16 - Meningitis and Subarachnoid Haemorraghe Flashcards
What are the main differences between the three types of extracerebral haemorraghe? e.g mechanism, CT appearance, presentation, risk factors and management
What is the function of the subarachnoid space?
- Between arachoid and pia mater and contains CSF
- CSF can compensate when there is an increase in ICP by decreasing in volume
How does CSF drain from the ventricular system and spinal canal back to the blood?
Cilliary action of ependymal cells and vascular pulsations cause it to move and then reabsorbed into the sagittal sinuses via arachnoid granulations
What layer of the brain is the Circle of Willis situated in?
SUBARACHNOID
What is the epidemiology of subarachnoid haemorraghes?
- 6% of all strokes
- More prevalent in females 1.6:1
- Most under 50 (50-55)
- More common in black and Finnish
- 50% mortality, 60% long term problems after
What are some risk factors for a subarachnoid haemorraghe?
- Smoking
- Hypertension
- Excess alcohol consumption
- Predisposition to aneurysm formation e.g EDS
- Family history
- CKD, Marfan’s, Neurofibromatosis
- Trauma
- Cocaine use
How does a subarachnoid haemorraghe present?
- Thunderclap headache (sudden onset and severe, diffuse and sentinel can start up to a week before)
- Loss of consciousness and confusion
- Meningism (neck stiffness, photophobia, headache)
- Focal neurology
- History of sentinel bleed (previous headache)
- May present as cardiac arrest due to Cushing’s after bleed
What is the general pathophysiology of a subarachnoid haemorraghe?
- Rupture of a berry aneurysm or AVM in the circle of Willis and 80% non-traumatic
- Risk factors for developing aneurysms are the same as CVS e.g hypertension, genetic predisposition
Where do berry aneurysms in the cerebral circulation normally occur?
- ACA (30%): can compress optic chiasm and frontal lobe/pituitary
- PCA (25%): can compress occulomotor nuclei so ipsilateral third nerve palsy
- Bifurcation of MCA into superior and inferior (20%)
- Most in anterior circulation as lots of birfurcations and these are weaker
Why are large cerebral arteries affected by aneurysms more than the smaller ones?
- Small ones are less likely to rupture
- Intracranial large communicating arteries lack external elastic lamina and have thin adventitia so are weaker
Why may someone have sentinel headaches in the months before a subarachnoid haemorraghe and why do they get meningism when the aneurysm ruptures?
- Minor leaks from the aneurysm
- Blood gets into the subarachnoid space which is irritant
What happens when there is a bleed into the subarachnoid space that causes the early brain injury?
- Microthrombi can be released and occlue smaller distal arteries
- Vasoconstriction due to irritation by blood
- Cerebral oedema due to general inflammatory response of tissue hypoxia
- Apoptosis of brain cells
What are some cellular changes that occur when there is a subarachnoid haemorraghe?
- Oxidative stress due to reperfusion
- Release of inflammatory mediators activating microglia/paths
- Platelet activation so formation of thrombi
What are some systemic complications with a subarachnoid haemorraghe?
- Sympathetic activation due to Cushing’s response
- Myocardial necrosis due to sympathetic activation so appears as MI on ECG
- Systemic inflammatory response
- Can also get early rebleeding, acute hydrocephalus by blood blocking CSF drainage, global cerebral ischaemia
What imaging investigations do we do into a suspected subarachnoid haemorraghe and what signs would we see on the images?
- CT head without contrast as contrast will look like blood
- Filling of basal cisterns in five point star pattern
- May be blood in the ventricles
- Once confirmed do angiography to confirm location and do surgical planning