27. STROKE 400L ABUAD LECTURE.pptx

STROKE DR. O.A. OGUNNIYI ABUAD CASE 1 MR AZ, 70yo HTN, T2DM poor medication adherence Found unresponsive in his room ~ 10a.m., in a pool of urine O/eGCS 8/15, anisocoria, facial deviation to the LFT, no motor response on the RT BP = 212/118mmHg, PR = 60 CASE 2 Mrs BY, 65 yr...

STROKE DR. O.A. OGUNNIYI ABUAD CASE 1 MR AZ, 70yo HTN, T2DM poor medication adherence Found unresponsive in his room ~ 10a.m., in a pool of urine O/eGCS 8/15, anisocoria, facial deviation to the LFT, no motor response on the RT BP = 212/118mmHg, PR = 60 CASE 2 Mrs BY, 65 yr , T2DM with good medication & follow up adherence Sudden onset slurred & incoherent speech after breakfast, assoc with inability to walk Examination – Conscious, GCS 15/15, dysarthric, Rt facial nerve palsy LUE = 4/5. RUE = 2/5 LLE = 3/5. RLE = 0/5 BP = 138/70mmHG CASE 3 A 42 year old male banker Sudden onset headache, 2 episodes of vomiting Brief L.O.C. o/e GCS 14/15, pupils normal & reactive, no CN deficits, +ve Kernigs sign, no motor deficits BP = 150/90mmHG LECTURE OBJECTIVES Definitions (Stroke, TIA, ) Classifications Epidemiology (including risk factors) Clinical evaluation Presentation – attention to neurovascular syndromes Investigations Management (AIS, ICH, SAH) Complications Prevention INTRODUCTION The International Classification of Diseases (ICD) system recently classified cerebrovascular disorders chiefly as TIA, cerebral ischemic stroke, Intracerebral hemorrhage (ICH), or Subarachnoid hemorrhage (SAH) in its 11th revision. STROKE “Rapidly developing clinical signs of focal (or global) disturbance of cerebral function, lasting more than 24 hours or leading to death, with no apparent cause other than that of vascular origin.” TRANSIENT ISCHAEMIC ATTACK - “Transient ischemic attacks are episodes of temporary and focal dysfunction of vascular origin, which are variable in duration, commonly lasting from 2 to 15 minutes, but occasionally lasting as long as a day (24 hours). They leave no persistent neurological deficit.” UPDATES IN DEFINITIONS: AHA/ASA 2013 Ischaemic stroke - An episode of neurological dysfunction caused by focal cerebral, spinal, or retinal infarction Stroke caused by ICH – Rapidly developing clinical signs of neurological dysfunction attributable to a focal collection of blood within the brain parenchyma or ventricular system that is not caused by trauma. Stroke caused by subarachnoid hemorrhage – Rapidly developing signs of neurological dysfunction and/or headache because of bleeding into the subarachnoid space (the space between the arachnoid membrane and the pia mater of the brain or spinal cord), which is not caused by trauma. UPDATES IN DEFINITIONS ii Stroke caused by cerebral venous thrombosis - Infarction or hemorrhage in the brain, spinal cord, or retina because of thrombosis of a cerebral venous structure. Strokenot otherwise specified - An episode of acute neurological dysfunction presumed to be caused by ischemia or hemorrhage, persisting ≥24 hours or until death, but without sufficient evidence to be classified as one of the above. Classification of Stroke Broadly classified into 1. Ischemic stroke (80%) i) Thrombotic (50%) ii) Embolic (30%) 2. Haemorrhagic Stroke (20%) i) Intracerebral haemorrhage (15%) ii) Subarachnoid haemorrhage (5%) Clinical classification of stroke 1- Completed stroke Complete focal neurological deficit at onset and lasting > 24hrs. 2- Progressive stroke/Stroke in evolution symptoms worsening gradually or in stepwise fashion over hrs or days with symptoms lasting >24 hrs 3- Transient ischemic attack (TIA) symptoms lasting < 24hrs Blood supply to the Brain Anterior Circulation Circle of Willis Posterior Circulation  RISK FACTORS Non-modifiable Modifiable Age Hypertension Diabetes mellitus Race Alcohol Cigarette smoking Male Dyslipidemia gender Physical inactivity Cardiac risk factors Previous stroke Hemoglobinopathies Vasculitis – HIV, syphilis, Family hx Connective tissue diseases Causes of Hemorrhagic Stroke Chronic hypertension (rupture of Charcot-Bouchard aneurysms, Saccular aneurysms) AV malformations Amyloid angiopathy, Anticoagulant therapy (Warfarin, Heparin) Antiplatelets Angioma (Cavernous hemangioma) Amphetamines and other Drugs-cocaine, sympathomimetics  PATHOPHYSIOLOGY ISCHAEMIC STROKE Pathophysiology of Hemorrhagic Stroke Explosive entry of blood into the brain parenchyma structurally disrupts neuronal activity by 1. Compression of neurons and vessels leading to additional ischemic damage 2. Cerebral oedema 3. Splitting neuronal planes 4. Vasospasm from Direct neurotoxicity of blood 5. The above 4 mechanisms leading to severely elevated Intracranial pressure leading to brain herniation and death CLINICAL FEATURES; Ischemic & ICH General features – LOC, vomiting, seizures, HA MCA distribution – contralateral weakness (face & arm > leg);+ aphasia (R), + sensory neglect (L) PCA distribution – Homonymous hemianopia + other motor deficits Internal capsule – sensorimotor loss (face=arm=leg), marked dysarthria, no cortical deficits eg aphasia) STROKE SYNDROMES Continuum (Minneap Minn) 2017;23(1):40–61. COMMON BRAINSTEM STROKE SYNDROMES Continuum (Minneap Minn) 2017;23(1):40–61 Lacunar Syndromes = Small vessel syndromes Indicate occlusion of perforating arteries in the subcortex, brainstem, or cerebellum, oftenassociated with chronic hypertension and diabetes mellitus. may be clinically silent, (only seen on imaging), or result in stroke syndromes involving densely packed white matter tracts with specific localization patterns. The most commonly described small vessel syndromes include 1. pure motor 2. pure sensory 3. sensorimotor 4. ataxic hemiparesis, and 5. dysarthria-clumsy hand syndrome. A less common, but striking, small vessel syndrome manifests as hemiballism from infarction in the subthalamic nucleus. LACUNAR SYNDROMES Pay attention to ALL INVESTIGATIONS Imaging – non-enhanced CT Brain Blood workup – FBC, ESR, Glucose, lipid profile, E & U, Cr, (± HIV, VDRL, Clotting profile, autoantibodies for individual cases), lipid profile ECG, ECHO ± Carotid Doppler (ischaemic stroke) CXR, For stroke in the young – screen for vasculitides, genotype (esp in our environment), Principles of Acute Ischaemic Stroke Care (1) achieve timely recanalization of the occluded artery and reperfusion of the ischemic tissue (2) optimize collateral flow (3) avoid secondary brain injury. MANAGEMENT; General measures Stabilise; ABCs If applicable care of the unconscious patient (HDU/ICU, careful nursing, attention to airway and vital signs, regular turning & skin care, oral hygiene via suctioning, irrigation of the eyes ± taping, sphincter care, feed – IV, NG, PEG) Monitor blood pressure Assess swallowing (gag reflex ± swallow test); NPO for the 1st 24 hours post stroke ISOTONIC IVFs ONLY Early physiotherapy Insulin for elevated blood glucose (Known DM or not) MANAGEMENT; Indications for antihypertensive use in acute ischemic stroke BP > 220/120mmHg on more than 2 occasions or MAP > 140 (EXCLUDE pain, raised ICP,) Associated hypertensive emergencies - Acute pulmonary edema - Acute kidney dysfunction - Hypertensive encephalopathy - Aortic dissection DO NOT CRASH/RAPIDLY LOWER THE BP  Current trends in management of AIS Emergency triage & initial evaluation; (including immediate stabilization of ABCs). Evaluation also r/o stroke mimics Investigations; ALL patients -non-contrast neuroimaging (CT still standard of care); RBS; SPO2; serum E, U, Cr; FBC (+ platelets); ECG;; ECHO & Carotid Doppler (not emergent) Selected patients – toxicology screen; CXR; Definitive AIS Rx – Thrombolysis (rtPa) within a specific time-frame (4.5 hours); For patients out of therapeutic window & those with contraindications to thrombolysis , commence ASA 300mg General measures – adequate positioning, avoid hypoxia, manage fever/hyperthermia  Current trends in management of AIS contd BP management; no intervention in 1st 24 hours unless BP > 220/120mmHg, or presence of medical emergency that warrants antihypertensive Rx (acute kidney injury, myocardial infarction, heart failure, aortic dissection) DO NOT CRASH THE BP!!!! Aim for gradual reduction using titratable parenteral antihypertensives; 15% - 25% reduction in SBP or MAP over 1st 24 hours ***Thrombolysis-eligible patients must have BP < 180/110mmHG*** Maintain euvolemia using isotonic fluids Blood glucose management – avoid hypoglycemia. Treat hyperglycemia; Target 140 – 180mg/dl (7.8 – 10mmol/L) Monitor and manage complications; cerebral edema with ↑ICP, DVT, contractures, pressure ulcers Rehabilitation and secondary prevention  MANAGEMENT; ISCHEMIC THROMBOLYSIS; within 3 – 4.5 hours of stroke onset (standard of care) Tab ASA 300mg daily Statin therapy Maintain cerebral perfusion (euvolemia) (IVFs 3L/24hours) DVT prophylaxis (SC LMWH/heparin) Anticipate and Rx complications  CURRENT TRENDS IN MANAGEMENT OF ICH Rapid triage and ER evaluation Emergency non-contrast brain imaging (CT scan) Blood workup - RBS, serum chemistry, clotting profile, PT_INR , platelet count , TT, toxicology Evaluate for other causes of ICH especially if elderly, atypical location of bleed (lobar), absence of risk factors Attention to euvolemia, oxygen saturation, euglycemia, treat hyperthermia (>38⁰C) Monitor for and manage complications – early neurologic deterioration (hematoma expansion, edema), Treat clinical seizures; no room for prophylactic anticonvulsants  MANAGEMENT; INTRACEREBRAL HAEMORRHAGE Maintain cerebral perfusion Manage raised ICP Rx of elevated BP to prevent hematoma expansion Intermittent pneumatic compression stockings for DVT prophylaxis NO NSAIDS/ASA Prophylactic anticoagulation in the acute phase (individualized basis) NEUROSURGERY IN SELECTED CASES Management Of ICH DVT prophylaxis – Avoid anticoagulants in the 1st 48 – 72 hours post-ICH -Use of anticoagulants in ICH should be on a case by case basis; -also based on availability of non-pharmacologic (mechanical) alternatives (pneumatic compression stockings) Blood pressure management – High BP associated with early neurologic deterioration, hematoma expansion, dependency, death. -For SBP 160 - 220mmHg lowering to 140mmHg considered safe -For SBP > 220mmHg ; aggressive reduction (must be with a titratable agent with facilities for intensive monitoring)  CARDIOEMBOLIC STROKE Most commonly caused by atrial fibrillation (–responsible 4 ~ half of all cardioembolic strokes) Secondary stroke prevention differs in cardioembolic strokes especially that due to atrial fibrillation Variability in the estimated risk of stroke in Afib depending on presence of other risk factors Presentation Of Cardioembolic Stroke Neurologic symptoms that are maximal at onset. A stroke syndrome that localizes to a large artery territory, particularly when there is clinical evidence of cortical involvement, also suggests a cardioembolic source. Evidence of multiple foci of concurrent or sequential ischemia, particularly in multiple cerebrovascular or systemic vascular beds, is also strongly suggestive of cardioembolism.  SECONDARY STROKE PREVENTION IN CARDIOEMBOLIC STROKE Use of risk stratification scores in Afib - CHADS2 (CCF- 1, HTN- 1, Age > 75yrs 1, DM -1, previous stroke/TIA -1). Tscore ≥ 2 (anticoag) - CHA2DS2- VASc [CCF – 1, HTN – 1, Age ≥ 75yrs – 2, DM – 1, previous stroke, TIA/ thromboembolism – 2,Vascular Dx (previous M.I., P.A.Dx, aortic plaque – 1, Age 65 – 74yrs - 1 Sex category (female) – 1]. Tscore ≥ 2 (anticoag) - Target – INR of 2 – 3 Treatment of stroke with Afib includes rate +/- rhythm control RISK OF BLEEDING DURING ANTICOAGULATION IN CARDIOEMBOLIC SROKE HAS-BLED score (HTN SBP > 160mmHG – 1, Abnormal renal or liver fxn – 1 each, Stroke – 1, History of bleeding predisposition – 1, Labile INR – 1, Elderly Age > 65yrs – 1, Drugs esp NSAIDS +/- antiplatelets, excess alcohol – 1each,). Tscore ≥ 3 (cautious) ASSIGNMENT LOOK UP - HEMORR₂HAGES  COMPLICATIONS OF STROKE CNS – repeat stroke, hematoma growth (ICH), hemorrhagic conversion, cerebral edema, raised ICP (± herniation), hydrocephalus, seizures RS - Aspiration, aspiration pneumonia, hypostatic pneumonia, pulmonary edema, pulmonary embolism CVS - Arrhythmias, cardiogenic shock, Endocrine - ↑RBS, disturbance of salt & water homeostasis GUS – UTI GIT - Stress (Cushing’s) ulcers, GI bleeding, paralytic ileus, malnutrition COMPLICATIONS Limb – DVT, contractures, adhesive capsulitis Skin – decubitus ulcers Psychology – Depression REHABILITATION & SECONDARY PREVENTION Lifestyle modifications Rx of risk factors (HTN, DM, infections, prophylaxis in Afib), ASA (or other antiplatelet) for life if ischemic Statin (regardless of lipid levels) if ischemic Physiotherapy Occupational therapy Speech therapy Assisted living/ adaptation of home to deficits RISK STRATIFICATION IN TIA Historically regarded as benign …no longer so Decision on evaluation following a TIA - admit or not to admit for evaluation Neuroimaging for TIA – MRI Depends on the calculated future risk of stroke The ABCD2: age ≥ 60 years (1 point); BP ≥ 140/90 mm Hg at presentation (1 point); clinical features: unilateral weakness (2 points) or speech/language impairment without weakness (1 point); duration ≥6 0 minutes (2 points) or 10 to 59minutes (1 point); and DM (1 point). ABCD2 score can vary from 0 to 7 SUBARACHNOID HEMORRHAGE; Nontraumatic/aneurysmal Neurologic emergency Accounts for ~5% of all strokes Occurs at a younger age than other types of stroke High mortality SAH Intracranial aneurysms Risk of rupture dependent on other factors SAH; Risk Factors Non-modifiable Modifiable Age Hypertension Female gender Cigarette smoking Previous hx of SAH Heavy alcohol use FHx of SAH Sympathomimetic drug Hx of aneurysm in 1st ab(use) degree relatives NEJM CLINICAL FEATURES OF SAH Sudden severe headache +/- L.O.C Focal features may suggest cause or complication - 6th cranial nerve palsy – Raised ICP - 3rd cranial nerve palsy – posterior communicating /PCA/superior cerebellar artery - Paraparesis & abulia; anterior communicating artery - Hemiparesis + aphasia/neglect; MCA aneurysm - Impaired L.O.C & impaired upgaze; Hydrocephalus - Unilateral visual loss & bitemporal hemianopia; ICA aneurysm DIAGNOSIS OF SAH Non-contrast enhanced CT Lumber puncture (if CT is negative) CT/MR angiography CONTINUUM: Lifelong Learning in Neurology 2018 MANAGEMENT OF SAH General measures as for other strokes Prevent rebleeding (Tx aneurysm) Prevent vasospasm; Nimodipine 60mg 4 hourly * 21days Anticipate and Rx complications; hydrocephalus Bedrest(including no bathroom privileges) & supportive management; control HTN, analgesics for headaches, DVT prophylaxis, laxatives Definitive Aneurysm Rx BEYOND SCOPE OF THIS LECTURE Neurosurgery Microvascular clipping Endovascular coiling COMPLICATIONS Rebleed Vasospasm and delayed cerebral infarction Hydrocephalus Cardiopulmonary; arrhythmias, neurogenic pulmonary edema Hyponatremia ; SIADH or cerebral salt wasting DVT Seizures  QUESTIONS?