Subarachnoid haemorrhage Flashcards

1
Q

Define subarachnoid haemorrhage (SAH)

A

Spontaneous bleeding into the subarachnoid space (between arachnoid mater and pia mater), often catastrophic

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2
Q

How common is it? Who gets SAH?

A

Incidence 9/100 000/yr;

Typical age: 35–65.

  1. 6x more common in women
  2. 1x more common in black ethnicity
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3
Q

What % of strokes is caused by SAH?

A

5%

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4
Q

What are the risk factors for SAH?

A
  • previous aneurysmal SAH
  • HTN
  • Smoking
  • FH - x3-5
  • ADPKD (autosomal dominant polycystic kidney disease)
  • alcohol
  • cocaine
  • bleeding disorders
  • Marfan syndrome/ Ehlers Danlos syndrome
  • Aortic coarctation
  • Pseudoxanthoma elasticum
  • Neurofibromatosis type I
  • SBE (mycotic aneurysms)

*Many of these genetic syndromes are associated with Berry aneurysms.

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5
Q

What is the aetiology of SAH?

A

80% - rupture of intracranial saccular aneurysms (non-traumatic)

20% - non-aneurysmal perimesencephalic SAH, arteriovenous malformations, arterial dissections, use of anticoagulants, and other rare conditions

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6
Q

Where do most cerebral aneurysms occur?

A

Cerebral aneurysms arise at the bifurcation of major arteries that form the circle of Willis. The majority are located at:

  • anterior communicating/anterior cerebral artery junction (Acom/ACA),
  • distal internal carotid artery/posterior communicating artery junction (ICA/Pcom),
  • and middle cerebral artery bifurcation (MCA).
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7
Q

What are the symptoms associated with SAH?

A
  • Sudden onset excruciating headache, typically occipital (“thunderclap”) - often lasting 1-5min. Speed of onset is diagnostic.
  • Sometimes preceded by a “sentinel” headache - perhaps from small warning leak from offending aneurysm (80%)
  • Vomiting
  • Collapse
  • Seizure
  • Coma/drowsiness may last for days
  • Photophobia
  • Confusion
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8
Q

What are the signs of SAH on examination?

A
  • Neck stiffness
  • Kernig’s sign (takes 6h to develop)
  • Retinal, subhyaloid and vitreous bleeds (Terson’s syndrome; increased mortality ~5)
  • Focal neurology may suggest aneurysm site (e.g. pupil changes = 3rd nerve palsy with PCA aneurysm) or intracerebral haematoma
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9
Q

Which conditions present similarly?

A
  • Meningitis
  • Migraine
  • Intracerebral bleed
  • Cortical vein thrombosis
  • Dissection of carotid/vertebral artery
  • Benign thunderclap headache (triggered by Valsalva maneouvres eg cough, coitus)
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10
Q

What investigations would you do for subarachnoid haemorrhage? Describe when these should be done.

A
  • Urgent non-contrast CT - detects >95% of SAH within 1st 24hrs
  • LP - if CT is negative but history is suggestibe of SAH. Needs to be done >12hours after headache onset to allow RBC breakdown for +ve xanthochromic sample (yellow, due to bilirubin differentiates between old blood from SAH vs “bloody tap”)

Other:

  • Electrolytes - may show hyponatraemia (<131mmol/L)
  • FBC - leukocytosis in SAH common
  • Clotting profile - elevated INR and PTT time
  • Troponin I - may be elevated but less than in MI
  • ECG - half of all patients have abnormal ECG on admission. Common cardiac findings in SAH include: Arrhythmias and ischaemic changes// Prolonged QTc // ST segment/T-wave abnormalities.
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11
Q

How do you manage SAH? (not on Sofia)

A

Refer all to neurosurgery .

Re-examine CNS often; chart BP, pupils, and GCS. Repeat CTif deteriorating.

Maintain cerebral perfusion by keeping well hydrated, but aim for SBP <160mmHg.

Nimodipine (60mg/4h PO for 3wks, or 1mg/h IVI) is a Ca2+ antagonist that reduces vasospasm and consequent morbidity from cerebral ischaemia.

Surgery:

  • endovascular coiling vs surgical clipping (requiring craniotomy): the decision depends on the accessibility and size of the aneurysm, though coiling is preferred where possible (fewer complications, better outcomes).
  • Do catheter or ct angiography to identify single vs multiple aneurysms before intervening.
  • Newer techniques such as balloon remodelling and flow diversion can be helpful in anatomically challenging aneurysms.
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