Stroke Flashcards
When to start Warfarin after Ischaemic Stroke/TIA
NICE guidelines:
Ischaemic Stroke
> to wait 2 weeks before starting anticoagulation in ischaemic stoke to reduce risk of haemorrhage transformation
TIA
> in the absence of cerebral infarction or haemorrhage, anticoagulation therapy should begin as soon as possible
Acute Stroke - Initial Mx
KEEP
Blood glucose, Hydration, O2 Sats, Temp within normal limits
BUT DO NOT lower High BP in acute phase UNLESS Cx e.g. Hypertensive encephalopathy
ASPIRIN 300mg PO/PR as soon as Haemorrhagic stroke has been excluded
If in AF, do not start anticoagulation until haemorrhage excluded, usually not until 14d post onset of ischaemic stroke
If cholesterol > 3.5mmol/L commence statin at 48h
Thrombolysis - ABSOLUTE Contraindications
Prev intracranial haemorrhage Prev stroke or traumatic brain injury in last 3m Seizure at onset of stroke Active bleeding Intracranial neoplasm Lumbar puncture in last 7d GI haemorrhage in last 3w Pregnancy Suspected SAH Oesophageal varices Uncontrolled HTN >200/120
Thrombolysis - RELATIVE Contraindications
Concurrent anticoagulation INR > 1.7 Haemorrhagic diathesis Active diabetic haemorrhagic retinopathy Suspected intracardiac thrombus Major surgery/trauma in preceding 2w
Indications for Thrombolysis in Acute Stroke
- Administer within 4.5h of onset of Sx (unless as part of a clinical trial)
- Haemorrhage has definitively been excluded (i.e. Imaging has been performed)
Alteplase currently recommended by NICE
Ischaemic Stroke - Mx dependent on vessel affected:
For individuals aged up to 60 years who suffer an acute MCA territory ischaemic stroke complicated by massive cerebral oedema, surgical decompression by hemicraniectomy should be offered within 48 hours of stroke onset.
Patient’s presenting with a confirmed acute proximal MCA or distal internal carotid artery or basilar artery occlusion may benefit from intra-arterial clot retrieval. Ideally, patients should undergo the procedure within 6 hours of symptom onset. Three recently published randomised trials established the safety and efficacy of intra-arterial clot retrieval in addition to intravenous thrombolysis for eligible patients presenting with acute stroke. Patients who are ineligible for IV thrombolysis who present within the appropriate time-frame with large vessel occlusion may also benefit from intra-arterial clot retrieval.
Stroke - Mx: Guidelines
The Royal College of Physicians (RCP) published guidelines on the diagnosis and management of patients following a stroke in 2004. NICE also issued stroke guidelines in 2008, although they modified their guidance with respect to antiplatelet therapy in 2010.
Selected points relating to the management of acute stroke include:
blood glucose, hydration, oxygen saturation and temperature should be maintained within normal limits
blood pressure should not be lowered in the acute phase unless there are complications e.g. Hypertensive encephalopathy*
aspirin 300mg orally or rectally should be given as soon as possible if a haemorrhagic stroke has been excluded
with regards to atrial fibrillation, the RCP state: ‘anticoagulants should not be started until brain imaging has excluded haemorrhage, and usually not until 14 days have passed from the onset of an ischaemic stroke’
if the cholesterol is > 3.5 mmol/l patients should be commenced on a statin. Many physicians will delay treatment until after at least 48 hours due to the risk of haemorrhage transformation
*the 2009 Controlling hypertension and hypotension immediately post-stroke (CHHIPS) trial may change thinking on this but guidelines have yet to change to reflect this
Stroke - Secondary Prevention: Clopidogrel and Dipyridamole
NICE also published a technology appraisal in 2010 on the use of clopidogrel and dipyridamole
Ischaemic Stroke: 300mg aspirin is given as soon as haemorrhagic stroke has been excluded with imaging
Aspirin should be commenced at a dose of 300mg for 2 weeks as soon as possible.
Lifelong anti-platelet therapy should be continued thereafter. Clopidogrel 75mg is preferred to be started 14 days after an ischaemic stroke.
Recommendations from NICE include:
clopidogrel is now recommended by NICE ahead of combination use of aspirin plus modified release (MR) dipyridamole in people who have had an ischaemic stroke
aspirin plus MR dipyridamole is now recommended after an ischaemic stroke only if clopidogrel is contraindicated or not tolerated, but treatment is no longer limited to 2 years’ duration
MR dipyridamole alone is recommended after an ischaemic stroke only if aspirin or clopidogrel are contraindicated or not tolerated, again with no limit on duration of treatment
NICE - Secondary Prevention: Carotid Endarterectomy
With regards to carotid artery endarterectomy:
recommend if patient has suffered stroke or TIA in the carotid territory and are not severely disabled
should only be considered if carotid stenosis > 70% according ECST** criteria or > 50% according to NASCET*** criteria
- *European Carotid Surgery Trialists’ Collaborative Group
- **North American Symptomatic Carotid Endarterectomy Trial
Stroke > Starting anticoagulants
Moderate-large areas of cerebral infarction are subject to the risk of haemorrhagic transformation within the acute period - usually defined as 10-14 days. With this in mind, patients with AF should be cautiously commenced on therapeutic dose formal anticoagulation 10-14 days after stroke onset in the absence of spontaneous haemorrhagic transformation.
Stroke> Starting Anticoagulants: Example Question
A 65-year-old lady with a history of diabetes and newly diagnosed atrial fibrillation (AF) was admitted to hospital with a moderate-large sized embolic stroke. Her blood pressure on admission was 165/90 mmHg with a heart rate of 95 beats per minute.
An MRI brain was performed 24 hours after admission which showed a moderate to large area of infarction involving the anterior 2/3 of the left middle cerebral artery territory without haemorrhagic transformation.
With regards to management of her AF and stroke prevention, the most appropriate decision would be to commence which of the following?
An adjusted dose intravenous heparin infusion Therapeutic dose low molecular weight heparin (LMWH) and transition to oral anticoagulation in 10-14 days > Aspirin and wait 10-14 days before commencing formal anticoagulation Warfarin with LMWH bridging therapy OR calculate the CHADS-vasc score and make a decision
Moderate-large areas of cerebral infarction are subject to the risk of haemorrhagic transformation within the acute period - usually defined as 10-14 days. With this in mind, patients with AF should be cautiously commenced on therapeutic dose formal anticoagulation 10-14 days after stroke onset in the absence of spontaneous haemorrhagic transformation.
The use of aspirin and/or low dose heparin/LMWH for venous thromboembolism (VTE) prophylaxis can be considered within 24 hours of symptom onset.
CHADS2 or CHADS-Vasc scores are used to estimate the risk of embolic stroke in patients with atrial fibrillation and assist with deciding on whether or not to anti-coagulate a patient. This patient scores highly enough to be started on formal anticoagulation, but this is not the focus of the question in this case. The focus is on the timing of anticoagulation in this clinical setting.
Intermittent Pneumatic Compression
Patients admitted with stroke are very likely to be at high risk of developing a thromboembolic event due to reduced mobility, but low molecular weight heparin is associated with haemorrhagic transformation. NICE advises that patients admitted within three days of an acute stroke should have intermittent pneumatic compression considered. This should be provided for 30 days or until the patient is mobile or discharged.
Stroke - PFO: Example Question
A 45 year old woman presents to the Accident and Emergency department after a road traffic accident where she sustains multiple injuries including an open fracture of her left tibia and fibula. The following day she has an open reduction and internal fixation of the left tibia and fibula and remains in hospital for physiotherapy. She is quite immobile during this period and then develops subsequent painful swelling and erythema of the left calf. Subsequent ultrasonogrphy confirms a left sided above knee Deep Vein Thrombosis.
Before treatment starts, she develops sudden onset weakness in her right leg and right arm, dysarthric speech and a reduction in conscious level. Subsequent CT scanning confirms the presence of a left sided infarct in the middle cerebral artery territory. Doppler investigation of the carotids show 20% stenosis on the left side and 10% on the right side. 24hr tape shows average heart rate 52bpm with 1.5s pauses maximum, sinus bradycardia
Which following feature from further investigation would best explain this womans presentation?
Anti phospholipid antibody positive Protein C deficiency > Patent foramen ovale (PFO) Hypercholeserolaemia Dilated cardiomyopathy on ECHO
This unfortunate lady has developed a thrombus as a result of her recent operation and subsequent immobility. Part of the thrombus has embolised into her left middle cerebral artery.
One would normally expect the source of the embolus to be from the carotids or from the heart. However, the minimal carotid stenosis and lack of history of atrial fibrillation make this less likely. The finding of a PFO on an ECHO would explain how a thrombus from the leg would reach the brain rather than the lungs.
PFOs are extremely common and have been found in 25-30% of people at autopsy. PFOs have been linked to an increase risk in stroke. There is also some evidence that subclinical DVTs in the presence of a PFO may be one cause for cyptogenic stroke http://content.onlinejacc.org/article.aspx?articleid=1120253
Evidence is however limited that PFO closure will reduce risk of stroke.
The other options except E are all risk factors for stroke but cannot explain the mechanism of embolism with near normal carotids and sinus rhythm. E is not associated with an increased risk of embolic stroke.
Stroke - Thrombolysis: Contraindications
A 76-year-old right-handed female presents with sudden onset flaccid right upper and lower paralysis with complete dysphasia. Her daughter reports her to have been well two hours ago.
On examination, the patients score 0/5 on her right upper and lower limb, at least 4/5 on both left limbs (examination was difficult due to her dysphasia), with a loud carotid bruit. She is also now in atrial fibrillation, a new diagnosis for her. She is well known to the stroke team: 6 weeks ago, she was admitted with a right middle cerebral artery ischaemic stroke, leaving her with minimal residual weakness on her discharge.
During her admission, she was found to have 85% carotid stenosis in her right internal carotid artery and 75% in her left internal carotid artery, for which she declined surgery. Her other past medical history includes hypertension, type 2 diabetes mellitus and dyslipidaemia. She does not take any anticoagulants. A CT head demonstrates a hypodensity in the left middle cerebral artery area distribution, consistent with an acute ischaemic stroke with no areas of haemorrhagic transformation.
What is the most appropriate next course of action?
Intravenous alteplase Clopidogrel 75mg > Aspirin 300mg Treatment dose low molecular weight heparin Warfarin
This patient has clearly had a new ischaemic stroke. Her NIHSS score and presentation within 4.5 hours would be sufficient to warrant consideration of thrombolysis. However, the key here is to identify the contraindication to thrombolysis: refusing carotid surgery recently is NOT a contraindication. However, a recent stroke or head trauma within 3 months is. The appropriate management would be to load the patient with 300mg aspirin. Clopidogrel 75mg is preferred 14 days after an ischaemic stroke. Anticoagulation is typically started 14 days after the acute stroke, possibly sooner in patients with small infarct sizes and hence a low risk of haemorrhagic transformation.
Thrombolysis Indications: Example Question
A 56-year-old female was admitted to the Emergency Department with a 90-minute history of new onset weakness in her left arm and leg. She stated that she was out shopping when the weakness suddenly came on. Since the onset of the weakness she has noticed some regained strength but still felt definite weakness. She had a past medical history comprising new atrial fibrillation for which she was undergoing investigation, hypertension, hypercholesterolaemia and asthma. She also had a perforated gastric ulcer 16 years ago. She was prescribed amlodipine 5mg OD, bisoprolol 2.5mg OD, atorvastatin 20mg OD, Clenil modulite 200mcg BD and aspirin 75mg OD. She declined formal anticoagulation regarding her atrial fibrillation. When questioned specifically, she denied the presence of any visual loss, headache, vomiting, loss of consciousness or cardiac symptoms. She smoked 20 cigarettes per day and did not consume alcohol.
On examination she was alert and walking with a hemiplegic gait. Her blood pressure was 168/74 mmHg, heart rate 78bpm, respiratory rate of 18/min, temperature of 37.2 C and oxygen saturations of 99% on air. Other than an irregularly irregular pulse, examination of the cardiovascular, respiratory and gastrointestinal systems were unremarkable.
Examination of the central neurological system revealed normal cranial nerves 2-12, with equal and reactive pupils, normal fundoscopy and a GCS of 15. Examination of the peripheral nervous system revealed the presence of power 3/5 in all muscles of the left upper and lower limbs, with decreased tone and absent deep reflexes. Power was otherwise 5/5 in all other muscle groups, with downgoing plantar reflexes. Sensation and coordination testing was unremarkable.
Initial investigations revealed the following results:
Hb 179 g/l
MCV 99 fl
Platelets 452 * 109/l
WBC 12.2 * 109/l
ECG: atrial fibrillation 74 bpm no acute changes
CT head scan: no evidence of intracranial haemorrhage, mass shift or space occupying lesions
What is the next best management step?
Commence intravenous heparin > Commence thrombolysis therapy Arrange urgent haematology consult Commence aspirin 300mg and admit to stroke unit Commence immediate amlodipine 5mg OD
This lady has suffered an ischaemic stroke and fulfils the criteria for urgent thrombolysis. There are no absolute contraindications to thrombolysis and this will maximize the probability of regaining full function of the affected limbs. The other management options may serve a role but in the hyperacute setting of the above options initiating thrombolysis is the most appropriate management option.
Stroke Mx: NG Feed associated Hyperglycaemia
NG feed associated hyperglycaemia:
The Joint British Diabetes Society 2012 guidelines recommend a target BM of between 6 and 12 mmol/l for hyperglycaemic patients on NG feed with insulin to be started when BM over 12 mmol/l. The insulin regime of choice is a biphasic insulin such as humulin M3, with a mixture of intermediate and short acting insulin, prescribed twice daily, at the start and middle of the NG feed
Example Question:
A 74-year-old female has been admitted to the stroke unit following a significant right middle cerebral artery infarct. A dense left side sensori-motor syndrome and significantly impaired swallowing mechanisms were noted. Nursing staff insert a nasogastric (NG) tube after the patient failed her swallow screen and NG feed is immediately started. Around 72 hours after the feed was commenced, her blood sugar was noted to be 16 mmol/l, with no serum or urinary ketones. Her only past medical history was paroxysmal atrial fibrillation and no known diagnosis of diabetes mellitus. She took aspirin 75mg only prior to admission. What is the optimal management of her hyperglycaemia?
Prescribe 6 units actrapid as required when BM > 10 mmol/l Stop the NG feed > Prescribe biphasic insulin twice daily Prescribe warfarin as per loading regime Repeat the BM in 4 hours time, no action at present
The most likely cause of this patients raised blood sugar is NG feed associated hyperglycaemia.
Patients with hyperglycaemia should never be prescribes PRN actrapid nor should the NG feed be stopped, as the patient demonstrates no signs of aspiration and has no other means of obtaining nutrition.
Stroke: Thrombolysis and Intra-arterial clot retrieval - Example Question
A 67-year-old male presents to the hospital with 2 hours of acute onset right sided weakness and speech difficulties.
A CT cerebral angiogram shows proximal left middle cerebral artery (LMCA) thrombosis.
Seven days prior to this presentation he underwent a laparotomy for bowel obstruction secondary to an incarcerated umbilical hernia. In the absence of IV thrombolysis which of the following emergency therapies may benefit the patient?
> Intra-arterial clot retrieval Prasugrel Mannitol Intravenous heparin infusion Rosuvastatin
Patient’s presenting with a confirmed acute proximal MCA or distal internal carotid artery or basilar artery occlusion may benefit from intra-arterial clot retrieval. Ideally, patients should undergo the procedure within 6 hours of symptom onset.
Recent abdominal surgery is an exclusion criterion for intravenous thrombolysis which is why the patient in this question may benefit from intra-arterial clot retrieval.
Three recently published randomised trials established the safety and efficacy of intra-arterial clot retrieval in addition to intravenous thrombolysis for eligible patients presenting with acute stroke. Patients who are ineligible for IV thrombolysis who present within the appropriate time-frame with large vessel occlusion may also benefit from intra-arterial clot retrieval.
All other answers have not been proven to benefit the patient in the emergency setting.
A statin based therapy should however be initiated in all ischaemic stroke patients as part of their secondary prevention regimen.
Posterior Circulation Infarct Mx- Example Question
A 48 year old male presents with a sudden onset occipital headache onset 2 and half hours ago, associated with slurred speech, vomiting and unsteadiness in all movements. In the 90 minutes after admission to A&E, it was noted that the patient became increasingly drowsy, deteriorating from a GCS of 15 on admission to E3 V4 M5. On examination, pupils are equal, his speech is dysarthric and bilateral plantars are downgoing. You are unable to illicite more formal power, tone or sensation examination in the patient. An initial CT head is unremarkable but a following MRI head with diffusion weighting sequences demonstrates restricted diffusion in bilateral cerebellar hemisphers with significant swelling around the cerebellum, brainstem and aqueduct. GCS currently 14/15 at 10 hours post-event. You have initiated aspirin 300mg and inserted a nasogastric tube. What is the appropriate management?
Add clopidogrel 300mg Start warfarinsation Thrombolysis > Discuss with neurosurgery for decompressive posterior craniectomy Hourly neuro observations with empirical anti-seizure medications
This patient is critically unwell. He has presented with a posterior circulation infarct significant oedema around a very tight part of the neuro-anatomy. Although pupils are currently equal and reactive, the drop in GCS is a major concern. It may not be possible to illicit upper motor neurone signs in the hyperacute phase after a stroke. The most concerning complication at this stage is progression towards obstructive hydrocephalus from CSF flow blockage at the aqeduct or 3rd or 4th ventricle. Prophylactic posterior craniectomy must be considered in such a young patient, discussion with neurosurgery is essential.
Stroke - Mx >4.5h onset: Example Question
A 57 year old gentleman was brought to the emergency department by ambulance following a collapse 2 hours earlier. His partner witnessed him fall to the floor, and stated that he had not been moving his right arm and leg since. She said that he had been well before this episode. The ambulance crew reported that he had had a generalised tonic-clonic seizure, which was terminated after 6 minutes with 5mg of diazepam. On examination he was drowsy, with a Glasgow coma score of 10 out of 15, and his blood pressure was 165/92mmHg. He had a right sided facial droop and there was no movement in his right arm or leg. He was known to be a smoker, and he took amlodipine for hypertension. He was not on any other medications.
An urgent CT head scan was performed immediately which demonstrated loss of differentiation between the grey and white matter in the left frontal and parietal lobes, but no acute haemorrhage.
What is the most appropriate initial management?
> Aspirin 300mg for 2 weeks Intravenous alteplase 900 micrograms/kg Aspirin + dipyridamole 25/200mg Clopidogrel 75mg Warfarin
This patient presents with a sudden onset of neurological deficit, with lateralising signs. This history is strongly suggestive of a stroke, and the CT head findings suggest an ischaemic cause.
Acute management of ischaemic stroke involves keeping the patient nil by mouth until swallow assessment is performed, nasogastric tube insertion if dysphagia is problematic, and admission to a high dependency stroke unit for close monitoring.
If presentation is within 4.5 hours of onset thrombolysis with a recombinant tissue plasminogen-activator (such as alteplase) can be considered, which has been shown to improve neurological outcome. This patient presents at 2 hours, but his seizure at the onset of stroke precludes the use of thrombolytic therapy (see table).
If presentation is beyond 4.5 hours, or thrombolysis is contraindicated, aspirin should be commenced at a dose of 300mg for 2 weeks as soon as possible. Lifelong anti-platelet therapy should be continued thereafter. Aspirin in combination with dipyridamole is only recommended if clopidogrel is contraindicated. Warfarin is not indicated in the immediate management of stroke, though may be started if the patient is shown to have atrial fibrillation. This is usually delayed for 2 weeks, due to risk of haemorrhagic transformation if given before this.
Stroke Types - Classification
The Oxford Stroke Classification (also known as the Bamford Classification) classifies strokes based on the initial symptoms.
The following criteria should be assessed:
- unilateral hemiparesis and/or hemisensory loss of the face, arm & leg
- homonymous hemianopia
- higher cognitive dysfunction e.g. dysphasia
Total Anterior Circulation Infarcts
- unilateral hemiparesis and/or hemisensory loss of the face, arm and leg
- homonymous hemianopia
- higher cognitive dysfunction e.g. dysphasia
Total anterior circulation infarcts (TACI, c. 15%)
- involves middle and anterior cerebral arteries
- all 3 of the above criteria are present
Partial Anterior Circulation Infarcts
- unilateral hemiparesis and/or hemisensory loss of the face, arm and leg
- homonymous hemianopia
- higher cognitive dysfunction e.g. dysphasia
Partial anterior circulation infarcts (PACI, c. 25%)
- involves smaller arteries of anterior circulation e.g. upper or lower division of middle cerebral artery
- 2 of the above criteria are present
Lacunar Infarcts
Lacunar infarcts (LACI, c. 25%)
- involves perforating arteries around the internal capsule, thalamus and basal ganglia
presents with 1 of the following:
1. unilateral weakness (and/or sensory deficit) of face and arm, arm and leg or all three.
2. pure sensory stroke.
3. ataxic hemiparesis
Posteror Circulation Infarcts
Posterior circulation infarcts (POCI, c. 25%) involves vertebrobasilar arteries presents with 1 of the following: 1. cerebellar or brainstem syndromes 2. loss of consciousness 3. isolated homonymous hemianopia
Lateral Medullary Syndrome / Wallenberg’s syndrome
Lateral medullary syndrome (posterior inferior cerebellar artery)
- aka Wallenberg’s syndrome
- ipsilateral: ataxia, nystagmus, dysphagia, facial numbness, cranial nerve palsy e.g. Horner’s
- contralateral: limb sensory loss
