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Dr Samed Talibi FY1 Department Mitchell MB BS Trauma and Orthopaedics Capt. James of Hospitals BirminghamMRCP University
1/20/13
Objectives Revision Stroke and TIA basics Presentation Differentials Risk factors Investigation Treatment Pathophysiology Classification Relevant scoring systems Predominantly drawn out through Cases
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Know when to request senior help Safe management post stroke (ward cover)
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Bandwagon
Neurophobia
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Context
5 minutes in England 40 seconds in USA Third commonest cause of death in UK Lifetime risk 1 in 4 men 1 in 5 women (2-3 times higher than breast cancer) 1/3 all strokes in under 65s Largest cause of complex disability in 1/20/13 adults
CASE 1
A 79 year old woman
HPc
Unable to rise up from her bed on waking Weakness of her right arm & leg Confused Atrial fibrillation Hypertension Osteoarthritis Warfarin Amlodipine Ramipril Paracetamol
Mhx
Dhx
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On examination
she is fully conscious difficulty finding words unable to clearly express the course of events mild weakness in the right upper & lower limb
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CT Head
Glucose and electrolytes and LFTS FBC ESR CXR and ECG Carotid doppler Cardiac echo Carotid ultrasound Young stroke screen
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Acute CT Head
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Why do we do CTs?
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CT Head 24hrs+
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A.
If less than 3 hours since onset of stroke symptoms require thrombolysis If greater than 3 hours medical management
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A.
3. 4.
5. 6.
More than a minimal neurological deficit Stroke symptoms must be present for at least 30 minutes Not significantly improve before treatment Symptoms must be distinguishable from an episode of generalized ischaemia (i.e. syncope)/seizure/migraine disorder Time of onset <3 hours (At the Moment!) No CT scan evidence of ICH
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Penumbra salvageable with thrombolysis and/or neuro-protective agents Reperfusion injury and ischaemic cascade targeted by neuro-protective agents IV thrombolysis (t-PA) given within 3 hours improves functional outcome and reduces neurological impairment (twice as effective in first 1.5Hrs)
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Aspirin 300 mg initially and for 2 weeks Then definitive long-term anti-thrombotic treatment -clopidogrel
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IV fluids avoid 5% Dextrose & excess fluid administration Swallowing Nil orally initially Assessment within first hour! SALT assessment + IV fluids Temporary NG feed if appropriate at 24hrs PEG placement if appropriate (rare!) Try to ensure nutrition in all patients O2 if Sa02 < 94 % Hypertension if >220mmMg, (180 post thrombolysis) GTN infusion Avoid hyperthermia PR/PO Paracetamol if necessary Blood glucose maintain normoglycaemia Statin after 48hrs Antidepressants shown to be useful in stroke related depression late Anticonvulsants where needed
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2 Stroke Prevention
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The mortality from the acute event is about 20 % Approximately 50 %of patients are alive after five years Death at 1 year
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Case 2
80 Yr old man Wife woken in the night by thrashing and fell out of bed Speech disturbance What else in history is important?
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History
90%+ of neurological diagnosis Says it in the name STROKE NEGATIVE symptoms May evolve acutely though consider the differentials
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Examination
The next 9% of neurological diagnosis Formal neurological examination but targeted Involves:
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Differentials of Stroke
Numerous but there are the usual suspects: SAH Seizure Space occupying lesion Migraine equivalent Venous sinus thrombosis Infective
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Inflammatory
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Mechanism is still unclear May present without headache History critical Positive symptoms/aura
1/20/13 !!Migrainous infarct!!
given full- dose anticoagulation treatment (initially full-dose heparin and then warfarin [INR 23]) unless there are comorbidities that preclude its use.
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satisfying when diagnosis made but this is very much a process Simply keep an open mind, investigate appropriately, report what you find not what you think you should find
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ETS U 1/20/13
A&E SHO reported 6th nerve palsy A&E SpR reported 3rd MAU SHO reported 4th MAU senior review reverted to 3rd Who was right? Underlying cause?
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Stroke
Defined by WHO as a clinical syndrome consisting of
rapidly developing clinical signs of focal (at times global) disturbance of cerebral function lasting more than 24 h or leading to death no apparent cause other than that of vascular origin
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Case 2
80 Yr old man Wife woken in the night by thrashing and fell out of bed Speech disturbance
Classification
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new higher cerebral dysfunction (e.g. dysphasia, visuospatial disorder) homonymous visual field defect ipsilateral motor and/or sensory deficit of at least two areas of face, arm and leg
Unilateral weakness (and/or sensory deficit) of face/arm/leg or all three Pure sensory stroke Ataxic hemiparesis
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What was all that really about? Classification helps to direct management and prognostication but also LOCALISATION
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67 year old, type 2 diabetic, hypertensive Reports episode of left arm weakness, sudden onset that day, 20mins Resolved Neuro NAD, BP 134/88
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If ABCD2 score > 4 aspirin (300 mg daily) started immediately specialist assessment and investigation within 24 hours of onset of symptoms measures for 2o prevention introduced as soon as the diagnosis is confirmed, including discussion of individual risk factors NICE guidance applies 1/20/13
AGE 67 BP 134/88 Clinical weak L arm Duration 20 mins Diabetic Yes TOTAL ABCD2 score
1 0 1 1 1 5
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If the patient has AF, how would you calculate their risk factor for a stroke?
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CHADS-VASc Therapy
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Neurological deficit of presumed vascular origin lasting less than 24 hours Most really last minutes Brain Infarction occurs with ischaemia > 1 hour This is an area that is evolving If there is a deficit on examination at presentation likely a stroke
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TIA Risk
Transient cerebral ischaemia is a sign of impending the risk of a permanent neurological deficit rises dramatically after a patient has experienced a TIA Approximately 60 %of patients with a completed stroke have had premonitory TIAs TIA may be due to low flow with inadequate collateral blood supply embolic TIAs are usually single and more prolonged
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1 Prevention of Stroke
Most common treatable risk factor Direct relationship BP Stroke 5-6 mmHg drop reduces stroke by 42% Treatment of Systolic HTN in elderly reduced stroke by 37%
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The mortality from the acute event is about 20 percent Approximately 50 percent of patients are alive after five years Irreversible damage begins at immediately at the core The surrounding area (penumbra) may be viable for up to 6 hours Process of stroke injury at cellular level called the ischaemic cascade ATP depletion, Membrane pumps fail, Calcium mediated cytotoxic reactions and release of excitatory neurotransmitters such as glutamate Another target for therapeutic interventions
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Carotid endarterectomy (CEA) should be considered for patients with large vessel atherothrombotic disease in the internal carotid artery that causes low flow or embolic TIAs CEA should be done quickly 1-2/52 Virtually all patients with atrial fibrillation who have a history of stroke or TIA should be treated with warfarin in the absence of contraindications (60% RRR in AF) Falls not as great a risk as traditionally taught
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Final case
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Final case
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Final case
Cerebellar and other posterior circulation strokes present quite differently Many are very subtle Brainstem strokes often combine cranial nerve signs with long tract signs many syndromes Can present with dizziness/vertigo or impaired conciousness - TIA is not the most likely diagnosis in elderly with frequent episodes of vertigo or (pre) syncope!
1/20/13
Summary
We have discussed the basics of stroke, presentation, history, examination, investigation and management
We have given an overview of the guidelines and scoring systems which give a framework to current clinical practice.
We have attempted to make this relevant to the expected standard of a good FY1
Further study needs to be tailored to your purpose not everyone needs to be a stroke physician
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