Focal CNS Infections - PowerPoint PPT Presentation

1 / 69
About This Presentation
Title:

Focal CNS Infections

Description:

Focal CNS Infections Donnie Tyler MD Department of Neurosurgery University of Mississippi Medical Center Anatomic Relationships of the Meninges Bone Epidural Abscess ... – PowerPoint PPT presentation

Number of Views:107
Avg rating:3.0/5.0
Slides: 70
Provided by: 22012811
Category:
Tags: cns | focal | infections

less

Transcript and Presenter's Notes

Title: Focal CNS Infections


1
Focal CNS Infections
  • Donnie Tyler MD
  • Department of Neurosurgery
  • University of Mississippi Medical Center

2
Anatomic Relationships of the Meninges
  • Bone
  • Epidural Abscess
  • Dura Mater
  • Subdural Empyema
  • Arachnoid
  • Meningitis
  • Pia Mater
  • Brain

3
Anatomic relationships of the Brain
  • Frontal Lobe
  • Frontal and Ethmoidal Sinuses
  • Sella Turcica
  • Sphenoidal sinuses
  • Temporal Lobe
  • Middle Ear, Mastoid, Maxillary Sinuses
  • Cerebellum, Brain Stem
  • Middle Ear, Mastoid

4
Brain Abscess
  • 50 - Local Source
  • otitis media, sinusitis, dental infection
  • 25 Hematogenous spread
  • adults - 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

5
Brain Abscess - pathology
  • Location
  • temporal gt frontal gt other lobes
  • gt10 are multiple
  • Stages - based on histologic findings
  • 1. 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

6
Early Abscess (Cerebritis) Poorly localized
area of discoloration and softening.
7
Later Cerebritic / Early Abscess Stage
increasing necrosis of center with beginnings of
capsule formation
8
Mature abscess (Late Stage) - dense fibro-gliotic
capsular wall and purulent center
9
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 lung
  • multiple organisms including anaerobic strep.,
    bacteroides, enterobacter (proteus)
  • Post Traumatic Abscess include
  • Staph. aureus and Enterobacteriaceae

10
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.
11
Pyogenic meningitis note the neutrophils are
collected in the subarachnoid space.
12
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.

13
Abscess CT presentation
  • CT appeareance dependent on stage
  • Cerebritic 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.

14
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

15
Intraparenchymal abscess
16
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.

17
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

18
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 lt 2 weeks
  • The patients should show improvement in the first
    2 weeks of treatment

19
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 treatment
  • Intervention, 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.

20
Brain Abscess - surgical treatment
  • modern methods
  • Needle aspiration - recommended for thin walled
    (immature) or multiple lesions
  • Surgical excision - only can be performed on
    mature abscess
  • Historical methods
  • Tube drainage - 34 morality
  • marsupialiaztion - remove overlying cortex and
    pack - 23 mortality
  • Decompressive craniectomy with spontaneous
    migration of abscess

21
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.

22
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)

23
Mortality / Morbidity
  • pre-CT era - 40-60 morality
  • post 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

24
Multiple abscesses in a 6 year old
25
Presumed source of polymicrobial abscesses.
26
Cerebellar Abscess from open skull fracture.
27
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
  • gt50 stem from a paranasal sinusitis
    (fronto-ethmoidal)
  • trauma or surgery
  • progression of an epidural abscess, ostermyelitis

28
Etiologies of SDE
  • paranasal sinusitis - 67-75
  • otitis-14
  • post neurosurgical - 4
  • trauma -3
  • meningitis (mainly peds) - 2
  • congenital heart disease - 2
  • other 7

29
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 - 31

30
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

31
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

32
Management of Subdural empyema
  • Craniotomy - relatively emergency to debride and
    drain
  • wide craniotomy is used because of septations /
    loculations
  • Antibiotics - initially
  • Vancomycin and chloramphemicol OR Cefotaxime and
    flagyl
  • Modify based on culture results

33
  • Meningitis progression to subdural empyema

34
Subdural Empyema
35
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

36
Mixed Abscess Location
37
Spinal Epidural Abscess
  • clinical presentation
  • back pain
  • fever
  • spine tenderness
  • major risk factors
  • diabetes
  • IV drug abuse
  • chronic renal failure
  • alcoholism

38
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

39
Spinal Epidural Abscess
  • Average time course
  • Back pain to root problems - 3 days
  • Root problems to weakness - 4.5 days
  • Weakness to paraplegia - 24 hours

40
Spinal Epidural Abscess
  • Epidemeology
  • .2-1.2 / 10,000 hospital admissions
  • 40-60 years old
  • incidence increasing

41
Spinal Epidural Abscess -source
  • Hematogenous spread
  • Skin infections
  • Parenteral infections (IVDA)
  • Bacterial endocarditis
  • UTI
  • Respiratory infection
  • Dental abscess

42
Spinal Epidural Abscess -source
  • direct
  • decubitus ulcer
  • psoas abscess
  • trauma
  • pharyngeal infection
  • mediastinitis
  • pyelonephritis

43
Spinal Epidural Abscess -source
  • Following spinal procedures
  • open procedure
  • for example disectomy
  • closed procedure
  • LP
  • Epidural catheter
  • No source in 50 of patients in some series

44
Spinal Epidural Abscess - location
  • Cervical 15
  • Thoracic - 50
  • Lumbar - 35
  • Posterior to the Cord - 82

45
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 gt3 days
  • absence of neurological deficit (controversial)

46
Spinal Epidural Abscess - treatment
  • Antibiotics
  • 3rd generation cephalosporin
  • PLUS
  • Vancomycin - until MRSA is ruled out
  • PLUS
  • Rifampin po
  • Duration of treatment
  • 3-4 weeks IV followed by 4 weeks of po
  • mortality 18-23

47
Discitis with local osteomyelitis and epidural
empyema
48
Parasitic Infections - Cysticercosis
  • Most common parasitic infection in CNS
  • Caused 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

49
Parasitic Infections - Cysticercosis
  • Infection with the larva
  • animals (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

50
Parasitic Infections - Cysticercosis
  • Common routes of infection
  • Food (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)

51
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

52
Parasitic Infections - Cysticercosis
  • Location
  • meningeal 27-56
  • parenchymal 30-63
  • ventricular 12-18 (may cause hydrocephalus)
  • mixed - 23
  • Clinical
  • symptoms of increased intracranial pressure

53
Parasitic Infections - Cysticercosis
  • serology
  • antibody titers significant if 164 in the serum
    and 18 in the CSF
  • CT scan
  • ring enhancing / calcified lesions, multiple

54
Parasitic Infections - Cysticercosis
  • Treatment
  • Steroids - symptomatic relief
  • Antihelmintic drugs
  • Praziquantal - (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

55
Cystercercus cellulosae - (3-20 mm)regular round
thin walled cyst, produces only mild
inflammationlarva in cyst

56
Parasitic Infections - Echinococcosis
  • Hydatid Cyst - caused by ingestion of the dog
    tapeworm
  • (Uruguay, Australia, New Zealand)
  • Treatment - Surgical excision without cyst
    rupture
  • Cyst is full of worms
  • Adjunctive treatment
  • Albendazole - 400mg po BID for 28 days

57
Echinococcus Cyst intraoperative
58
Fungal Infections
  • Cryptococcosis - most common fungal infection in
    CNS diagnosed in live patients
  • Cryptococcoma (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 patients
  • rare in healthy individuals
  • Aspergillosis
  • Coccidiomycosis - normally causes meningitis

59
Cryptococcosis
60
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.)
61
Mucor aggressive and locally destructive
infection.
62
Toxoplasmosis
  • CNS manifestations
  • Mass lesion (most common)
  • Meningoencephalitis
  • Encephalopathy

63
Toxoplasmosis
  • CT findings
  • Mass 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

64
Toxoplasmosis
  • Treatment
  • Pyrimethamine 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

65
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.

66
Toxoplasmosis
67
Toxoplasmosis
68
Texas Tapeworm
69
END
Write a Comment
User Comments (0)
About PowerShow.com