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Central Nervous SystemInfections
Clinical Aspects
I m r a n I Al i M .D .
P r o f e s sor of N eu r o l ogyUn i ve rs it
y of T o l edoC o ll ege of M ed i c i ne
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CNS Infections
Objectives Describe the epidemiology/ pathogenesis/
microbiology/ clinical presentation/diagnosis/ basic treatment of common CNS infections
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CNS Infections
Brain Acute Bacterial
Meningitis S. Pneumoniae Subdural Empyema Brain abscess
Viral Meningitis Viral Encephalitis
HSE
HIV
Spinal Cord Epidural Abscess
Viral myelitis
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CNS Anatomy
To understand central nervous systeminfections - pathogenesis, presentations - it isnecessary to recall the basics of CNS anatomy brain and spinal cord are surrounded by the
leptomeninges (pia mater and arachnoid)
pia mater is continuous and tightlyadherent to the brain
arachnoid encloses parenchyma and piamater loosely
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CNS Anatomy
Cerebral spinal fluid (CSF) - located in thespace between the pia mater and thearachnoid mater (a.k.a. - the subarachnoidspace) secretion of CSF mostly by cells in the
choroid plexus (in the lateral, 3rd, 4thventricle)
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CNS Anatomy
CSF Composition: derived from blood plasma
Small amount of protein ( 50% serum), less specific gravity, and
more chloride (n-118-132) than blood plasma Total amount is 140-150 cc on average Opening pressure is approximately 8-16 cm water
(80-160 mm), > 20 cm water is abnormal!
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CNS Anatomy
Dura mater Adherent to the periosteum and skull
except for four rigid septa falx cerebri, falx cerebelli, tentorium
cerebelli, diaphragma selli Brain sits on the cranial fossa
Anterior fossa is actually the roof of thefrontal and ethmoid sinuses
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CNS Anatomy
Blood -Brain barrier Capillaries in the CNS have tight
junctions (no fenestrations in general)
and are surrounded by the foot processesof nearby astrocytes this forms the relatively impermeable
blood brain barrier Blood brain barrier does not generally
allow large molecules to enter CNS by
diffusion
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CNS Infections
CNS is well protected- difficult for organisms to penetrate into brain (also
difficult for
good
things like antibiotics,complement, and antibodies as well)
CNS is a tightly enclosed space and so even
very small amounts of organisms causinginflammation (edema) can have devastatingconsequences
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CNS Infections
CNS infections are grouped by anatomicallocation Encephalitis - infection of brain
parenchyma Meningitis - infection of leptomeninges
Myelitis - infection of spinal cord tissue Neuritis - infection of peripheral nerves Organisms enter CNS via bloodstream,
neuronal pathways, or direct inoculation
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Acute Bacterial Meningitis
Meningitis - inflammation of the meninges if the brain parenchyma is also involved, it is
called meningoencephalitis if brain and spinal cord tissue are also
involved, it is meningoencephalomyelitis
Acute bacterial meningitis infection of meninges due to bacteria with
clinical presentation within 24 - 48 hours
sine qua non is CSF leukocytosis
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Acute Bacterial Meningitis
Epidemiology and Etiology 3 cases per 100,000 in US rate is over 15x higher in underdeveloped
countries epidemics are also common in addition
to the high endemic rate Common organisms are S. pneumoniae,
N. meningitidis, H. influenzae, L.
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Acute Bacterial Meningitis
0 - 4 week s : Group B streptococcus ( S.agalactiae ), E. coli, L. monocytogenes
< 18 y / o : H. flu (type b greatly decreased,other strains increasing), N. meningitidis, S
pneumoniae
18 - 50 y / o : N. meningitidis, S pneumoniae >50 y / o : N. meningitidis, S pneumoniae , L.
monocytogenes, GNR
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Epidemiology of ABM
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Risk Factors in the Elderly
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Acute Bacterial Meningitis
H. influenza Type b vaccine has greatly decreased the rate
of H. flu meningitis but invasive disease due toother encapsulated strains such as type f areincreasing
In patients >5 yo, meningitis may be associatedwith sinusitis, otitis, epiglottitis, pneumonia
Predisposing conditions: DM, alcoholism,
asplenia, CSF leak, hypogammaglobulinemia
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Acute Bacterial Meningitis
N. meningiditis Serotypes A,B,C, W135, and Y
commonly associated with meningitis Serotype B causes >50% of infections Vaccine is active against A, C, W135,
and Y Terminal complement deficiencies are
associated with increase in attack rate anddecrease in fatality rate
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associated with meningitis
Acute Bacterial Meningitis
S. pneumoniae # 1 cause of meningitis in 18 - 50 yo often associated with URI/LRTI or
endocarditis predisposing conditions: DM, alcoholism,
asplenia, CSF leak,hypogammaglobulinemia
vaccine covers most common serotypes
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Acute Bacterial Meningitis
L. monocytogenes Causes 2 - 3% of cases of meningitis but is
seen in neonates, pregnant women, elderly,immunocompromised
Ce ph a losporin s a r e no t ac tiv e a g a ins t L ist e riaa nd v a n c o m y c i n i s not r e li a bl y e ff ec tive
Ampicillin or Trimethoprim-sulfa aretreatments of choice
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ACUTE BACTERIAL MENINGITIS
Consider in patients with fever and any neurologic symptoms/cerebral dysfunctionTypical presentation-headache, fever, lethargy, confusion,vomiting, stiff neck - but presentation may be variable< 80% nuchal rigidity, Kernig
s or Brudzinski
s signsPapilledema:
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Acute Bacterial Meningitis
Kernigs
s sign patient lies supine with thigh
and knee flexed leg is passively extended and
this is resisted with meningealinflammation
Brudzinski
s sign passive flexion of the neck
causes passive flexion of pelvis/hips
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Acute Bacterial Meningitis
CID July 2002 :35; 46-52. Thomas, et al. Thediagnostic accuracy of Kernig
s sign, Brudzinski
s sign, and Nuchal Rigidity in Adults with suspected meningitis. Prospective study of meningeal signs prior to LP
Kernig
s sign and Brudzinski
s sign - sensitivity 5%:
positive predictive value - 27% nuchal rigidity - sensitivity 30%: positive predictive
value - 26%
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Acute Bacterial Meningitis
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Acute Bacterial Meningitis
CSF examination essential Contraindications to lumbar puncture
increased intracranial pressure platelet count
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Acute Bacterial Meningitis
CSF EXAMINATION Need to order
WBC withdifferential
Glucose Protein
Gram stain andculture Need 4-8 cc Always take more
than you need!
CSF EXAMINATION Special Studies
Cytology Cryptococcal Antigen
and India Ink VDRL AFB & Fungal Smear
& CS Viral Studies ?Latex agglutination
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Acute Bacterial Meningitis
Bacterial meningitis partially tx WBC >1000 with >60% PMNs Glucose often < 45 Protein may be increased Gram stain and culture positive 60 - 65% Latex agglutination may be helpful here Oral ATB (low dose) usually leaves CSF
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abnormal, especially glucose
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Acute Bacterial Meningitis
Treatment (begin within 3 0 minu t es ) Needs to cover the most commonly encountered
pathogens: treat for 10 -14 days Ceftriaxone 2 grams iv bid + Vancomycin if >2%
community incidence of high level S.pneumoniaeresistance + Ampicillin 4 grams q6 hours if patient > 50
or immunocompromised Dexamethasone used in children -lactam anaphylaxis - Tmp-smx + chloramphenicol.
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Acute Bacterial Meningitis
Dexamethasone in adults - 301 patients with bacterial meningitis
157 received Dexamethasone with ATB or 15minutes prior
144 ATB alone mortality and adverse outcome (Glasgow Outcome Scale)
improved with Dexamethasone, especially in the patientsubset with pneumococcal meningitis sensitive to PCN
NEJM 2002: 347: 20 : 1549 - 1556
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Complications
Raised intracranial pressure Seizures Hearing loss Hydrocephalus
Subdural Empyema Cerebral Infarction Cognitive Impairment
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Acute Viral Meningitis
Viral meningitis is often referred to asaseptic meningitis
meningitis without bacterial etiology -generally means viral etiology
Enteroviruses cause 80-85% of cases of
viral meningitis arbovirus, herpes virus, and HIV are also
common causes of aseptic meningitis
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Acute Viral Meningitis
Pathophysiology Mucosal colonization -->viremia -->
BBB crosses by virus (or may travelalong nerve endings) --> viral entry intosubarachnoid space --> spread of virus in
CSF --> inflammatory response specificfor the virus and consisting of lymphocytes begins: T-cell responseneeded to clear CSF
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Acute Viral Meningitis
Clinical manifestations Enterovirus meningitis in kids > 2 weeks old
sudden onset of fever, severe frontal headache, photophobia, nuchal rigidity and myalgias,vomiting, diarrhea, anorexia, cough, sore throat
usually occurs in the summer months
may also be associated with recognizableenteroviral syndromes (eg - classic rash of hand-foot-and-mouth disease, the painful mouth vesiclesof herpangina)
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Acute Viral Meningitis
Clinical manifestations Initial episode of HSV 2 infection often
associated with aseptic meningitis andsigns of genital tract infection
Initial episode of HIV infection may also
be associated with aseptic meningitis
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Acute Viral Meningitis
Diagnosis LP with
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Acute Viral Meningitis
Viral (aseptic) meningitis WBC usually
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Acute Viral Meningitis
Treatment Enterovirus: Consider use of IVIG if
patient is extremely ill Herpes virus: Acyclovir HIV: Consider triple drug therapy
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Chronic Meningitis
Definition Neurologic abnormalities or CSF
abnormalities of > 4 weeks duration
Etiology Infections: TB, Nocardia, Cryptococcus,
Syphilis, Lyme Disease
Noninfectious diseases: Behcet
s,Meningeal Carcinomatosis, Sarcoidosis
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Chronic Meningitis
Clinical Manifestations Often insidious onset of symptoms which
wax and wane over weeks but withgradual neurologic decline
Cranial neuropathies
Focal neurological signs such asweakness, ataxia, sensory loss
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Chronic Meningitis
Diagnosis and Treatment Diagnostic workup is very difficult and is
guided by a thorough history and physicalexam plus lumbar puncture(s)
Treatment is generally not empiric but is
guided by the most likely initial diagnosisif the patient is critically ill or preferably
by a confirmed diagnosis
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Chronic Meningitis
Fungal WBC 60 need special smears
and cultures
Tubercul osi s WBC < 1,000 Glucose > 100 AFB smear and culture
positive more than>85% need to examine10cc centrifuged fluidfor > 1 hour
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Chronic Meningitis
A 36 year old with 3 week history of progressive gait disorder,weakness and multiple cranial neuropathies.
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TB Meningitis
A 12 year old immigrant from South Asia with chronic cough andheadaches. Examination shows bilateral sixth nerve paralysis.
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Intracranial Abscess
Definition: abscess in brain parenchyma May or may not be associated with
meningeal involvement From contiguous foci - 50% From hematogenous dissemination - 25% From direct inoculation - 10% Primary abscess - 15%
I t i l Ab
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Intracranial Abscess
Pathogenesis - site of abscess gives a clue to itsorigin Frontal lobe: sinuses, teeth, direct inoculation Temporal lobe: otitis, mastoiditis, sphenoid
sinusitis Cerebellum: otitis, mastoiditis MCA circulation - hematogenous source (eg-
lung abscess, endocarditis) Beneath area of a wound - direct inoculation
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Intracranial Abscess
4 stages of abscess formation early cerebritis 1 - 3 days
late cerebritis 4 - 9 days early capsule 10 - 13 days late capsule > 14 days
Intracranial Abscess
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Intracranial Abscess Bacteriology
Otitis/mastoiditis - Strep, Bacteroides, GNR Sinusitis - same as otitis + S. aureus Teeth - Fusobacterium, anaerobes, strep
Wound - staph, strep, GNR, Clostridium Endocarditis - staph or strep Lung - actinomyces, anaerobes, strep, fusobacterium,
nocardia Immunocompromised - toxoplasmosis, fungi, GNR,
nocardia
Intracranial Abscess
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Intracranial Abscess
Clinical manifestations Space occupying lesion --> headache, N/V, seizures, mental status change, focalneurologic deficit deficit depends on location --
cerebellar abscess may have ataxia,temporal lobe may have visual fielddefect, etc
generally < 50% have fever with
presentation
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presentation
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Intracranial Abscess
Diagnosis MRI or CT scan with contrast are
diagnostic modalities of choice MRI is very sensitive Avoid LP
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Intracranial Abscess
Intracranial Abscess
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Intracranial Abscess
Treatment
Surgical drainage and management of increased ICP almost always required
Search for source Culture abscess for bacteria, fungi,
mycobacteria and obtain immediate gramstain, AFB stain and fungal smears to help
guide therapy Empiric ATB - metronidazole + 3rd gen
ceph+ nafcillin or vancomycin
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Encephalitis
Encephalitis means inflammation of the brain - it is characterized by alterations in
consciousness many non-infectious diseases can be
associated with encephalitis (eg- drug
reactions, vasculitis) in general, infectious encephalitis is due
to viral infection, less commonly
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bacterial, fungal, or tubercular infection
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Encephalitis - Common Viral Causes
Herpesviruses - HSV 1 and 2, VZV (only treatableform of encephalitis)
West Nile HIV Togaviruses - cause EEE (eastern equine encephalitis),
WEE (western EE), and VEE (Venezuelan EE) Flaviviruses - St. Louis encephalitis, West Nile virus Enteroviruses (e.g. poliovirus) Rhabdovirus rabies Paramyxoviruses measles
Encephalitis
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most viruses
Pathophysiology
Encephalitis
Pathogens enter brain parenchyema in severalways Hematogenous - occurs for many viral
infections, rickettsia, bacteria, fungi, and TB Retrograde peripheral transport - rabies,
varicella Exposed olfactory nerves - definitely the route
of entry for Naegleria and Acanthamoeba but inexperimental animals is also route of entry for
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Encephalitis
Clinical Manifestations Classic presentation is altered mental
status and personality changes, decreaseslevel of consciousness, focal neurologicfindings, and seizures
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Encephalitis
Diagnosis EEG often has a characteristic pattern
MRI in HSV encephalitis shows temporallobe involvement
LP often with mild pleocytosis
PCR for HSV is diagnostic
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Encephalitis
Treatment Intravenous Acyclovir is effective
treatment for encephalitis caused byHSV1/2 and VZV.
Ganciclovir and Foscarnet for CMV
HAART for HIV
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West Nile Encephalitis
A 79 year old with headaches, progressive weakness and encephalopathy.
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HIV Encephalitis
A 32 year old with poor memory, weakness and inability to comprehend.
l l l f
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Neurological Complications of
HIV Meningitis- acute or chronic
Encephalopathy Vacuolar myelopathy Peripheral neuropathy
distal symmetric polyneuropathy Mononeuritis multiplex
Myopathy
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Secondary Involvement
Opportunistic infections Toxoplasmosis, Cryptococcus meningitis,
CMV, PML Neoplasms
Lymphoma
Vascular Drug toxicity Nutritional and metabolic
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PML
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PML
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CNS Lymphoma
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M liti I f ti C
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Myelitis- Infectious Causes
Highlights Herpes Virus VZV
Picornavirus Enteroviruses, Polio
Flaviviruses West Nile, Japanese B,
St. Louis Retrovirus
HIV, HTLV-1
Bacterial Lyme, Syphilis
Fungal Aspergillus
Parasitic Schistosomiasis
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Clinical Presentation
Acute to sub acute onset Weakness involving arms and/or legs
Numbness and sensory loss Incontinence (bowel and/or bladder)
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Subdural Empyema
Definition - pyogenic infection of space between the dura and arachnoid
Subdural space is crossed by numeroussmall veins (emissary vessels) and dividedinto several anatomic compartments by the
falx cerebri, tentorium cerebelli, and base of the brain @ 20 % of all intracranial infections
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infection
Subdural Empyema
Organisms reach subdural space throughemissary vessels or direct extension of
osteomyelitis of the skull (as a sequalae of associated epidural abscess) Source of empyema
50 - 80 % frontal or ethmoid sinusitis 10-20% otitis media/mastoiditis 5% hematogenous dissemination of
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Subdural Empyema
Bacteriology aerobic streptococci, staphylococci, S.
pneumoniae, H. influenzae, anaerobes,other gram - negative organisms,
polymicrobic infections are common
Epidemiology 4:1 males to females usually 2nd and 3rd decades of life
Subdural Empyema
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Clinical Manifestations Acts like a rapidly expanding mass lesion Fever, focal headache that later generalizes,
vomiting, altered mental status Focal neurologic signs appear then spread and
expand rapidly to include hemiparesis,seizures
Due to rapid spread < 50% have papilledema Occasionally patients progress neurologically
in weeks, rather than hours
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Subdural Empyema
Diagnosis MRI is diagnostic and very sensitive
CT scan will miss some subduralempyemas
CSF + in 14% of cases but LP is contra-
indicated
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Subdural Empyema
Treatment Neurosurgery for burr holes or
craniotomy Aggressive management of increased ICP
including use of dexamethasone
Culture of empyema fluid May need simultaneous debridement of
sinuses, mastiod, or ear
Subdural Empyema
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Treatment
Antibiotics indicated for a minimum of threeweeks need to cover anaerobes, GNR, GPC
Metronidazole + Ceftriaxone + Nafcillin or Vancomycin would be good empiric therapy
pending culture results
Prognosis 75% mortality if comatose, otherwise @ 15% 42% of survivors develop seizures
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Epidural Abscess
Abscess located between bone and the duramater
Intracranial epidural abscess generallyspills over into the subdural space andforms an associated subdural empyema aswell (81% of the time) etiology/pathogenesis/microbiology/
diagnosis/therapy same as for subduralempyema
Epidural Abscess
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Intracranial epidural abscess
Inflammation of the face or scalp may be present otherwise clinical manifestationsare the same
Spinal epidural abscess is different fromintracranial epidural abscess in spinal canal, dura mater is not adherent
to the vertebra but epidural space is adistinct fat filled anatomic space withoutemissary vessels
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dissemination
Spinal Epidural Abscess
Spinal epidural abscess Spinal canal anatomy allows easy
longitudinal but not subdural spread Ne u ro l og i c a l e m erge n cy!
Etiology
Bacteria enter epidural spinal space bydirect extension from vertebralosteomyelitis or hematogenous
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Spinal Epidural Abscess
Less often polymicrobial than intracranialepidural abscess
S aureus 60 -90% and often the sole pathogen followed by streptococci,anaerobes, and gram-negative rods
Abscess at time of diagnosis usually covers4 - 5 vertebra but may extend the wholelength of spine
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Spinal Epidural Abscess
Clinical manifestations Focal vertebral pain develops first, followed by
radiculopathy, then motor and/or sensorydeficits (sphincter function if lumbar location),and finally increasing paralysis
Patients may (or may not) have fever and appear quite ill Time course of evolution of clinical features can
be a few hours to days/weeks
Spinal Epidural Abscess
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Clinical manifestations Often see nuchal rigidity and severe focal tenderness
Diagnosis MRI is diagnostic modality of choice Myelogram (injection of radio-opaque dye into
arachnoid space) can be used as well to visualize thecord and look for compression (not preferred)
blood cultures are often positive, SED usuallyelevated
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Spinal Epidural Abscess
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p p Treatment
Immediate surgical drainage traditionalteaching
Case reports of recovery in selected patientswith antibiotics alone
Cover S. aureus, GNR, and anaerobes pending culture results
Vancomycin +3rd gen ceph +metronidazole
Prognosis if treated prior to paralysis/very poor if paralysis present >24 hours
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Recap
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