Subarachnoid haemorrhage Flashcards

1
Q

Why is subarachnoid haemorrhage important?

A
  • 5% of all strokes
  • high level of mortality and morbidity
  • 1/3 of survivors are dependent on carers
    1/2 have life-changing cognitive deficits
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2
Q

What are the causes of subarachnoid haemorrhage?

A
  1. Aneurysmal (ACOM, MCA bifurcation, PCOM)
  2. AVMs
  3. Trauma
  4. Moyamoya disease
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3
Q

What are the risk factors for SAH?

A
  1. age 40-60 years
  2. Hypertension
  3. Atherosclerosis
  4. Smoking
  5. Alcohol abuse
  6. Cocaine use
  7. Inherited conditions: Autosomal dominant polycystic kidney disease, collagen vascular disease.
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4
Q

How does SAH present?

A
  • Classical thunderclap headache - possible sentinel bleed headache
  • Nausea and vomiting
  • Altered consciousness
  • Neck stiffness
  • Photophobia
  • Coma
  • Seizures
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5
Q

How is SAH diagnosed?

A
  1. Unenhanced CT
  2. Lumbar puncture (after 12 hours symptom onset) for xanthochromia
  3. Digital subtraction CT angiography
  4. Cerebral angiography
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6
Q

How is SAH graded?

A

Clinically or radiologically

Clinically - WFNS:
1 - GCS 15 and no motor defect
2 - GCS 13-14 and no motor deficit
3 - GCS 13-14 with motor deficit
4 - GCS 7-12
5 - GCS <7
Radiologically - Fisher CT criteria
1 - no blood seen
2 - blood layers <1mm thick
3 - Localised clots or blood layers >1mm
4 - Non-subarachnoid blood or intraventricular involvement
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7
Q

What is the immediate management of SAH?

A

ABCDE approach to prevent secondary brain injury and focuses on neuroprotection.

A&B - control of airway in reduced consciousness and control of ventilation aiming pCO2 4.5-5.0 and pO2 >10
C - Optimise BP to prevent ischaemia from raised ICP or worsen bleed - target BP 80110. Nimodipine to prevent delayed cerebral ischaemia/vasospasm
D - seizure control and prevention of raised ICP, frequent pupil monitoring. Prompt CT scan.
E - Normothermia, normoglycemia. D/W neurosurgical centre.

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8
Q

What definitive management options are there for aneurysmal SAH?

A
  • Protective measures against secondary brain injury and delayed cerebral ischaemia.
  • Clipping or coiling of an aneurysm (ISAT trial 2002 - coiling had lower death and dependence but higher re-bleed risk).
  • prevention and treatment of other non-neurological conditions/complications
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9
Q

What is delayed cerebral ischaemia?

A
  • Neurological deterioration related to ischaemia (unrelated to treatment of the aneurysm) that persists for one hour and has no other cause.
  • May be caused by vasospasm:
    i) diagnosed by angiography or trans cranial doppler (Lindegaard ratio >3).
    ii) treated with:
  • nimodipine (Cochrane review found benefit in death and dependence)
  • Triple H therapy - only hypertension really used now
  • Endovascular interventions: angioplasty or vascodilator therapy
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10
Q

What are the complications following SAH and how are they managed?

A

Neurological:

  1. Obstructive hydrocephalus -> EVD
  2. Re-bleeding ->Re-coiling/clipping
  3. Seizures -> Exclude non-convulsive status, manage with AEDs.

Non-neurological:

  • Respiratory: VAP/aspiration/ARDS/neurogenic pulmonary oedema
  • CVS: Neurogenic stunned myocardium due NA release/Takotsubo cardiomyopathy/VTE
  • Metabolic: fever, hyperglycaemia/hypoglycaemia/SIADH/CSWS/DI
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