Focal CNS InfectionsFocal CNS Infections
Donnie Tyler MD
Department of Neurosurgery
University of Mississippi Medical Center
Anatomic Relationships of the Meninges
BoneEpidural Abscess
Dura MaterSubdural Empyema
ArachnoidMeningitis
Pia Mater
Brain
Anatomic relationships of the Brain
Frontal LobeFrontal and Ethmoidal Sinuses
Sella TurcicaSphenoidal sinuses
Temporal LobeMiddle Ear, Mastoid, Maxillary Sinuses
Cerebellum, Brain StemMiddle Ear, Mastoid
Brain Abscess
50% - Local Sourceotitis media, sinusitis, dental infection
25% Hematogenous spreadadults - lung abscess, bronchiectasis and empyema
children - cyanotic congenital heart disease (4-7%)
pulmonary AVM - Osler-Weber-Rendu syndrome (5%)
rarely bacterial endocarditis
10% trauma / surgery
Brain Abscess - pathology
Locationtemporal > frontal > other lobes
>10% are multiple
Stages - based on histologic findings1. Early cerebritis - poorly demarcated from surrounding brain
2. Late cerebritis - reticular marix (collagen precursor) and developing necrotic center
3. Early capsule formation - neovascularity, necrotic center, developing capsule
4. Late capsule formation - collagen capsule, necrotic center, gliosis surrounding capsule
Early Abscess (Cerebritis) – Poorly Early Abscess (Cerebritis) – Poorly localized area of discoloration and localized area of discoloration and
softening. softening.
Later Cerebritic / Early Abscess Stage – increasing necrosis of center with beginnings of capsule
formation
Mature abscess (Late Stage) - dense fibro-gliotic capsular wall and
purulent center
Brain Abscess - microbiology
Streptococcus most frequent (33-50%), Multiple organisms(80-90%) of cases, May also include anaerobes (Bacteroides sp.)
When secondary to frontal-ethmoidal sinusitis:Strep. Milleri, Strep. Anginosus
When from otitis media, mastoiditis, or lungmultiple organisms including anaerobic strep., bacteroides,
enterobacter (proteus)
Post Traumatic Abscess include:Staph. aureus and Enterobacteriaceae:
Abscess wall – inner portion formed by a layer of neutrophils and fibrin, middle layer with mainly
fibrin (Blue on trichrome stain) and the outer portion with reactive glia.
Pyogenic meningitis – note the neutrophils are collected in the subarachnoid space.
Brain Abscess - Clinical Presentation
Symptoms are non-specific for abscess and are normally due to increased intracranial pressure / mass effect: Headache, Nausea/Vomiting, or Lethargy. Occasionally Seizures.
Abscess – CT presentation
CT appeareance dependent on stageCerebritic stage – thick diffuse ring of enhancement,
further diffusion on contrast into central lumen or lack of decay of contrast on delayed scan 30-60 minutes later.
Capsular stage – faint rim present on pre contrast CT. (Necrotic center with edematous surrounding brain makes the collagen capsule easier to see.). Thin ring on enhancement and there is decay of enhancement on delayed scans.
Abscess – MRI presentation
MRI presentation also varies with capsule formation
Early Cerebritic stage – hyperintense in T2 with poor contrast enhancement on T1.
Later Cerebritic Stage – central region of necrosis is hyperintense to brain on T2, rim is isointense to mildly hyperintense on T1. The capsule enhances with contrast.
Early and Late Capsule Stages – Capsule is easily visible on unenhanced scans as a well deliniated isointense to slightly hyperintence ring with becomes hyperintense with contrast on T1. Capsule is hypointense on T2
Intraparenchymal abscess
Initial management of Brain Abscess
Blood Cultures (rarely helpful)
LP role is dubious because of risk of transtentorial herniation. CSF is typically abnormal but cultures are usually negative.
initiate antibiotic therapy (preferably after biopsy specimen is obtained), regardless of which management mode is chosen.
Brain Abscess Antibiotics
If pathogen is unknown or S aureus is suspected:Vancomycin - Adult 1 gm q 12 hours
PLUS
3rd generation cephalosporin (e.g Claforan)
PLUS
Metronidazole Adult (30mg/kg/d) divided q12 or q6 hours
OR
Chloramphenicol Adult 1 gm IV q 12 hours
OR
for post traumatic abscess use po rifampin 9mg/kg/d qd
Brain Abscess - medical treatment
Medical therapy alone is more successful if:The treatment is begun before complete encapsulation
The lesion is 0.8-2.5cm in diameter or less
(3.0 cm is the typical cutoff)
The duration of symptoms is < 2 weeks
The patients should show improvement in the first 2 weeks of treatment
Brain Abscess - surgical treatment, indications
significant mass effect exerted by lesion
proximity to ventricle
poor neurological condition
Inability to obtain weekly CT scans
In patient undergoing medical treatmentIntervention, if neurological deterioration occurs, anatomic
progression of abscess towards ventricles, or after 2 weeks of therapy if abscess is enlarged. Also consider if there is no decrease in abscess size by 4 weeks of treatment.
Brain Abscess - surgical treatment
modern methodsNeedle aspiration - recommended for thin walled (immature)
or multiple lesions
Surgical excision - only can be performed on mature abscess
Historical methodsTube drainage - 34% morality
marsupialiaztion - remove overlying cortex and pack - 23% mortality
Decompressive craniectomy with spontaneous migration of abscess
Treatment of Brain Abscess in 1895
If symptoms of abscess exist – trephine the skill at once.
If there are localizing symptoms open over that region.
If pus is not found in the epi/sub dural spaces and the brain bulges very much and is not seen to pulsate then instert a grooved director to 2.5 inches, if no pus the redirect and reinsert.
1895 medicine continued
When pus is found, incise the brain overlying he cavity. Scrape out the granulation tissue in the abscess cavity.
Irrigate with hot salt solution. Place a rubber drainage tube to externally drain.
Close dura and skin. Slowly remove the rubber tube over the next 4-7
days.(Pennicillin – 1943)
Mortality / Morbidity
pre-CT era - 40-60% moralitypost CT era - 0-10% (Improvement due to better antibiotics, surgical methods and
ability to diagnose earlier)neurologic disability 45%late focal or generalized seizures - 27%hemiparesis - 29%
Multiple abscesses in a 6 year old
Presumed source of polymicrobial abscesses.
Cerebellar Abscess from open skull fracture.
Subdural Empyema
Located in the potential space between the dura and the arachnoid.
May spread rapidly due to lack of anatomical boundaries.
Less mass effect than brain abscess
Surgical Emergency
Usually from a local source of infection>50% stem from a paranasal sinusitis (fronto-ethmoidal)
trauma or surgery
progression of an epidural abscess, ostermyelitis
Etiologies of SDE
paranasal sinusitis - 67-75%
otitis-14%
post neurosurgical - 4%
trauma -3%
meningitis (mainly peds) - 2%
congenital heart disease - 2%
other 7%
Subdural Empyema - clinical
fever -95%
focal neurological deficit (mainly hemiparesis) - 80-90%
nuchal rigidity - 80%
headache 77%
Seizures - 50-60%
Forehead or eye swelling from emissary vein thrombosis - 30%
Vomiting - 20%
Male to female ratio - 3:1
Subdural Empyema - evaluation
CT of head both with and without contrast
LP - hazardous - risk of transtentorial herniation
Location -
convexity 70-80%
falcine 10-20%
32/10,000 autopsies
Subdural empyema - Bacteriology
Aerobic Streptococcus - 30-50%
Staphylococcus - 15-20%
Microaerophilic and anaerobic strep - 15-25%
Anaerobic Gm negative rods- 5-10%
other 5-10%
Management of Subdural empyema
Craniotomy - relatively emergency to debride and drainwide craniotomy is used because of septations /
loculations
Antibiotics - initiallyVancomycin and chloramphemicol OR Cefotaxime and
flagyl
Modify based on culture results
Meningitis progression to subdural empyema
Subdural Empyema
Intracranial Epidural Abscess
Localized between dura and bone
sharply defined - mainly be dural adherence to bone at suture lines
focal osteomyelitis
associated with subdural empyema
Management and etiology same as subdural empyema
Mixed Abscess Location
Spinal Epidural Abscess
clinical presentationback pain
fever
spine tenderness
major risk factorsdiabetes
IV drug abuse
chronic renal failure
alcoholism
Spinal Epidural Abscess - Exam
myelopathic distal to lesion
deterioration of exam with time
classic presentation of a “skin boil” in 15% of patients
Patients complain of excruciating pain localized to the spine
Also may note bowel/bladder disturbances
Spinal Epidural Abscess
Average time courseBack pain to root problems - 3 days
Root problems to weakness - 4.5 days
Weakness to paraplegia - 24 hours
Spinal Epidural Abscess
Epidemeology.2-1.2 / 10,000 hospital admissions
40-60 years old
incidence increasing
Spinal Epidural Abscess -source
Hematogenous spreadSkin infections
Parenteral infections (IVDA)
Bacterial endocarditis
UTI
Respiratory infection
Dental abscess
Spinal Epidural Abscess -source
directdecubitus ulcer
psoas abscess
trauma
pharyngeal infection
mediastinitis
pyelonephritis
Spinal Epidural Abscess -source
Following spinal proceduresopen procedure
for example disectomy
closed procedureLP
Epidural catheter
No source in 50% of patients in some series
Spinal Epidural Abscess - location
Cervical – 15%
Thoracic - 50%
Lumbar - 35%
Posterior to the Cord - 82%
Spinal Epidural Abscess - treatment
Surgery goal is to determine causative organism and debridement
is necessary
immobilization - infected segments may become unstable
Non-surgical management indications:patients with prohibitive operative risk factors
involvement of an extensive length of the spinal canal
complete paralysis for >3 days
absence of neurological deficit (controversial)
Spinal Epidural Abscess - treatment
Antibiotics3rd generation cephalosporin
PLUS
Vancomycin - until MRSA is ruled out
PLUS
Rifampin po
Duration of treatment3-4 weeks IV followed by 4 weeks of po
mortality 18-23%
Discitis with local osteomyelitis and epidural empyema
Parasitic Infections - Cysticercosis
Most common parasitic infection in CNSCaused by larval stage of Taenia solium- pork tapeworm
Incubation period from months to decades 83% of cases show symptoms within 7 years of
exposure
Infection with the adult form - tapeworm in gut man is the only know permanent host for the worm
eggs are excreted in the feces - does not cause neurocysticercosis
Parasitic Infections - Cysticercosis
Infection with the larvaanimals (pigs) serve as an intermediate host
larva burrow through the small bowel to gain access to the systemic circulation
mainly infect the following sites:Brain (60-92% of cases)
Skeletal muscle
Eye
Subcutaneous Tissue
Parasitic Infections - Cysticercosis
Common routes of infectionFood (usually vegetables) or water containing eggs from
human feces
Fecal - Oral autoinfection (poor sanitation habits)
Autoinfection from reverse peristalsis - (theory possibly offered by patients who autoinfected themselves)
Parasitic Infections - Cysticercosis
cystercercus cellulosae - (3-20 mm)regular round thin walled cyst,
produces only mild inflammation
larva in cyst
cystercercus racemosus - (4-12 cm)active growing
grape like clusters
intense inflammation
no larva in cyst
Parasitic Infections - Cysticercosis
Location:meningeal 27-56%
parenchymal 30-63%
ventricular 12-18% (may cause hydrocephalus)
mixed - 23%
Clinical symptoms of increased intracranial pressure
Parasitic Infections - Cysticercosis
serologyantibody titers significant if 1:64 in the serum and 1:8 in
the CSF
CT scanring enhancing / calcified lesions, multiple
Parasitic Infections - Cysticercosis
TreatmentSteroids - symptomatic relief
Antihelmintic drugsPraziquantal - (DOC for intestinal infestation) -
50mg/kg divided tid for 15 days
Albendazole -15mg/kg divided bid po tid for 3 months
Niclosamide - may be given orally for GI infestation
Cystercercus cellulosae - (3-20 mm)regular round thin walled cyst,
produces only mild inflammationlarva in cyst
Parasitic Infections - Echinococcosis
“Hydatid Cyst” - caused by ingestion of the dog tapeworm
(Uruguay, Australia, New Zealand)
Treatment - Surgical excision without cyst ruptureCyst is full of worms
Adjunctive treatmentAlbendazole - 400mg po BID for 28 days
Echinococcus Cyst – intraoperative
Fungal Infections
Cryptococcosis - most common fungal infection in CNS diagnosed in live patientsCryptococcoma (mucinous pseudocyst) - occurs almost entirely
in the HIV population
3-10mm, most commonly in the basal ganglia
Candidiasis - most common fungal infection in CNS diagnosed in dead patientsrare in healthy individuals
Aspergillosis
Coccidiomycosis - normally causes meningitis
Cryptococcosis
Aspergillosis – Abscess in the centrum ovale. (Also may cause diffuse cerebritic infections) Note many satellite lesions common among fungal infections.
(Patient was on steroid therapy for leukemia.)
Mucor – aggressive and locally destructive infection.
Toxoplasmosis
CNS manifestationsMass lesion (most common)
Meningoencephalitis
Encephalopathy
Toxoplasmosis
CT findingsMass lesion - comprises 70-80% of cerebral masses in
AIDS patients
large low density area with mild to moderate edema
Ring enhancement with contrast
most commonly in the basal ganglia
Often multiple
Most patients with CT diagnosed toxoplasmosis also have evidence of cerebral atrophy
Toxoplasmosis
TreatmentPyrimethamine 200mg loading dose then 75-100mg/d
PLUS
Sulfadiazine 75mg/kg po loading dose then 25mg/kg/q6 hours
PLUS
Folic Acid 5-40mg/d (usually 10mg with each dose of Pyrimethamine)
Should show radiologic response in 3 weeks. If response is good then continue dose for 6-12 weeks then reduce by 50% and continue for life
Toxoplasmosis
Biopsy in following settings:negative toxo titers
(keep in mind the patient may be anergic)
accessible lesions atypical for toxo (non-enhancing, not in basal ganglia, etc)
in patients with extraneural infections or malignancies that may involve CNS
Single lesion
The role of biopsy for non-enhancing lesions is less well defined as the diagnosis normally does not influence therapy (most are PML or the biopsies are non-diagnostic), it may, however, be useful for prognostic purposes.
Toxoplasmosis
Toxoplasmosis
Texas Tapeworm
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