Stroke PDF

Stroke Definitions Stroke: a ''neurological deficit of cerebrovascular cause that persists beyond 24 hours or is interrupted by death within 24 hours'' (WHO). Brain Attack ''Transient Ischaemic Attack (TIA)'': stroke symptoms that resolve completely within 24 hours '...

Stroke Definitions Stroke: a ''neurological deficit of cerebrovascular cause that persists beyond 24 hours or is interrupted by death within 24 hours'' (WHO). Brain Attack ''Transient Ischaemic Attack (TIA)'': stroke symptoms that resolve completely within 24 hours ''Acute Ischaemic cerebrovascular syndrome'' Epidemiology: Stroke is a major health problem; 56 000 people die as a result of a stroke. 11% of all deaths, 1/3 most common form of death. MOST common cause of adult disability. Half patients' dependent on others for everyday needs. Half of stroke survivors do not have full restoration of function. 1 Signs of Stroke: FAST - the Face Arm Speech Test Assessment of three specific symptoms of stroke: – Facial weakness - can the person smile? Has their mouth or eye drooped? – Arm weakness - can the person raise both arms? – Speech problems - can the person speaks clearly and understand what you say? 2 Types of Stroke Ischaemic (85%) Following thrombosis or embolism. Interruption of blood supply (oxygen, nutrients) to neurons. Neuronal death leads to loss of function. Haemorrhagic (15%) Intracranial bleeding. Damage can be caused by compression of tissue from an expanding haematoma, direct toxic effects of blood cells (free iron) and interruption of blood supply to neurons. Surgical interventions required. Brain Attack Ischemic stroke involves an interruption to the blood flow to the brain causing hypoxia and hypoglycaemia. Can be GLOBAL – entire brain following cardiac arrest. Can be FOCAL – particular region characterized by intense foci (core) and penumbra (area surrounding the core where neuronal death is delayed). Pathophysiology Immediate consequence of the ischemic insult at the core: Rapid depletion of oxygen leads to a cessation of oxidative phosphorylation, glucose and glycogen stores consumed within only 2-3 minutes. Accumulation of lactate and increases in CO2 tension produces acidosis – inhibition of active transport mechanisms. Loss of calcium homeostasis. Breakdown of membrane phospholipids and the release of free fatty acids. Anoxic depolarization/excessive release of glutamate into extracellular space and glutamate transporter reversal. 3  Oedema: neuronal swelling resulting from influx of ions and H2O. Necrotic cell death in core. Risk factors Age: The chance of having a stroke approximately doubles for each decade of life after age 55. Heredity (family history) and race. Gender: More common in men than in women, however more than half of total stroke deaths occur in women. Prior stroke, TIA or heart attack. Risk factors (that can be controlled): High blood pressure Cigarette smoking Diabetes mellitus Carotid or other artery disease Atrial fibrillation or other heart disease including dilated cardiomyopathy, heart valve disease, and some types of congenital heart defects. Sickle cell disease High blood cholesterol Poor diet (sodium, saturated fat, cholesterol) Physical inactivity and obesity Hypertension Lifestyle changes to promote a healthy cardiovascular system e.g. Blood Pressure (BP) increase by 5 mm Hg increases stroke risk by 35-40%, decrease BP by 10 mm Hg decreases stroke risk by 40% Strategies for treatment of stroke Enhance survival of patient. Rapid action treatments aimed to prevent further strokes. Prevention of further neuronal loss, repair of damaged neurons (damage limitation). 4  Help patient restore lost function? Neurorestoration – replacement of lost neurons. Acute Stroke management: (NICE guidelines) Ensure that people who have had a suspected TIA who are at high risk of stroke (ABCD score of 4 or above*) have: – Aspirin (300 mg) started immediately. – Specialist assessment and investigation within 24 hours of symptom onset. – Measures for secondary prevention introduced. Admit anyone with a suspected stroke directly to an acute stroke unit following initial assessment. Screen swallowing on admission before giving any oral food, fluid or medications. ABCD score A – age (≥60 years, 1 point) B – blood pressure at presentation (≥140/90 mmHg, 1 point) C– clinical features (unilateral weakness= 2 points or speech disturbance without weakness= 1 point) D– Duration of symptoms (≥ 60 minutes, 2 points or 10–59 minutes, 1 point). Complications Some of the long-term deficits arising from stroke Physical Communicative Cognitive Emotional Motor deficits, Paralysis Language Agnosia Depression difficulties abnormal muscle tone Impairment of Anxiety disorder Dysarthria Memory Ataxia coordination (Dementia) Apathy Dysphasia Confusion Catastrophic Dysphagia Dysphonia reaction Impairments of Visual/hearing loss Dyspraxia Attention Pathologic affect Perception Sensory deficits problem- Psychosis, Mania 5  Solving Bipolar disorder Insight are rare Some definitions… Ataxia uncoordinated muscle movements (often presenting as difficulty in walking). Dysphagia is the inability to swallow. Dysphasia (also known as aphasia) is difficulty using and understanding spoken and written language. Agnosia inability to recognize objects, persons, sounds, shapes, or smells. Dysarthria is the motor speech disorder (misfunction of muscles in face resulting in an inability to form words) Dysphonia is when a stroke affects the muscles in the voice box, changing the way the voice sounds and making it hard to moderate the voice. Dyspraxia (or apraxia) is difficulty with complicated tasks, which means that the person may find it hard to speak or understand conversation. General treatment interventions 1. Fluid and electrolyte control Excessive hydration or inadequate sodium suppl. May result in hyponatremia ---- forcing fluid into neurons ---- increase the damage from ischemia. Hyponatremia ----- seizures ----- increase the metabolic demand on compromised neurons. Therefore, initiate fluid therapy with a solution at least 0.45% saline. 2. Hyperglycemia control with insulin therapy to keep glucose conc. < 155 mg/dl, since hyperglycemia may adversely affect ischemic infarction outcome and have 3-fold higher 30-day mortality rate than patients without hyperglycemia, may be due to sympathetic response to stroke. 3. Maintain blood pressure for 1-2 days after stroke onset (because hypotension may decrease cerebral blood flow --- expand ischemia) 4. Assess the patient in general daily needs (nutrition, urination, defecation) because of compromised ability due to neurological deficiency. 6 Pharmacological management of stroke 1. Heparin/ LMWH Used in progressive embolic stroke only, to avoid conversion to hemorrhagic stroke. 2. Thrombolytics In acute ischemic stroke to restore the blood flow more rapidly to neurons and prevent damage (within 2-3 hrs). If occlusion persists for 3-7 hours ----- permanent neurological damage. Treatment with tP-A should be initiated as soon as possible after the onset of stroke symptoms, preferably within 90 minutes. Rapid diagnosis by C'T scans of ischemic stroke and immediate administration of tP-A increases its efficacy and may limit the potential for hemorrhagic conversion of ischemic stroke. The dose of tP-A should not exceed 0.85 mg/kg administered over 60 minutes, since higher doses increase the risk of intracranial hemorrhage. Thrombolytic agents Tissue Plasminogen Activator (tPA) Alteplase (Bayer). Administered within 3 hours of stroke onset improves clinical outcome (death, disability) at 3 months. 0.90 mg/kg (max 90 mg): 10% initially by I.V. injection, remainder by I.V. infusion over 60 minutes. Not appropriate for hemorrhagic stroke, increased risk of intracranial bleeding. T-PA is a serine protease enzyme which acts as a “clot-buster”. Tissue Plasminogen Activator (tPA) Plasminogen → Plasmin ↓ Thrombus ---→ Proteolytic degradation products 7  Anti-platelet drugs – Decrease platelet aggregation, inhibit thrombus formation. – Help prevent further strokes, do not restore the damage caused by initial ischaemic event. Aspirin – Cyclooxygenase inhibitor reduces thromboxane 2 synthesis in platelets. – Reduces likelihood of platelet aggregation. – Single dose (150 – 300 mg) given soon after ischemic event, followed by 75 mg/d to prevent further cardiovascular events. – Aspirin decreases the risk of stroke by about 15%: this effect is uniform across aspirin doses from 50 to 1500 mg/d. – Problems with aspirin…… Aspirin plus Dipyridamole (NICE guidelines) – Phosphodiesterase inhibitor, increases [cAMP] and acts as a vasodilator, also an Adenosine uptake inhibitor, increases extracellular [Adenosine], blocks platelet activation via adenosine receptors. – Modified Release (MR) dipyridamole (Persantine Retard) in combination with aspirin should be used as part of the prevention of stroke or heart attack in people who have had a stroke for a period of two years from the most recent event. – After 2 years, or if the patient can’t tolerate MR dipyridamole, treatment should revert to standard care (including long-term treatment with low-dose aspirin). – Dipyridamole absorption is PH-dependent and concomitant treatment with gastric acid suppressors (such as a proton pump inhibitor) will reduce drug availability. Clopidogrel – Plavix (Bristol-Myers Squibb) and Iscover (Sanofi-Aventis) Clopilet (Sun Pharmaceuticals). 8  – Irreversible blockade of the adenosine diphosphate (ADP) receptor on platelet cell membranes to reduce platelet activation. – UK NICE guidelines suggest Clopidogrel should be used on its own (within its license) for people who can’t take low-dose aspirin and have either experienced a stroke or heart attack or have symptomatic peripheral arterial disease. – Contraindications: Severe neutropenia (Incidence: 1/2,000) Thrombotic thrombocytopenic purpura (TTP) (Incidence: 4/1,000,000 patients treated) Hemorrhage – The incidence of hemorrhage may be increased by the co-administration of aspirin. – Gastrointestinal hemorrhage (incidence: 2 %), Cerebral haemorrhage (Incidence: 0.1 to 0.4%). Treatment of depression following stroke Post stroke depression can be treated with conventional antidepressant medication. No particular advantage of one class over another. Prophylactic treatment with fluoxetine during the first 6 months post-stroke is associated with significant increase in survival in both depressed and non- depressed patients. Antidepressants can have side-effects such as falls, increased bleeding, seizures, and sedation. Rehabilitation Restoration of function, relearning skills and abilities. Physiotherapy (e.g. learning to walk). Speech and language therapy (e.g. learning to talk). Occupational therapy (e.g. shopping). Psychologist/Psychiatrist (adapting psychologically). Learning new skills. Adapting to some of the limitations caused by a stroke. 9 e.g. smaller meals to avoid choking, physical changes to home, wearing incontinence pads, communicating in different ways, mobility aids. 10