improvement, intravenous antibiotics should be considered after a culture with sensitivities is performed. Treatment includes frequent suctioning of debris and drainage from the ear prior to each instillation of topical otomicrobials. If the ear becomes dry, prophylactic antibiotics should be considered in the young child with a tympanostomy tube. If the ear fails to become dry, consideration should be given to intact canal wall tynv panomastoidectomy with removal of infected mucus membrane, granulation tissue, and infected bone.20 If there is no response to short-term intravenous antibiotics or surgery, the child should be treated for osteomyelitis of the temporal bone with a prolonged course of intravenous antibiotics (ie, 6 weeks).11
Figure 1 . Tympanoscferosis typically appears as an irregular whitish plaque in the tympanic membrane and moves with pneumatic otoscopy.
Cholesterol granuloma, also known as the "blue drum syndrome," is the sequela of chronic MEE. It has also been labeled idiopathic hemotympanum because the bluish appearance of the TM looks like there is blood in the middle ear. In actuality, the middle ear is filled with granulation and cholesterol crystals. Cholesterol granuloma is often difficult to distinguish by appearance from the more common hemotympanum that may be the result of either trauma or the accumulation of hemorrhagic fluid in the middle ear cavity.
The diagnosis of cholesterol granuloma is made by otomicroscopy. As with other chronic middle ear conditions, computed tomography is essential to exclude cholesteatoma. Both computed tomography and magnetic resonance imaging may be necessary to differentiate a cholesterol granuloma of the petrous apex from a congenital cholesteatoma of the same region. Other causes of a bluish TM include a high-riding jugular bulb, a glomus rumor, or an aberrant carotid artery. Treatment typically includes intact canal wall tympanomastoid surgery and placement of a tympanostomy tube.
The exact pathogenesis of tympanosclerosis remains unclear, but is thought to be hyalinization of the TM secondary to inflammation, trauma, or both.11 It is seen commonly in children with a history of AOM or OME, and following myringotomy or myringotomy with tube placement. Most cases are asymptomatic. In extensive cases, there may be a conductive hearing loss due to decreased elasticity of the TM or decreased mobility of the ossicular chain. Tympanosclerosis has been reported to occur in 5% to 7% of all children by the age of 6 years.21
The diagnosis is made by pneumatic otoscopy or otomicroscopy (Fig. 1). The central TM is usually more affected than the periphery.4 The major concern is to exclude a cholesteatoma behind an intact TM. In most cases, pneumatic otoscopy will provide reassurance by confirming that the tympanosclerotic plaque moves with the remainder of the TM. In cases where there is still doubt, referral to an otolaryngologist is suggested. The use of computed tomography may also be helpful.
Most cases of tympanosclerosis do not affect hearing and so do not require any treatment. The best treatment is the prevention of persistent fluid or recurrent episodes of AOM. Reconstruction of the ossicular chain or TM may be necessary in those severe cases with a significant conductive hearing loss.
Cholesteatoma is the presence of keratinizing squamous epithelium in the middle ear or pneumatized portion of the mastoid. Several mechanisms account for their development. A primary acquired cholesteatoma occurs when a deep retraction pocket (Fig. 2) forms secondary to persistent negative middle ear pressure from eustachian tube dysfunction (keratin accumulating in the pocket eventually forms an epitheliallined cyst). A secondary acquired cholesteatoma is caused by squamous ingrowth into the middle ear through a perforation of the TM.
Figure 2. A retraction pocket of the tympanic membrane may signify a developing cholesteatoma.
The diagnosis is made by careful pneumatic otoscopy or otomicroscopy (Fig. 3). Secretions or debris should be carefully suctioned so that the entire TM may be carefully inspected for the presence of a retraction pocket or perforation. Referral to an otolaryngologist and computed tomography are essential in any suspected case of cholesteatoma.
Prevention is the key to the initial management. Treatment of long-standing fluid with tympanostomy tubes prevents the development of retraction pockets that may ultimately form a primary acquired cholesteatoma. Deep retraction pockets not responsive to conservative treatment with ventilation may necessitate excision of the affected portion of the TM and tympanoplastic repair. The management of cholesteatoma is complicated and a function of its location and extent. Options range from middle ear exploration with excision of disease to mastoidectomy. A specific controversy in pediatrie otology is the use of intact wall tympanomastoidectomy versus an open cavity (radical or modified radical) mastoidectomy.
Figure 3. A small cholesteatoma (pearl) behind an intact tympanic membrane.
Patients with AOM routinely have involvement of the mastoid because of the direct connection between the middle ear and the mastoid. Acute mastoiditis is said to have developed when there is destruction of bone or formation of a subperiosteal abscess. The spread of infection from the middle ear into the mastoid can follow one or more routes: (1) laterally into the retroauricular soft tissues, with displacement of the pinna and blunting of the retroauricular sulcus; (2) anteriorly into the external auditory canal, causing sagging of the canalwall skin; (3) posteriorly into the sigmoid sinus; (4) medially into the vestibular labyrinth or petrous apex; (5) superiorly into the middle cranial fossa, forming an epidural abscess; or (6) inferior medially into the mastoid tip, forming a Bezold's abscess. Coalescent mastoiditis develops when the normal bony structures of the mastoid antrum are destroyed by the infectious process.
Acute mastoiditis presents with fever and postauricular erythema and swelling plus other common symptoms of AOM, including hearing loss and otalgia. Coalescent mastoiditis takes days to weeks to develop and is associated with postauricular swelling and erythema, pain, and otorrhea in some cases (Fig. 4). The TM may have a range of findings from AOM to those of OME. The diagnosis of acute mastoiditis is confirmed by computed tomography of the temporal bone. One should look for changes in the normal bony architecture (ie, loss of the bony septae within the mastoid; Figs. 5 and 6).
Figure 4. An example of postauricular swelling and erythema seen in a child with acute mastoiditis. Note the blunting of the retroauricular sulcus.
Figure 5. Computed tomography of the temporal bone (coronal section) illustrates fluid in the middle ear and the mastoid in a patient with acute mastoiditis. The external canal is also opacffied because of the large amount of otorrhea.
Figure 6. Computed tomography of the temporal bone (axial section) in a patient with acute coalescent mastoiditis. Note the toss of bony septae within the mastoid, a classic finding.
Uncomplicated acute mastoiditis with minimal bone destruction and pus collection may be managed successfully with just intravenous antibiotics and wide-field myringotomy to decompress the middle ear and provide a specimen for culture. Instead of wide-field myringotomy, a tympanostomy tube may be placed to provide long-term ventilation. A mastoidectomy is necessary when there is (1) significant bone destruction, (2) a poor response to intravenous antibiotic therapy, or (3) an impending intracranial complication. The goals of mastoid surgery are to drain the pus, obtain cultures, and remove infected bone.
Petrositis results from extension of mastoiditis into the petrous portion of the temporal bone. This complication occurs only in those individuals with a pneumatized petrous apex, or approximately 30% of the population.11 Obstruction of the normal drainage of the petrous apex may result in an acute coalescent process, and a higher incidence of intracranial complications.
Symptoms and signs of petrositis include a classic triad (Gradenigo syndrome): (1) retrobulbar pain, (2) persistent otorrhea, and (3) ipsilateral abducens nerve palsy. The diagnosis of petrositis is confirmed by computed tomography.
Treatment includes surgical drainage of the petrous apex, intravenous antibiotics, and placement of a tympanostomy tube. In at least one series, affected children treated with intravenous antibiotics and a conservative mastoidectomy (without drainage of the petrous apex) had resolution of their infections.7
Labyrinthitis that results from bacterial infection of the temporal bone occurs in two forms: serous or suppurative. In serous labyrinthitis, bacterial toxins from a middle ear infection spread into the labyrinth. A mixed hearing loss may result - die conductive component from the otitis media and the sensorineural component from invasion of the labyrinth by bacterial toxins. With suppurative Iabyrinthitis, there is actual bacterial invasion either through the round window or around the annular ligament of the oval window. Another route spreads from a meningitis into the cochleovestibular apparatus.
Serous Iabyrinthitis presents with vestibular symptoms. The physical examination identifies either AOM or OME; spontaneous, constant horizontal nystagmus with past pointing; and a variable mixed hearing loss. Suppurative Iabyrinthitis presents with the same or perhaps more severe vestibular symptoms and sensorineural hearing loss.
Management is directed at the underlying infection. Intravenous antibiotics are necessary, and surgical therapy ranges from myringotomy to mastoidectomy, depending on the extent of disease. Actual surgical drainage of the labyrinth may be required in cases of suppurative Iabyrinthitis that respond poorly to conservative therapy.
Facial Naive Paralysis
The exact mechanism by which the facial nerve becomes paralyzed as a complication of otitis media remains unknown, but this is thought to occur by either a direct inflammatory effect, exposure to toxins, or ischemia.22 Rarely, facial nerve paralysis may result from direct compression of the nerve by a cholesteatoma. The incidence of facial paralysis secondary to AOM in the preantibiotic era has been reported as 1.20Xo.22 In the antibiotic era, the incidence in adults ranges between 0.1% and D.2%.22'23 In view of how common AOM is in the pediatrie population and how rarely facial paralysis is seen, the incidence may be less in children.
Similar to other complications of otitis media, the evaluation of the child with a facial paralysis begins with a careful examination of the ear with either an otoscope or an otomicroscope. One should look for evidence of AOM or cholesteatoma. Computed tomography is essential to confirm the extent of disease and identify other pathology such as a cholesteatoma or neoplasm as the cause of the facial paralysis. Electrical testing of the nerve is usually not necessary unless function of the nerve fails to return.
Management begins with aggressive treatment of the middle ear disease with intravenous antibiotics and wide-field myringotomy. Placement of a tympanostomy tube for more chronic ventilation is also an option, especially if there is recurrent or chronic ear disease.24 Mastoidectomy or facial nerve decompression remains controversial, but is not necessary in most cases.7 When facial nerve paralysis is secondary to a cholesteatoma, treatment should include intravenous antibiotics and surgical management of the cholesteatoma.
INTRACRANIAL COMPLICATIONS OF OTITIS MEDIA
Bacterial meningitis is the most common intracranial complication of AOM. It develops by (1) hematogenous spread from either a generalized bacteremia or a retrograde thrombophlebitis, (2) direct spread from die middle ear to the meninges through bony dehiscences or preformed pathways, or (3) spread from the inner ear through either the round window or other routes in children with a history of trauma or congenital malformations. Organisms responsible for bacterial meningitis include those associated with otitis media, more commonly (S. pneumoniae) or less commonly (S. pyogenes and H. influenzae type B).25
Antibiotic coverage can be tailored pending results of the cerebrospinal fluid culture and sensitivity. Treatment of an otitic meningitis may include wide-field myringotomy or placement of a tympanostomy tube. Rare cases caused by cholesteatoma may also receive a mastoidectomy. Even in the antibiotic era, the mortality rate from meningitis remains significant - 7% in 58 patients described by Gower et al.26 The use of dexamethasone early in the course of treatment to prevent hearing loss or other neurologic sequelae remains controversial.27
An epidural abscess usually destroys the bone adjacent to the dura. Frank pus or granulation tissue may then accumulate in the potential space between the dura and the bone. An epidural abscess is usually due to chronic infection with or without cholesteatoma and may be found incidentally at the time of mastoid surgery. The mechanisms of this complication appear to be either retrograde thrombophlebitis or direct spread of infection through preformed pathways.
Figure 7. Computed tomography of the brain with contrast (axial section) demonstrates an epidural abscess, with a hypodense region surrounded with ring enhancement. There is no evidence of a mass effect.
The symptoms of an epidural abscess are often low grade and include otalgia or headache over the involved region. ??, the patient may be totally asymptomatic with the abscess discovered as an incidental finding during a mastoidectomy. In most cases, the diagnosis of an epidural abscess is made by computed tomography or magnetic resonance imaging (Fig. 7). Results of lumbar puncture in affected patients are usually normal, and an epidural abscess rarely produces a mass effect.4
Treatment consists of surgical drainage of the abscess into the mastoid cavity and removal of any granulation. Management of mis intracranial complication should also include treatment of the underlying ear disease, such as removal or exteriorization of a cholesteatoma.
A subdural empyema is a collection of pus in the subdural space from either direct extension of infection or retrograde thrombophlebitis. Fortunately, this is a rare complication of AOM in developed countries, because it carries a mortality rate of 13% to 55%.28<29 The presenting signs and symptoms include headache, seizures, and an altered state of consciousness. The child usually appears toxic. The diagnosis is made by contrast-enhanced computed tomography or magnetic resonance imaging. Treatment includes intravenous antibiotics and neurosurgical drainage. Corticosteroids may be employed to reduce brain swelling, and anticonvulsant therapy may also be required. After the patient's condition has stabilized, the underlying ear disease should be treated.
Similar to the other intracranial complications, the incidence of otitis brain abscess has decreased dramatically since the advent of antibiotic therapy.1 The mechanism of spread is thought to be either hematogenous from a distant source or direct extension through the mastoid or internal auditory canal. An epidural abscess may develop up to a month after an episode of AOM, and the temporal lobe is usually involved more than the cerebellar region.4 A large abscess may rupture into the lateral ventricle, resulting in a fulminant meningitis.
The signs and symptoms of a brain abscess are a reflection of the mass effect of the abscess and infection of the surrounding brain tissue (cerebritis). They include fever, headache, nausea, vomiting, irritability, and malaise. Occasionally, mere may be seizures and signs of increased intracranial pressure, such as papilledema or a bulging fontanelle in an infant. Contrast-enhanced computed tomography demonstrates a hypodense region with ring enhancement within the brain parenchyma. If the intracranial pressure is markedly elevated, a lumbar puncture may be contraindicated because of the risk of herniation.
Initial treatment includes intravenous antibiotics, typically a third-generation cephalosporin, plus either penicillin, vancomycin, or metronidazole, pending the results of culture.30'31 High-dose intravenous steroids may be used to reduce cerebral edema. Although small abscesses may be treated conservatively with medical management alone, most require neurosurgical drainage or excision. Mortality rates in recent series range from 0% to 20%.27 As with other otitic complications, the underlying ear disease should be treated when the patient's condition has stabilized.
Otitic hydrocephalus is increased cerebrospinal fluid pressure in the absence of a mass effect associated with AOM. Obstruction of one or more of the venous sinuses, typically the sigmoid sinus, results in decreased absorption of cerebrospinal fluid and hydrocephalus. This otitic complication usually occurs several weeks following an episode of AOM.
Otitic hydrocephalus is a complication of older children and adolescents. The symptoms and signs include headache, drowsiness, nausea, vomiting, papilledema, and an ipsilateral abducens palsy. Computed tomography is the first step, to exclude a mass effect. The diagnosis is made by an elevated cerebrospinal fluid pressure on lumbar puncture with fluid that is otherwise normal.
The treatment of increased cerebrospinal fluid pressure may include drainage by repeated lumbar punctures, placement of a lumbar drain, or medical treatment with diuretics, typically acetazolamide. The underlying ear disease should also be treated.
Lateral Sinus Thrombosis
Lateral sinus thrombosis results from the direct extension of a mastoid infection into the lateral venous sinus. A coalescent mastoiditis or infected cholesteatoma may cause thrombosis of small venules that then propagate into the sigmoid sinus. Granulation tissue overlying the sigmoid sinus may cause inflammation and subsequent thrombus formation within the sinus. In the pre-antibiotic era, lateral sinus thrombosis was the second most common cause of otitic death, exceeded only by meningitis.31
The symptoms and signs of a lateral sinus thrombosis include spiking fevers ("picket fence fevers"), headache, malaise, and signs of increased intracranial pressure. There may be a positive Griesinger's sign - edema over the posterior mastoid secondary to thrombosis of the mastoid emissary vein. There may be a progressive anemia as well. The diagnosis is confirmed by magnetic resonance angiography that reveals flow voids and thrombus formation within the sigmoid sinus.
The initial medical treatment of lateral sinus thrombosis is broad-spectrum intravenous antibiotics. Surgical treatment should include drainage of the mastoid with exploration of the dura overlying the sigmoid sinus and posterior fossa.
Treatment of the thrombus within the sinus remains controversial.31 Some authors recommend removal of the thrombus. However, most believe that intravenous antibiotics and surgical debridement of the mastoid are sufficient. Thrombus removal should be considered in cases of increased intracranial pressure that fail to improve. A thrombolytic agent delivered by interventional radiology can be used to dissolve the dot. The other method of clot removal is by surgical exploration following aspiration of the sinus to confirm the absence of blood flow. After evacuation of the dot, the sinus is packed.
Rarely, in the face of septic thrombophlebitis unresponsive to medical management, ligation of the internal jugular vein may be necessary. Likewise, anticoagulation is also not typically required because the sigmoid sinus usually recanalizes with time. Repeat magnetic resonance angiography studies may be required to confirm return of blood flow within the sinus.
Although otitis media remains common in pediatrie patients, complications have fortunately become rare in the antibiotic era. Due to attempts to limit antibiotics because of an increased incidence of resistant pathogens in the past decade, the clinician should remain vigilant for the development of such complications. Failure of a child with otitis media to respond to appropriate medical therapy should alert the clinician to a possible impending complication. Likewise, children with suspected intratemporal complications should be promptly referred to an otolaryngologist.
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