S9) Subarachnoid Haemorrhage and Meningitis Flashcards
What are the 3 layers of the meninges and describe them?
The 2 layers of the dura are firmly adhered to each other except where they split. These are:
– To enclose venous sinuses
– To form dural septa (4 important ones)
Identify 4 important dural septa
- Falx cerebri (between/ divides cerebral hemispheres)
- Falx cerebelli (between/ divides cerebellar hemispheres)
- Tentorium cerebelli (supports the occipital lobes and separates it from the cerebellum)
- Diaphragma sella (covers the superior surface of the pituitary gland and has a hole in it to allow passage of the infundibulum)
Differentiate between the extradural (epidural) and subdural bleeds in terms of what causes it, what is the presentation like, and what it would look like on an CT scan
Describe the structure of the subarachnoid space.
Located between arachnoid and pia
Contains enlarged regions called cisterns
• Occur where brain moves away from skull
What does the subarachnoid space contain?
CSF
The subarachnoid space is filled with CSF. What is the function of the CSF?
– Physical support of neural structures - makes the brain buoyant
– Excretion (of brain metabolites)
– Intracerebral transport (hormone releasing factors)
– Control of chemical environment
– Volume changes reciprocally with volume of intracranial contents
• Blood — i.e. it will reduce its volume in the case of a raised ICP as a compensatory mechanism
What forms CSF?
• Formed by choroid plexuses - which are capillaries in loose connective tissue which filter plasma from the blood to produce CSF (and extra-choroidal structures)
What is the flow of CSF?
Flow:
- Lateral ventricles
- -3rd ventricle-(aqueduct of Sylvius)
- -4th ventricle (median and lateral apertures)
- subarachnoid space (small amount into spinal cord) , also into cistern where CSF will be drained into venous blood via the arachnoid granulations that project into the dural venous sinuses
Propelled by newly formed fluid, ciliary action of ventricular ependyma, vascular pulsations
What is subarachnoid haemorrhage?
Extravasation of blood into the subarachnoid space
Can occur in trauma but we are going to be talking about non-traumatic (spontaneous)
What is the epidemiology of SAH?
▪ ~6% of all strokes
▪ Slightly more females 1.6:1
▪ More likely in black, Finnish and Japanese populations
▪ Average age of onset is 50-55 yrs
▪ 50% mortality, 60% suffer some longer term morbidity following the event
Identify the risk factors for SAH
– Hypertension
– Smoking
– Excess alcohol consumption
– Predisposition to aneurysm formation
– Family history
– Associated conditions:
o Chronic kidney disease (resultant effect on vessel wall)
o Marfan’s syndrome (effect on connective tissues of vessels)
o Neurofibromatosis (unclear mechanism, if any link)
– Trauma
– Cocaine use
How do patients with SAH present?
– Thunderclap headache (48%) - sudden and painful headache - explosive in onset and severe, often reported as worst headache ever or even ‘like being hit on the head with a cricket bat’
– Dizziness
– Orbital pain
– Diplopia
– Visual loss (anterior communicating artery aneurysm)
What is the pathophysiology of SAH?
▪ Usually occur following rupture of an aneurysm in the circle of Willis
Accounts for 80% non-traumatic
• Rupture of AVMs -10%
What and how do aneurysms arise?
Aneurysm is a weakness in a vessel (usually artery) wall which can cause an abnormal bulge.
Aneurysms develop due to pressures on the arterial wall (vessels in subarachnoid space)
May be a genetic predisposition to aneurysm formation
May be caused by haemodynamic effects at branch points in the circle of Willis (e.g. higher resulting flow rate in progressively smaller branches, turbulence)
Most are berry aneurysms (as they look like berries).
Describe the features of aneurysms - in relation to SAH.
– Usually at bifurcation points
– Large cerebral arteries in anterior circle of Willis most affected
– Intracranial arteries lack external elastic lamina and have thin adventitia
– Small aneurysms (<5mm) unlikely to rupture
What are the common areas of aneurysms to be found in terms of SAH? (mostly berry aneurysms)
Common sites, making up 75% of all aneurysms:
– Anterior communicating artery / proximal anterior
cerebral artery (30%)
▪ Can compress the nearby optic chiasm and may affect frontal lobe or even pituitary
– Posterior communicating artery (25%)
▪ Can compress the adjacent oculomotor nerve causing an ipsilateral third nerve palsy
– Bifurcation of the middle cerebral artery as it splits into superior and inferior divisions (20%)
Identify the risk factors for aneurysm formation causing SAH?
– Same as cardiovascular- hypertension, smoking etc
– Alcohol ++
Identify the typical symptoms and examination findings of SAH.
Clinical features
▪ Thunderclap headache:
• Explosive in onset and severe, often reported as worst headache ever or even ‘like being hit on the head with a cricket bat’
- Diffuse pain
- Can last from an hour to a week
▪ Frequently loss of consciousness and confusion
▪ Meningism
• Neck stiffness • Photophobia • Headache
▪ May be focal neurology
▪ May be history of sentinel bleed (previous headache)
▪ May present as cardiac arrest (if intracranial pressure rises rapidly following bleed leading to profound Cushing response)
What complications can arise from a subarachnoid haemorrhage?
– Early brain injury:
o Microthrombi
▪ These may occlude more distal branches
o Vasoconstriction
▪ As a result of blood in the CSF ‘irritating’ cerebral arteries
o Cerebral oedema
▪ General inflammatory response to tissue hypoxia and extravasated blood
o Apoptosis of brain cells
– Cellular changes:
o Oxidative stress
▪ Maybe related to reperfusion?
o Release of inflammatory mediators
▪ Can activate many pathways as well as activation of microglia
o Platelet activation
▪ Formation of thrombi
– Systemic complications:
o Sympathetic activation
▪ Early Cushing response
o Myocardial necrosis
▪ Due to sympathetic activation
▪ Interestingly, SAH has typical ECG features
o Systemic inflammatory response
▪ Can affect multiple systems
What is the first line investigation you would do for a subarachnoid haemorrhage?
– CT head scan - do an urgent non-contrast CT scan (don’t do contrast as blood acts as a contrast)
– Will detect 93% if done within 24 hours of bleed
Small amounts of blood can be hard to see on CT scan.
- Prominent filling of the basal cisterns in a five pointed ‘star’ pattern
- Blood may be seen within the ventricles (maybe due to
reflux from subarachnoid space)
If we have a convincing history, but negative CT scan, what should we do next?
– Lumbar puncture
– CSF analysis
What are we looking for in the lumbar puncture?
– Increased opening pressure (as there is now additional volume in the subarachnoid space)
– Frank blood or xanthochromia may be seen
▪ Xanthochromia is a yellow colouring of the CSF due to metabolism of haemoglobin to bilirubin within the subarachnoid space
▪ Seen at least 12 hours post bleed
▪ More specific than frank blood for SAH (helps exclude a bloody/traumatic tap)
– High protein (blood constituents and haemoglobin)
– White cells often not raised
– Glucose not affected
– High red cell count
When performing a lumbar puncture, why do we need to wait at least 6 hours (12+ is preferable) for a SAH?
We need time for the lysis of red blood cells to take place (release of bilirubin) and therefore gives the CSF with a yellow tinge after centrifuging it - known as Xanthochromia
We need to be able to differentiate it from the traumatic tap - this is where as we perform the lumbar puncture, we go through other blood vessels on our way to the subarachnoid space and .: can get blood leaking into the CSF as a result and making it hard to diagnose the cause behind the bleed.
