ischaemic stroke Flashcards
define ischaemic stroke
a clot blocks blood flow to an area of the brain
neurological dysfunction due to ischaemia and death of brain, spinal cord, or retinal tissue following vascular occlusion or stenosis.
define haemorrhagic stroke
bleeding occurs inside or around brain tissue
neurological dysfunction caused by a focal collection of blood from rupture of a blood vessel within the brain (intracerebral haemorrhagic stroke) or between the surface of the brain and the arachnoid tissues covering the brain (subarachnoid haemorrhagic stroke).
define ischaemia
- insufficient blood flow to the brain to meet metabolic demand
- This leads to poor oxygen supply or cerebral hypoxia, and may in turn lead to the death of brain tissue or cerebral infarction
- Ischaemia may be reversible
- Infarction is irreversible
pathway from ischaemia to infarction
Tissue hypoperfusion
- Dysfunction
Early & reversible failure of the Na+ K+ pump
- Some cellular oedema
Progressive failure Na+ K+ pump until an irreversible ‘tipping point’ is reached
- Sudden influx Na+ ions
Cytotoxic oedema
BBB opens for macromolecules
- Vasogenic oedema
BBB opens for RBC’s
- Haemorrhage into the infarct
define TIA
A brief episode of neurological dysfunction caused by focal brain and/or retinal ischaemia, with clinical symptoms typically lasting < 1 hour, and without evidence of acute infarction
what are the ages of a infarct
Hyperacute (1st 6 hours) late hyperacute (6 to 24 hours) Acute (up to 7 days) Subacute (up to 4 months) Chronic (after 4 months)
treatment for hyperacute infarct
The only approved therapy is intravenous thrombolysis with Alteplase within 4.5 hours of onset of stroke symptoms
Thrombolysis may not be given until haemorrhage has been excluded
Ix for stroke
unenhanced CT - highly sensitive for the detection of acute haemorrhage
FBC, U&Es, glucose, ESR, lipid profile ECG CXR CT head scan consider doppler USS of carotids CT is sensitive to the detection of stroke mimics e.g. tumour, arterial venous malformation (AVM) that could be the cause of the neurological defect
signs of cerebral infarct on CT
- Hypoattenuating
- Cortical-sub cortical
- Within a vascular territory
role of unenhanced CT
- Eliminate haemorrhage as a cause as itll preclude thrombolysis
- look for any early features of ischaemia
- exclude other intracranila pathologies that may mimc a stroke and determine further investigations
- May show a target - thrombosed vessel
- Identify infarctions that are too big, too old for thrombolysis (increased risk of haemorrhage) - based on hyppattenuation
role of MRI
Detection and diagnosis of acute infarction - Diffusion weighted imaging - Positive from 2 hours to 3 weeks - Useful ----- Previous CVD makes CT difficult ----- Difficult location for CT - posterior fossa ------ Equivocal case - query tumour? ------ Sensitivity - TIA clinic MRA and MRV
Immediate recognition of stroke done by which tools
outside of hospital - FAST
Exclude hypoglycaemia in people with sudden onset of neurological symptoms as the cause of these symptoms.
at ED use ROSIER
criteria to do CT
immediately at least within one hour
indications for thrombolysis or thrombectomy
on anticoagulant treatment
a known bleeding tendency
a depressed level of consciousness (GCS below 13)
unexplained progressive or fluctuating symptoms
papilloedema, neck stiffness or fever
severe headache at onset of stroke symptoms
thrombectomy might be indicated, perform imaging with CT contrast angiography following initial non-enhanced CT. Add CT perfusion imaging (or MR equivalent) if thrombectomy might be indicated beyond 6 hours of symptom onset.
oxygen therapy and sugar control
give oxygen only if their sats drop below 95%
maintain blood glucose between 4 and 11 mmol.l
who to offer thrombectomy
within 6 hours of symptom onset plus IV thrombolysis
- acute ischaemia stroke
- confirmed occlusion of the proximal anterior circulation demonstrated by CTA or MRA
last known to be well between 6 hours and 24 hours previously (including wake-up strokes):
- who have acute ischaemic stroke and confirmed occlusion of the proximal anterior circulation demonstrated by CTA or MRA and
- if there is the potential to salvage brain tissue, as shown by imaging such as CT perfusion or diffusion-weighted MRI sequences showing limited infarct core volume
Tx foe cerebral venous sinus thrombosis
full-dose anticoagulation treatment (initially full-dose heparin and then warfarin [INR 2 to 3]
when do you give BP medications
- hypertensive encephalopathy
- hypertensive nephropathy
- hypertensive cardiac failure/myocardial infarction
- aortic dissection
- pre-eclampsia/eclampsia.
Blood pressure reduction to 185/110 mmHg or lower should be considered in people who are candidates for intravenous thrombolysis.
attempt to reduce it after 2 weeks
earliest CT sign
hyperdense segment of a vessel which needs to be differentiated from a calcified cerebral embolus
most commonly affected vessel in stroke
middle cerebral artery
early hyperacute signs on CT
loss of grey-white matter differentiation, and hypoattenuation of deep nuclei
cortical hypodensity with associated parenchymal swelling with resultant gyral effacement
acute signs on CT
With time the hypoattenuation and swelling become more marked resulting in a significant mass effect. This is a major cause of secondary damage in large infarcts.
subacute signs on CT
As time goes on the swelling starts to subside and small amounts of cortical petechial haemorrhages result in elevation of the attenuation of the cortex. This is known as the CT fogging phenomenon 5.
Imaging a stroke at this time can be misleading as the affected cortex will appear near normal.
contrast CT or MRI will show you wrong
old infarct how does it look
well demarcated
very low density similar looking to CSF
negative mass effect
old infarct how does it look
well demarcated
very low density similar looking to CSF
negative mass effect
role of CT angiography
may identify thrombus within an intracranial vessel, and may guide intra-arterial thrombolysis or clot retrieval
what is a time attenuation curve
As contrast passes through the brain it causes a transient hyperattenuation directly proportional to the amount of contrast in the vessels of that region
how do you calculate cerebral blood flow
cerebral blood volume divide mean transit time
reduction in the CBV represents what
irreversible infarction
what can u use to distinguish ischaemia from infarction
CBF and CBV maps
if you have a large core infarct and do thrombolysis what risk does it increase
secondary haemorrhage
causes of ischaemic stroke
occluded by thrombus ((often as a complication of atherosclerosis)
Embolus of fatty material from an atherosclerotic plaque or a clot in a larger artery or the heart (often as a complication of atrial fibrillation or atherosclerosis of the carotid arteries).
causes of haemorrhagic stroke
Intracerebral haemorrhage – bleeding within the brain parenchyma or ventricular system. The main cause of intracerebral haemorrhage is high blood pressure.
Subarachnoid haemorrhage – bleeding into the subarachnoid space from a cerebral blood vessel, aneurysm or vascular malformation.
rarer causes of stroke
Cerebral venous thrombosis — more likely in patients with a prothrombotic tendency, for example, related to pregnancy, infection, dehydration or malignancy.
Carotid artery dissection — tends to occur in younger people and may be preceded by neck trauma.
risk factors of stroke
age men COCP Cardiovascular disease such as angina, myocardial infarction and peripheral vascular disease Previous stroke or TIA Atrial fibrillation Carotid artery disease Hypertension Diabetes Smoking Vasculitis Thrombophilia
early complications of stroke
Haemorrhagic transformation of ischaemic stroke.
Cerebral oedema.
Seizures.
Venous thromboembolism — pulmonary embolism
hydration and nutritional difficulties
pressure sores
spasticity with pain and/or contractures
Cardiac complications — cardiac complications (myocardial ischemia, congestive heart failure, atrial fibrillation, and arrhythmias) are common due to shared aetiology.
Infection — people with stroke are at increased risk of infection including aspiration pneumonia, urinary tract infection, and cellulitis from infected pressure sores.
long term complications
mobility sensory problems continence problems pain fatigue problems with swallowing, hydration adn nutrition sexual dysfunction skin problems visual problems cognitive problems difficulties with activities of daily living emotional and psychological problems communication problems financial problems
mobility complications from stroke
hemiparesis or hemiplegia
ataxia
falls
spasticity and contractures
when do you suspect a TIA
sudden onset, focal neurological deficit which has completely resolved within 24 hours of onset and cannot be explained by another condition such as hypoglycaemia
- Unilateral weakness or sensory loss.
- Dysphasia.
- Ataxia, vertigo, or incoordination.
- Syncope.
- Sudden transient loss of vision in one eye (amaurosis fugax).
- Homonymous hemianopia.
- Cranial nerve defects.
when do u suspect stroke
longer than 24 hours onset
- Confusion, altered level of consciousness and coma.
- Headache – sudden, severe and unusual headache which may be associated with neck stiffness. Sentinel headache(s) may occur in the preceding weeks.
Weakness − sudden loss of strength in the face or limbs.
Sensory loss – paraesthesia or numbness.
Speech problems such as dysarthria.
Visual problems – visual loss or diplopia.
Dizziness, vertigo or loss of balance — isolated dizziness is not usually a symptom of TIA.
Nausea and/or vomiting.
Specific cranial nerve deficits such as unilateral tongue weakness or Horner’s syndrome (miosis, ptosis, and facial anhidrosis).
Difficulty with fine motor co-ordination and gait.
Neck or facial pain (associated with arterial dissection
when to suspect a posterior circulation strok
Symptoms of acute vestibular syndrome — acute persistent continuous vertigo dizziness with nystagmus nausea or vomiting head motion intolerance new gait unsteadiness.
what do you ask in the histroy
clinical features mentioned such as
headache
vomiting
decreased level of consciousness
time of onset, activity at onset
risk factors mentioned CVS disease smoking alcohol
PMH - miscarriage thromboembolic events past myocardial infarct (MI) • recent chest pain suggesting recent MI (or thoracic root aortic dissection) • atrial fibrillation • rheumatic fever as a child • valvular heart disease or valve replacement • symptoms of heart failure • palpitations • pacemaker PVD
FH of stroke or hyperlipidaemia or hypercoagulability
current medications such as anticoagulants, HRT or illicit
always take a collateral history ie witness ambulance personnel family members
What has MRI showed in terms of TIA lasting longer than an hour
associated with a new infarction
what conditions have a sudden onset
stroke
epilepsy
trauma
what conditions have subacute onset that build up over hours or days
infectious
inflammatory
metabolic
malignant
main differentials for stroke/TIA
blackouts/syncope
epilepsy
migraine with aura
metabolic, particularly hypoglycaemia
Mx of stroke acutely
MDT involved who
- aspirin 300 mg AFTER CT SCAN daily for 2 weeks then clopidogrel 75 mg daily long-term.
- Thrombolysis w altpeplase - tissue plasminogen activator
- refere to stroke unit
- monitor BP
secondary prevention
A statin should also be offered if the patient is not already on statin therapy.
aspirin
stop smoking
LONG TERM Nurses Speech and language (SALT) Dieticians Physiotherapy Occupational therapy Social services Optometry and ophthalmology Psychology Orthotics speech therapy liaison between district services and social workers
Diagnostic of which area is affected
diffusion weighted MRI
how do u initially manage a stroke pt
reassure pt monitor GCS CT/MRI to distinguish bloods - glucose, U&Es, FBC - polycythaemia, ESR ECG- AF,MI NBM
