Stroke Management -

Stroke Management Professor Phyo Kyaw Myint Clinical Chair in Medicine (Old Age) Outline Definition/classification Diagnosis Acute management - Hyperacute stage - Acute physiological monitoring and management Complications of thrombolysis and management

Definition Stroke is a clinical syndrome characterised by rapidly developing clinical symptoms and/or signs of focal neurological deficit lasting more than 24 hours and thought to be of vascular origin [Warlow et al, 1996]. This definition arbitrarily distinguishes stroke from a Transient Ischaemic Attack (TIA) where symptoms last less than 24 hours. However, the distinction between them is

controversial [Albers et al, 2002]. Classification Anatomical classification Oxfordshire Community Stroke Project (OCSP) Classification TACS Total Anterior Circulation Stroke PACS Partial Anterior Circulation Stroke LACS Lacunar Stroke

POCS Posterior Circulation Stroke PICH- Primary Intracerebral Haemorrhage Undetermined Pathophysiological classification Ischaemic Stroke

Haemorrhagic stroke Ischaemic stroke Small deep infarcts (lacunar) Cardio-embolic Large artery infarcts Artery-to-artery embolism Extracranial occlusion Intracranial atherosclerosis

Arterial dissection (carotids/vertebral) Arteritis Cryptogenic Haemorrhagic stroke (ICH) Primary Amyloid angiopathic or hypertensive) Secondary - AVM - Aneurysm - Coagulopathy (warfarin) Hyperacute phase (< 6hrs)

Need to be quick: time is brain Need to triage in A&E as potential thrombolysis NIHSS and OCSP classification if FAST positive Face Arm Speech Test (FAST) screening for paramedics/nurses Harbison. Stroke 2003;34;71-76. Stroke mimics miscellaneous SAH TGA vertigo MS syncope/presyncope 3.1% dementia psychogenic

migraine confusional state 3.6% SDH tumour PN palsy toxic/metabolic 18.2% seizures 0.0% 5.0% 10.0%

15.0% 20.0% % of all stroke mimics (n=670) 25.0% 30.0% Note Problems of clinical diagnosis Approximately 75% of conditions mimicking strokeofare neurological within 6 hours onset

How many of these can be identified by CT? ~15% of non-stroke disorders (e.g. SDH) diagnosed by CT rest diagnosed clinically/with other tests CT < 6hrs of ischaemic stroke often normal If CT is normal Often need stroke specialist or neurologist to confirm clinical diagnosis of stroke before thrombolysis or thrombectomy: Avoid thrombolysis for migraine, focal epilepsy, functional weakness, ischaemic deficit after subarachnoid haemorrhage! Clinical pointers for thrombolysis Likely to be eligible Known time of onset

Abnormal vascular signs (AF, PVD) Unilateral neurological signs Can assign an OCSP classification Increasing NIH score Likely to be not eligible

prior cognitive impairment LOC early Seizure can walk now ( too mild) Indications for urgent CT scan are

Suspected SAH or infective pathology e.g. meningitis/encephalitis Patients on anticoagulation Patients with deteriorating or fluctuating level of consciousness When thrombolysis treatment is considered appropriate History of or suspicious of head injury and/or sub/extradural haematoma Thrombectomy in ischaemic stroke As soon as possible after the onset of stroke symptoms CT scan and a CT or MR angiogram to confirm the presence of a major vessel occlusion. under sedation, but sometimes general anaesthesia is used. A delivery catheter is inserted, usually through the femoral artery in the groin,

and advanced into the occluded artery using Xray guidance. A clotretrieval device attached to a guidewire is introduced through the delivery catheter to the site of the occlusion, to remove the clot and reestablish blood flow to the affected part of the brain. Many patients will also have had initial treatment with intravenous thrombolysis. Analysis of the five trials and the Catalan population-based SONIIA registry revealed that the observed number needed to treat (NNT) of 5 to reach a modified Rankin scale (mRS) score of 0-2 only applies to approximately 1 % of all stroke patients. (Breuer et al. 2016) Thrombolysis Symptoms and signs of clinically definite acute stroke. Time of stroke onset is known and treatment can be started within 4.5 hours of onset

CT or MRI brain scan has reliably excluded both intracranial haemorrhage and structural brain lesions which can mimic stroke. The patient was independent in activities of daily living before this stroke. Major surgery, trauma (e.g. major fall at time of stroke) or gastrointestinal or urinary tract haemorrhage within the previous 3 weeks. Arterial puncture at a non-compressible site within a week. Current/recent oral anticoagulant therapy with INR > 1.4. Current heparin therapy (including LMWH) Known defect of clotting or platelet function or low platelet (<10 5/mm cu) Pregnancy and/or breast feeding

Hypoglycaemia (blood glucose <2.7 mmol/L)- or hyperglycaemia (blood glucose > 22.1 mmol/L) Patient has other life threatening illness with guarded prognosis Severe stroke assessed by NIHSS score > 25 Epileptic seizure at the onset of stroke Prior stroke within last 3 months History of prior stroke and concomitant diabetes Systolic blood pressure > 185 mmHg or diastolic blood pressure > 110 mmHg Minor or rapidly improving neurological symptoms prior to treatment Known or suspected history of intracranial structural pathology including SAH, sub/extradural haematoma or neoplasm Haemorrhagic retinopathy Systematic disease which potentially can lead to haemorrhage (e.g. acute pancreatitis, oesophageal varices, severe liver disease) Rankin 0-1 at day 90 (adjusted OR with 95% CI) N =2776

mRS 0-1at Day 90 Adjusted odds ratio with 95% confidence interval by stroke onset to treatment time (OTT) ITT population (N=2776) Expanded Time Window 4.5 hrs NNT Lansberg et al, 2009, Stroke Pooled data set of the first 6 major randomized acute stroke trials

3.6 for patients treated between 0 and 90 minutes, 4.3 with treatment between 91 and 180 minutes, 5.9 with treatment between 181 and 270 minutes, and 19.3 with treatment between 271 and 360 minutes. The NNT for harm estimates for the corresponding time intervals are 65, 38, 30, and 14. IST-3 Lancet Neurology 2013 FINDINGS (N=3035) Mortality at 18 months, 349% Vs. 351% (p=0.85) 350% cf. 314% had an OHS score of 0-2 (p=0024). A favourable shift in the distribution of OHS grades (p=0002).

Treatment was associated with significantly higher overall self-reported health (adjusted mean difference in EQ utility index 0060; p=0019). IST-3 provides evidence that thrombolysis with intravenous alteplase for acute ischaemic stroke does not affect survival, but does lead to statistically significant, clinically relevant improvements in functional outcome and health-related quality of life that are sustained for at least 18 months. Immediate management steps General and Supportive measures Establish correct diagnosis (as above) Attend ABC (Airways, Breathing and Circulation) if appropriate Monitor conscious level and neuro-observation Normalise physiological parameters such as oxygenation, glycaemic

control, temperature Blood pressure (BP) monitoring Swallowing assessment Hydration Prevention of complications e.g. DVT, bedsores, aspiration Specific measures Admit to an acute stroke unit Thrombolysis should be considered in appropriate cases and offered if the service is available locally Ischaemic stroke due to carotid or vertebral dissection need a special management Anticoagulation is not recommended in newly diagnosed atrial fibrillation

Special circumstances Carotid dissection younger patients without vascular risk factors preceding episode of cervical strain or injury Urgent carotid imaging is indicated Anticoagulation should be considered and discussion should be made with a stroke consultant. Special circumstances Blood pressure monitoring in these patients is vital. Systolic blood pressure (SBP) should be kept at least below 180 mm Hg and mean arterial pressure

(MAP) should be lower than 130 mmHg Seizures should be treated after the first occurrence. Prophylactic anticonvulsant is not currently recommended in UK and European guidelines. Neurosurgical opinion should be sought when appropriate especially if there is evidence of hydrocephalus or raised intracranial pressure. Main results of STICH trial showed no evidence of an overall benefit of early surgery when compared to initial conservative treatment [Mendelow et al, 2005]. For all secondary causes of ICH, the underlying aetiology should be addressed and treated if possible (e.g. aneurysm, anticoagulation). Complications due to thrombolysis Anaphylaxis Haemorrhage

Intra-cerebral haemorrhage Allergic reactions Anaphylactoid reaction, laryngeal oedema, orolingual angioedema, rash, and urticaria usually respond to conventional therapy many of these patients received concomitant ACEI therapy Most cases resolved with prompt treatment; there have been rare fatalities as a result of upper airway haemorrhage from intubation trauma Other Adverse Reactions

-Nausea and/or vomiting, hypotension and fever ICH Symptomatic ICH contemporaneous neurological worsening (Levy et al, 1994) any CT-documented haemorrhage that was temporally related to deterioration in the patients clinical condition in the judgement of the clinical investigator (NINDS, 1995) an increase of 4 or more points in the NIHSS score within 36 hours from treatment initiation associated with any intracranial blood on CT. (PROACT II, 2001) Non-symptomatic ICH

Risk factors for ICH post throbolysis Stroke severity, cerebral oedema or mass effect on CT prior to Rx ECASS 2- rtPA, h/o CHF, extent of parenchymal hypoattenuation on baseline CT, increasing age PROACT II- baseline hyperglycaemia > 200mg/dL Protocol violation! ?? Post thrombolytic unfractionated heparin use

Management of Bleeding Complications Guided by (1) the location and size of the hematoma (2) the likelihood that the bleeding can be controlled mechanically (3) the risk of neurological worsening or death (4) the interval between administration of the drug and the onset of haemorrhage If bleeding is suspected For all potentially life-threatening haemorrhages, including suspected intracranial bleeding, ongoing infusion of a thrombolytic drug should be stopped immediately. FBC, APTT, PT/INR, and fibrinogen. Grouped and matched if transfusions are needed (at least 4 U of packed red blood cells, 4 to 6 U of cryoprecipitate or fresh frozen plasma, and 1 U of single donor platelets). These therapies should be made available for urgent administration. Management of Bleeding Complications

Could it be controlled mechanically? -Compression Treat hypotension or hypovolemic shock Urgent CT of the brain is needed if an intracranial haemorrhage is suspected; if bleeding is demonstrated neurosurgical consultation Surgery is delayed until the fibrinolytic state is corrected. For patients with severe non-neurological haemorrhage, emergency imaging studies should be performed before prescribing any surgical or medical therapy. Surgical interventions usually are delayed until the fibrinolytic state is corrected. Surgical vs. medical therapy Surgical removal Superficial Clot volume 20-80 ml Worsening neurological status Relatively young Midline shift/raised ICP Cerebellar haematoma >3 cm/

causing hydrocephalus Medical therapy Large haematoma with moribund patient (GCS<5) Oriented patient with small haematoma Visit us ACTRA Aberdeen The key objective of the ACTRA is to promote the health and independence of older people through research which: increases knowledge about novel risk factors and prognostic markers for common conditions of older age facilitates the interaction between clinical and experimental researchers and provides training for

students and staff interested in ageing-related research identifies personalised optimal treatment targets for relevant outcomes develops and tests new therapies, and undertakes lifestyle, clinical and service interventions that aim to improve the health and healthcare of ageing populations Thank you for your attention

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