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RAJKUMARI AMRIT KAUR COLLEGE OF NURSING Lajpat Nagar, New Delhi-110024 A Medical-Surgical Nursing Presentation
CVD or CVA is a term that refers to a functional abnormality of the central nervous system that occurs when the normal blood supply to the brain is disrupted. Brain & cerebral nerve cells are extremely sensitive to a lack of oxygen; if the brain is deprived of oxygenated blood for 2-3 mins, both the brain & nerve cells begin to die with irreversible outcome.
Related anatomy of brain and its blood supply Four vessels supply the brain: • Two internal carotid arteries (anterior circulation: most of the frontal, parietal &temporal lobes, basal ganglia, part of diencephalon.) • Two vertebral arteries (posterior circulation: middle & lower part of temporal lobes, occipital lobes, cerebellum, brain stem and part of diencephalon.) The Circle of Willis is the joining area of several arteries at the bottom (inferior) side of the brain. At the Circle of Willis, the internal carotid arteries branch into smaller arteries that supply oxygenated blood to over 80% of the cerebrum.
Related anatomy of brain and its blood supply Cerebral circulation- • Anterior circulation- MCA, ACA, and Anterior choroidal artery • Posterior circulation- Vertebral artery, Basilar artery and Posterior cerebral artery
Clinical stroke syndrome Cluster of signs and symptoms produced due to the occlusion of an artery (due to an atherothrombotic lesion or an emboli or dissection) supplying a particular region of the brain. Classification-  Large vessel stroke within the anterior circulation  Large vessel stroke within the posterior circulation  Small vessel disease of either vascular bed
STROKE WITHIN THE ANTERIOR CIRCULATION
Which arteries occlusion results in the stroke within the anterior circulation? Question number- 01
Cerebral hemisphere in coronal section
Complete MCA SYNDROME-
PARTIAL SYNDROME- Lacunar stroke within the internal capsule produces pure motor or sensory motor stroke contralateral to the side of lesion. Lacunar infarct of putamen, Globus pallidus- predominantly parkinsonian features Brachial syndrome- weakness of hand and arm Frontal opercular syndrome- Broca’s aphasia with facial weakness with or without arm weakness Proximal part of the superior division involved- clinical features of motor weakness, sensory disturbances and Broca's aphasia. If dominant hemisphere- Wernicke’s aphasia without weakness with contralateral homonymous superior quadrantanopia If non dominant hemisphere- Hemineglect, spatial agnosia without weakness. Occlusion of lenticulostriate branches If superior division of M1 involved If inferior division of M2 involved
M2 SYNDROMES
ANTERIOR CEREBRAL ARTERY-
ANTERIOR CEREBRAL ARTERY- •A1 segment- from internal carotid to anterior communicating artery branches to anterior limb of internal capsule, inferior part of caudate, anterior hypothalamus A2 segment- distal to anterior communicating artery- supplies frontal pole, entire medial part of cerebral hemispheres. A1 segment occlusion rarely produces clinical syndrome because collateral flow through anterior communicating artery and collaterals from MCA and PCA.
ANTERIOR CEREBRAL ARTERY- A2 SEGMENT- • c/l paralysis of foot and leg, paresis of arm • c/l cortical sensory loss of foot and leg -urinary incontinence. • c/l grasp and suckling reflex -abulia, slowness, delay -gait apraxia • If both A2 segments arise from a single anterior cerebral stem, it may affect both hemispheres, b/l pyramidal signs, paraparesis or quadriparesis and urinary incontinence
ANTERIOR CHOROIDAL ARTERY-
ANTERIOR CHOROIDAL ARTERY SYNDROME- • Supplies posterior limb of internal capsule, white matter posterolateral. • Complete syndrome rare due to collaterals from MCA, PCA, and ICA. • Syndrome comprises- c/l hemiplegia c/l hemianesthesia c/l homonymous hemianopia • Anterior choroidal strokes are usually due to in-situ thrombosis of the vessel.
INTERNAL CAROTID ARTERY SYNDROME-
STROKE WITHIN THE POSTERIOR CIRCULATION
THE POSTERIOR CIRCULATION-
BASILAR ARTERY SYNDROME-
DEFINITION CVA or stroke may be defined as the abrupt development of a focal neurological deficit as a consequence of disturbance in cerebral circulation, or irreversible brain injury resulting from cerebral ischemia.
Episodes of stroke and familial stroke have been reported from the 2nd millennium BC onward in ancient Mesopotamia and Persia. Hippocrates (460 to 370 BC) was first to describe the phenomenon of sudden paralysis that is often associated with ischemia. The word stroke was used as a synonym for apoplectic seizure as early as 1599. In 1658, in his Apoplexia, Johann Jacob Wepfer (1620– 1695) identified the cause of hemorrhagic stroke when he suggested that people who had died of apoplexy had bleeding in their brains. The term cerebrovascular accident was introduced in 1927, reflecting a "growing awareness and acceptance of vascular theories and recognition of the consequences of a sudden disruption in the vascular supply of the brain“. HISTORY
Stroke is a major public health concern. The prevalence of stroke in the general population varies from 40 to 270 per 100,000 in India. Approximately 12% of all strokes occur in those aged <40 years. It is the third biggest killer in India after heart attacks and cancers. The percentage is higher for people aged 65 and older. Family members may have a genetic tendency for stroke or share a lifestyle that contributes to stroke. Higher levels of Von Willebrand factor are more common amongst people who have had ischemic stroke for the first time Men are 25% more likely to suffer strokes than women, yet 60% of deaths from stroke occur in women. INCIDENCE
RISK FACTORS MODIFIABLE RISK FACTOR NON-MODIFIABLE RISK FACTORS Hypertension Smoking Atrial fibrillation Hyperlipidemia History of Transient Ischemic Attack or CVA Thrombogenic substances Valvular disease Drug abuse Obesity Diabetes Diet Cardiac diseases Emotional stress Age Gender Race Genetics
CAUSES Ischemia Thrombosis Cerebral embolism Cerebral hemorrhage Compression
WHAT ARE THE WARNING SIGNS OF CVA? Question number- 02
WARNING SIGNS OF CVA  Transient hemiparesis  loss of speech  hemi-sensory loss.  severe occipital or nuchal headaches  vertigo or syncope  Paresthesia  transient paralysis, epistaxis and retinal hemorrhages.  Manifestations of deficit must persist longer than 24 hours to be diagnostic of stroke.  TIAs are focal neurologic deficits lasting less than 24 hours.
TEMPORAL CLASSIFICATION OF STROKE 1. Transient ischemic attack 2. Stroke in evolution / progressive stroke 3. Completed stroke/ established stroke
WHAT IS TRANSIENT ISCHEMIC ATTACK? Question number- 03
1. Transient ischemic attack These are brief, transient and focal disturbances of neurological function that clear with little or no residual deficit within 24 hrs. Most of them last for only 7 to 10 minutes. Also called as “little strokes”.40% of the client develop stroke in 5 yrs. Causes Emboli Carotid artery stenosis Polycythemia Subclavian steal syndrome Hypertensive crisis Migraine Sign and symptoms of TIA Depend on type of vessel: Carotid: transient dysphasia, hemi paresis or monocular vision disturbances. Vertebrobasilar: brief unconsciousness, vertigo, alternating hemiplegia and visual hallucination or Diplopia, etc. Treatment Primary interventions: Lowering high BP, cholesterol levels and weight Secondary interventions: Medications (anti coagulants, antiplatelets)and Surgery
When neurologic deficit occurs in stepwise manner. If the problem involves carotid artery distribution, the progression does not usually extend beyond 24 hours but if it involves the vertebrobasilar distribution, it can progress up to 72 hours. The symptoms may resolve or may worsen. When neurologic deficit appear to have ceased escalating. This may occur within minutes or may take 24 to 72 hrs. 2. Progressive stroke 3.Established stroke
TYPES OF STROKE Based on the causes it is basically of two types: A) Ischemic stroke B) Hemorrhagic stroke Ischemic strokes are further divided into: 1.Thrombotic stroke (61% cases) 2.Embolic stroke (24% cases) 3. Systemic hypoperfusion (Watershed stroke)
WHAT IS ISCHEMIC STROKE? Question number- 03
An ischemic stroke occurs when an artery in the brain becomes blocked. Ischemic (“is-skeem-ic”) stroke occurs when an artery to the brain is blocked.
THROMBOTIC STROKE Thrombus — a built-up clot — gradually narrows the lumen of the artery and impedes blood flow to distal tissue. Depending upon the type of vessels involved, it is divided into two types: Large vessel disease Small vessel disease Symptoms develop gradually  Large vessel disease  Common are internal carotid, middle cerebral, anterior & posterior cerebral, vertebral, and basilar arteries.  Small vessel disease:  Intra cerebral arteries, branches of the Circle of Willis, middle cerebral artery, and arteries arising from the distal vertebral and basilar artery.  Micro-atheromas.
EMBOLIC STROKE Blockage of arterial access to a part of the brain by an embolus :- A traveling particle or debris in the arterial bloodstream originating from elsewhere. Most commonly, a clot but may be air, broken fragment of atherosclerotic plaque, cancerous cell or bacterial particle. Blockage is sudden in onset; symptoms usually are maximal at start. Embolic stroke can be divided into further categories: - those with known cardiac source those with an arterial source those with unknown source
Systemic hypoperfusion (Watershed stroke) The reduction of blood flow to all parts of the body due to:- Cardiac pump failure Reduced cardiac output Bleeding
Pathophysiology of Ischemic stroke Ischemia Acidosis- ion imbalance Intracellular calcium increased and release of neurotoxins. Cell membrane & protein breakdown & Formation of free radical. Cell injury & cell death. Warning signs of ischemic stroke.
FAST It is an acronym used as a mnemonic to help detect and enhance responsiveness to stroke victim needs. The acronym stands for Facial drooping, Arm weakness, Speech difficulties and Time. 1. Facial drooping 2. Arm weakness 3. Speech difficulties 4. Time
HEMORRHAGIC STROKE Accounts for 15% of strokes. It results from bleeding into brain tissues itself (intracerebral or intraparenchymal hemorrhage) or into the sub-arachnoid space or intraventricular hemorrhage. Hemorrhage means escape of blood from a ruptured blood vessel in the brain. Sites for hemorrhage: -  Subdural  Subarachnoid  Intraventricular  Intracerebral Causes of Hemorrhagic stroke  Hypertension  Bleeding disorders  Angiopathy  Trauma  Drugs (cocaine, methamphetamines)  Aneurysm  Inflammatory diseases of arteries
WHAT DO YOU MEAN BY ANEURYSM? Question number- 04
Aneurysm Ballooning out of the wall Rupture of the dome of the aneurysm Stimulation of SNS & release of vasoactive substances Loss of auto-regulation HTN HYPOTENSION RAISED ICP Risk of re-bleed reduced CBF decreased CBF ischemia vasospasm infarction ANEURYSM
WHAT ARE THE SYMPTOMS OF CEREBRAL HAEMORRHAGE? Question number- 05
Symptoms of a cerebral Hemorrhage  Sudden onset of symptoms  Weakness  Numbness or pins and needles of the face, arm or leg, usually on one side of the body  Paralysis on one side of the body  Slurring speech or difficulty finding words  Severe headache  Nausea & Vomiting  Drowsiness  Unconsciousness  Dizziness  Difficulty walking or loss of balance  Confusion.  Flat affect, lack of spontaneity, slowness and lack of interest in surroundings  Cognitive impairment such as perseveration and amnesia  Urinary incontinence  Vertebrobasilar region:  Dizziness  Nystagmus
DIAGNOSTIC TESTS CT scan LUMBAR PUNCTURE
MANAGEMENT
APPROACH TO THE PATIENT Emergency Management • Oxygenation @ 2-4 l/mt • Cardiac and pulse oximetry monitoring • Vital sign monitoring • GCS • IV lines • Medications • Radiology • NPO Medical Management IDENTIFY THE STROKE EARLY • CAB, Neurological assessment, GCS • History: history of warning signs • Risk factors for atherosclerotic and cardiac disease, including hypertension, diabetes mellitus, tobacco use. • Physical examination • Standardized assessment tools can be used e.g. NIHSS (National institute of health stroke scale) • Vital signs • Hunt Hess scale if haemorrhagic stroke
NATIONAL INSTITUTE OF HEALTH STROKE SCALE
HUNT HESS SCALE
Tissue plasminogen activator (t-PA):- Thrombolytic agents are used to treat ischemic stroke by dissolving the blood clot that is blocking the normal blood flow to the brain. Dosage and administration: - • Within 4½ hr tPA is given (0.9 mg/kg over 1 hour) Side effects: - • Bleeding is the most common side effect of t- PA administration. The patient should be closely monitored for any sign of bleeding. THROMBOLYTIC THERAPY
Therapy for patients with ischemic stroke nor receiving t-PA • Intra-arterial thrombolytics: e.g. Heparin • Antihypertensive: Are given rarely to reduce the BP in acute phase, as it acts as a compensatory mech. to perfuse the brain. • Anticoagulation: Anti platelets and Anti Thrombotic e.g. Heparin, low dose aspirin × 4 to 10 days. • Long term anticoagulants e.g. warfarin, aspirin • Osmotic diuretics e.g. Mannitol • Analgesic: -If headache e.g. codeine,stronger narcotics are avoided. • Vasodilators • Anticonvulsants: Phenytoin (dilantin), phenobarbital, barbiturates, sedatives. • Elevate the head end of the bed to promote venous drainage and to lower increased ICP. • Intubation with an endotracheal tube to establish patent airway if necessary • Continuous hemodynamic monitoring. Other pharmacological management-
WHICH OF THE FOLLOWING IS CONTRAINDICATED IN HAEMORRHAGIC STROKE? QUESTION NUMBER- 06 CHOOSE AMONG THE OPTIONS GIVEN BELOW- 1) ASPIRIN 2) HARTMAN SOLUTION 3) Tranexamic acid (TXA)
Surgical mx • Craniotomy for evacuation of hematoma. • Carotid endarterectomy • Carotid stenting SURGICAL MANAGEMENT
Surgical mx •Decompressive craniotomy • Aneurysm treatment Coil embolization Cliping SURGICAL MANAGEMENT
SPECIFIC DEFICIT AFTER CVA Pain DECREASE STAMINA
SPECIFIC DEFICIT AFTER CVA CONTRACTURE Changes in sensation •Feeling less sensitive – this is called hypoesthesia. •Feeling less sensitive to temperature. •Feeling more sensitive- this is called hyperesthesia and can affect a range of your senses such as your taste, hearing or touch. •Feeling unaware of your position and movement in your limbs. •Experiencing altered sensations – this is sometimes called dysesthesia or paraesthesia.
NURSING MANAGEMENT
Assessment: •Neurological assessment •Vital signs •Careful history •CAB •Ongoing Monitoring Nursing Process
The major nursing care planning goals for the patient and family may include:  Improve mobility.  Avoidance of shoulder pain.  Achievement of self-care.  Relief of sensory and perceptual deprivation.  Prevention of aspiration.  Continence of bowel and bladder.  Improved thought processes.  Achieving a form of communication.  Maintaining skin integrity.  Restore family functioning.  Improve sexual function.  Absence of complications.
NURSING DIAGNOSIS 1. Altered tissue perfusion r/t increased ICP, infarcted brain area. • ICP monitoring • Neurological assessment • Avoid causes of restlessness, e.g. full bladder • Temperature regulation • Activities like Straining at stool should be avoided • Proper positioning
NURSING DIAGNOSIS 2. Altered Physical mobility r/t paralysis • Change the position 2 hourly & position him in prone position for 10-15 mins. • Do not place a pillow under the affected knee & avoid acute hip flexion. • Prevent foot drop by using footboard & ROM exercises • At night use night splints. • Exercises in bed • Sitting up: Raise the head end of the bed slowly Help him to sit up by supporting the affected side  Wheel chair
NURSING DIAGNOSIS 3. Self-care deficit r/t paralysis • Help them in using paralyzed arm as much as possible but avoid a tendency to do everything with affected arm. • When they can sit up, encourage them to use the affected limb • Assist them in carrying out ADL • Involve the family members actively in their care. • Promote psychological and social support.
NURSING DIAGNOSIS 4. High risk for injury r/t paralysis • Keep bed side rails up • Frequent skin inspection • Safe environment • Eye care • Mouth care • Supervise their activities .
NURSING DIAGNOSIS 5.High risk for aspiration r/t loss of swallowing reflex • Assess for breath sounds every 2-4 hourly • Do tracheo-bronchial suctioning • While giving mouth care, place the patient with the head turned to one side. • Place in lateral position to allow the drainage of secretions • Monitor ABG and other parameters. .
NURSING DIAGNOSIS 6. Altered nutrition less than body requirement r/t inability to swallow • Monitor intake output of the patient • Needs patience and care to prevent choking and aspiration • Small and frequent feeds should be administer to the patient. • High fiber diet is to be provided to prevent constipation.
NURSING DIAGNOSIS 7.Altered elimination pattern r/t incontinence dehydration, immobility and deterioration in LOC. • Observe the patient to identify characteristics of voiding pattern (e.g. freq., amount, constant dribbling) • Maintain intake/output • Whenever possible try to keep him catheter free by: • Offering bedpan or urinal frequently • Take patient to commode frequently. • Develop a bowel training program • Give foods known to stimulate defecation • Initiate a suppository and laxative regimen • Institute a bowel program. • Enemas are avoided in presence of increased ICP.
NURSING DIAGNOSIS 9. Impaired communication r/t aphasia secondary to CVA. • Explain all the procedures before carrying out them. • Do not whisper at the bed side. • Never shout or blame the patient • Don’t discuss about the patient’s condition with the relative at the bed side • Be calm, gentle and patient • Help the family members to communicate with the patient and encourage them to talk effectively.
Rehabilitation Stroke rehabilitation may include some or all of the following activities: - 1. Therapy for communication disorders 2. Strengthening motor function 3. Mobility training 4. Range of motion therapy 5. Constraint-induced therapy 6. Electrical stimulation 7. Robotic technology Inpatient rehabilitation units.  Outpatient units.  Skilled nursing facilities.  Home-based programs.
RESEARCH INPUTS- Optimal delay time to initiate anticoagulation after ischemic stroke in atrial fibrillation (START): Methodology of a pragmatic, response-adaptive, prospective randomized clinical trial. Epub 2019 Aug 18. Aims: To determine if there is an optimal delay time to initiate anticoagulation after atrial fibrillation-related stroke that optimizes the composite outcome of haemorrhagic conversion and recurrent ischemic stroke. Sample size estimates: The study will enroll 1500 total subjects split between a mild to moderate stroke cohort (1000) and a severe stroke cohort (500). Methods and design: This study is a multi-center, prospective, randomized, pragmatic, adaptive trial that randomizes subjects to four arms of time to start of anticoagulation. The four arms for mild to moderate stroke are: Day 3, Day 6, Day 10, and Day 14. The time intervals for severe stroke are: Day 6, Day 10, Day 14, and Day 21. Allocation involves a response adaptive randomization via interim analyses to favor the arms that have a better risk-benefit profile. Study outcomes: The primary outcome event is the composite occurrence of an ischemic or hemorrhagic event within 30 days of the index stroke. Secondary outcomes are also collected at 30 and 90 days. Discussion: The optimal timing of direct oral anticoagulants post-ischemic stroke requires prospective randomized testing. A pragmatically designed trial with adaptive allocation and randomization to multiple time intervals such as the START trial is best suited to answer this question in order to directly inform current practice on this question.
RESEARCH INPUTS- MRI-Guided Thrombolysis for Stroke with Unknown Time of Onset Epub 2018 May 16. Abstract Background: Under current guidelines, intravenous thrombolysis is used to treat acute stroke only if it can be ascertained that the time since the onset of symptoms was less than 4.5 hours. We sought to determine whether patients with stroke with an unknown time of onset and features suggesting recent cerebral infarction on magnetic resonance imaging (MRI) would benefit from thrombolysis with the use of intravenous alteplase. Methods: In a multicenter trial, we randomly assigned patients who had an unknown time of onset of stroke to receive either intravenous alteplase or placebo. All the patients had an ischemic lesion that was visible on MRI diffusion-weighted imaging but no parenchymal hyperintensity on fluid-attenuated inversion recovery (FLAIR), which indicated that the stroke had occurred approximately within the previous 4.5 hours. We excluded patients for whom thrombectomy was planned. Conclusions: In patients with acute stroke with an unknown time of onset, intravenous alteplase guided by a mismatch between diffusion-weighted imaging and FLAIR in the region of ischemia resulted in a significantly better functional outcome and numerically more intracranial haemorrhages than placebo at 90 days. (Funded by the European Union Seventh Framework Program; WAKE-UP ClinicalTrials.gov number, NCT01525290; and EudraCT number, 2011-005906-32 .).
CONCLUSION The onset of stroke is a dramatic and discouraging event both for the person having the stroke and their family. A person may go from complete independence to complete dependence in a matter of minutes. All nursing staff have important roles and responsibilities when caring for people with a stroke. These include: Physiological monitoring and maintenance of homeostasis. Reduce morbidity and prevent mortality.
BIBLIOGRAPHY-  Black M Joyce, Hawks Jane Hokanson. Medical-surgical nursing: clinical management for positive outcomes. 7th ed. Elsevier publishers:2005; 2107-36.  Harrison’s Principles Of Internal Medicine.20th ed. Page no- 3069-78.  Smeltzer Suzanne C, Bare Brenda G. Brunner & Suddarth’s Textbook of medical-surgical nursing. 11th ed. lippincott williams & wilkins:2009; 2206-25.  Monahan, Sands. et al. Phipp’s medical surgical nursing: health and illness perspective. 8th ed. Elsevier publishers:2007; 1861-72.  Chintamani; textbook of medical-surgical nursing; published by: Elsevier; 7th edition; page no- 1466-90  http://www.google.co.in/? gws_rd=cr&ei=HBbHUqnQO4qJrAf8hoDIDA#q=stroke+reha bilitation+pdf  https://www.stroke.org.uk/sites/default/files/physical_eff ects_of_stroke.pdf  https://pubmed.ncbi.nlm.nih.gov/31423922/  https://pubmed.ncbi.nlm.nih.gov/29766770/ ANY DOUBT? PLEASE ASK.

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stroke. cardiovascular accident and stroke

  • 1.
    RAJKUMARI AMRIT KAURCOLLEGE OF NURSING Lajpat Nagar, New Delhi-110024 A Medical-Surgical Nursing Presentation
  • 2.
    CVD or CVAis a term that refers to a functional abnormality of the central nervous system that occurs when the normal blood supply to the brain is disrupted. Brain & cerebral nerve cells are extremely sensitive to a lack of oxygen; if the brain is deprived of oxygenated blood for 2-3 mins, both the brain & nerve cells begin to die with irreversible outcome.
  • 3.
    Related anatomy ofbrain and its blood supply Four vessels supply the brain: • Two internal carotid arteries (anterior circulation: most of the frontal, parietal &temporal lobes, basal ganglia, part of diencephalon.) • Two vertebral arteries (posterior circulation: middle & lower part of temporal lobes, occipital lobes, cerebellum, brain stem and part of diencephalon.) The Circle of Willis is the joining area of several arteries at the bottom (inferior) side of the brain. At the Circle of Willis, the internal carotid arteries branch into smaller arteries that supply oxygenated blood to over 80% of the cerebrum.
  • 4.
    Related anatomy ofbrain and its blood supply Cerebral circulation- • Anterior circulation- MCA, ACA, and Anterior choroidal artery • Posterior circulation- Vertebral artery, Basilar artery and Posterior cerebral artery
  • 5.
    Clinical stroke syndrome Clusterof signs and symptoms produced due to the occlusion of an artery (due to an atherothrombotic lesion or an emboli or dissection) supplying a particular region of the brain. Classification-  Large vessel stroke within the anterior circulation  Large vessel stroke within the posterior circulation  Small vessel disease of either vascular bed
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    Which arteries occlusionresults in the stroke within the anterior circulation? Question number- 01
  • 8.
    Cerebral hemisphere incoronal section
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    PARTIAL SYNDROME- Lacunar strokewithin the internal capsule produces pure motor or sensory motor stroke contralateral to the side of lesion. Lacunar infarct of putamen, Globus pallidus- predominantly parkinsonian features Brachial syndrome- weakness of hand and arm Frontal opercular syndrome- Broca’s aphasia with facial weakness with or without arm weakness Proximal part of the superior division involved- clinical features of motor weakness, sensory disturbances and Broca's aphasia. If dominant hemisphere- Wernicke’s aphasia without weakness with contralateral homonymous superior quadrantanopia If non dominant hemisphere- Hemineglect, spatial agnosia without weakness. Occlusion of lenticulostriate branches If superior division of M1 involved If inferior division of M2 involved
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    ANTERIOR CEREBRAL ARTERY- •A1segment- from internal carotid to anterior communicating artery branches to anterior limb of internal capsule, inferior part of caudate, anterior hypothalamus A2 segment- distal to anterior communicating artery- supplies frontal pole, entire medial part of cerebral hemispheres. A1 segment occlusion rarely produces clinical syndrome because collateral flow through anterior communicating artery and collaterals from MCA and PCA.
  • 18.
    ANTERIOR CEREBRAL ARTERY- A2SEGMENT- • c/l paralysis of foot and leg, paresis of arm • c/l cortical sensory loss of foot and leg -urinary incontinence. • c/l grasp and suckling reflex -abulia, slowness, delay -gait apraxia • If both A2 segments arise from a single anterior cerebral stem, it may affect both hemispheres, b/l pyramidal signs, paraparesis or quadriparesis and urinary incontinence
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  • 20.
    ANTERIOR CHOROIDAL ARTERYSYNDROME- • Supplies posterior limb of internal capsule, white matter posterolateral. • Complete syndrome rare due to collaterals from MCA, PCA, and ICA. • Syndrome comprises- c/l hemiplegia c/l hemianesthesia c/l homonymous hemianopia • Anterior choroidal strokes are usually due to in-situ thrombosis of the vessel.
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  • 34.
    DEFINITION CVA or strokemay be defined as the abrupt development of a focal neurological deficit as a consequence of disturbance in cerebral circulation, or irreversible brain injury resulting from cerebral ischemia.
  • 35.
    Episodes of strokeand familial stroke have been reported from the 2nd millennium BC onward in ancient Mesopotamia and Persia. Hippocrates (460 to 370 BC) was first to describe the phenomenon of sudden paralysis that is often associated with ischemia. The word stroke was used as a synonym for apoplectic seizure as early as 1599. In 1658, in his Apoplexia, Johann Jacob Wepfer (1620– 1695) identified the cause of hemorrhagic stroke when he suggested that people who had died of apoplexy had bleeding in their brains. The term cerebrovascular accident was introduced in 1927, reflecting a "growing awareness and acceptance of vascular theories and recognition of the consequences of a sudden disruption in the vascular supply of the brain“. HISTORY
  • 36.
    Stroke is amajor public health concern. The prevalence of stroke in the general population varies from 40 to 270 per 100,000 in India. Approximately 12% of all strokes occur in those aged <40 years. It is the third biggest killer in India after heart attacks and cancers. The percentage is higher for people aged 65 and older. Family members may have a genetic tendency for stroke or share a lifestyle that contributes to stroke. Higher levels of Von Willebrand factor are more common amongst people who have had ischemic stroke for the first time Men are 25% more likely to suffer strokes than women, yet 60% of deaths from stroke occur in women. INCIDENCE
  • 37.
    RISK FACTORS MODIFIABLE RISKFACTOR NON-MODIFIABLE RISK FACTORS Hypertension Smoking Atrial fibrillation Hyperlipidemia History of Transient Ischemic Attack or CVA Thrombogenic substances Valvular disease Drug abuse Obesity Diabetes Diet Cardiac diseases Emotional stress Age Gender Race Genetics
  • 38.
  • 39.
    WHAT ARE THEWARNING SIGNS OF CVA? Question number- 02
  • 40.
    WARNING SIGNS OFCVA  Transient hemiparesis  loss of speech  hemi-sensory loss.  severe occipital or nuchal headaches  vertigo or syncope  Paresthesia  transient paralysis, epistaxis and retinal hemorrhages.  Manifestations of deficit must persist longer than 24 hours to be diagnostic of stroke.  TIAs are focal neurologic deficits lasting less than 24 hours.
  • 42.
    TEMPORAL CLASSIFICATION OFSTROKE 1. Transient ischemic attack 2. Stroke in evolution / progressive stroke 3. Completed stroke/ established stroke
  • 43.
    WHAT IS TRANSIENTISCHEMIC ATTACK? Question number- 03
  • 45.
    1. Transient ischemicattack These are brief, transient and focal disturbances of neurological function that clear with little or no residual deficit within 24 hrs. Most of them last for only 7 to 10 minutes. Also called as “little strokes”.40% of the client develop stroke in 5 yrs. Causes Emboli Carotid artery stenosis Polycythemia Subclavian steal syndrome Hypertensive crisis Migraine Sign and symptoms of TIA Depend on type of vessel: Carotid: transient dysphasia, hemi paresis or monocular vision disturbances. Vertebrobasilar: brief unconsciousness, vertigo, alternating hemiplegia and visual hallucination or Diplopia, etc. Treatment Primary interventions: Lowering high BP, cholesterol levels and weight Secondary interventions: Medications (anti coagulants, antiplatelets)and Surgery
  • 46.
    When neurologic deficitoccurs in stepwise manner. If the problem involves carotid artery distribution, the progression does not usually extend beyond 24 hours but if it involves the vertebrobasilar distribution, it can progress up to 72 hours. The symptoms may resolve or may worsen. When neurologic deficit appear to have ceased escalating. This may occur within minutes or may take 24 to 72 hrs. 2. Progressive stroke 3.Established stroke
  • 47.
    TYPES OF STROKE Basedon the causes it is basically of two types: A) Ischemic stroke B) Hemorrhagic stroke Ischemic strokes are further divided into: 1.Thrombotic stroke (61% cases) 2.Embolic stroke (24% cases) 3. Systemic hypoperfusion (Watershed stroke)
  • 48.
    WHAT IS ISCHEMICSTROKE? Question number- 03
  • 49.
    An ischemic strokeoccurs when an artery in the brain becomes blocked. Ischemic (“is-skeem-ic”) stroke occurs when an artery to the brain is blocked.
  • 50.
    THROMBOTIC STROKE Thrombus —a built-up clot — gradually narrows the lumen of the artery and impedes blood flow to distal tissue. Depending upon the type of vessels involved, it is divided into two types: Large vessel disease Small vessel disease Symptoms develop gradually  Large vessel disease  Common are internal carotid, middle cerebral, anterior & posterior cerebral, vertebral, and basilar arteries.  Small vessel disease:  Intra cerebral arteries, branches of the Circle of Willis, middle cerebral artery, and arteries arising from the distal vertebral and basilar artery.  Micro-atheromas.
  • 51.
    EMBOLIC STROKE Blockage ofarterial access to a part of the brain by an embolus :- A traveling particle or debris in the arterial bloodstream originating from elsewhere. Most commonly, a clot but may be air, broken fragment of atherosclerotic plaque, cancerous cell or bacterial particle. Blockage is sudden in onset; symptoms usually are maximal at start. Embolic stroke can be divided into further categories: - those with known cardiac source those with an arterial source those with unknown source
  • 52.
    Systemic hypoperfusion (Watershedstroke) The reduction of blood flow to all parts of the body due to:- Cardiac pump failure Reduced cardiac output Bleeding
  • 53.
    Pathophysiology of Ischemicstroke Ischemia Acidosis- ion imbalance Intracellular calcium increased and release of neurotoxins. Cell membrane & protein breakdown & Formation of free radical. Cell injury & cell death. Warning signs of ischemic stroke.
  • 54.
    FAST It is anacronym used as a mnemonic to help detect and enhance responsiveness to stroke victim needs. The acronym stands for Facial drooping, Arm weakness, Speech difficulties and Time. 1. Facial drooping 2. Arm weakness 3. Speech difficulties 4. Time
  • 56.
    HEMORRHAGIC STROKE Accounts for15% of strokes. It results from bleeding into brain tissues itself (intracerebral or intraparenchymal hemorrhage) or into the sub-arachnoid space or intraventricular hemorrhage. Hemorrhage means escape of blood from a ruptured blood vessel in the brain. Sites for hemorrhage: -  Subdural  Subarachnoid  Intraventricular  Intracerebral Causes of Hemorrhagic stroke  Hypertension  Bleeding disorders  Angiopathy  Trauma  Drugs (cocaine, methamphetamines)  Aneurysm  Inflammatory diseases of arteries
  • 57.
    WHAT DO YOUMEAN BY ANEURYSM? Question number- 04
  • 58.
    Aneurysm Ballooning out ofthe wall Rupture of the dome of the aneurysm Stimulation of SNS & release of vasoactive substances Loss of auto-regulation HTN HYPOTENSION RAISED ICP Risk of re-bleed reduced CBF decreased CBF ischemia vasospasm infarction ANEURYSM
  • 59.
    WHAT ARE THESYMPTOMS OF CEREBRAL HAEMORRHAGE? Question number- 05
  • 60.
    Symptoms of acerebral Hemorrhage  Sudden onset of symptoms  Weakness  Numbness or pins and needles of the face, arm or leg, usually on one side of the body  Paralysis on one side of the body  Slurring speech or difficulty finding words  Severe headache  Nausea & Vomiting  Drowsiness  Unconsciousness  Dizziness  Difficulty walking or loss of balance  Confusion.  Flat affect, lack of spontaneity, slowness and lack of interest in surroundings  Cognitive impairment such as perseveration and amnesia  Urinary incontinence  Vertebrobasilar region:  Dizziness  Nystagmus
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    APPROACH TO THEPATIENT Emergency Management • Oxygenation @ 2-4 l/mt • Cardiac and pulse oximetry monitoring • Vital sign monitoring • GCS • IV lines • Medications • Radiology • NPO Medical Management IDENTIFY THE STROKE EARLY • CAB, Neurological assessment, GCS • History: history of warning signs • Risk factors for atherosclerotic and cardiac disease, including hypertension, diabetes mellitus, tobacco use. • Physical examination • Standardized assessment tools can be used e.g. NIHSS (National institute of health stroke scale) • Vital signs • Hunt Hess scale if haemorrhagic stroke
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    NATIONAL INSTITUTE OFHEALTH STROKE SCALE
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    Tissue plasminogen activator(t-PA):- Thrombolytic agents are used to treat ischemic stroke by dissolving the blood clot that is blocking the normal blood flow to the brain. Dosage and administration: - • Within 4½ hr tPA is given (0.9 mg/kg over 1 hour) Side effects: - • Bleeding is the most common side effect of t- PA administration. The patient should be closely monitored for any sign of bleeding. THROMBOLYTIC THERAPY
  • 69.
    Therapy for patientswith ischemic stroke nor receiving t-PA • Intra-arterial thrombolytics: e.g. Heparin • Antihypertensive: Are given rarely to reduce the BP in acute phase, as it acts as a compensatory mech. to perfuse the brain. • Anticoagulation: Anti platelets and Anti Thrombotic e.g. Heparin, low dose aspirin × 4 to 10 days. • Long term anticoagulants e.g. warfarin, aspirin • Osmotic diuretics e.g. Mannitol • Analgesic: -If headache e.g. codeine,stronger narcotics are avoided. • Vasodilators • Anticonvulsants: Phenytoin (dilantin), phenobarbital, barbiturates, sedatives. • Elevate the head end of the bed to promote venous drainage and to lower increased ICP. • Intubation with an endotracheal tube to establish patent airway if necessary • Continuous hemodynamic monitoring. Other pharmacological management-
  • 70.
    WHICH OF THEFOLLOWING IS CONTRAINDICATED IN HAEMORRHAGIC STROKE? QUESTION NUMBER- 06 CHOOSE AMONG THE OPTIONS GIVEN BELOW- 1) ASPIRIN 2) HARTMAN SOLUTION 3) Tranexamic acid (TXA)
  • 71.
    Surgical mx • Craniotomyfor evacuation of hematoma. • Carotid endarterectomy • Carotid stenting SURGICAL MANAGEMENT
  • 72.
    Surgical mx •Decompressive craniotomy •Aneurysm treatment Coil embolization Cliping SURGICAL MANAGEMENT
  • 74.
    SPECIFIC DEFICIT AFTERCVA Pain DECREASE STAMINA
  • 75.
    SPECIFIC DEFICIT AFTERCVA CONTRACTURE Changes in sensation •Feeling less sensitive – this is called hypoesthesia. •Feeling less sensitive to temperature. •Feeling more sensitive- this is called hyperesthesia and can affect a range of your senses such as your taste, hearing or touch. •Feeling unaware of your position and movement in your limbs. •Experiencing altered sensations – this is sometimes called dysesthesia or paraesthesia.
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    Assessment: •Neurological assessment •Vital signs •Carefulhistory •CAB •Ongoing Monitoring Nursing Process
  • 78.
    The major nursingcare planning goals for the patient and family may include:  Improve mobility.  Avoidance of shoulder pain.  Achievement of self-care.  Relief of sensory and perceptual deprivation.  Prevention of aspiration.  Continence of bowel and bladder.  Improved thought processes.  Achieving a form of communication.  Maintaining skin integrity.  Restore family functioning.  Improve sexual function.  Absence of complications.
  • 79.
    NURSING DIAGNOSIS 1. Alteredtissue perfusion r/t increased ICP, infarcted brain area. • ICP monitoring • Neurological assessment • Avoid causes of restlessness, e.g. full bladder • Temperature regulation • Activities like Straining at stool should be avoided • Proper positioning
  • 80.
    NURSING DIAGNOSIS 2. AlteredPhysical mobility r/t paralysis • Change the position 2 hourly & position him in prone position for 10-15 mins. • Do not place a pillow under the affected knee & avoid acute hip flexion. • Prevent foot drop by using footboard & ROM exercises • At night use night splints. • Exercises in bed • Sitting up: Raise the head end of the bed slowly Help him to sit up by supporting the affected side  Wheel chair
  • 81.
    NURSING DIAGNOSIS 3. Self-caredeficit r/t paralysis • Help them in using paralyzed arm as much as possible but avoid a tendency to do everything with affected arm. • When they can sit up, encourage them to use the affected limb • Assist them in carrying out ADL • Involve the family members actively in their care. • Promote psychological and social support.
  • 82.
    NURSING DIAGNOSIS 4. Highrisk for injury r/t paralysis • Keep bed side rails up • Frequent skin inspection • Safe environment • Eye care • Mouth care • Supervise their activities .
  • 83.
    NURSING DIAGNOSIS 5.High riskfor aspiration r/t loss of swallowing reflex • Assess for breath sounds every 2-4 hourly • Do tracheo-bronchial suctioning • While giving mouth care, place the patient with the head turned to one side. • Place in lateral position to allow the drainage of secretions • Monitor ABG and other parameters. .
  • 84.
    NURSING DIAGNOSIS 6. Alterednutrition less than body requirement r/t inability to swallow • Monitor intake output of the patient • Needs patience and care to prevent choking and aspiration • Small and frequent feeds should be administer to the patient. • High fiber diet is to be provided to prevent constipation.
  • 85.
    NURSING DIAGNOSIS 7.Altered eliminationpattern r/t incontinence dehydration, immobility and deterioration in LOC. • Observe the patient to identify characteristics of voiding pattern (e.g. freq., amount, constant dribbling) • Maintain intake/output • Whenever possible try to keep him catheter free by: • Offering bedpan or urinal frequently • Take patient to commode frequently. • Develop a bowel training program • Give foods known to stimulate defecation • Initiate a suppository and laxative regimen • Institute a bowel program. • Enemas are avoided in presence of increased ICP.
  • 86.
    NURSING DIAGNOSIS 9. Impairedcommunication r/t aphasia secondary to CVA. • Explain all the procedures before carrying out them. • Do not whisper at the bed side. • Never shout or blame the patient • Don’t discuss about the patient’s condition with the relative at the bed side • Be calm, gentle and patient • Help the family members to communicate with the patient and encourage them to talk effectively.
  • 87.
    Rehabilitation Stroke rehabilitation mayinclude some or all of the following activities: - 1. Therapy for communication disorders 2. Strengthening motor function 3. Mobility training 4. Range of motion therapy 5. Constraint-induced therapy 6. Electrical stimulation 7. Robotic technology Inpatient rehabilitation units.  Outpatient units.  Skilled nursing facilities.  Home-based programs.
  • 88.
    RESEARCH INPUTS- Optimal delaytime to initiate anticoagulation after ischemic stroke in atrial fibrillation (START): Methodology of a pragmatic, response-adaptive, prospective randomized clinical trial. Epub 2019 Aug 18. Aims: To determine if there is an optimal delay time to initiate anticoagulation after atrial fibrillation-related stroke that optimizes the composite outcome of haemorrhagic conversion and recurrent ischemic stroke. Sample size estimates: The study will enroll 1500 total subjects split between a mild to moderate stroke cohort (1000) and a severe stroke cohort (500). Methods and design: This study is a multi-center, prospective, randomized, pragmatic, adaptive trial that randomizes subjects to four arms of time to start of anticoagulation. The four arms for mild to moderate stroke are: Day 3, Day 6, Day 10, and Day 14. The time intervals for severe stroke are: Day 6, Day 10, Day 14, and Day 21. Allocation involves a response adaptive randomization via interim analyses to favor the arms that have a better risk-benefit profile. Study outcomes: The primary outcome event is the composite occurrence of an ischemic or hemorrhagic event within 30 days of the index stroke. Secondary outcomes are also collected at 30 and 90 days. Discussion: The optimal timing of direct oral anticoagulants post-ischemic stroke requires prospective randomized testing. A pragmatically designed trial with adaptive allocation and randomization to multiple time intervals such as the START trial is best suited to answer this question in order to directly inform current practice on this question.
  • 89.
    RESEARCH INPUTS- MRI-Guided Thrombolysisfor Stroke with Unknown Time of Onset Epub 2018 May 16. Abstract Background: Under current guidelines, intravenous thrombolysis is used to treat acute stroke only if it can be ascertained that the time since the onset of symptoms was less than 4.5 hours. We sought to determine whether patients with stroke with an unknown time of onset and features suggesting recent cerebral infarction on magnetic resonance imaging (MRI) would benefit from thrombolysis with the use of intravenous alteplase. Methods: In a multicenter trial, we randomly assigned patients who had an unknown time of onset of stroke to receive either intravenous alteplase or placebo. All the patients had an ischemic lesion that was visible on MRI diffusion-weighted imaging but no parenchymal hyperintensity on fluid-attenuated inversion recovery (FLAIR), which indicated that the stroke had occurred approximately within the previous 4.5 hours. We excluded patients for whom thrombectomy was planned. Conclusions: In patients with acute stroke with an unknown time of onset, intravenous alteplase guided by a mismatch between diffusion-weighted imaging and FLAIR in the region of ischemia resulted in a significantly better functional outcome and numerically more intracranial haemorrhages than placebo at 90 days. (Funded by the European Union Seventh Framework Program; WAKE-UP ClinicalTrials.gov number, NCT01525290; and EudraCT number, 2011-005906-32 .).
  • 90.
    CONCLUSION The onset ofstroke is a dramatic and discouraging event both for the person having the stroke and their family. A person may go from complete independence to complete dependence in a matter of minutes. All nursing staff have important roles and responsibilities when caring for people with a stroke. These include: Physiological monitoring and maintenance of homeostasis. Reduce morbidity and prevent mortality.
  • 91.
    BIBLIOGRAPHY-  Black MJoyce, Hawks Jane Hokanson. Medical-surgical nursing: clinical management for positive outcomes. 7th ed. Elsevier publishers:2005; 2107-36.  Harrison’s Principles Of Internal Medicine.20th ed. Page no- 3069-78.  Smeltzer Suzanne C, Bare Brenda G. Brunner & Suddarth’s Textbook of medical-surgical nursing. 11th ed. lippincott williams & wilkins:2009; 2206-25.  Monahan, Sands. et al. Phipp’s medical surgical nursing: health and illness perspective. 8th ed. Elsevier publishers:2007; 1861-72.  Chintamani; textbook of medical-surgical nursing; published by: Elsevier; 7th edition; page no- 1466-90  http://www.google.co.in/? gws_rd=cr&ei=HBbHUqnQO4qJrAf8hoDIDA#q=stroke+reha bilitation+pdf  https://www.stroke.org.uk/sites/default/files/physical_eff ects_of_stroke.pdf  https://pubmed.ncbi.nlm.nih.gov/31423922/  https://pubmed.ncbi.nlm.nih.gov/29766770/ ANY DOUBT? PLEASE ASK.