5 - stroke pathophysiology and clinical management Flashcards
when is someone in a hyper-acute stroke unit and when is repatriation?
- <48 hrs — HASU
- repatriation at 72 hours
what is the WHO definition of a stroke?
a clinical syndrome characterised by the rapid onset of focal or global cerebral deficit lasting more than 24 hours or leading to death with no other apparent cause than a vascular one
- RAPID ONSET
- FOCAL OR CEREBRAL
- LAST MORE THAN 24 HRS (if less = TIA)
what are the 2 main subtypes of stroke?
- ischaemic = 85%
- haemorrhagic = 15%
- intracerebral
- subarachnoid
what are typical imaging appearances in an ischaemic stroke?
- wedged-shaped hypodensity with complete loss of grey-white matter differentiation
- localised swelling with sulcal effacement
- in a recognisable arterial territory
what are some hyper acute ischaemic changes seen in scanning?
what would a stroke look like on CT angiogram?
how much tPA is given over one hour?
1mg/kg
what is the aim of intravenous thrombolysis?
dissolve thrombus to allow reperfusion
intravenous thrombolysis is only beneficial if administered when?
<4.5 hours after stroke
what % of UK patients are eligible for intravenous trhombolysis?
12%
what are 2 significant risks of intravenous thrombolysis?
- haemorrhage — 1/30
- angioedema — not usually too harmful, allergic reaction, 1/14
what is mechanical thrombectomy?
stent retriever used to pull clot out
what is the treatment window from onset for mechanical thrombectomy?
<6 hours
what estimated % of people are eligible for thrombectomy?
10-15%
describe secondary prevention of ischaemic stroke
> identify cause — athero-thrombo-embolism (50%), cardioembolic (20%), small vessel disease (25%), miscellaneous rare causes (5%)
> aspirin (1x daily for 2 weeks) then clopidogrel long term
> statin
> BP management (systolic BP <130 mmHg long-term)
> atrial fibrillation — anticoagulation if risk:benefit favourable
> carotid revascularisation
how does ICH lead to herniation syndromes?
very large haematomas — pushing structures over to the side — causes herniation syndromes
second injury in ICH?
toxic products such as thrombin, Hv, heme, iron in haematoma — damage surrounding brain tissue
what do heme and iron trigger?
inflammatory action — worsens damage
what is the target systolic BP over first 24 hours in hyper acute setting?
130-140 mmHg
why is there uncertainty for intensive BP lowering for larger haematomas (>30ml)?
raise intracranial pressure — can reduce cerebral perfusion pressure — could cause ischaemia by dropping BP dramatically
what are risks in infratentorial ICH? what does the infratentorium region include?
- brainstem compression, herniation syndromes, hydrocephalus
- region below tentorium. includes brainstem and cerebellum (relatively small space)
what neurosurgery procedures can be carried out for an infratentorial ICH?
- EVD = external ventricular drain — to relieve hydrocephalus. goes into frontal horn of lateral ventricle to relieve pressure above when there is a blockage below in posterior fossa
- posterior fossa decompression — remove some of posterior cranium
- haematoma evacuation — remove mass
neurosurgery for supratentorial ICH?
- early haematoma evacuation in the stable patient
- haematoma evacuation in the detiorating patient
- external ventricular drainage for hydrocephalus
are the majority of ICH infra or supratentorial?
supra
what is the ABC hyper acute care bundle?
A : anticoagulant reversal : deliver reversal agent <90 min from arrival
B : blood pressure lowering : deliver intensive bp lowering with needle-to-target time < 60 min (time from giving 1st dose to reaching the target BP)
C : care pathway : refer patients with good pre-morbid function and any of the following to neurosurgery
- GCS < 9
- posterior fossa ICH
- obstructed 3rd/4th ventricle
- haematoma volume > 30ml
what is the most common structural cause of ICH?
hypertensive microangiopathy — due to high BP on deep arteries of the brain
what is cerebral amyloid angiopathy?
- a structural cause of ICH
- amyloid protein builds up in arteries in particular at cortico-subcortical junction, particularly posterior aspect of brain — vessels fragile and prone to rupture — causes lobar bleeds and bleeding over surface of brain — cortical superficial siderosis — bleeding in sulci
