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Intracranial Complications of Otitis Media
Built from Haynes-Glasscock-Shambaugh Surgery of the Ear, Seventh Edition
What’s inside
10 sections · 150 slides
Overview
- Scope of intracranial complications of otitis media
Historical perspective
- Hippocrates 460 BC: ear pain with fever feared fatal Celsus and Avicenna described frequent complications Morgagni: ear infection first, brain abscess second Lebert 1856 described brain abscess pathology Confirmed abscess follows an otologic infection
- Morand 1768: first successful operation for abscess MacEwen reported a successful operative series Korner 1908: series with a 50% recovery rate Otologic interest peaked in the 1920s Abscess stayed an otologic operation until sulfonamides
- Purulent meningitis was the most dreaded complication Most frequent cause of death from otitis media Treatment of generalized meningitis rarely succeeded Effort therefore went into prevention by early surgery Bone-invading AOM and COM operated before complication Otitis media was the commonest non-meningococcal source
- Infective lateral sinus thrombosis described in 1826 Lebert described otitic sinus thrombosis pathology 1856 Zaufal proposed an operation 1880, attempted it 1884 Lane 1889 and Ballance 1890 established the surgery Jugular vein ligation debated for decades Antibiotics settled it in favour of non-ligation
- Both spread within temporal bone to fatal intracranial disease Jansen 1895 described draining the infected labyrinth Gradenigo 1904: otorrhoea, V nerve pain, VI nerve palsy Caused by petrous apex cell infection with meningitis Kopetsky, Almour and Eagleton drained the petrous apex Petrositis vanished once antibacterials treated AOM
- 1928-1933: 1 in 40 hospital deaths from otitic complication Meningitis commonest, then sinus thrombosis, then abscess 1949-1954: only 1 in 400 deaths from otologic disease A tenfold reduction in under 20 years Lateral sinus thrombosis nearly vanished as a cause of death Meningitis persists as the commonest complication
- Pneumococcal conjugate vaccines reduced pneumococcal meningitis PCV 20 covers more serotypes; impact not yet determined H. influenzae and pneumococcal vaccines cut virulence Complications still occur despite vaccination Resistance patterns shift with antibiotic use and geography
- Complications occur despite adequate oral AOM antibiotics Cultures negative at surgery in 33-51% of series Incomplete treatment delays and alters symptom course Presentation alone cannot exclude a complication Imaging essential in acute mastoiditis Neurosurgeon may be consulted before the otologist
- Headache and otalgia in a patient with COM Fever, neck stiffness, altered mental status Such symptoms are unusual in uncomplicated COM Image with high-resolution CT and MRI Awareness of these signs lowers mortality
- Higher threshold now for aggressive surgical intervention Some advocate purely medical primary management Radical mastoidectomy no longer the default operation Canal wall up or modified radical often sufficient in COM Under-treatment remains the greater danger Sigmoid sinus and fossa dura must be exposed when needed
Factors that influence spread
- Virulence of the organism and antibiotic sensitivity Host resistance and immune status Adequacy of antibiotic therapy Anatomic pathways and bony barriers to spread Natural and surgical drainage of pneumatic spaces Complications follow uncontrolled or undertreated OM
- Bacteriology of acute and chronic otitis media
- At risk of otitis media and of its complications Atypical pathogens more likely Immunosuppressive drugs a common cause Congenital or acquired immunodeficiency also relevant Fewer objective signs of severity may be present
- Poorly pneumatized bones extend intracranially more often Previous attacks of otitis media also predispose Middle ear cleft has bony barriers against spread Barriers eroded by infection, granulation or cholesteatoma Fracture creates passages that bypass these defences
- Mastoid volume approximately 5 cc Middle ear cavity capacity approximately 0.9 cc Mastoid drains into the smaller middle ear cavity Middle ear then drains via the Eustachian tube Inadequate drainage lets infected secretions accumulate Accumulated pus erodes through and extends intracranially
- Routes of intracranial spread
- Most frequent manner of intracranial spread Nearly always the route in chronic suppurative OM In AOM caused by coalescent mastoiditis In COM usually cholesteatoma, less often osteomyelitis Erosion exposes soft tissue of neighbouring structure Protective granulations form as last line of defence
- Sequence of spread by bone erosion
- Complication weeks after AOM onset, or long-standing COM Prodrome of partial or intermittent involvement Intermittent facial weakness before complete palsy Recurrent mild vertigo before purulent labyrinthitis Meningismus before diffuse purulent meningitis At surgery: bone dehiscence with granulation over it
- Treat the complication itself Always remove the bone-eroding suppurative focus Complete mastoidectomy exenterates diseased cells Neglecting the focus risks recurrence Or a poor response to medical treatment
- Occurs in AOM or acute exacerbation of COM Normal openings: oval and round windows Internal auditory canal, cochlear aqueduct Endolymphatic duct and sac Developmental dehiscence, patent suture, hypotympanum Fracture, prior surgery, perilymph fistula, scar tract
- History of skull fracture or temporal bone surgery Previously healed otitis media or repeated meningitis Complication early in the acute infection Thus mimics extension by thrombophlebitis At surgery: dehiscence not caused by bone erosion Intracranial complication after suppurative labyrinthitis
- Treat the complication itself Close the pathway Evacuate any pus within the temporal bone Labyrinth drained when meningitis came via the IAC Done at the same time as antimicrobial therapy
- Korner 1902: spread through intact bone via venules Progressive thrombophlebitis of small venules Occurs in AOM or acute exacerbation of COM Spreads via veins contiguous with pneumatized spaces Or via a previously thrombosed dural venous sinus
- Rich venous network within the temporal bone Communicates with extracranial and diploic veins Extracranial veins accompany the arterial supply Mastoid emissary veins link the systems to sigmoid sinus Sigmoid drains superior and inferior petrosal sinuses All dural venous sinuses are interconnected
- Complication early, sometimes within a day or two Usually within the first 10 days of infection No meningismus prodrome before purulent meningitis At surgery bony walls of ear and mastoid are intact Mucoperiosteum inflamed and bleeds easily No coalescent abscess, bone not dehiscent
- Site of abscess by vascular route
Impending intracranial complication
- Persistent otorrhoea is the first warning Discharge becomes particularly foul-smelling Pus more viscous, thicker and creamier May be blood-stained Scanty discharge signals poor drainage Scanty discharge means complication is imminent
- Pain is an ominous sign of impending complication Typically deep and boring in nature Accompanied by change in quality of the pus Generalized headache may be the worst ever experienced Deep boring otalgia heralds worsening neurologic status
- High-grade fever and toxaemia Altered sensorium and irritability Photophobia Neck stiffness and generalized malaise Stiffness means organisms have reached the CSF space
- Eradication of disease Establishment of adequate drainage Thorough complete mastoidectomy for eradication All diseased air cells exenterated Pus drained wherever encountered All diseased or dead tissue removed
- AOM causing meningitis: antibiotics plus myringotomy and tube Overwhelming disease with cholesteatoma: canal wall down Goal is a disease-free ear Wide meatoplasty is equally important Permits drainage and easy inspection of the cavity
- Meningitis most common in traditional series Brain abscess and lateral sinus thrombosis next Then otitic hydrocephalus Subdural and epidural processes least common Subdural empyema is the rarest of all
Meningitis
- Inflammatory response to infection of pia-arachnoid and CSF Subarachnoid space continuous around brain and cord Also around the optic nerves So infection usually involves the whole cerebrospinal axis Localized meningitis confined next to a suppurative focus No viable organisms in the CSF in localized disease
- Most frequent complication in the preantibiotic era Antimicrobials raised recovery from 10% to 86% Recovery from otogenic meningitis was 59% Pneumococcal meningitis fatality now 8-37% Still the commonest intracranial complication of AOM AOM often predominates over COM as the cause
- S. pneumoniae a major pathogen associated with AOM Growing rate of multidrug-resistant pneumococcal strains Serotype vaccines cut pneumococcal and Hib meningitis Concern over non-vaccine pneumococci and other pathogens Anaerobes may cause more severe infection Supports broad initial coverage and obtaining cultures
- Recovery of anaerobes from CSF is a warning sign May indicate intraventricular rupture of a brain abscess Polymicrobial CSF infection from otogenic causes uncommon So mixed growth deserves a search for another focus
- Retrograde thrombophlebitis, bone erosion, preformed pathways Labyrinth via round and oval windows an important route Nager and Kaplan: perineural spaces to internal auditory canal Less frequently via the endolymphatic ducts Proctor: spread via labyrinth and petrous apex Can also follow middle ear and mastoid surgery
- Abnormal communication: subarachnoid space to air-filled ear Causes: chronic ear disease, iatrogenic, temporal bone fracture After irradiation of temporal bone tumours Spontaneous, as in idiopathic intracranial hypertension Or from a congenital malformation Repair often recommended once detected
- Hearing loss, seizures and cognitive impairment 5-35% of survivors have bilateral sensorineural hearing loss Hearing loss often associated with pneumococcal meningitis Sequelae drive the case for corticosteroids Audiological follow-up mandatory after recovery
- Paparella described three phases Acute phase: leukocyte infiltration Fibrous stage: fibrous proliferation in perilymph spaces Ossification stage follows Worst disease in basal turn near the round window Pathology same as tympanogenic labyrinthitis
- Often unrecognized as otogenic Otologic cause suspected when otorrhoea or old ear disease Must exclude otitis media even without those features Symptoms develop rapidly when associated with AOM Earliest: headache, fever, vomiting, photophobia Irritability, restlessness; seizures in infants
- Brudzinski: neck flexion causes hip and knee flexion Or leg cannot be flexed without moving the other leg Kernig: cannot extend leg with thigh flexed, supine Both are classic physical signs of meningitis Diagnostic accuracy is variable Interpret with other forms of assessment
- Obtain CT and/or MRI when a complication is suspected High-resolution temporal bone CT often the first step Typically the imaging modality of choice Bony detail best visualized with CT Rapid CT shortens scan time, useful in children Excludes congenital malformation permitting CSF leak
- CT or MRI generally advised before lumbar puncture To exclude intracranial hypertension and mass effect Aim is to prevent brain herniation Debated: imaging may delay tap and antibiotics Delay can increase mortality Selective imaging when herniation risk is high
- Better resolution of intracranial tissue Shows middle ear fluid and inflammatory brain changes Ideal for assessing intracranial complications No bone detail, so ear-bone relationship not shown Both CT and MRI often obtained together Non-contrast CT plus contrasted MRI limits contrast load
- CSF analysis and culture the diagnostic gold standard Fluid often cloudy or xanthochromic Raised white cell count, low glucose, high protein Gram stain then culture identifies the pathogen Sensitivity testing guides drug choice Sample the ear too if pus is present
- Only 44% grow if antibiotics given before culture Blood cultures advised before antibiotics Especially when lumbar puncture is delayed PCR detects bacteria days after antibiotics started PCR sensitivity 87-100%, specificity 98-100% 16S rRNA detection also highly sensitive and specific
- Third-generation cephalosporin plus vancomycin Cephalosporins bactericidal and cross the blood-brain barrier Active against beta-lactamase producers and gram negatives Low toxicity Vancomycin added for penicillin-resistant pneumococci
- Cochrane review: reduced hearing loss and neurologic sequelae Non-significant reduction in mortality overall Greater mortality reduction in S. pneumoniae infection Children: severe hearing loss 11% down to 7.3% Adults: hearing loss 21.9% down to 15.7%
- 4-day regimen of dexamethasone used in the studies 0.6 mg/kg/day divided into four daily doses This is the recommended regimen Start before or with the first dose of antibiotics Timing matters more than dose in these trials
- AOM with intact drum: myringotomy and fluid evacuation Fluid sent for examination and culture Coalescent mastoiditis: complete mastoidectomy With middle ear exploration After trauma, repair CSF leak once infection resolves CT reveals fracture line or tegmen dehiscence
- Mastoid surgery needed to make the ear disease-free And to provide adequate drainage Intact canal wall versus canal wall down case by case Critically ill patients may need a staged compromise Remove the bulk of disease now, eradicate fully later
Brain abscess
- Focal suppuration within brain parenchyma Surrounded by a region of encephalitis Bimodal age: children and the fourth decade Male to female ratio nearly 3:1 in most series Less important cause now in developed countries COM far more likely than AOM to cause abscess
- Most series: cerebrum, especially temporal lobe Majority of cerebellar abscesses are otogenic Several studies found cerebellum more frequent Abscess typically ipsilateral to the ear disease Cerebellar abscess has greater likelihood of death
- Mortality of otogenic abscess continues to decline Several series report no deaths in cerebral or cerebellar cases Permanent sequelae more common with brain abscess Hemiparesis and decreased cognitive function Dysmetria and dysarthria
- Multiple organisms often present Polymicrobial cultures with high incidence of anaerobes Streptococcus and Staphylococcus common gram positives E. coli, Proteus, Klebsiella, Pseudomonas gram negatives Host immune status shapes the microbiology H. influenzae rarely found in otogenic abscess
- Contiguous focus such as otitis media Haematogenous spread from a distant focus For example chronic pyogenic lung disease Head injury or cranial surgery An immunocompromised state
- Venous thrombophlebitis or direct dural extension Through the tegmen or posterior fossa bone Osteitis or granulation causes retrograde thrombophlebitis Dural vessels end in white matter, producing encephalitis Encephalitis progresses to necrosis and liquefaction Capsule with granulation tissue by about 2 weeks
- Well-encapsulated temporal lobe abscess on MRI
- Stages in the formation of a brain abscess
- Proinflammatory mediators damage surrounding tissue Encapsulation better defined on the cortical side Ventricular side of the capsule is thinner So abscesses rupture medially into the ventricle Rather than into the subarachnoid space Maturity depends on oxygen, organism and host immunity
- Toxic, drowsy patient with deep bony otologic pain Often prolonged otorrhoea from chronic suppurative OM Triad: headache, high fever, focal neurologic deficit Complete triad is not always present Symptoms may precede full abscess formation by 2 weeks Papilledema frequent in stage 3 of formation
- Cerebellar abscess: dizziness, ataxia, nystagmus, vomiting Temporal lobe lesions may cause seizures Signs of meningitis usually also present Nausea, vomiting, photophobia, nuchal rigidity Hearing loss commonly accompanies these signs Deficits depend on abscess location
- Earlier detection and improved outcomes Hypodense area with surrounding oedema This configuration is the ring sign Non-contrast: low attenuation, later a peripheral rim With contrast: uniform ring enhancement almost always seen
- Superior to CT for subtle parenchymal change Detects extension into subarachnoid space or ventricle T1: low signal centre, hyperintense capsule T2: high signal in areas of necrosis DWI hyperintense, low ADC from viscous pus Separate CT still needed for temporal bone detail
- Serial CT or MRI follows response to treatment Confirms resolution and times surgical intervention Some reimage every 2 weeks for new complications Others reimage at 6 weeks or if symptoms worsen Symptoms improve weeks before imaging appearance does Stop antibiotics once imaging shows resolution
- Hospitalize and start high-dose antimicrobials immediately Empiric cover: cefotaxime, ceftriaxone or ceftazidime Plus vancomycin and metronidazole Metronidazole covers the commonly found anaerobes Six-week courses typically recommended Duration guided by findings on reimaging
- Rarity prevents a standardized evidence-based algorithm Newer IV antibiotics can resolve small abscesses alone Some monitor clinical and radiological response closely Operate if no improvement, expansion, or mass effect Some report success with antibiotics plus tympanomastoidectomy Neurosurgical consultation is essential
- Aspiration versus excision of a brain abscess
Otogenic suppurative thrombophlebitis
- Venous thrombosis plus suppuration in the mastoid cavity Thrombus forms after inflammation reaches the intima Mural thrombus may propagate and occlude the lumen Septic emboli and sinus extension produce further disease Mortality fell from 100% to 0-25% over 30 years Can follow either AOM or COM
- Shift from beta-haemolytic streptococcus predominance Now S. pneumoniae, S. aureus including MRSA Enterococcus, Pseudomonas, Klebsiella, Proteus Bacteroides and other anaerobes Mixed flora common, particularly in COM Drug-resistant strains increasingly prevalent
- Mattos: culture-positive S. pneumoniae 33% in both eras Multidrug-resistant S. pneumoniae 13% before 1998 Rose to 55% between 1998 and 2013 Frequent antibiotic use yields negative operative cultures Cultures negative in 25-80% of modern series
- Pathogenesis of sigmoid sinus thrombophlebitis
- Overlying infection, granulation, perisinus abscess Or cholesteatoma incites sinus wall inflammation Direct extension through an eroded bony plate Or haematogenous spread from emissary veins Sigmoid most susceptible: adjacent to mastoid air cells
- Mural thrombus may become occlusive Retrograde spread: transverse, petrosal, sagittal, cavernous And into the vein of Labbe Distally into jugular vein and right atrium Intracranial: abscess, raised pressure, papilledema, infarct Distal: jugular foramen syndrome, lower cranial nerve palsy
- Prevalence may be elevated versus general population Elevated lipoprotein apolipoprotein levels reported Factor V Leiden mutation Antibodies against beta-2 glycoprotein and cardiolipin Some abnormalities are heritable Haematology input may guide long-term anticoagulation
- Seen where access to antibiotics is limited Rapid onset of acute otomastoiditis Otorrhoea, severe otalgia, headache, fever, leukocytosis Otorrhoea foul-smelling and blood-stained Deep boring otalgia heralds worsening neurology Picket fence fever from periodic septic emboli
- Early antibiotics mask the classic symptoms COM a more common precipitant with good access to care After AOM, otologic signs may be mild Symptoms may last over 2 weeks, even 2 months Under one third present with fever Picket fence rare; white cell count may be normal
- Neurologic features may predominate over otologic ones Headache the commonest presenting symptom in many series Diplopia from cranial nerve VI paresis Cranial nerve VII paresis and lethargy Papilledema, nausea, vomiting, photophobia, phonophobia Nuchal rigidity and ataxia from raised pressure
- Proptosis, ptosis, chemosis, ophthalmoplegia: cavernous sinus Griesinger's sign: mastoid tenderness, erythema, oedema Pathognomonic for sigmoid sinus thrombophlebitis Reflects thrombosis of mastoid emissary veins Firm, cord-like, tender neck: internal jugular thrombosis Palsy of IX, X, XI may herald jugular bulb occlusion
- CT and MRI are the current imaging tools of choice Cerebral angiography abandoned: may dislodge the clot CT shows coalescent mastoiditis and sinus plate erosion Contrast CT may show the delta sign Empty triangle: clot ringed by enhancing dura and veins Seen in up to one third of cases only
- Sigmoid sinus thrombosis on MRI and venography
- MRI more sensitive than CT for sinus thrombosis CT sensitivity 72-84% against MRI as gold standard Early thrombus: intermediate T1, low T2 signal Deoxyhaemoglobin-rich clot behaves this way Mature clot with methemoglobin: bright on T1 and T2 MRV separates slow flow from occlusive thrombus
- Historical test for lateral venous sinus thrombosis Spinal needle, manometer, record resting CSF pressure Compress each internal jugular vein, then both Positive: no rise on diseased side, prompt contralateral rise False positive when one sigmoid sinus is smaller, often left False negative with good collateral circulation
- Sinus thrombosis mandates serial imaging for progression And a search for other intracranial and extracranial disease Coexistent complication rate 80% before antibiotics Modern series still report 40% or greater Common: meningitis, epidural or intracranial abscess Also otitic hydrocephalus and jugular vein thrombosis
- Start empiric parenteral antibiotics at diagnosis Range of potential pathogens is broad Common regimen: ceftriaxone, vancomycin, metronidazole Culture-directed therapy best but often impossible Six weeks of parenteral therapy usually recommended Shorter or oral courses used by some clinicians
- Most surgeons perform urgent mastoidectomy with tube Removes thrombogenic perisinus inflammation and granulations Drains perisinus abscess Aims to prevent propagation and intracranial spread Sigmoid sinus decompressed in part or in whole Exposed sinus wall inspected and palpated
- Eroded, open sinus wall: infected clot may be debrided Rubbery clot under intact wall: some aspirate to test flow Venotomy then evacuates clot, sparing medial dural wall Routine venotomy now falls out of favour Risks: distal propagation, emboli, sinus rupture IJV ligation only for persistent sepsis or septic emboli
- Some cases managed with antibiotics and tube alone May suffice in selected patients Mastoidectomy still indicated with cholesteatoma And with coalescent mastoiditis or sigmoid bone erosion Also aggressive infection or neurologic symptoms And when other intracranial complications coexist
- Goal: expedite recanalization after surgery And prevent propagation and septic embolization Unfractionated or low molecular weight heparin used Aspirin used perioperatively by some Then continued LMWH or transition to oral warfarin Reported durations range from 3 weeks to 12 months
- Concern about haemorrhagic complications Recanalization and recovery rates similar without it Sinuses recanalize in as little as 6 weeks without it After perisinus debridement and targeted antibiotics Recanalization is not essential for clinical recovery Collateral venous circulation may matter more
- Bleeding complications in 7% or fewer treated cases May prevent propagation, embolization and sequelae Consider when clot extends beyond the sigmoid sinus Transverse, cavernous sinus or internal jugular involvement Also with neurologic change or known embolic events And with persistent fever; evidence is case series only
Otitic hydrocephalus
- Raised intracranial pressure after acute or chronic OM No meningitis, abscess or abnormal CSF composition No dilation of the ventricles occurs Better termed otitis-associated intracranial hypertension Hydrocephalus is a misnomer coined by Symonds Usually arises with sigmoid sinus thrombophlebitis
- Symonds' proposed mechanism of otitic hydrocephalus
- Precise mechanism remains unknown Attributed to reduced CSF absorption in sinus thrombophlebitis Sagittal sinus thrombus not essential after all Lateral sinus thrombosis alone may raise CSF pressure Worse when the dominant outflow tract is obstructed And when collateral circulation is inadequate
- Cerebral venous outflow patterns vary widely Collateral tracts therefore vary between individuals Adequate collaterals absorb the loss of one sinus Dominant sinus obstruction is less well tolerated Explains variable occurrence after lateral sinus thrombosis
- Onset weeks after AOM or years after COM onset Features are those of any raised intracranial pressure Headache, nausea and vomiting, drowsiness Blurred vision and diplopia Diplopia due to abducens nerve palsy Papilledema frequent; risk of permanent vision loss
- Pressure changes displace the brainstem Displacement stretches one or both abducens nerves Nerve runs from pons to Dorello's canal Long intracranial course makes it vulnerable So VI palsy is a false localizing sign
- Lumbar puncture only if imaging shows it is safe Opening pressure elevated CSF cytology and biochemistry are normal MRI with MRV is the imaging modality of choice Superior evaluation of the venous sinuses Diffuse brain oedema without ventricular dilatation
- Eradicate ear disease and lower intracranial pressure Reduce symptoms and prevent permanent visual loss Multidisciplinary: ENT, neuro-ophthalmology, neurosurgery Decompress the diseased sinus and dura surgically Remove excess granulation tissue Recovery may precede recanalization by months
- Diuretics may temporarily reduce pressure Mannitol, furosemide or acetazolamide used Serial lumbar punctures for persistent hypertension Short-term measure only Ventriculoperitoneal shunt for refractory cases Optic nerve sheath fenestration to halt visual loss
Subdural empyema and epidural abscess
- Collection of pus between dura mater and arachnoid Almost always fatal before antibiotics Now the rarest complication of otitis media Rapid deterioration is characteristic A surgical emergency once diagnosed
- Pathways to subdural empyema
- Subdural space is normally only a potential space Divided into several large compartments Boundaries: foramen magnum and tentorium cerebelli Also the base of the brain and the falx cerebri Confined spaces allow rapid evolution Empyema quickly becomes a fatal mass lesion
- Headache of abrupt onset and unusual severity Fever and vomiting accompany it Rapidity of deterioration points to the diagnosis MRI is the imaging modality of choice Superior for presence and extent of infection Distinguishes epidural from subdural infection
- Parafalcine subdural collection on CT and MRI
- Multiple discrete loculated collections may be seen No bone artefact on MRI Heightened contrast between bone, CSF and parenchyma Multiplanar imaging capability Characterizes sterile, bloody and infected collections CT cannot perform these functions
- A surgical emergency Prognosis depends on promptness of diagnosis and drainage Lumbar puncture is contraindicated It may precipitate cerebellar tonsillar herniation Emergency neurosurgical drainage is the treatment With high-dose intravenous antimicrobials
- Potential space between dura and overlying bone Usually first manifests as granulation tissue In direct continuity with the otitic suppuration At surgery granulation is commoner than frank abscess Commonest site: posterior fossa, over the sigmoid sinus A perisinus abscess; then middle fossa above tegmen
- Acute coalescent mastoiditis erodes bone Sigmoid sinus plate, Trautmann's triangle, tegmen Pocket of granulation or pus expands as bone gives way Along the sinus and the posterior and middle fossae COM granulation invades perisinus and tegmen cells Acute exacerbation can convert silent granulation to abscess
- May present with fever, otalgia, low-grade headache Often clinically silent Rarely symptomatic unless large May be an incidental finding at surgery for another problem Usually visible on modern preoperative imaging Absence of localizing signs is why imaging is needed
- Thin-cut temporal bone CT best shows bone erosion Of tegmen, sigmoid plate or posterior fossa plate Contrast CT may show dural enhancement Larger abscess: rim-enhancing lentiform low-density collection Gadolinium MRI more sensitive for dural enhancement T1 signal between CSF and white matter
- Temporal lobe abscess with inferior epidural abscess
- Granulation over sinus or fossa bone prompts exploration Remove surrounding bone until normal dura is seen Drain the abscess through the mastoidectomy Scrape or trim granulation parallel to the dural plane Do not perforate dura: risks CSF leak and brain infection Craniotomy unnecessary for most otogenic epidural abscess
- All patients receive culture-directed antibiotics Most cases still managed surgically Small abscesses reported to resolve with IV antibiotics With tympanostomy tube placement alone Others resolved after cortical mastoidectomy Without dural manipulation or abscess drainage
Summary
- Recognizing an intracranial complication
- Three routes: erosion, preformed pathway, thrombophlebitis Bone erosion is late; thrombophlebitis is early Intact bone at surgery does not exclude spread Always remove the temporal bone focus of suppuration Close any preformed pathway or CSF leak Wide meatoplasty completes the drainage
- Empiric cover: cephalosporin, vancomycin, metronidazole Metronidazole for anaerobes in abscess and sinus disease Dexamethasone 0.6 mg/kg/day for 4 days in meningitis Give it before or with the first antibiotic dose Roughly 6 weeks of parenteral therapy for abscess Anticoagulation remains selective and evidence-poor
- Complications are rarer but not eliminated Patients are often critically ill Significant morbidity and mortality persist Suspect when ear infection meets neurologic symptoms Or when symptoms plateau after initial improvement Close follow-up ensures complete disease resolution
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- Haynes-Glasscock-Shambaugh Surgery of the Ear, Seventh Edition
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