Subarachnoid haemorrhage Flashcards
Clinical features of SAH
-thunderclap headache
- nausea/vomiting
-decreased LOC
-photophobia & neck stiffness ( irritation of meninges by blood)
- seizures
-focal neurological signs
-raised ICP
WHat is a SAH?
Rupture of the cerebral vessels, usually from circle of Willis, into subarachnoid space ( can also bleed into ventricles)
Causes of SAH
1) Intracranial aneurysms
-ACA/ACOM
-MCA
-PCOM
-Basilar artery bifurcation
2) AVM
3) trauma
Risk factors for SAH
-smoking
-alcohol abuse
- cocaine use
-hypertension
-male
-age (40-60 peak risk)
How is SAH diagnosed?
-Non contrast CTH
-CTA can be used to differentiate underlying cause
- LP >12 hrs after symptom onset if CT non-diagnostic - CSF sent for xanthochromia
Grading of SAH
World federation of Neurosurgeons
1 - GCS 15, no deficit
2 - GCS 13-14, no motor deficit
3 - GCS 13-14, with motor deficit
4 - GCS 7-12 +/- motor deficit
5 - GCS <6 +/- motor deficit
How to manage patient with SAH?
A&B - Intubation as needed
Neuroprotective ventilation - PaO2 >10, PaCO2 4.5-5
Head elevated to promote venous drainage
Tube ties not tight
C -SBP<160 or MAP <110 - use labetalol as needed
SBP should be maintained >100 with fluids/vasopressors
D- Monitor pupils, assess neurology, normothermia, normoglycaemia
E - securing of aneurysm - coiling or clipping
Neurological complications of SAH
1) Vasospasm or delayed cerebral ischaemia
- neurological deterioration related to ischaemia that persists for 1hr with no other cause
-most common 4-10 days post SAH
- can be demonstrated on CTA or DSA
- treat with nimodipine -60mg every 4 hrs for 21 days
- hypertensive therapy -
2) Obstructive hydrocephalus - CTH -treat with EVD
3) Re-bleed
4) Seizures -AEDs
Other complications of SAH
1) Neurogenic pulmonary oedema - massive chatecholamine surge causes pulm. artery hypertension and injury to capillary alveolar membrane
2) Neurogenic stunned myocardium syndrome - noradrenaline release results in intracellular calcium depletion and myocyte death - causes ECG changes, arrhthmias, transient LV dysfunction, may have trop rise
3) Fever - associated with worse outcomes
If not infective cause, can be due to hypothalamus change to set point
4) Hyperglycaemia - marker of severity in SAH
5) Disorders of sodium balance
What is the pathophysiology of cerebral salt wasting?
Can occur following brain injury (particularly SAH &TBI) and causes polyuria, hyponatraemia and hypovolaemia as a result of losing sodium through the kidneys.
Diagnosis of cerebral salt wasting
Serum sodium - low
Urine sodium - high (>40meq/l)
Serum osmolality - high
urine osmolality - high
Evidence of hypovolaemia - raised haematocrit, raised urea
Treatment of CSW
1) FLuid replacement and correction of sodium - n.saline fluid resuscitation
Which disorders of sodium balance may occur with SAH
1) cerebral salt wasting
2) SIADH
3) Cranial DI
