2023 Stroke Symposium PDF

Stroke symposium Dr J. Ganesalingam Consultant Neurologist Brighton and Sussex University Hospital INCIDENCE OF STROKE  Over 152,000 people in UK have a stroke per year  Currently 1.3 million stroke survivors in the UK  Stroke is the fourth largest cause of death (7%)  Cost of stoke to...

Stroke symposium Dr J. Ganesalingam Consultant Neurologist Brighton and Sussex University Hospital INCIDENCE OF STROKE  Over 152,000 people in UK have a stroke per year  Currently 1.3 million stroke survivors in the UK  Stroke is the fourth largest cause of death (7%)  Cost of stoke to society is £26 billion per year Rise in young stroke in UK  Between 2002-2008 and 2010-2017, there was a 67% increase in the incidence of stroke in those under 55 yrs. Impact of having stroke 73% of stroke survivors lack confidence.  63% live in fear of another stroke.  44% find it difficult to talk about their stroke and its effect on their lives.  56% feel friends and family treat them differently.  55% are unable to care for family in the same way as before.  44% had broken up with their partner or considered doing so.  Aims of the symposium The pathophysiology, clinical assessment and early management of stroke.  Stroke recovery and rehabilitation.  Service user’s experience  Contents  Lectures face to face: ◦ 2.05 to 2.25pm  Stroke pathophysiology and treatment  Dr Ganesalingam, Consultant Neurologist ◦ 2.25pm to 2.50pm  Case studies by Dr Hervey, Consultant Stroke physician ◦ 2.50pm to 3.10pm  Jessica Fryer, Lead Occupational Therapist ◦ 3.10pm to 3.30pm  Speech and Language therapist by Lynsey Keeley, Principal SALT ◦ 3.30pm BREAK 3.45pm to 4.45pm patient educators in breakout groups  4.45pm to 5pm Summary  Stroke pathophysiology and treatment Dr J. Ganesalingam Consultant Neurologist Learning objectives To describe the pathophysiology of ischaemic and haemorrhagic stroke  To differentiate the clinical presentations in relation to the vascular territories.  To describe the principles behind the acute treatment of stroke  Case study Mrs P, 65 yr old female  Whilst making breakfast around 8am, she noticed an abrupt onset of right arm and leg weakness.  Husband noted a right facial droop and her speech sounded abnormal.  The husband called 999  TIME IS BRAIN  1.9 million neurones die/minute in stroke Clinical assessment Sudden onset of focal neurological or monocular symptoms.  Symptoms and signs should fit within a vascular territory.  Negative symptoms rather than positive symptoms.  Examination Vascular territories Classic stroke presentations      ACA infarct ◦ Predominantly the contralateral lower limb Left MCA infarct ◦ Dysphasia, right sided weakness/numbness Right MCA infarct ◦ Neglect, left sided weakness/numbness Brainstem infarct ◦ May involve diplopia, visual field defect, facial weakness, facial weakness, contralateral limb weakness/numbness, incoordination Note UMN facial weakness: upper face spared due to bilateral innervation. ◦ Compared with Bells palsy: unilateral LMN facial weakness Case study She was blue-lighted into hospital and assessed by the stroke team in A&E at 9.40am (1hr 40min after onset)  Clinically it was felt that she had a left MCA stroke with a NIHSS of 12.  At this stage – unclear whether infarct of bleed  Causes of stroke Thromboembolic ISCHAEMIC Brain infarct HEMORRHAGIC Brain vessel thrombosis Circle of Willis Arterio-venous Dysplasia Intracerebral hemorrhage Emboli from extracranial thrombosis TIA Computed Tomography ACA infarct MCA infarct PCA infarct Ischemic infarct: Frequently, up to 50%, there is delay in CT imaging within 48 h “Normal CT” at admission of an ischemic stroke with left hemiparesis| Large infarct in the area of middle brain artery causing compressive effect, 48h after admission HAEMORRHAGE Hemorrhagic Stroke Admission CT of hemorrhagic stroke with left hemiparesis and persistent headacne Subdense appearance and severe compressive effect of extented oedema around hematoma, 48h after admission Critical Ischaemia High metabolic demand of brain – no glucose stores  Physiological blood flow–50ml/100g/min  <20ml/100g/min – electrical function stops – neurones still alive, potentially salvageable – reversible ischaemia – limited time  <10ml/100g/min – neuronal death within minutes – irreversible ischaemia – cerebral infarction  CT perfusion imaging Case study  CT scan performed No signs of ischaemia Hyperdense clot in the left MCA territory Efficacy of thrombolysis is time dependent CT perfusion demonstrating a mismatch has allowed extension of thrombolysis window to 9 hours for selected patients. Case study Onset of stroke 8am  Arrival in A&E: 9.40am  CT scan completed: 10.05am  Therefore time from onset is 2hrs 5min  No contraindications  Decision made to proceed to thrombolysis with tPA  Tissue Plasminogen Activation Case study  Length of clot is an independent predictor of the efficacy of thrombolysis As hyperdense clot was long on CT with no improvement in the NIHSS after 20minutes so proceed to mechanical thrombectomy Stent retrieval After mechanical thrombectomy Case study The patient was taken to the ward to recover.  The next day she was noted to have some improvement in the strength in the right arm and leg.  A MRI Brain scan was performed.  Normal MRI brain INFARCT ON MRI – DWI sequence Cytotoxic oedema of cells leads to restricted diffusion of water molecules Case study Whilst on the ward, the patient is:  Commenced on Aspirin after 24 hours. After two weeks this will switch to Clopidogrel.  Investigations are performed to determine the aetiology.  Rehabilitation from SALT, Physio, OT  Nutrition via input from dietician, SALT.  Mode of action of antiplatelets Avoiding stroke and TIA Vascular Risk Factors Hypertension – shearing forces – endothelial injury, and prothrombotic state  Hyperlipidaemia – lipid accumulation in foamy macrophages  LDL – oxidised to free radicals – promote inflammation  Diabetes – promotes prothrombotic state, facilitates platelet adhesion  Smoking – prothrombotic state, platelet activation and adhesion, endothelial injury  Underlying cause? Carotid stenosis Anticoagulation Virchov’s triad Stroke pathophysiology Stroke pathophysiology Stroke pathophysiology Stroke pathophysiology  Endothelial injury ◦ Increased vascular permeability, leukocyte adhesion  Accumulation of lipoproteins ◦ Including LDL and its oxidised forms  Monocyte adhesion to the endothelium ◦ Followed by migration into the intima and transformation into macrophages and foam cells. Platelet adhesion  Factor release  ◦ From activated platelets, macrophages inducing smooth muscle cell recruitment.  Smooth muscle cell proliferation Haemorrhagic stroke  Treatment ◦ Aggressive lowering of BP 130-139mmHg  Use iv GTN or iv labetalol ◦ Reverse clotting derangement  Prothrombin complex concentrate and drug reversal agents (if on anticoagulation) Classification of Stroke The five TOAST (Trial of ORG 10172 in acute stroke treatment), subtypes of ischemic stroke are:  ●Large artery atherosclerosis  ●Cardioembolism  ●Small vessel occlusion  ●Stroke of other determined etiology  ●Stroke of undetermined etiology  Stroke: a multidisciplinary approach A multidisciplinary input is vital      Nursing and medical staff Functional and movement disability – OT/physiotherapy Communication and swallowing function – S&LT Nutritional support – Dieticians Social service Thank you! Feedback