BySiti Nur Shafiqah Binti Fazil Mohammad Hazim Fikri Bin Adnan Mohd. Amirul Hafifi Bin Khairulzaman Nor Akma Binti Sulaiman Norashikin Binti Naim Zafirah Hani Binti Ramli Atika Azura Binti Abdul Rashed Public: weakness, usually permanent on one side, often with loss of speech. ´Stroke is a clinical syndrome characterized by rapidly developing clinical symptoms and/or signs of focal, and at times global, loss of cerebral function, with symptoms lasting more than 24 hours or leading to death, with no apparent cause other than that of vascular originµ. ~ Academy of Medicine, Malaysia .Ischemic Hemorrhage . .blood accumulates and compresses the surrounding brain tissue .Sudden loss of fx dt loss of blood supply to an area that controls that fx.results from a weakened vessel that ruptures and bleeds into the surrounding brain. .Usually caused by partial/complete blockage of an artery that supplies the brain. Intracere ral hemorrhage Cortico l Large vessel h Lacuna r Small arteries ertension .Mesothelioma Brainstem .Em olism Hemorrhagic (15%) .Em olism .Throm osis .atheroma Anterior circulation Posterior circulation .Su arachnoid hemorrhage .Ischemic (85%) . NON-MODIFIABLE Age Sex Ethnicity/race Family history of stroke MODIFIABLE Hypertension (systolic and diastolic) Cigarette smoking Diabetes Mellitus Atrial fibrillation Coronary heart disease Hyperlipidemia Obesity and physical inactivity Raised homocysteine level High dietary salt intake Heavy alcohol consumption Previous stroke . Atherothromboembolism (50%) 2. Intracranial small vessel disease (penetrating artery disease) (25%) 3. Cardiogenic embolism (20%) Other causes: Arterial dissection Trauma Vasculitis Metabolic disorder Congenital disorder .Three main causes of ischaemic stroke are: 1. . Caused by : Extracranial embolism Intracranial thrombosis Decreased cerebral blood flow Initiate ischaemic cascade Necrosis of brain tissue Cerebral infarction Stroke . prosthetic valve) Mural thrombi ( MI.1.Embolism May arise from the heart or extracranial arteries Sources of cardiogenic emboli : Valvular thrombi (MS. AF) . IE. 2.Thrombosis Large vessels (including carotid artery system) Small vessels (comprising intracerebral arteries. including the Circle of Willis & posterior circulation) . . 3. polycythemia vera) . multiple myeloma.Flow disturbances Inadequate cerebral blood flow due to : Decreased cerebral perfusion pressure Hematologic hyperviscosity ( sickle cell disease. Less common cause : polycythemia. arteritis) . Any process that causes dissection of the cerebral arteries (trauma. and prolonged vasoconstriction from migraine headache disorders. fibromuscular dysplasia of the cerebral arteries. sickle cell anemia. protein C deficiency. thoracic aortic dissection. Loss of perfusion to a portion of the brain unleashed the ischemic cascade On cellular level : Ischemic neurons become depolarized (ATP depleted) Membrane ion-transport systems fail Calcium influx release neurotransmitters (including glutamate) Activates N-methyl-D-Aspartate (NMDA) & other excitatory receptors on other neurons . arachidonic acid.Neurons become depolarized Further calcium influx Further glutamate release Local amplification of initial ischemic insult + Massive calcium influx activates various degradative enzymes destruction of the cell membrane and other essential neuronal structures + Free radicals. and nitric oxide are generated by this process further neuronal damage . Intracerebral and subarachnoid hemorrhage . The extravasation forms a roughly circular or oval mass that disrupts the tissue and grows in volume as the bleeding continues. Neurological deficit .Blood vessel ruptures Explosive entry of blood into the brain parenchyma. Swelling of brain tissue (cerebral edema) Adjacent brain tissue is distorted and compressed. Subarachnoid hemorrhage Common : ruptured aneurysm .Intracranial hemorrhage Common : chronic high BP Weakens the arteries burst 2.1. . The presentation are dependant on what portion of the brain is damage. coma and death. The areas of the brain affected by the stroke depend on the particular artery that is affected. . Presentation of patient of stroke varies from mild confusion to altered level of consciousness. Ischemic stroke Cortical Lacunar Brainstem Hemorrhagic stroke . . . . Anterior (carotid) artery circulation Middle cerebral artery Aphasia Hemiparesis / plegia Hemianopia cerebral artery personality changes Anterior . Posterior (vertebrobasilar) artery circulation Supply: Brainstem Cerebellum Occipital . Symptoms: Dizziness Diplopia Dysarthria Dysphagia Dystaxia . Aphasia Agnosia Apraxia hemineglect Loss of consciousness Drowsy . . Alert Normal cognitive function (absence of cortical signs) . lacunar strokes tend to occur in areas located away from the surface of the brain. Because of the way blood vessels divide in the brain.Definition: strokes caused by the occlusion of a small branch of a larger blood vessel. where many of the smaller blood vessel branches are located. Pure motor stroke Pure Sensory Sensorimotor Ataxic Hemiparesis Dysarthria Clumsy-Hand Syndrome . . distribution of the basilar or vertebral arteries "cardinal" feature of an ipsilateral peripheral cranial nerve involvement. and a contralateral weakness or sensory deficit . - dangerous: small portion but have many functions. Wallenberg's syndrome Horner·s syndrome Hemiparesis : corticospinal tract Diplopia: occulomotor Facial numbness and weakness: 5th and 7th cranial nerve Nystagmus and vertigo: vestibular Dysphagia and dysartria: 9th and 10th . : most patient die. but usually patient with hemorrhagic stroke present with severe headache which sometimes preceed with vomitting. . Dangerous within 24 hours. Differences between intracerebral and subarachnoid can only be found radiologically. However. Definite differences between hemorrhagic and infarction can only be seen radiologically. Clinical manifestation is almost the same. in severe hemorrhage. it·s difficult to distinguish between the two. AVM) Encephalitis Head injury Relapsing multiple sclerosis Conversion disorder Hyperviscosity syndrome Peripheral nerves lesion ( guillaine barre syndrome) . brain tumor. Metabolic/toxic encephalopathy Epileptic seizures ( Todd s palsy) Hemiplegic migrain Structural intracranial lesion ( subdural hematoma. should be considered if cardiac embolism is suspected Ct brain -should be done as soon as possible in all patient to exclude or confirm hemorrhage . serum creatinine. diabetis mellitus or blood clotting problem ECG. ABG . FBC. coagulation profile. lipid profile. blood glucose. ESR. liver function test. echocardiography. chest X-ray .to detect common vascular risk factor and markers of rarer causes such as atherosclerosis. serum electrolytes. MRI brain and MRA . which supply blood to the brain. Lumbar puncture .should be done if subarachnoid hemorrhage is suspected and CT brain is negative .this is used to find out whether there has been a narrowing of the blood vessels in the neck (the carotid arteries).should be considered if CT is negative (CT scan unable to differentiate ischemic and hemorrhagic stroke especially perfomed >10 days after stroke) Doppler or Duplex ultrasound scan . Acute management Long-term management . Airway Breathing Circulation check the patient can protect can protect his/her airway and swallow w/o evidence of aspiration check that the patient is breathing adequately. anti-arrhythmics drug and inotropic drug as appropriate screen for sign of dehydration and give fluids parenterally or by nasogastric tube if necessary assess nutritional status and provide nutritional supplements if necessary. and blood pressure adequate and treat w fluid replacement. start feeding via a nasogastric tube if the patient is dysphagic. check O2 saturation and give O2 if saturation < 95% check peripheral perfusion. if dysphagia persist for a day or two. pulse. consider alternative routes for essential medications Hydration Nutrition Medication . evidence of hypertensive encephalopathy or aortic dissection. turn immobile patient regularly . maintain nutrition. do not lower the blood pressure in the fist few week since the cerebrel perfusion may decrease. provide a pressure-relieving mattress. give antipyretics since raised brain temperature may increase infarct volume Pressures area check pressure areas and introduce measures to reduce the risk for bedsores : treat infection.BP unless there is heart failure or renal failure. BP often returns towards the patient·s normal level within the first few days check blood glucose and treat w insulin when levels are > 11.1 mmol/L. monitor closely to avoid hypoglycemia Blood glucose Temperature check for pyrexia and investigate and treat underlying cause . avoid urinary catheterization unless the patient is in acute urinary retention or incontinence is threatening pressure areas CT/MRI.Incontinenc e check for constipation and urinary retention and treat appropriately. ESR. INR. blood glucose. ECG Investigatio n . FBC. urea n electrolyte. Primary prevention (ie before a stroke) Secondary prevention (ie preventing further stroke) . Further management of the stroke patient centre on identification and treatment of risk factor and rehabilitation to restore function. treat . Medical therapy Risk factor should be identified and addressed Risk factor are : HPT ² treat and monitor Smoking ² stop Lifestyle ² more active (exercise) Alcohol ² moderate intake/stop High cholesterol ² statins.surgery Sleep apnoea . diet Raised hematocrit ² reduce Atrial fibrillation ² anticoagulate Obesity ² weight reduction Diabetes ² good control Severe carotid stenosis . Antihypertensive therapy Recognition and good control of high BP is the major factor in both 1st and 2nd stroke prevention. Clopidogrel and dipyrimadole are also used Combined aspirin 75 mg daily and dipytidamole 200 mg twice daily possibly provide optimal prophylaxis against further thromboembolic stroke or TIA. Sustained severe HPT needs treatment. Antiplatelet therapy Long-term soluble aspirin(75 mg daily) reduces substantially the incidence of further infarction following thromboembolic TIA or stroke. Transient HPT often seen following stroke usually does not require treatment provided diastolic pressure does not rise > 100 mmHg. BP should be lowered slowly to avoid any sudden fall in perfusion. Anticoagulants Heparin and warfarin shoud be given when there is atrial fibrillation . . Other measures Polycythaemia and any clotting abnormalities should be treated. Percutanous transluminal angioplasty (stenting) is an alternative. The value of surgery for asymtomatic carotid stenosis is debatable. Endarterectomy has a mortality around 3% and a similar risk of stroke. Statin therapy should be given for all Surgical approaches Internal carotid endarterectomy Surgery is recommended in TIA or stroke patient with internal carotid stenosis >70%. Successful surgery reduces the risk of further TIA/stroke by around 75%. coordinates disability-related medical care and trains caregivers. Rehabilitation after stroke Optimal care is on a stroke rehabilitation unit that provides multidisciplinary services. Physiotherapy* Speech therapy* Occupational therapy* . relieving contractures and teaching patients to use walking aids. Is particularly useful in the few weeks in reducing spasticity. . The benefits of physiotherapy for longer-term outcome are still inadequately researched. Baclofen and/or botulinum toxin are sometimes helpful in the management of severe spasticity. . Return of speech is hastened by conversation generally. If swallowing is unsafe because of the risk of aspiration. Video-fluoroscopy while attempting to swallow is helpful. either nasogastric feeding or percutanous gastrostomy will be needed. Speech therapists have a vital understanding of aphasic patients· problem and frustration. . such as stair rails. the occupational therapists play a valuable role in assessing the requirement for and arranging the provision of various aids and modifications in the home. Following recovery. hoists or wheelchairs. aspirin. warfarin Thrombolytics-streptokinase. clopidogrel. Anti-platelet. urokinase.t-PA Antihypertensive agents ACE inhibitors Beta-blockers Hydralazine Lipid lowering drugs . ticlopidine Anticoagulants-heparin. . ANTIPLATELETS Inhibition of prostaglandin mechanism Aspirin Ticlodipine, clopidogrel Abciximab, integrelin Inhibition of ADP-induced platelet aggregation Blockade of GP llb/llla receptors on platelets irreversibly inactivates platelet cyclooxygenase 1 (through acetylation)and suppresses the production of thromboxane A2 Interfere with platelet aggregation Anuclear platelet cannot synthesize new enzyme during its 10 day lifetime Irreversibly inhibit binding of ADP to its receptors on platelets Thus, inhibit activation of GP llb/IIIa receptors required for platelets to bind to fibrinogen and to each other IXa.Xa.ANTICOAGULANTS Heparin serve as a calatytic template to accelerate the antithrombin reaction antithrombin inhibits clotting factor proteases by forming stable complexes with them it interacts with activated factors (thrombin)IIa. providing anticoagulant effect within minutes . Warfarin Antagonist of vitamin K inhibit the synthesis of Vitamin K dependent clotting factors: factor II factor VII factor IX factor X . THROMBOLYTICS Streptokinase Combines with ciculating plasminogen to form an activator complex: convert plasminogen plasmin Preferentially activate plasminogen bound to fibrin confines fibrinolysis to the formed thrombus and avoids systemic activation t-PA (Alteplase. Reteplase) . ANTIHYPERTESIVE AGENTS IV betablockers hydralazine ACE inhibitors are recommended limited effect on cerebral circulation . lisinopril. enapril. irbesartan.angiotensinogen Captopril.candesartan Block angiotensin 2 receptor Do not have effect on bradykinin Similar benefits like ACE inhibitor Angiotensin 2 receptor vasoconstriction Aldosterone secretion Increase peripheral vascular resistance Increased sodium. valsartan. ramipril Inhibit peptidyl dipeptidase enzyme Decreased formation of angiotensin 2 Decreased breakdown of bradykinin ACE inhibitors Angiotensin 1 Angiotensin 2 Angiotension receptor blocker Losartan. Increase water retention Increased blood pressure . Labetalol . acting primarily on arteries and arterioles. This drug causes direct vasodilation. . which in turn prompts a reflex elevation in heart rate and cardiac output. This results in a decreased peripheral resistance. LIPID LOWERING DRUGS HMG CoA Reductase Inhibitor Bile acids binding resin Nicotinic acid Fibric acid derivatives Cholesterol absorption inhibitors . pravastatin. simvastatin. fluvastatin MOA: .HMG CoA reductase inhibitor Lovastatin.analogs of 3-hydroxy-3-methylglutarate -competitive inhibitors of 3-H-3-M coenzyme A (HMG CoA reductase) which catalyze mevalonate biosynthesis HMG CoA mevalonate HMG CoA re uctase ihibitor Decreased de novo synthesis of cholesterol Increase LDL receptor number Increased LDL uptake by hepatocytes Decreased plasma LDL . cholestipol. MOA: -decreased intracellular lipase activity Increased lipoprotein lipase activity Decrease catabolic rate of HDL MOA: .Bile acid binding resin (cholestyramine. gemfibrozil) Cholesterol absoprtion inhibitor (ezetimibe) MOA: inhibit intestinal absorption of dietry and biliary cholesterol -reduce hepatic cholesterol stores -increase hepatic uptake of LDL from plasma. Enterohepatic cycling interupted More cholesterol neede to form bile acid Outcome: Increased de nove synthesis of cholesterol Increased LDL Nicotinic acid (niacin) Fibrates (clofibrate. benzafibrate. colesevelam) MOA: binds to bile acid in the intestine and prevents reabsorbtion .activate peroxixome proliferatoractivated receptor -Increased expression of lipoprotein lipase -Increased catabolism of VLDL . air bed. regardless of their age. felt unable to prevent outbursts and this compounded their feelings of guilt. The fees for physiotherapy and speech therapist treatment. Loss of self esteem makes depression common Financial Need to buy some equipment for the patients for example. wheel chair. increase anger and feelings of frustration. Most of the females lost interest in their appearance. medication. low-esteem and despair. lose independence and are financially embarrassed .Phychosocial Sexual relationships changed. Many become unemployable. pampers. Family members must be educated about how to take care of stroke patient Both the family and stroke patient must go for counseling in order to over come the problem Physiotherapy and speech therapy have an important psychological role. . as it will increase confidence of stroke patients to live their life.