Stroke Flashcards
What is a neurovascular unit?
It is a functional unit of the CNS.
Composed of neurons, glial cells and endothelium (including BBB).
How does a stroke occur?
There is a hypoperfusion of the endothelial lumen which causes a reduction in available glucose and O2. This leads to reduction in ATP synthesis and so any processes requiring ATP will be affected.
Membrane transport is the ATP dependent process mostly affected, where this is the process underlying the generation of AP.
An AP is an ‘all or nothing’ pattern of firing. Therefore if there is a low ATP in the NVU the AP won’t set off and so move from the ability of achieving neuronal transmission to total cessation. I.e. the symptoms of stroke will present suddenly, without any progression in symptoms.
What are the typical symptoms of stroke?
Sudden onset- this is due to the loss of AP firing, so any gradual onset symptoms would imply an alternative diagnosis.
Focal- Since only a branch of the cerebrovasculature is affected, only the NVU in this area are impacted.
Loss of function- Since have a cessation of AP.
Collection of symptoms can relate back to the vascular territory of hypoperfusion.
Symptoms do not typically migrate in a stroke syndrome since the loss of AP is a sudden change, commonly visual and sensory symptoms will migrate in common stroke mimics.
Episodes do not typically stereotype- i.e. the symptoms do not repeat in an identical fashion, in relation to a stroke this would mean embolization to the same vessel, which is highly unlikely.
What is capsular warning syndrome?
Intermittent hypoperfusion of the lenticulostriate arteries/the equivalent in the PCA and ACA leads to the appearance of intermittent/fluctuating impairments. These recurrent events recur over minutes to hours and so is different from non vascular stereotyping occurring over days/weeks/years.
What are the different groups of stroke mimics?
Group 1- Readily identifiable on imaging i.e. cerebral abscess, brain tumour, MS, subdural haematomas, where MRI may be more useful than CT.
Group 2- Distinguishable from stroke on clinical grounds i.e. BPPV, vestibular neuronitis, Bell’s palsy, syncope syndrome etc.
Group 3- Exclusion from stroke syndrome requires specialist stroke assessment using brain imaging i.e. migraine with aura, focal seizures, functional syndrome etc.
What are some types of stroke mimics?
1) BPPV- Vertigo is a common presentation of stroke syndrome and common stroke mimics. Vertigo on changing positions, associated vomiting, examine and confirm with Dix-Hallpike test and Epley maneuver.
2) Vestibular neuronitis- Sudden onset vertigo, since isolated presentation of vertigo it is less likely to be stroke. Head thrust test will confirm the diagnosis.
3) Transient Global Amnesia- Dysfunction of ‘episodic’ memory, whilst procedural memory stays in tact. Px memory affected at the stages of registration, storage and retrieval, where Px will repeatedly ask the same Qs and once the TGA resolves, they have no recollection of the event, having a ‘gap’ in their memory.
4) Migraine with aura- There is a migration of symptoms due to cortical spreading depression.
5) Functional syndrome
6) Apparent neurological deficits- Areas of gliosis (scarring of the brain) exist, where during ‘optimal conditions’ the Px functions normally. In suboptimal conditions i.e. hypoglycaemia, hypoxia, sepsis, dehydration, poor sleep there is underperformance and so symptoms become apparent.
7) Focal seizures
What are some possible chameleons of stroke?
Venous infarct Small cortical strokes Limb shaking TIA Occipital stroke Stroke amnestic syndromes Stroke mimicking vestibular dysfunction
What is the cause of the stroke?
What are the complications of stroke?
Complications arise as a result of Px being in a state of having had a stroke. Sensory/functional loss from the stroke do not constitute the complciations.
Recurrent stroke
Immobility- Pressure sores, DVT, constipation
Raised ICP- hydrocephalus, malignant oedema.
Infections
Mood/cognitive issues
Post stroke fatigue
Post stroke pain
Spasticity, contractures, secondary epilepsy
How are complications of stroke prevented?
Anticipate them!
Surveillance- daily review of obs, mood, chest, bowel etc
Timely bloods- CRP looking for infection, Hb
How would you manage and prevent the complications of stroke?
Complications of a stroke:
-Care bundle; admit to stroke unit, revascularisation*, surveillance, nutritional support, secondary prevention, rehabilitation.
*Revascularisation:
IV alteplase in 4.5hr therapy window
Thrombectomy in Px with large vessel occlusion, in 6hr therapy window.
NIHSS- examination of stroke Px giving clues about aetiology, prognosis, therapy, recovery and/or deterioration.
Secondary prevention of a stroke:
- Aeitology
- Antithrombotic therapy
- BP control
- Lipid control
- Glycaemic control
- Carotid endarterectomy
- Lifestyle changes i.e. smoking cessation, weight loss, optimising sleep, exercise etc.
How is an intracerebral hemorrhage managed?
The haematoma will result in an increased ICP therefore need to anticipate this and manage with BP control, correcting clotting derangements, managing glycaemic control.
Can also consider neurosurgery for managing increased ICP, although this requires a balance between surgical accessibility and neurological stability.
What are the prognostic groups of stroke Px?
Unstable- Requiring multiple assessments to evaluate the usefulness of interventions.
Stable but high risk of stroke complocations- Need close surveillance
Stable- Standard attention and review.
What is the current pathway for stroke presentation?
Call 999
Paramedic do FAST test
If +ve then refer to LRI ED, where stroke team are alerted.
If -ve then discuss other possible routes.
What are the 5 priorities following a stroke presentation to ED?
Confirm diagnosis, weigh Px, find out if for thrombolysis, bloods, CT, obs Identify any contraindications Gain consent/assent Imaging Bolus and infusion
What are the indications of alteplase?
- Alteplase can be administered within 4.5 hrs
- Disabling impairments (NIH >4, dysphasia, inability to self care or mobilise independently, visual field defect, dysphagia).
- No contraindications
What are the contraindications of alteplase?
Blood pressure > 185/110 mmHg after 2 attempts to reduce levels
Seizure at onset of stroke
Symptoms suggestive of a subarachnoid haemorrhage
Stroke/head injury within the last 3 months
Active internal bleeding
Severe haematology abnormalities
INR>1.7 or APTT>40
On dabigatran with abnormal APTT or thrombin time >100 seconds
On rivaroxaban / apixaban / edoxaban
On high-dose LMWH
Platelet count <50 x 109/L
etc
What are the relative contraindications of alteplase?
What are the optimal areas to image for a stroke presentation?
Pipes- Blood vessels using CT angiography (may use MR). Confirms large vessel occlusion so would be the starting point for thrombectomy. Can also show evidence of good collateral circulation.
Parenchyma- Explore the tissue, using non contrast CT or MRI
Perfusion- Identify tissue at risk- hypo perfused to give symptoms but no cell death.
Penumbra- Identify tissue at risk- hypo perfused to give symptoms but no cell death. Use perfusion scans which will represent areas of hypoperfusion on one image and areas of infarction on another image of the same area- the area of penumbra = hypo perfused area - the infarct volume.
What are the important points of consenting a Px for thrombolysis?
The earlier the treatment is given the better the odds of recovery.
Giving alteplase:
- 1/3 benefit compared to not having alteplase.
- 1/10 have a chance of full recovery.
- 1/50 chance of allergic reaction.
Practical details of giving the infusion, details of monitoring.
Explain the risk of bleeding.
What is thrombolytic therapy?
The use of alteplase in an ischaemic (80% of all strokes) stroke.
Steps of stroke management:
1) FAST +ve
2) ED notified
3) Px imaged and haemorrhagic stroke ruled out, contraindications assessed, consent obtained.
4) Alteplase adminstered
Alteplase:
Given if Px presents within 4.5hrs of stroke onset.
Dose calculated based of weight.
10% given as an initial bolus over 1-2 minutes.
Remaining 90% given as an infusion over 1hr.
How is a Px on thrombolytic therapy monitored?
Potential of many complications.
Monitored neurologically and haemodynamically every 15 mins during the infusion, checking pulse, BP, GCS, pupil reaction, asking about headaches, vision changes etc.
If any suspected anaphylaxis or bleeding then infusion paused and Px is imaged.
After 24hrs the Px will undergo a CT head to pick up any potential causes of raised ICP, which were not apparent on regular monitoring.
What are the complications of thrombolysis?
Adverse effect of thrombolysis and alteplase
Evolution of stroke causing rising ICP-
- Oedema
- Hydrocephalus
Seizure
Infection
Metabolic disturbance
Bleeding is the main and feared risk of alteplase infusion. If this is the case, pause the alteplase treatment, image, give reversal drugs, blood transfusion, may require surgery also. Extracerebral haemorrhage- -Thin thready pulse, drop in BP - Maleena - Distended abdomen
Intracerebral haemorrhage-
- Neurological decline
- New headache
- Rising BP
- N+V
Why is alteplase not effective with large vessel occlusion?
Alteplase is a fibrinolytic agent, so therefore requires a communication with fibrin. In larger vessels, the thrombus is such that most of the firbin is hidden and so can’t communicate with the alteplase, rendering it ineffective.
What is thrombectomy?
The management of choice in large vessel occlusion stroke, pre stroke MRS score of 0/1, NIHSS>/= 5/
Within 6hrs of stroke symptoms onset.
At the time of the CT, patient should also have a CT angiography, where the quality of collateral circulation should also be assessed.
What is the process of a thrombectomy?
- Catheter inserted through the femoral artery then through the carotid.
- A microcatheter is pushed out (from the point at the carotid artery) and pushed along through the offending clot.
- A Merci Retriever is pushed through the catheter and the catheter withdrawn.
- The stent will open up, where the blood flow will push the stent up against the clot, adhering the clot to the stent.
- A balloon at the level of the carotid catheter is inflated to stop any blood flow, and create blood flow illusion towards the carotid artery balloon*.
- The stent is withdrawn along with the adhered clot, through the carotid balloon.
*This creates a ‘vacuum’ so that if any pieces of the clot were to break off, they are removed from the body as opposed to being allowed to distally circulate.
What is a haemorrhagic transformation?
Complication of an ischaemic stroke, usually post cardioembolic strokes. This is because this is a sudden event, where the collateral arteries do not have time to be recruited and so there is a lack of protection of the BBB, as opposed to carotid disease which is a more gradual course.
BBB dysfunction leads to peripheral blood extravasation into the brain.
Developing 2-14 days post stroke
Can still give anti-platelets as treatment, if indicated.
What is the importance of AF in stroke?
A common cause of stroke, where the outcomes are more severe due to lack of collateral circulation mobilisation.
AF is becoming more prominent due to the aging population.
Can identify AF through clinical examination, ECG and prolonged cardiac monitoring.
As a primary prevention technique CHA2DS2VASc score is used to identify the risk of stroke.
HASBLED is used to identify the bleeding risk of a Px.
Mainstay secondary prevention is anticoagulation, where DOACS (rivaroxaban, apixaban, edoxaban and dabigatran) are preferred to Warfarin.
If anticoagulation is contraindicated then left atrial appendage closure is recommended as the alternative method of secondary prevention.
What is the importance of temporal arteritis and stroke?
Increases the risk of ischaemic stroke.
Need to start high dose steroid therapy, even without the confirmation of a diagnosis.
What is the importance of metabolic syndrome in stroke?
Metabolic syndrome is a combination of obesity, dyslipidaemia, insulin resistance and HTN.
This is a risk to developing a stroke and so stroke prevention would include measures such as; -Weight loss -Good BP control -Lipid control -Glycaemic control -Smoking cessation -Alcohol reduction -Optimisation of sleep etc.
What are the complications of metabolic syndrome?
- Vasculopathy- stroke, IHD, PVD
- Obstructive sleep apnoea- Even with good BP control, there can be nocturnal spikes in BP which can lead to a ‘hypertensive’ ICH.
- Non-alcoholic steatohepatitis can lead to liver cirrhosis.
- Malignancy
- Osteoarthritis
- Chronic venous insufficiency leading to ulcers, complex regional pain syndrome.
- Difficulties with conception.
- Cognitive dysfunction- Can include cerebrovascular disease or a normal sleep deprived brain.
What is the importance of carotid disease and stroke?
Disease progression at the carotid artery due to;
1) Disturbance of laminar flow at the carotid bifurcation, therefore usual location of carotid stenosis.
2) Endothelial damage- This can be due to turbulent flow, HTN, toxins (from smoking) etc.
Arethomatous plaques are the equivalent of ‘scar tissue’, growing over the damaged endothelium. The plaque progression depends on the cells involved, i.e. a diabetic Px or one with controlled dyslipidaemia will have a macrophage dense plaque with foam cells.
A stable plaque has a nice layer of endothelium over the plaque, so regardless of the reduced lumen size, is unlikely to embolise.
An unstable plaque has a raw top layer engaging in inflammation/clotting so will easily embolise.
What are the secondary preventative management plans for stroke induced by carotid disease?
Either through plaque stabilisation or plaque removal.
1) BMT (Best medical therapy)- Induces endothelial repair and reduce repeated injury, which in turn would reduce the promotion of plaques. I.e. Smoking cessation, aggressive BP control, dual antiplatelet therapy, high dose statin therapy, maintenance of good glycaemic control in diabetics.
2) Carotid endarterectomy- Additional benefit beyond that of BMT, good recovery where the disease is ipsilateral. Threshold is 50% lumen reduction, need to assess the risk of surgery and the time in which the stroke occurred (unstable plaque provides a benefit, stable plaque either no benefit or even harm). Risk of stroke recurrence reduces over time and so CEA becomes unbeneficial after some time.
3) Carotid stenting- Although an option, is not as beneficial as CEA, and post surgery there is a risk of death and stroke.
