10.3 SAH and Meningitis Flashcards
What is the Epidemiology for SAH?
~6% of all strokes
Slightly more females 1.6:1
Mostly under 50
50% mortality; 60% suffer some longer term morbidity following the event
What are the Risk factors for SAH?
Hypertension Smoking Excessive Alcohol Trauma Cocaine use Family history Predisposition to aneurysm formation Associated conditions (Marfan's syndrome, CKD, Neurofibromatosis)
What is the pathophysiology of SAH?
Usually occur following rupture of an aneurysm in the circle of Willis. Most are berry aneurysms. Common sites include:
- Anterior communicating artery (30%)
- Posterior communicating artery (25%)
- Bifurcation of the middle cerebral artery (20%)
What does bleeding into the subarachnoid space cause? (3 broad categories)
- Early brain injury
- Cellular changes
- Systemic complications
Outline what happens in the early brain injury caused by bleeding into the subarachnoid space.
- Microthrombi formation -may occlude more distal branches
- Vasoconstriction -results from blood in the CSF ‘irritating’ cerebral arteries
- Cerebral oedema -general inflammatory response due to tissue hypoxia and extravasated blood
- Apoptosis of brain cells
Outline what happens in the cellular changes of the brain caused by bleeding into the subarachnoid space.
- Oxidative stress -related to reperfusion?
- Release of inflammatory mediators -activates many pathways as well as activation of microglia
- Platelet activation -formation of thrombi
Outline what systemic complications take place as a result of bleeding into the subarachnoid space.
- Systemic activation -early Cushing’s response
- Myocardial necrosis -due to sympathetic activation, typical ECG features (ST elevation, T wave inversion)
- Systemic inflammatory response -can affect multiple systems
What are the clinical features of SAH?
Thunderclap headache - diffuse pain, lasts hours to weeks
Frequently loss of consciousness and confusion
Meningism (neck stiffness, photophobia, headache)
May be focal neurology
History of sentinel bleed (slow bleed causing previous headache before thunderclap headache)
May present as cardiac arrest (Cushing’s response)
What investigations would be required for a SAH?
CT head - blood is hyperdense - seen as a ‘star pattern’ due to filling of the Basal Cisterns (blood may also be seen in the ventricles due to reflux from sub arachnoid space)
CT angiogram if bleed confirmed = direct visualisation
Lumbar puncture
Outline the technique for a lumbar puncture
Find the iliac crests (L4/L5 level)
Give local anaesthetic
Insert needle and feel for pop of ligamentum flavum
Remove needle stylet and collect CSF in sterile containers (dont aspirate! allow to drip!)
Take 3 samples (traumatic tap may cause blood in CSF)
What are the Lumbar puncture findings in a SAH?
Increased opening pressure (more volume from bleed = more pressure)
Frank blood or Xanthochromia (yellow colouring from bilirubin) may be seen (Xanthochromia more specific for SAH than frank blood (helps exclude a traumatic tap))
High protein (blood constituents and haemoglobin)
White cells often not raised; Glucose not affected
High red cell count
What is the treatment for a SAH?
ABC approach (support airway, give oxygen, support circulation with fluids and nimodipine to alleviate cerebral vasospasm) Neurological observations - look for trends indicating raised ICP (Cushings triad) Neurosurgery - Craniectomy, Coiling, Clipping
What is Coiling and why is it used in SAH?
Insertion of (Frequently) a platinum wire into the aneurysm sac, which causes thrombosis of blood within the aneurysm itself Performed by neuroradiologists
What is Clipping and why is it used in SAH?
Placement of a spring clip aroudn the neck of the aneurysm, causing it to lose blood supply and ‘shrivel up’
Performed by neurosurgeons
What typical organisms affects which ages in meningitis?
Neonates - E.coli, Listeria monocytogenes
Children - Haemophilus influenza type B, Neisseria meningitidis
Elderly - Streptococcus pneumoniae, Listeria monocytogenes
