Session 10: Subarachnoid Haemorrhage and Meningitis Flashcards
Epidemiology of SAH.
6% of all strokes.
More common in females than males 1.6:1
Most are under 50
Prognosis of SAH.
50% mortality
60% suffer some longer term morbidity following the event if they survive.
Risk factors of SAH.
Hypertension
Smoking
Excess alcohol consumption
Predisposition aneurysm formation
FH
Trauma
Cocaine use
Give associated conditions with SAH.
CKD
Marfan’s syndrome
Neurofibromatosis
What is the most common pathophysiology of an SAH?
A rupture of an aneurysm in the circle of Willis.
Why might there be an aneurysm in the circle of Willis?
Genetics
Haemodynamic effects at branch point in the circle of Willis leading to turbulent flow.
What are the most common type of aneurysm in SAH?
Berry aneurysm
Common sites of aneurysm in circle of willis leading to SAH.
Anterior communicating artery/proximal ACA (30%)
Posterior communicating artery (25%)
Bifurcation of the middle cerebral artery as it splits into superior and inferior divisions (20%)
Specific structures at risk of Anterior communicating artery/proximal ACA aneurysm.
Can compress nearby optic chiasm leading to bitemporal hemianopia.
May affect frontal lobe or even pituitary.
Specific structures at risk of posterior communicating artery aneurysm.
Compression of CN III leading to ipsilateral third nerve palsy.
What will bleeding into the subarachnoid space cause?
Early brain injury
Cellular changes
Systemic complications
What causes early brain injury due to bleeding into subarachnoid space?
Microthrombi which can occlude more distal branches.
Also vasoconstriction as a result of blood in the CSF irritating cerebral arteries.
Cerebral oedema due to general inflammatory response.
Apoptosis of brain cells.
Explain the cellular changes in bleeding into subarachnoid space.
Oxidative stress
Release of inflammatory mediators and activation of microglia.
Platelet activation which will lead to formation of thrombi.
Systemic complications of bleeding into subarachnoid space.
Sympathetic activation and early cushing response.
Myocardial necrosis due to sympathetic activation.
Systemic inflammatory response.
Clinical features of SAH.
Thunderclap headache
Frequently loss of consciousness and confusion
Meningism
Can have focal neurology
Can have a history of sentinel bleed
May present as cardiac arrest (profound Cushing response)
Features of thunderclap headache.
Explosive in onset and severe commonly described as being hit on the head with a cricket bat.
Diffuse pain
Can last from an hour to a week.
Features of meningism.
Neck stiffness
Photophobia
Headache
Investigations of SAH
CT head
CT angiogram if a bleed is confirmed
Lumbar puncture
What will a CT head look like in SAH?
Five pointed star pattern
Blood may be seen within the ventricles
Why is a CT angiogram performed if the bleed is confirmed?
To allow direct visualisation of bleeding aneurysm of aneurysm sac.
This is important for planning surgery
Explain LP technique.
Feel for iliac crests at around L4/L5
Give local anaesthetics
Insert LP needle between spinous processes and through the supraspinous and interspinous ligaments.
Feel the give as you pass through the ligamentum flavum and dura.
Remove needle and collect CSF in sterile containers.
LP findings in SAH.
Increased opening pressure
Frank blood or xanthochromia
HIgh protein
White cells often not raised
Glucose not affected
High red cell count