Neuro - Encephalitis Flashcards

1
Q

What is encephalitis?

A

Inflammation of the brain parencyma.Can be:- Infective: usually viral from haematogenous spread to the CNS. May also be bacterial, fungal or TB.- non-infective e.g. autoimmune (NMDA-R, VGKC)

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2
Q

How does encephalitis present?

A
  1. personality change
  2. headaches
  3. seizures
  4. reduced consciousness
  5. visual disturbance
  6. confusion
  7. Fevers
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3
Q

Which viruses cause encephalitis?

A
  1. HSV-1 (most common)
  2. Enterovirus
  3. VZV
  4. EBV
  5. CMV
  6. Rabies
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4
Q

How would you diagnose encephalitis?

A
  1. History and examination
  2. Serology: CSF (PCR, cultures, gram stain and cell count, protein, glucose, cytology, autoantibodies), blood, sputum, FBC, clotting, LFTs, U&Es, TFTs, toxicology, B12 and folate, pregnancy test, HIV. 3. Radiology: CXR, CT head, MRI brain.
  3. Others: EEG
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5
Q

What are the differential diagnoses for encephalitis?

A
  1. Infection - meningitis, HIV, cerebral abscess, sepsis
  2. Vascular - infarction, haemorrhage, PRES#
  3. Malignancy - lymphoma, metastases.
  4. Inflammation - vasculitis, autoimmune
  5. Metabolic dysfunction - thyroid disease, steroids, low sodium, uraemia, hepatic encephalopathy.
  6. Psychiatric disorders
  7. Toxicology/overdose
  8. NEAD
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6
Q

How is infective encephalitis treated?

A

Typically aciclovir (10mg/kg TDS) for viral particularly HSV +/- cephalosporin (3rd gen) cover for bacterial.

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7
Q

What is the prognosis of HSV encephalitis?

A

Treated HSV encephalitis has a mortality of around 10%. Untreated around 80%.Complication rates are high in those who survive and can result in variable level of disability.

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8
Q

How would your treatment differ in someone who is immunocompromised?

A

Assess for HIV infection and low threshold for covering CNS fungal infection.

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9
Q

Describe the CSF findings in viral, bacterial, fungal and TB meningitis.

A

Viral: Clear colourless fluid, normal glucose, low protein, lymphocytosis,
Bacterial: turbid yellow/colourless fluid, low glucose, high protein, neutrophilia
Fungal: Turbid fluid, low glucose, high protein, fibrin web, lymphocytes
TB: Turbid fluid, low glucose, high protein, lymphocytes

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10
Q

What is PRES and what is the aetiology?

A

PRES is a clinico-radiological syndrome. The pathogenic hallmarks are failure of cerebral autoregulation and the development of vasogenic oedema.

The posterior regions of the brain may be more susceptible to failed autoregulation due to relatively less sympathetic innervation.

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11
Q

What are the associated features of PRES?

A

Hypertension and associations

It is the rate of BP rise rather than the absolute pressure which is most of concern

Pre-eclampsia and eclampsia

Renal failure

Guillain-Barre Syndrome (autonomic instability)

Inflammation and endothelial dysfunction

Sepsis

Autoimmune disease

Thrombotic microangiopathies

Drugs

Anything that can cause hypertension or endothelial damage

Chemotherapeutics

Anti-inflammatory

Pro-inflammatory, VEGF-I, TKI

Sympathomimetics

Carbamazepine

Lithium

Linezolid

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12
Q

What are the differentials to PRES?

A

Reversible cerebral vasoconstriction syndrome (RCVS)

PRES and RCVS may coexist [5]   
Demyelination 

Progressive multifocal leukoencephalopathy (PML)         

Autoimmune or paraneoplastic encephalitis

Viral encephalitis

Toxic leukoencephalopathy 

Acute hepatic encephalopathy

Osmotic demyelination syndrome        

Cerebral venous thrombosis

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13
Q

How would you manage a patient with PRES?

A

Blood pressure management

Individualised targets
Lower MAP 20-25% in 2 hours [7]
Neuroprotective measures

Anti-convulsive therapy and EEG monitoring

Steroids and diuresis are often used for vasogenic oedema

Renal replacement therapy if required

Ensure magnesium is corrected

Withdraw potentially offending agents

In SLE-related PRES: corticosteroids and cyclophosphamide

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14
Q
A
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