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In the 1970s the World Health
Organization defined stroke as a "neurological
deficit of cerebrovascular cause that persists
beyond 24 hours or is interrupted by death within
24 hours",
Stroke occure when there is ischemia to a
part of brain or haemorrhage into the brain that
results in death of the brain cells. (Lewies)
Non modifiable Risk factors:-
Age
Gender
Ethnicity
Race
Family history
Heredity
Hypertension:- Increase systolic BP & diastolic BP
increase chances to rupture the blood vessels.
Heart disease:- Arterial fibrillation, myocardial
infraction, valve abnormalities or Endocardiatis
increase risk of stroke.
DM
Smoking:- Excessive smoking causes arterial damage.
Excessive alcohol consumption
Metabolic syndrome
Drug abuse:- Cocaine causes vasoconstriction
Obesity:- It causes HTN, DM & elevated blood lipid
level.
Stroke is divided in to two major categories,
those are:-
Ischemic Stroke
Hemorrhagic stroke
Definition:-
Ischemic stroke results from inadequate blood
flow to the brain from partial or complete occlusion of
artery.
Types:-
A person experiencing stroke losses 1.9 million
neurons neurons each minutes .
 Ishemic stroke are further divided in to two types,
those are:-
Thrombotic
Embolic
Cerebral thrombosis is a narrowing of the artery
by fatty deposits called plaque.
The plaque can cause a clot to form, which block
the passage of blood through the artery.
Thrombotic stroke are associated with DM or
HTN.
Both the disease enhance atherosclerosis.
Extent of stroke depands upon rapidity of onset,
size of leision & presence of collateral circulation.
Ischemic stroke symptoms progress in the first 72
hours as infraction & cerebral edema increase.
It is the stroke due to occlusion of small penetrating
artery.
It is commonly occure in basal ganglia, thalamus,
internal casule. It generally a symptomatic but
sometimes causes hemiplasia, leg or face weakness, leg
ataxia, decrease cognitive function.
An Embolus is a blood clot or other debris circulating in the
blood.
When it reach an artery in the brain that is too narrow to
pass through, it lodges there & block the flow of blood.
Majority of embolus originate in the endocardial layer of
heart. Here the plaque breaking from the endocardium &
enter the circulation.
The embolus travel upward to the cerebral circulation &
ludge the where the vissel narrow or bifurcate.
The heart condition which raise emboli are MI, infective
Endocardiatis, rheumatic fever, Vulvular prosthesis, fat from
long bone fracture.
Symptoms are seen rapidly.
CR:- Headache, neurologic deficit depends upon amount of
brain tissue involve.
• PATHOPHYSIOLOGY:-
• DUE TO ETIOLOGY ( THROMBUS OR EMBOLUS)
 OBSTRUCTION IN THE BLOOD VESSELS
 CEREBRAL BLOOD FLOW DECREASE TO LESS THEN 25ml PER MINUTE
 ISCHEMIC CASCADE BEGINS
 NEURONE ARE NO LONGER ABLE TO MAINTAIN AEROBIC RESPIRATION
 MITOCHONDRIA SWICH TO MAINTAIN ANAROBIC RESPIRATION
 PRODUCTION OF LARGE AMOUNT OF LACTIC ACID
 CHANGE IN Ph
 INEFFICIANT ANAEROBIC RESPIRATION
 NEURONE INCAPABLE OF PRODUCING SUFFICIENT QUANTITIES OF ATP
 DEPOLARIZATION PROCESS HAMPER
 CELL MEMBRANE FAIL TO MAINTAIN ELECTROLYTE BALANCE IN
PENUMBRA REGION(area surrounding an ischemic event)
 EXCESSIVE INFLUX OF CELLULAR CALCIUM & RELEASE GLUTAMATE
 ACTIVATE DAMAGING PATHWAY
 DESTRUCTION OF CELL MEMBRANE, VASOCONSTRICTION
Visual field deficits:- It occur due to disturbance in primary
sensory pathway between the eye & visual cortex.
Loss of peripheral vision:- difficulty seeing in night, unaware
of object
Diplopia:- Double vision
Motor loss:-
Damage in upper motor neurone on one hemisphere
causes damage to the opposite side of the body.
Hemiparesis:- Weakness of the face, arm & leg on opposite
site.
Hemiplasia:- Paralysis of the face, arm,& leg on opposite
site of leision.
Ataxia:- Staggering, unsteady gait, unable to keep the feet
together. Dysphasia:- Difficulty in swallowing
Sensory deficits:-
Difficult in interpreting visual, tactile & auditory
stimuli,
Agnosias:- Deficite in the ability to recognise previously
familiar objects.
Verbal deficits:-
Dysarthria:- Difficulty of speaking caused by paralysis
of muscles responsible for producing speech
Excessive Aphasia:- Inability to express oneself.
Receptive aphasia:- Inability to understand the
language
Global:- Both excessive aphasia & receptive aphasia
Cognitive Deficits:-
Short & long term memory loss
Decrease attention span
Impaired ability to concentrate.
Poor abstract reasoning
Altered judgement
Emotional deficit:-
Decrease tolerance to stressful situation
Depression
Fear, hostility, anger
Feeling of isolation
Assess whether there is loss of gag reflex, cough reflex,
altered respiratory pattern, cardiovascular status & gross
neurological deficit.
Identify Transient ischemic attack which results from
temporary ischemia to a specific region of the brain which
manifested as sudden loss of motor, sensory & visual
function. It is the pre stroke which suggest patient will
develop stroke & irreversible damage.
CT Scan:- It identify size & location of lesion &
differentiation between ischemic & hemorrhagic stroke.
CTA( Computerised tomographic angiography):-
Visualization of vasculature which done at the time of CT
scan.
MRI:- Provide clear picture the CT scan
PET:- It shows metabolic activity of the brain & shows
extent of tissue damage
SPECT:- Single photon emission computed
tomography:-
Angiography to determine the cerebral atherosclerosis
Transcranial Doppler ultrasonography:- To measure
the velocity of blood flow in the measure cranial
arteries.
Skull X-ray
Brain scan
EEG
Lumber pumpture:- If RBC found in the CSF then
haemorrhage is subarachnoid space.
Control of hypertension
Control of DM
Treatment of underlying cardiac problem
Anticoagulation therapy for the patient with arterial
fibrillation
No smoking
Limiting alcohol
Stenting of carotid artery
Innitial management:-
Ensure patient airway
Maintain adequate oxygenation with
supplemental o2
Establish IV assess for normal saline
Maintain BP according to the guideline
Obtain CT Scan immediately
Position Head midline
Position HOB 30 degree if no symptom of shock
Anticipate thrombolytic therapy for ischemic
stroke
Ongoing management:-
Monitor vital sign& neurologic, including level of
consciousness.
Monitor motor & sensory function, pupil size &
reactivity
Medication:-
Those with arterial fibrillation are treated with low
dose warfarin with target INF of 2-3
Thrombolytic therapy:- Used to treat ischemic stroke
by dissolving the blood clot that blocking the blood flow
to the brain.
Surgical therapy:-
Endarterectomy:- removal of lesion from the carotid
artery to improve blood flow
Transluminalangioplasty:- There is insertion of a balloon
to open a stenosed artery
EC-IC bypass:- Anasomosis a branch of external artery to
an intracranial artery to increase the cerebrl perfusion.
Endarterectomy
Transluminalangioplasty
EC-IC bypass:-

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Stroke

  • 1.
  • 2. In the 1970s the World Health Organization defined stroke as a "neurological deficit of cerebrovascular cause that persists beyond 24 hours or is interrupted by death within 24 hours", Stroke occure when there is ischemia to a part of brain or haemorrhage into the brain that results in death of the brain cells. (Lewies)
  • 3. Non modifiable Risk factors:- Age Gender Ethnicity Race Family history Heredity
  • 4. Hypertension:- Increase systolic BP & diastolic BP increase chances to rupture the blood vessels. Heart disease:- Arterial fibrillation, myocardial infraction, valve abnormalities or Endocardiatis increase risk of stroke. DM Smoking:- Excessive smoking causes arterial damage. Excessive alcohol consumption Metabolic syndrome Drug abuse:- Cocaine causes vasoconstriction Obesity:- It causes HTN, DM & elevated blood lipid level.
  • 5. Stroke is divided in to two major categories, those are:- Ischemic Stroke Hemorrhagic stroke
  • 6. Definition:- Ischemic stroke results from inadequate blood flow to the brain from partial or complete occlusion of artery. Types:- A person experiencing stroke losses 1.9 million neurons neurons each minutes .  Ishemic stroke are further divided in to two types, those are:- Thrombotic Embolic
  • 7. Cerebral thrombosis is a narrowing of the artery by fatty deposits called plaque. The plaque can cause a clot to form, which block the passage of blood through the artery. Thrombotic stroke are associated with DM or HTN. Both the disease enhance atherosclerosis. Extent of stroke depands upon rapidity of onset, size of leision & presence of collateral circulation. Ischemic stroke symptoms progress in the first 72 hours as infraction & cerebral edema increase.
  • 8. It is the stroke due to occlusion of small penetrating artery. It is commonly occure in basal ganglia, thalamus, internal casule. It generally a symptomatic but sometimes causes hemiplasia, leg or face weakness, leg ataxia, decrease cognitive function.
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  • 10. An Embolus is a blood clot or other debris circulating in the blood. When it reach an artery in the brain that is too narrow to pass through, it lodges there & block the flow of blood. Majority of embolus originate in the endocardial layer of heart. Here the plaque breaking from the endocardium & enter the circulation. The embolus travel upward to the cerebral circulation & ludge the where the vissel narrow or bifurcate. The heart condition which raise emboli are MI, infective Endocardiatis, rheumatic fever, Vulvular prosthesis, fat from long bone fracture. Symptoms are seen rapidly. CR:- Headache, neurologic deficit depends upon amount of brain tissue involve.
  • 11. • PATHOPHYSIOLOGY:- • DUE TO ETIOLOGY ( THROMBUS OR EMBOLUS)  OBSTRUCTION IN THE BLOOD VESSELS  CEREBRAL BLOOD FLOW DECREASE TO LESS THEN 25ml PER MINUTE  ISCHEMIC CASCADE BEGINS  NEURONE ARE NO LONGER ABLE TO MAINTAIN AEROBIC RESPIRATION  MITOCHONDRIA SWICH TO MAINTAIN ANAROBIC RESPIRATION  PRODUCTION OF LARGE AMOUNT OF LACTIC ACID  CHANGE IN Ph  INEFFICIANT ANAEROBIC RESPIRATION  NEURONE INCAPABLE OF PRODUCING SUFFICIENT QUANTITIES OF ATP  DEPOLARIZATION PROCESS HAMPER  CELL MEMBRANE FAIL TO MAINTAIN ELECTROLYTE BALANCE IN PENUMBRA REGION(area surrounding an ischemic event)  EXCESSIVE INFLUX OF CELLULAR CALCIUM & RELEASE GLUTAMATE  ACTIVATE DAMAGING PATHWAY  DESTRUCTION OF CELL MEMBRANE, VASOCONSTRICTION
  • 12. Visual field deficits:- It occur due to disturbance in primary sensory pathway between the eye & visual cortex. Loss of peripheral vision:- difficulty seeing in night, unaware of object Diplopia:- Double vision Motor loss:- Damage in upper motor neurone on one hemisphere causes damage to the opposite side of the body. Hemiparesis:- Weakness of the face, arm & leg on opposite site. Hemiplasia:- Paralysis of the face, arm,& leg on opposite site of leision. Ataxia:- Staggering, unsteady gait, unable to keep the feet together. Dysphasia:- Difficulty in swallowing
  • 13. Sensory deficits:- Difficult in interpreting visual, tactile & auditory stimuli, Agnosias:- Deficite in the ability to recognise previously familiar objects. Verbal deficits:- Dysarthria:- Difficulty of speaking caused by paralysis of muscles responsible for producing speech Excessive Aphasia:- Inability to express oneself. Receptive aphasia:- Inability to understand the language Global:- Both excessive aphasia & receptive aphasia
  • 14. Cognitive Deficits:- Short & long term memory loss Decrease attention span Impaired ability to concentrate. Poor abstract reasoning Altered judgement Emotional deficit:- Decrease tolerance to stressful situation Depression Fear, hostility, anger Feeling of isolation
  • 15. Assess whether there is loss of gag reflex, cough reflex, altered respiratory pattern, cardiovascular status & gross neurological deficit. Identify Transient ischemic attack which results from temporary ischemia to a specific region of the brain which manifested as sudden loss of motor, sensory & visual function. It is the pre stroke which suggest patient will develop stroke & irreversible damage. CT Scan:- It identify size & location of lesion & differentiation between ischemic & hemorrhagic stroke. CTA( Computerised tomographic angiography):- Visualization of vasculature which done at the time of CT scan.
  • 16. MRI:- Provide clear picture the CT scan PET:- It shows metabolic activity of the brain & shows extent of tissue damage SPECT:- Single photon emission computed tomography:- Angiography to determine the cerebral atherosclerosis Transcranial Doppler ultrasonography:- To measure the velocity of blood flow in the measure cranial arteries. Skull X-ray Brain scan EEG Lumber pumpture:- If RBC found in the CSF then haemorrhage is subarachnoid space.
  • 17. Control of hypertension Control of DM Treatment of underlying cardiac problem Anticoagulation therapy for the patient with arterial fibrillation No smoking Limiting alcohol Stenting of carotid artery
  • 18. Innitial management:- Ensure patient airway Maintain adequate oxygenation with supplemental o2 Establish IV assess for normal saline Maintain BP according to the guideline Obtain CT Scan immediately Position Head midline Position HOB 30 degree if no symptom of shock Anticipate thrombolytic therapy for ischemic stroke
  • 19. Ongoing management:- Monitor vital sign& neurologic, including level of consciousness. Monitor motor & sensory function, pupil size & reactivity Medication:- Those with arterial fibrillation are treated with low dose warfarin with target INF of 2-3 Thrombolytic therapy:- Used to treat ischemic stroke by dissolving the blood clot that blocking the blood flow to the brain.
  • 20. Surgical therapy:- Endarterectomy:- removal of lesion from the carotid artery to improve blood flow Transluminalangioplasty:- There is insertion of a balloon to open a stenosed artery EC-IC bypass:- Anasomosis a branch of external artery to an intracranial artery to increase the cerebrl perfusion.