@ Stroke seminar

STROKE
INTRODUCTION:
Stroke is an acute interruption of blood flow to a portion of brain, resulting in cell death and loss of
associated neurologic function in the area
DEFINITION:
Stroke (or ‘Cerebrovascular accident’) is a syndrome of rapidly developing clinical signs of focal
(or global) disturbance of cerebral function, with symptoms lasting 24 hours or longer or leading to
death with no apparent cause other than of vascular origin.
- WHO definition
or
Transient Ischaemic Attack (TIA) or ‘mini stroke’ is where those symptoms resolve in 24 hours
(usually under 30 minutes).
EPIDERMIOLOGY:
 Worldwide, 3 million women and 2.5 million men die from stroke every year- however;
men are 25% more likely to suffer strokes than women.
 The Prevalence of stroke is approximately 1.5/1000 which rises with age to 10/1000 at the
age of 75.

RISK FACTOR(MODIFIABLE FACTORS)
 High Blood Pressure
High blood pressure, or hypertension, is a leading cause of stroke and the most significant
controllable risk factor.
 Smoking
The nicotine and carbon monoxide in cigarette smoke damage the cardiovascular system
and pave the way for a stroke.
 The use of birth control pills combined with cigarette smoking can greatly increase the risk
of stroke.
 Diabetes
It is an independent risk factor for stroke.
 Diet
Diets high in saturated fat, trans fat and cholesterol can raise blood cholesterol levels. Diets
high in sodium (salt) can increase blood pressure. Diets with high calories can lead to
obesity.
 Physical Inactivity
Physical inactivity can increase your risk of stroke, heart disease, overweight/obesity,
high blood pressure, high blood cholesterol and diabetes.
 Obesity
Excess body weight and obesity are linked with an increased risk of high blood pressure,
diabetes, heart disease and stroke.
 High Blood Cholesterol
Large amounts of cholesterol in the blood can build up and cause blood clots — leading to a
stroke. Also, it appears that low HDL ("good”) cholesterol is a risk factor for stroke
 Carotid Artery Disease
 Artheosclerosis
 Peripheral Artery Disease
 Atrial Fibrillation
 Atrial fibrillation, increases stroke risks fivefold.
 Other Heart Disease

 Coronary Heart Disease
 Cardiomyopathy
 Valve Diseases
 Congenital Heart Disease
 Sickle Cell Disease (Sickle Cell Anemia)
“Sickled” red blood cells which are less able to carry oxygen to the body’s tissues and
organs. These cells also tend to stick to blood vessel walls, which can block arteries to the
brain and cause a stroke.
NON MODIFIABLE RISK FACTORS
 Age
 The likelihood of having a stroke increases with age for both males and females.
Although stroke is more common among the elderly, a lot of people under 65 also have
strokes.
 Family History
 greater risk.
 Race
 African-Americans have a much higher risk of death from a stroke than Caucasians do..
Hispanics and Latinos also have unique risks for stroke.
 Gender
 Women have more strokes than men and stroke kills more women than men. Women tend
to live longer than men and are older when they have a stroke. Factors that may increase
stroke risks for women include pregnancy, history of preeclampsia/eclampsia or
gestational diabetes, oral contraceptive use (especially when combined with smoking) and
post-menopausal hormone therapy.
 Prior Stroke, TIA or Heart Attack
 A person who’s had one or more Transient ischemic Attack is almost 10 times more likely
to have a stroke than someone of the same age and sex who hasn't.

PATHOPHYSIOLOGY:
The blood flow to the brain is managed by two internal carotidsanteriorly and two vertebral arteries
posteriorly (the circle of Willis). Ischemic stroke is caused by deficient blood and oxygen supply to
the brain while hemorrhagic stroke is caused by bleeding or leaky blood vessels.
Ischemic Stroke Pathophysiology:
 Ischemic occlusion generates thrombotic and embolic conditions in the brain.
 In thrombosis, the blood flow is affected by narrowing of vessels due to atherosclerosis. The
build‐up of plaque will eventually constrict the vascular chamber and form clots, causing
thrombotic stroke.
 In an embolic stroke, decreased blood flow to the brain region causes an embolism; the
blood flow to the brain reduces, causing severe stress and untimely cell death (necrosis).
 Necrosis is followed by disruption of the plasma membrane, organelle swelling and leaking
of cellular contents into extracellular space ,and loss of neuronal function.

 Other key events contributing to stroke pathology are inflammation ,energy failure,loss of
homeostasis, acidosis, increased intracellular calcium levels, excitotoxicity, free
radical‐mediated toxicity, cytokine‐mediated cytotoxicity, complement activation,
impairment of the blood–brain barrier, activation of glial cells, oxidative stress and
infiltration of leukocytes.
Hemorrhagic Stroke Pathophysiology:
 Stress in the brain tissue and internal injury cause blood vessels to rupture, leading to
compression of brain tissue from an expanding haematoma.
 It produces toxic effects in the vascular system, resulting in infarction.
 It is classified into intracerebral and subarachnoid haemorrage.
 In intracerebral haemorrage (ICH), blood vessels rupture and cause abnormal accumulation
of blood within the brain
 The main reasons for ICH are hypertension, disrupted vasculature, excessive use of
anticoagulants and thrombolytic agents.
 In subarachnoid haemorrage, blood accumulates in the subarachnoid space of the brain dura
typically caused by head injury or cerebral aneurysm.
CLASSIFICATION:
The two main types of stroke are:
 Ischemic stroke.
 Hemorrhagic stroke.

Ischemic Stroke
o Most strokes (87%) are ischemic strokes.1 An ischemic stroke happens when blood flow
through the artery that supplies oxygen-rich blood to the brain becomes blocked.
o Blood clots often cause the blockages that lead to ischemic strokes.
Hemorrhagic Stroke
o A hemorrhagic stroke happens when an artery in the brain leaks blood or ruptures (breaks
open). The leaked blood puts too much pressure on brain cells, which damages them.
o High blood pressure and aneurysms—balloon-like bulges in an artery that can stretch and
burst—are examples of conditions that can cause a hemorrhagic stroke.
There are two types of hemorrhagic strokes:
Intracerebral hemorrhage: It is the most common type of hemorrhagic stroke. It occurs when an
artery in the brain bursts, flooding the surrounding tissue with blood.
Subarachnoid hemorrhage: It is a less common type of hemorrhagic stroke. It refers to bleeding
in the area between the brain and the thin tissues that cover it.
SIGNS AND SYMPTOMS:
 The presence of a stroke is generally indicated by the development of sudden-onset facial
weakness, arm drift or drop, abnormal speech, eyesight changes and confusion.
 The UK system for diagnosis includes the FAST screen (face, arm, speech and time) and
was advocated by the Department of Health.

 In most stroke cases, the symptoms only affect one side of the body (unilateral) and the
defect in the brain is on the contralateral side (opposite),
If the area of the brain affected contains one of the three prominent Central Nervous system
pathways- the spinothalamic tract, corticospinal tract, and dorsal column (medial lemniscus),
symptoms may include:
 Hemiplegia and muscle weakness of the face
 Numbness
 Reduction in sensory or vibratory sensation.
 In addition to the above pathways, the brainstem also consists of the 12 cranial nerves. A
stroke affecting the brainstem can therefore produce symptoms relating to deficits in the
cranial nerves:
 Altered smell, taste, hearing or vision.
 Ptosis and weakness of the extra ocular muscles
 Decreased reflexes: Gag, swallow, pupil reflexes to light.
 Nystagmus

 Weakness in sternocleidomastoid muscle with inability to turn head
 Tongue weakness
If the cerebral cortex is involved, the CNS pathways can be again affected, but can also produce the
following symptoms:
 Aphasia (inability to speak or understand language from involvement of Wernicke’s or
Broca’s area)
 Apraxia (altered voluntary movement)
 Visual field defect
 Memory Deficits (involvement of Temporal lobe)
 Hemi neglect (involvement of the Parietal lobe)
 Disorganised thinking, confusion, hypersexual gestures (with involvement of the frontal
lobe)
 Anosognosia (persistent denial of the existence of a, usually stroke-related deficit).
If the cerebellum is involved, the patient may have the following:
 Trouble walking
 Altered movement coordination
 Vertigo/ disequilibrium
 Loss of consciousness, headache and vomiting usually occur more often in haemorrhagic
stroke than in ischemia because of the increased intracranial pressure from the leaking blood
compressing on the brain. If symptoms are maximal at onset, the cause is more likely to be a
subarachnoid haemorrhage or an embolic stroke.

DIAGNOSTIC EVALUATION:
 History and Neurological Examination and
 A non contrast head CT scan.
CT imaging will help to distinguish between an infarct and a haemorrhagic stroke- bleeding
is shown within or around the brain. If no bleeding is seen, a presumptive diagnosis of
ischaemic stroke is made.
 A Doppler ultrasound study of the carotid arteries (to detect stenosis) or dissection.
 An electrocardiogram and echo (to identify arrhythmias and resultant clots in the heart
which may embolise).
 A Holter monitor study to identify intermittent arrhythmias.
 An Angiogram of the cerebral vasculature (if a bleed is thought to have originated from an
aneurysm or arteriovenous malformation.)
 Blood tests to determine hypercholesterolemia, bleeding diathesis and some rarer causes
such as homocysteinuria.
MANAGEMENT:
Emergency management:
• ICH is a neurological emergency and initial management should be focused on assessing the
patients airway, breathing capability, blood pressure and signs of increased intracranial
pressure. The patient should be intubated based on risk of aspiration, impending ventilatory
failure (PaO2 < 60 mmHg or pCO2 > 50 mmHg), and signs of increased intracranial
pressure.

• Emergency measures for ICP control are appropriate for stuporous or comatose patients, or
those who present acutely with clinical signs of brainstem herniation. The head should be
elevated to 30 degrees, 1.0–1.5 g/kg of 20% mannitol should be given by a rapid infusion,
and the patient should be hyperventilated to a pCO2 of 30–35 mmHg.
• These measures are designed to lower ICP as quickly as possible prior to a definitive
neurosurgical procedure (craniotomy, ventriculostomy, or placement of an ICP monitor) can
be done.
• A number of these patients will present after a fall so particular attention should be directed
to lacerations, skeletal fractures, stabilization of the cervical spine.
Blood pressure
• Elevated blood pressure is seen in 46%–56% of patients with ICH.
• recommended maintaining a mean arterial pressure below 130 mmHg in patients with a
history of hypertension
• In patients with elevated ICP who have an ICP monitor, cerebral perfusion pressure (MAP–
ICP) should be kept >70 mmHg
Early hemostatic therapy
• According to guidelines devised by the American Heart Association Stroke Council, if
bleeding is suspected the following measures should be taken:
1) blood should be drawn to measure the patient’s hematocrit, hemoglobin, partial
thromboplastin time, prothrombin time/INR, platelet count, and fibrinogen
2) blood should be typed and cross-matched if transfusions are needed (at least 4 U of
packed red blood cells, 4–6 U of cryoprecipitate or fresh frozen plasma, and 1 U of
single donor platelets
• These therapies should be made available for urgent administration.
• Antifibrinolytic agents such as e-aminocaproic, tranexemic acid, aprotinin, and activated
recombinant Factor VII (rFVIIa) have been receiving attention for early hemostatic therapy
in patients with no underlying coagulopathy.

MANAGEMENT OF ICP:
• Therapeutic goal of treating elevated ICP is to maintain ICP < 20 mmhg while maintaining
cerebral perfusion pressure >70 mmhg.
• An intravenous sedative such as propofol (0.6–6.0 mg/kg/h) or fentanyl (0.5–3.0 μg/kg/h)
should be given to the agitated patient to attain a motionless state. Thereafter, therapy
should be directed at controlling blood pressure with vasopressors such as dopamine and
phenylephrine if the CPP is < 70 mmHg or with antihypertensive agents if the CPP is > 70
mmHg.
• If ICP does not respond to sedation and cerebral perfusion management, osmotic agents and
hyperventilation should be considered.
MEDICAL MANAGEMENT :
 Osmotic agents : (mannitol, glycerol, and sorbitol), each has characteristic advantages and
disadvantages.
 Sorbitol and glycerol are metabolized by the liver and interfere with glucose metabolism.
However, sorbitol is infrequently used due to a short half life and poor penetration into the
cerebrospinal fluid (CSF). Glycerol has a half-life less than one hour but it penetrates into
the cerebrospinal fluid the best. Mannitol is commonly used because it is renally
metabolized, has a half-life up to 4 hours, and achieves intermediate concentrations within
the CSF
• Large ICH associated with elevated intracranial pressure refractory to these measures is fatal
in most patients but a barbiturate coma may considered as a last resort to try to reduce
intracranial pressure.
 Anticonvulsant therapy
• The 30-day risk of seizures after ICH is about 8%. Seizures most commonly occur at the
onset of hemorrhage and may even be the presenting symptom.
• American Heart Association suggest prophylactic antiepileptic treatment may be considered
for 1 month in patients with intracerebral hemorrhage and discontinued if no seizures are
noted.

• Acute management of seizures entail administering intravenous lorazepam (0.05–0.10
mg/kg) followed by an intravenous loading dose of phenytoin or fosphenytoin (15–20
mg/kg), valproic acid (15–45 mg/kg), or phenobarbital (15–20 mg/kg)
 Fever control
• Fever after ICH is common and should be treated aggressively because it is independently
associated with a poor outcome.
• Sustained fever in excess of 38.3 °C (101.0 °F) should be treated with acetaminophen and
cooling blankets.
• Patients should be physically examined and should undergo laboratory testing or imaging to
determine the source of infection.
• Fever of neurologic origin is diagnosis of exclusion and may be seen when blood extends
into the subarachnoid or intraventricular .
• Intracerebral hemorrhage patients with persistent fever that is refractory to acetaminophen
and without infectious cause may require cooling devices to become normothermic.
Adhesive surface-cooling systems and endovascular heat-exchange catheters are better at
maintaining normothermia than conventional treatment
SURGICAL MANAGEMENT:
• Ventricular drains should be used in patients with or at risk for hydrocephalus. Drainage can
be initiated and terminated according to clinical performance and ICP values.
• Surgical clipping. a tiny clamp is placed at the base of the aneurysm, to stop blood flow to
it. This clamp can keep the aneurysm from bursting, or it can keep an aneurysm that has
recently hemorrhaged from bleeding again.
• Coiling (endovascular embolization). Using a catheter is inserted into an artery and
guided to brain, tiny detachable coils will be placed into the aneurysm to fill it. This
blocks blood flow into the aneurysm and causes blood to clot.

• Surgical AVM removal.
• Stereotactic radiosurgery : Using multiple beams of highly focused radiation, stereotactic
radiosurgery is an advanced minimally invasive treatment used to repair blood vessel
malformations.
• Deep venous thrombosis prophylaxis
• Immobilized state due to limb paresis predisposes ICH patients for deep vein thrombosis
and pulmonary embolism. Intermittent pneumatic compression devices and elastic stockings
should be placed on admission.
Management of Ischemic stroke
• Recombinant tissue plasminogen activator (tPA) — also called alteplase (Activase) — is the
gold standard treatment for ischemic stroke.
• An injection of tPA is given in first three hours. Sometimes, tPA can be given up to 4.5
hours after stroke symptoms started.
NURSING MANAGEMENT OF STOKE:
Nursing Assessment
During the acute phase, a neurologic flow sheet is maintained to provide data about the following
important measures of the patient’s clinical status:
 Change in level of consciousness or responsiveness.
 Presence or absence of voluntary or involuntary movements of extremities.
 Stiffness or flaccidity of the neck.
 Eye opening, comparative size of pupils, and pupillary reaction to light.

 Color of the face and extremities; temperature and moisture of the skin.
 Ability to speak.
 Presence of bleeding.
 Maintenance of blood pressure.
Nursing Diagnosis
 Impaired physical mobility related to hemiparesis, loss of balance and coordination,
spasticity, and brain injury.
 Acute pain related to hemiplegia and disuse.
 Deficient self-care related to stroke sequelae.
 Disturbed sensory perception related to altered sensory reception, transmission, and/or
integration.
 Impaired urinary elimination related to flaccid bladder, detrusor instability, confusion, or
difficulty in communicating.
 Disturbed thought processes related to brain damage.
 Impaired verbal communication related to brain damage.
 Risk for impaired skin integrity related to hemiparesis or hemiplegia and decreased
mobility.
 Interrupted family processes related to catastrophic illness and caregiving burdens.
 Sexual dysfunction related to neurologic deficits or fear of failure.
NURSING INTERVENTION:
1. Improving Mobility and Preventing Deformities
 Position to prevent contractures; use measures to relieve pressure, assist in maintaining good
body alignment, and prevent compressive neuropathies.
 Apply a splint at night to prevent ﬂexion of affected extremity.

 Prevent adduction of the affected shoulder with a pillow placed in the axilla.
 Elevate affected arm to prevent edema and fibrosis.
 Position fingers so that they are barely flexed; place hand in slight supination.
2. Establishing an Exercise Program
 Provide full range of motion four or five times a day to maintain joint mobility, regain motor
control, prevent contractures in the paralyzed extremity, prevent further deterioration of the
neuromuscular system, and enhance circulation. If tightness occurs in any area, perform a
range of motion exercises more frequently.
 Exercise is helpful in preventing venous stasis, which may predispose the patient to
thrombosis and pulmonary embolus.
 Observe for signs of pulmonary embolus or excessive cardiac workload during exercise
period (e.g., shortness of breath, chest pain, cyanosis, and increasing pulse rate).
 Supervise and support the patient during exercises; plan frequent short periods of exercise,
not longer periods; encourage the patient to exercise unaffected side at intervals throughout
the day.
3. Preparing for Ambulation
 Start an active rehabilitation program when consciousness returns (and all evidence of
bleeding is gone, when indicated).
 Teach patient to maintain balance in a sitting position, then to balance while standing (use a
tilt table if needed).
 Begin walking as soon as standing balance is achieved (use parallel bars and have a
wheelchair available in anticipation of possible dizziness).
4. Preventing Shoulder Pain
 Never lift patient by the flaccid shoulder or pull on the affected arm or shoulder.

 Use proper patient movement and positioning (e.g., flaccid arm on a table or pillows when
patient is seated, use of sling when ambulating).
 Range of motion exercises are beneficial, but avoid over strenuous arm movements.
 Elevate arm and hand to prevent dependent edema of the hand; administer analgesic agents
as indicated.
5. Enhancing Self Care
 Encourage personal hygiene activities as soon as the patient can sit up; select suitable self-
care activities that can be carried out with one hand.
 Help patient to set realistic goals; add a new task daily.
 As a first step, encourage patient to carry out all self-care activities on the unaffected side.
 Make sure patient does not neglect affected side; provide assistive devices as indicated.
 Improve morale by making sure patient is fully dressed during ambulatory activities.
 Assist with dressing activities (e.g., clothing with Velcro closures; put garment on the
affected side first); keep environment uncluttered and organized.
 Provide emotional support and encouragement to prevent fatigue and discouragement.
6. Managing Sensory-Perceptual Difficulties
 Approach patient with a decreased field of vision on the side where visual perception is
intact; place all visual stimuli on this side.
 Teach patient to turn and look in the direction of the defective visual field to compensate for
the loss; make eye contact with patient, and draw attention to affected side.
 Increase natural or artificial lighting in the room; provide eyeglasses to improve vision.
 Remind patient with hemianopsia of the other side of the body; place extremities so that
patient can see them.

7. Assisting with Nutrition
 Observe patient for paroxysms of coughing, food dribbling out or pooling in one side of the
mouth, food retained for long periods in the mouth, or nasal regurgitation when swallowing
liquids.
 Consult with speech therapist to evaluate gag reflexes; assist in teaching alternate
swallowing techniques, advise patient to take smaller boluses of food, and inform patient of
foods that are easier to swallow; provide thicker liquids or pureed diet as indicated.
 Have patient sit upright, preferably on chair, when eating and drinking; advance diet as
tolerated.
 Prepare for GI feedings through a tube if indicated; elevate the head of bed during feedings,
check tube position before feeding, administer feeding slowly, and ensure that cuff of
tracheostomy tube is inflated (if applicable); monitor and report excessive retained or
residual feeding.
8. Attaining Bowel and Bladder Control
 Perform intermittent sterile catheterization during the period of loss of sphincter control.
 Analyze voiding pattern and offer urinal or bedpan on patient’s voiding schedule.
 Assist the male patient to an upright posture for voiding.
 Provide high fiber diet and adequate fluid intake (2 to 3 L/day), unless contraindicated.
 Establish a regular time (after breakfast) for toileting.
9. Improving Thought Processes
 Reinforce structured training program using cognitive, perceptual retraining, visual imagery,
reality orientation, and cueing procedures to compensate for losses.
 Support patient: Observe performance and progress, give positive feedback, convey an
attitude of confidence and hopefulness; provide other interventions as used for improving
cognitive function after a head injury.

10. Improving Communication
 Reinforce the individually tailored program.
 Jointly establish goals, with the patient taking an active part.
 Make the atmosphere conducive to communication, remaining sensitive to patient’s
reactions and needs and responding to them in an appropriate manner; treat the patient as an
adult.
 Provide strong emotional support and understanding to allay anxiety; avoid completing
patient’s sentences.
 Be consistent in schedule, routines, and repetitions. A written schedule, checklists, and
audiotapes may help with memory and concentration; a communication board may be used.
 Maintain patient’s attention when talking with the patient, speak slowly, and give one
instruction at a time; allow the patient time to process.
 Talk to aphasic patients when providing care activities to provide social contact.
11.Maintaining Skin Integrity
 Frequently assess skin for signs of breakdown, with emphasis on bony areas and dependent
body parts.
 Employ pressure relieving devices; continue regular turning and positioning (every 2 hours
minimally); minimize shear and friction when positioning.
 Keep skin clean and dry, gently massage the healthy dry skin and maintain adequate
nutrition
12. Improving Family Coping
 Provide counseling and support to the family.
 Involve others in patient’s care; teach stress management techniques and maintenance of
personal health for family coping.

 Give family information about the expected outcome of the stroke, and counsel them to
avoid doing things for the patient that he or she can do.
 Develop attainable goals for the patient at home by involving the total health care team,
patient, and family.
 Encourage everyone to approach the patient with a supportive and optimistic attitude,
focusing on abilities that remain; explain to the family that emotional lability usually
improves with time.
13. Helping the Patient Cope with Sexual Dysfunction
 Perform in depth assessment to determine sexual history before and after the stroke.
 Interventions for patient and partner focus on providing relevant information, education,
reassurance, adjustment of medications, counseling regarding coping skills, suggestions for
alternative sexual positions, and a means of sexual expression and satisfaction.
HEALTH TEACHING EDUCATION
 Teach patient to resume as much self care as possible; provide assistive devices as indicated.
 Have occupational therapist make a home assessment and recommendations to help the
patient become more independent.
 Coordinate care provided by numerous health care professionals; help family plan aspects of
care.
 Advise family that patient may tire easily, become irritable and upset by small events, and
show less interest in daily events.
DISCHARGE AND HOME CARE GUIDELINES
Patient and family education is a fundamental component of rehabilitation.
 Consult an occupational therapist. An occupational therapist may be helpful in assessing
the home environment and recommending modifications to help the patient become more
independent.

 Physical therapy. A program of physical therapy may be beneficial, whether it takes place
in the home or in an outpatient program.
 Antidepressant therapy. Depression is a common and serious problem in the patient who
has had a stroke.
PROGNOSIS:
People can get better after stroke. However, for the reasons mentioned, predicting the degree
and pace of recovery is very difficult. Much of the recovery after a stroke occurs early,
usually within the first six months. Most experts agree that the brain can continue to heal for up
to two years afterward.

JOURNAL ABSTRACT
KNOWLEDGE OF STROKE AMONG STROKE PATIENTS AND THEIR RELATIVES IN
NORTHWEST INDIA
Jeyaraj D, Guneet K
Year of publication : 2006
Volume : 5
Issue : 2
Background: The knowledge of warning symptoms and risk factors for stroke has not been
studied among patients with stroke in developing countries. Aims: We aimed to assess the
knowledge of stroke among patients with stroke and their relatives.
Settings and Design: Prospective tertiary referral hospital-based study in Northwest India.
Materials and Methods: Trained nurses and medical interns interviewed patients with stroke and
transient ischemic attack and their relatives about their knowledge of stroke symptoms and risk
factors.
Statistical Analysis: Univariable and mulivariable logistic regression were used.
Results: Of the 147 subjects interviewed, 102 (69%) were patients and 45 (31%) were relatives.
There were 99 (67%) men and 48 (33%) women and the mean age was 59.7±14.1 years. Sixty-
two percent of repondents recognized paralysis of one side as a warning symptom and 54%
recognized hypertension as a risk factor for stroke. In the multivariable logistic regression
analysis, higher education was associated with the knowledge of correct organ involvement in
stroke (OR 2.6, CI 1.1- 6.1, P =0.02), whereas younger age (OR 2.7, CI 1.1-7.0, P =0.04) and
higher education (OR 4.1, CI 1.5-10.9, P =0.005) correlated with a better knowledge regarding
warning symptoms of stroke.
Conclusions: In this study cohort, in general, there is lack of awareness of major warning
symptoms, risk factors, organ involvement and self-recognition of stroke. However younger age
and education status were associated with better knowledge. There is an urgent need for
awareness programs about stroke in this study cohort.

SUMMARY:
In this document, introduction, definition, epidermiology, risk factor(modifiable factors,
pathophysiology, classification, signs and symptoms, diagnostic evaluation, management,
management of icp, medical management , surgical management, nursing management of stoke,
nursing intervention, health teaching education, discharge and home care guidelines and
prognosis of stroke is studied in details.
CONCLUSION:
A stroke is a medical condition in which poor blood flow to the brain causes cell death. In
2015, stroke was the second most frequent cause of death after coronary artery disease,
accounting for 6.3 million deaths (11% of the total). Overall, two thirds of strokes occurred in
those over 65 years old. There are two main types of stroke: ischemic, due to lack of blood flow,
and hemorrhagic, due to bleeding. Both cause parts of the brain to stop functioning properly.
Signs and symptoms of a stroke may include an inability to move or feel on one side of the body,
problems understanding or speaking, dizziness, or loss of vision to one side. The main risk factor
for stroke is high blood pressure. Prevention includes decreasing risk factors, surgery to open up
the arteries to the brain in those with problematic carotid narrowing, and warfarin in people with
atrial fibrillation.

BIBLIOGRAPHY:
 Brunner and Suddarth’s . “A Text book of Medical Surgical Nursing”. Vol-2. 13th
edition, New Delhi , Wolters Kluwer; 2014, page no. 1958-1961.
 Lewis’s “Medical Surgical Nursing”, 7th edition. Published by Elsevier. Page no.
1397-1398.
REFERENCES:
 https://www.neurologyindia.com/
 https://www.cdc.gov/stroke/types_of_stroke.htm
 https://www.medicalnewstoday.com/articles/317111
 https://www.mayoclinic.org/diseases-conditions/stroke/symptoms-causes/syc-20350113

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