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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