Ischemic Stroke and Transient Ischaemic Attack

Ischemic Stroke and Transient Ischaemic Attack Definitions Stroke: acute neurological deficits that occurs when there is either thrombotic or embolic occlusion a cerebral artery or vein or there is a bleed around or in the brain Transient ischaemic attack: presets as an acute neurological deficit but the symptoms are temporary Epidemiology Second leading cause of death worldwide First is ischemic heart disease For most patients happens suddenly and unexpectantly Ischemic stroke is the most common type of stroke Large vessel disease is the most common 90% of TIAs last less than an hour 30% of suspected stroke patients have a stroke mimic Risk of stroke within 2 weeks after TIA is 10% Supply of the Cerebrum ACA: anteromedial area of the cerebrum MCA: majority of lateral cerebrum PCA: mixture of medial and lateral areas of posterior cerebrum Classification by Cause Ischemic stroke: Occlusion -> thrombi or embolic Bacterial endocarditis Cerebral venous thrombosis Carotid or vertebrobasilar arterial dissection Thoracic aortic dissection Patent foramen Intracerebral haemorrhage Subarachnoid haemorrhage Clinical Presentation If symptoms resolve within 24 hours -> TIA Focal neurological deficit that begun abruptly Hemiparesis Language dysfunction Vision loss Brainstem signs MCA ACA PCA Common symptoms – visual and perceptual Homonymous hemianopia with macular sparing Common symptoms Contralateral weakness/paralysis Cortical blindness: total loss of vision due to occipital lobe damage Contralateral sensory loss Contralateral facial drop Left MCA/dominant hemisphere Common symptoms Aphasia Prosopagnosia: difficulty recognising familiar faces Reading difficulties Broca’s Contralateral weakness/paralysis Wernicke’s Contralateral sensory loss Global Urinary incontinence Apraxia Cognitive/behavioural changes Difficulty planning and performing purposeful movements Aphasia or mutism or trouble comprehending Dysphagia Bilateral ACA Dysarthria Right MCA/non-dominant hemisphere More severe paralysis -> paraplegia Dysphagia Left neglect -> hemi spatial neglect Akinetic mutism: inability to speak or move Diplopia Other common symptoms – motor and sensory Dizziness/vertigo Unilateral weakness/numbness Gait ataxia Headache: sudden and severe Visuospatial deficits -> poor spatial awareness, difficulty with directions or Primitive reflexes: grasping, dressing sucking or snout reflexes Cognitive and consciousness changes Memory impairment Anosognosia -> unawareness or denial Parkinsonian symptoms of deficits Tremors Behavioural changes Rigidity Reckless behaviour Gait issues Poor judgement Esp encoding and reserving memories Impulsivity Disorientation Others Less common Gaze deviation Nausea and vomit Homonymous hemianopia CN deficits Altered consciousness Lethargy Confusion E.g. Horner’s syndrome or facial weakness Investigations Patients presenting with resolved symptoms who present within 48 hours: Urgent assessment -> within 24 hours in a facility with imaging e.g. rapid access TIA clinic or ED Clinical Diagnosis Initial investigations FBC U&E Coagulation studies Glucose ECG Lipids If on warfarin Check INR CT All patients presenting with a suspected stroke Identifies intracerebral haemorrhage May identify stroke mimics Detects early signs of focal ischemia CT angiography -> occluded or stenosed intracranial and making neck vessels Esp. if large vessel occlusion is present Should also exclude haemorrhage or space occupying lesion Findings: Hyperdense artery sign Loss of grey matter differentiation Insular ribbon sign loss Parenchymal hypodensity/cytotoxic oedema Perfusion studies with CT or MRI Show volume of potentially salvageable brain tissue Determine suitability for reperfusion therapy MRI Especially diffusion weighted more sensitive than CT for ischemic stroke detection Most helpful in: TIA Minor stroke where degree of ischemia is likely small Circulation events that affect the cerebellum or brainstem Investigations to identify causes such as cardiogenic or carotid stenosis. All patients should be investigated for atrial fibrillation If symptoms are within the carotid artery territory Carotid duplex ultrasound Key Info Ischemic penumbra Preserved by collateral circulation and may survive Stroke mimics Bell palsy Brain abscess Hyperglycaemia Hypoglycaemia Metabolic disorders Seizures Tumour Thoracic aortic dissection Subdural hematoma Migraine especially with aura symptoms Drug poisoning and illicit drugs Management of Transient Ischaemic Attack Immediate treatment is required to reduce risk of a subsequent stroke No radiological evidence of infarction Lifestyle modifications: Quitting smoking Low fat and low sodium diet Exercise regularly Avoid excessive alcohol consumption Immediate initiation with antiplatelet therapy Long term for all patients who are not on an anti-coagulant therapy Aspirin and dipyridamole are more effective than aspirin alone If have AFiB, cardio-embolic stroke from a cardiovalvular disease or recent MI -> use anticoagulation instead But do so once a haemorrhage has been excluded on CT If have a pre-existing AFiB Use DOACs for secondary stroke prevention Statin Cholesterol lowering med All patients Should be used in combination with lifestyle changes Blood pressure lowering All patients unless contradicted by symptomatic hypotension ACEi and diuretics Either together or separately Should be tailored as per patient factors and comorbidities. Diabetes management Hormone therapy Carotid surgery Reduces risk for disabling stroke and death Do not give reperfusion therapy to TIA patients Advice patients to seek urgent medical attention if stroke or TIA symptoms occur FAST – available in many languages Face: mouth dropping Arms: can the patient raise borth arms Speech: is speech slurred, can the patient comprehend speech Time: time is important – if any occur -> call 000 immediately Management of Acute Ischemic Stroke Immediate gaols Minimise brain injury Treating complications ABCDE assessment Reperfusion therapy Time critical Important to establish time of onset Require expert input and consideration of patient factors Assess need based on imaging results Types: Thrombolysis IV alteplase or IV Tenecteplase (pre Most effective taken within 4.5 hours of stroke symptom onset Can also be given within 4.5 to 9 hours in patients with potentially salvageable brain tissue on CT Commence as soon as a haemorrhagic stroke is excluded The main adverse effect is bleeding Including symptomatic intracranial haemorrhage The longer the time between stroke onset and initiation of thrombolysis -> higher risk of bleeding For patients with high blood pressure Ensure it is lowered beforehand If blood pressure is more than 180/110 mmHg -> lower BP -> Check local guidelines e.g. glyceryl trinitrate and labetalol After administration monitoring blood pressure and neurological status for at least 24 hours Absolute contradictions: Acute intracranial haemorrhage Extensive frank hypodensity on CT scan Active non-compressible systemic bleeding Systemic coagulopathy DOACs use within 48 hours with abnormal coagulation parameters unless a specific reversible agent is available Infective endocarditis Thoracic aortic dissection Relative contradictions Severe uncontrolled high BP Previous intracerebral haemorrhage Cranial or spinal surgery Endovascular thrombectomy When stroke us due to occlusion of a large vessel in carotid, proximal MCA or in some patients basilar artery Highly effective when done within 6 hours of symptom onset when detectable on CT May also be very effective for patients with salvageable brain tissue (detected on CT or MRI perfusion imaging) who present 6 to 24 hours after onset of stroke symptoms May be given together when indicated in a timely manner Safety of IV thrombolysis for patients taking DOACs is unknown. For patients who have taken it within 48 hours of considering thrombolysis: Endovascular thrombectomy alone Reversal of DOACs if possible, followed immediately by thrombolysis Coagulation testing with appropriate assay E.g. factor Xa assay for apixaban Antiplatelet therapy Can reduce subsequent risk Should be use immediately as part of secondary prevention measures in patients who are not eligible for reperfusion therapy Loading dose + long term drug therapy Neurosurgery Hemicraniectomy, posterior fossa decompression and ventricular drainage Indicated for extensive hemispheric infarction As causes cerebral oedema -> fatal in over 80% of patients Brain stem compression and hydrocephalus -> oedema surrounds large cerebellar infarcts Hemicraniectomy Consider within 48 hours of stroke onset Reduces disability Large space occupying cerebellar infarcts Posterior fossa decompression and ventricular drainage Supportive Care Assess swallowing ability before giving anything oral Gag reflex is not useful If dysphagia is present -> NBM and speech pathology assessment If dysphagia is transient -> fluids and drugs can be given parenterally for the first few days until swallowing improves Before NGT -> weigh harms and benefits BP Usually elevated in acute ischemic stroke Usually reduces spontaneously Avoid BP lowering meds in the first 48 hours Except in hypertensive encephalopathy or malignant hypertension If BP more than 220 mmHg and diastolic more than 110 mmHg cautious use of oral anti-hypertensives is recommended Aim to reduce BP by 20% Hyperglycaemia Associated with worse outcomes after a stroke If possible -> avoid IV fluids with glucose Monitor glucose concentration and maintain euglycemia DVT prevention Early mobilisation Adequate hydration Antiplatelet therapy If immobilised -> give low molecular weight heparin e.g. enoxaparin Monitor temperature for 72 hours If needed treat with paracetamol Raised temperature happens in 20 to 50% of patients after an episode Associated with poorer outcomes