Cns carlson 11 24 03 studyslide.com hypoxic anoxic brain injury

CNS_Carlson_11_24_03 download report transcript

CNS_Carlson_11_24_03 CNS infections

Margrit carlson, M.D.

November 2003

How are infections in the

CNS different?

Separated by the blood brain barrier

Immunologically distinct

Unique anatomic considerations dictate

The spread of infection within the CNS

Closed space

Limited capacity for regeneration or

Compensation for injury

Blood brain barrier

Between blood and brain formed by the

Tight junctions of the cerebral capillary

Endothelium

Between blood and CSF formed by the

Tight junctions of the choroid plexus

Epithelium

Immune response in the CNS

Access of immune effector cells to CNS


Is limited by the BBB

T lymphocytes can enter and exit the

CNS in small numbers

hypoxic anoxic brain injury

Low expression of MHC molecules limits

Antigen presentation

Entry into the CNS

Bypassing the blood brain barrier

 direct

Extension from a local focus,

Sinuses

Middle ear or mastoid

Dental source

 foreign body

 trauma

Entry through the BBB

Direct penetration of the choroid plexus

Epithelium into the CSF (meningitis)

Direct penetration of the capillary

Endothelium into the brain parenchyma

(encephalitis)

Disruption of the tight junctions

Transportation across the barrier inside

Leukocytes

Types of infections

Meningitis- subarachnoid

 encephalitis-brain parenchyma

 abscess

Subdural

Brain

Epidural

Cerebrospinal fluid in

Meningitis

Pressure

Normal 180mm

Glucose

Protein

2/3 of serum up to50

WBC

0-5

Bacterial

I

40

50-1500

50-5000P

hypoxic anoxic brain injury

Viral

N

N

N

100L

Chronic

I

10-45

45-500

25-1000L

I=increased

N =normal

P=polymorphonuclear leukocytes

L=lymphocyte

CSF parameters

Pressure

Normal 180mm

Glucose

2/3 of serum

Protein

50

WBC

0-5

Abscess

I

N

30-200

10-500 L

Encephalitis N

N

20-125

20-200 L

I=increased N =normal

P=polymorphonuclear leukocytes

L=lymphocyte

Acute meningitis

19 yo student is seen for sore throat x2

Days. His symptoms worsen and he

Develops a terrible headache and

Photophobia. He is brought to the ER

The next morning by his roommate. In

The ER he is hypotensive, confused,

Complaining of headache and

Photophobia. He has a seizure.

He is given antibiotics and taken for a

CT scan which is unremarkable.

CSF

RBC 10

WBC 1230 93% pmns

Glucose 33

Protein 276

Acute meningitis

hypoxic anoxic brain injury

Meningeal signs and symptoms worsen

Over a few days

Symptoms: headache, fever, neck

Stiffness, photophobia and vomiting.

Signs: nuchal rigidity, altered level of

Consciousness, seizures and cranial

Nerve palsies(sensorineural hearing

Loss)

Bacterial meningitis

0-4 weeks streptococcus agalactiae,

E. Coli, listeria monocytogenes

4-12 weeks H. Influenzae, E. Coli,

L. Monocytogenes, S.Agalactiae,

3mo-18 years H. Influenzae, N.

Meningiditis, S. Pneumoniae

18-50 years S. Pneumoniae, N.

Meningiditis

36 YO G3P2, 33 week IUP brought in by

Her sister for chest pain and confusion

Increasing over the last 3 days.

PE: temp was 38.5, she had

Photophobia but no nuccal rigidity. A

Vesicular rash was seen on her L chest

CSF: 320 RBC, 460 WBC, 50% lymphs

hypoxic anoxic brain injury

And 34% monos

Protein 623, glucose 91

Her MRI had diffuse meningeal

Enhancement

Meningitis in the

Immunocompromised host

Bacterial syphilis, listeria, nocardia

Viral

VZV, HSV

Fungal

Cryptococcus,

Coccidioidomycosis,

Histoplasmosis

Mycobacterial

Tuberculosis

44 yo construction worker had upper

Respiratory symptoms 1 month ago. He

Has had worsening fevers, a constant

Headache and photophobia for a month.

His thinking has been slowed and he

Had an episode of aphasia lasting 1 day.

Glucose 27

Protein 203

RBC

1

WBC

203

 45%lymphs/40% mono/5% eos

 MRI: enhancement of the basal

Cisterns, along the midbrain, pons, right

Optic tract, and the right caudate head.

CSF:

Chronic meningitis

Gradual onset and progression

Focal symptoms

hypoxic anoxic brain injury

Increased intracranial pressure

History of exposure

Immunocompromised ?

Symptoms of increased

Intracranial pressure

Headache

 nausea, vomiting

 altered mental status

 ataxia

 incontinence

 papilledema

 3rd or 6th nerve palsy

Infectious causes of chronic

Meningitis

Coccidioidomycosis, cryptococcus,

Histoplasmosis, sporotrichosis

Tuberculosis

Syphilis, lyme disease

HIV, enterovirus

Non-infectious causes of

Chronic meningitis

Behcet’s disease

Systemic lupus erythematosis

Sarcoidosis

Carcinomatous or lymphomatous

Meningitis

Granulomatous angiitis

Complications of chronic

Meningitis

Hydrocephalus

Vasculitis, cerebrovascular occlusion

Cranial nerve palsies

32 yo hispanic man has new onset

Confusion developing over 24 hours,

hypoxic anoxic brain injury

Aphasia, hallucinations and seizures

Following a bone marrow transplant for

CML. He has no known ill contacts. He

Has had mucositis

Putting it all together

Sudden or gradual onset?

 meningeal symptoms, encephalopathy?

 focal findings?

 fever ?

 predisposing conditions and exposures

 imaging

 LP results

 CSF:

Glucose 67

Protein 158

RBC 179

WBC 124 25% P /74% L

 his MRI shows diffuse periventricular

White matter disease and enhancement

In the temporal lobes.

Acute encephalitis

Fever

 headache

 altered level of consciousness: lethargy,

Confusion, stupor, coma

 seizures

 hypothalamic or pituitary dysfunction

Causes of acute encephalitis

Herpes simplex, varicella zoster

California, st louis, japanese, western

hypoxic anoxic brain injury

And eastern equine encephalitis viruses

Enteroviruses (coxsackie, echo and

Enteroviruses)

Post measles, post influenza

Encephalomyelitis

HSV pathogenesis

Retrograde transport of virus from

Mucous membranes to the sensory

Ganglia and rarely to the CNS

Anterograde transport from the sensory

Ganglia to the periphery during

Cutaneous exacerbations

33 yo with AIDS,CD4 cells 5, brought in

By his partner who has noticed he has

Become more forgetful and withdrawn

Over the last 3-6 months.

He’s had no fevers or headache. No

Recent infections. He has been off

Antiretrovirals because of side effects.

MRI showed diffuse atrophy

CSF

Glucose

Protein

RBC

WBC

88

78

1

12

74% lymphs

26% monos

Chronic encephalitis

Predominantly viral

hypoxic anoxic brain injury

Non-viral: neurosyphilis, lyme disease,

Neurotropic viruses:

Retroviruses: HTLV I and II, HIV

Herpes viruses: HSV, VZV and CMV

Chronic encephalitis

Other:

JC virus: progressive multifocal

Leukoencephalopathy

Subacute sclerosing panencephalitis

(measles)

Rubella

Creutzfeldt-jakob

HIV encephalopathy

AIDS dementia complex

7-27% of persons with CD4200 have

Some impairment including:

 decreased attention and concentration

 psychomotor slowing

 personality change, loss of initiative,

Drive, animation

 hyperreflexia, ataxia, frontal release

Signs

Pathogenesis of ADC

HIV is present in the CSF and brain in

Primary infection.

 HIV infects cells of monocyte lineage

(macrophages, microglia, multinucleated

Giant cells).

 viral burden (HIV qpcr) in CSF or brain

hypoxic anoxic brain injury

Correlates with neurologic disease.

Pathogenesis of ADC

Release of neurotoxins from

Macrophages (nitric oxide, arachidonic

Acid, quinolinic acid).

 cytokine mediated release of

Neurotoxins.

 direct toxicity of viral proteins, i.E.

Gp120.

73 yo man with a fever who is brought in

By his wife because he is confused and

Unable to move his right side.

He was complaining of a headache for a

Few days. He started vomiting this

Morning and was bumping into the wall

On his way to the bathroom.

Brain abscess

Hematogenous spread through the

Blood brain barrier

Direct extension via the the emissary

Veins into the cerebral venous

Circulation

Development of an abscess

Local area of cerebritis, inflammation

And edema (1-3 days)

hypoxic anoxic brain injury

Expansion and development of a

Necrotic center (4-9 days)

Formation of a ring enhancing capsule

By gliosis and fibrosis (14 days)

Clinical presentation

Headache with gradual worsening

 fever 50%

 focal neurologic signs

 seizures

 CSF: elevated protein, normal glucose

And mild leukocytosis

 increased ICP: nausea,vomiting,

Lethargy

Brain abscess

Location

Source

Organism

Treatment

Brain abscess

Paranasal sinuses

Otogenic infection

Frontal lobe

Temporal lobe,

Cerebellum

Hematogenous spread multiple lesions

MCA distribution

Post traumatic

Site of wound

Post operative

Site of surgery

Pathogens

Sinuses

Streptococci, haemophilus,

Bacteroides, fusobacterium

Otogenic as above, and pseudomonas

Endocarditis staphylococcus, viridans

hypoxic anoxic brain injury

Streptococci

Lung abscess streptococci, anaerobes,

Actinomyces

Trauma

Staph aureus

A 28 YO father of 3 develops worsening

Sinus headaches and is seen repeatedly

At an outside ER. He has low grade

Fevers. His headache becomes

Excruciating and he subsequently

Becomes unresponsive during his

Evaluation.

Brain abscess in the

Immunocompromised

AIDS

Toxoplasmosis, tuberculoma,

Cryptococcoma, coccidiodomycosis,

Blastomycosis

 transplant

Aspergillus, nocardia, candida,

Zygomycetes in addition to the above

35 YO man with 2 weeks of worsening

Headache, low grade fever and rash.

He also has had myalgias and L knee

Pain and swelling.

 he has no recent travel or outdoor

Activities, not sexually active x 6 months

CT scan is unremarkable

hypoxic anoxic brain injury

CSF: 2 RBC, 25 WBC;20%segs, 60%

Lymphs, 20% monocytes, glucose 64,

Protein 45.

Fever, headache,rash and

Mild CSF pleocytosis

Enterovirus

Primary HIV

Epstein barr

Secondary syphilis

Mycoplasma

Drug reaction

Neurosyphilis

Primary, chancre 10-90 days

 secondary,rash 4-10 weeks later (up to

6 months after initial infection

 meningeal within 1st year after infection

 meningovascular 4-7 years later

 parenchymal disease decades later

Syphilis

50-75% of exposed partners were

Infected.

 30-70% of those with secondary syphilis

Have CSF mononuclear pleocytosis,

Elevated protein or + RPR in CSF

 25% untreated patients have

Recurrances

 1/3 of untreated patients develop late

Sequelae