This document provides an outline and overview of key topics related to stroke. It begins with definitions and classifications of stroke, including transient ischemic attack (TIA) and different types of stroke. It then covers risk factors, pathophysiology, signs and symptoms, investigations, and management approaches for stroke. Specific sections address hemorrhagic versus ischemic stroke, localization of stroke syndromes, and differentiating features between anterior and posterior circulation strokes. Differential diagnoses are also listed. The document aims to present essential information on stroke for medical education purposes.
Hemiparesis is unilateral paresis, that is, weakness of the entire left or right side of the body (hemi- means "half"). Hemiplegia is, in its most severe form, complete paralysis of half of the body. Hemiparesis and hemiplegia can be caused by different medical conditions, including congenital causes, trauma, tumors, or stroke
Hypenension: Commonest cause of intracerebral haemorrhage.
Rupture of an intracranial aneurysm, angioma or A-V malformation: commonest cause of subarachnoid haemorrhage.
Haemorrhagic blood diseases: purpura, haemophilia.
Anticoagulants.
Trauma to the head: commonest of subdural haematoma.
II. Infective: ;
Encephalitis
Meningitis – Brain abscess.
III. Neoplastic: e.g. Meningioma.
IV. Demyelination: multiple sclerosis may present with hemiplegia.
V. Traumatic: e.g. Cerebral laceration and subdural haematoma.
VI. Hysterical: patient suffering from paralysis in the absence of organic lesion.
Hemiparesis is unilateral paresis, that is, weakness of the entire left or right side of the body (hemi- means "half"). Hemiplegia is, in its most severe form, complete paralysis of half of the body. Hemiparesis and hemiplegia can be caused by different medical conditions, including congenital causes, trauma, tumors, or stroke
Hypenension: Commonest cause of intracerebral haemorrhage.
Rupture of an intracranial aneurysm, angioma or A-V malformation: commonest cause of subarachnoid haemorrhage.
Haemorrhagic blood diseases: purpura, haemophilia.
Anticoagulants.
Trauma to the head: commonest of subdural haematoma.
II. Infective: ;
Encephalitis
Meningitis – Brain abscess.
III. Neoplastic: e.g. Meningioma.
IV. Demyelination: multiple sclerosis may present with hemiplegia.
V. Traumatic: e.g. Cerebral laceration and subdural haematoma.
VI. Hysterical: patient suffering from paralysis in the absence of organic lesion.
A spinal cord injury (SCI) is damage to the spinal cord that causes temporary or permanent changes in its function. Symptoms may include loss of muscle function, sensation, or autonomic function in the parts of the body served by the spinal cord below the level of the injury.
A spinal cord injury (SCI) is damage to the spinal cord that causes temporary or permanent changes in its function. Symptoms may include loss of muscle function, sensation, or autonomic function in the parts of the body served by the spinal cord below the level of the injury.
A Strategic Approach: GenAI in EducationPeter Windle
Artificial Intelligence (AI) technologies such as Generative AI, Image Generators and Large Language Models have had a dramatic impact on teaching, learning and assessment over the past 18 months. The most immediate threat AI posed was to Academic Integrity with Higher Education Institutes (HEIs) focusing their efforts on combating the use of GenAI in assessment. Guidelines were developed for staff and students, policies put in place too. Innovative educators have forged paths in the use of Generative AI for teaching, learning and assessments leading to pockets of transformation springing up across HEIs, often with little or no top-down guidance, support or direction.
This Gasta posits a strategic approach to integrating AI into HEIs to prepare staff, students and the curriculum for an evolving world and workplace. We will highlight the advantages of working with these technologies beyond the realm of teaching, learning and assessment by considering prompt engineering skills, industry impact, curriculum changes, and the need for staff upskilling. In contrast, not engaging strategically with Generative AI poses risks, including falling behind peers, missed opportunities and failing to ensure our graduates remain employable. The rapid evolution of AI technologies necessitates a proactive and strategic approach if we are to remain relevant.
The French Revolution, which began in 1789, was a period of radical social and political upheaval in France. It marked the decline of absolute monarchies, the rise of secular and democratic republics, and the eventual rise of Napoleon Bonaparte. This revolutionary period is crucial in understanding the transition from feudalism to modernity in Europe.
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This will be used as part of your Personal Professional Portfolio once graded.
Objective:
Prepare a presentation or a paper using research, basic comparative analysis, data organization and application of economic information. You will make an informed assessment of an economic climate outside of the United States to accomplish an entertainment industry objective.
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Synthetic fiber production is a fascinating and complex field that blends chemistry, engineering, and environmental science. By understanding these aspects, students can gain a comprehensive view of synthetic fiber production, its impact on society and the environment, and the potential for future innovations. Synthetic fibers play a crucial role in modern society, impacting various aspects of daily life, industry, and the environment. ynthetic fibers are integral to modern life, offering a range of benefits from cost-effectiveness and versatility to innovative applications and performance characteristics. While they pose environmental challenges, ongoing research and development aim to create more sustainable and eco-friendly alternatives. Understanding the importance of synthetic fibers helps in appreciating their role in the economy, industry, and daily life, while also emphasizing the need for sustainable practices and innovation.
The Roman Empire A Historical Colossus.pdfkaushalkr1407
The Roman Empire, a vast and enduring power, stands as one of history's most remarkable civilizations, leaving an indelible imprint on the world. It emerged from the Roman Republic, transitioning into an imperial powerhouse under the leadership of Augustus Caesar in 27 BCE. This transformation marked the beginning of an era defined by unprecedented territorial expansion, architectural marvels, and profound cultural influence.
The empire's roots lie in the city of Rome, founded, according to legend, by Romulus in 753 BCE. Over centuries, Rome evolved from a small settlement to a formidable republic, characterized by a complex political system with elected officials and checks on power. However, internal strife, class conflicts, and military ambitions paved the way for the end of the Republic. Julius Caesar’s dictatorship and subsequent assassination in 44 BCE created a power vacuum, leading to a civil war. Octavian, later Augustus, emerged victorious, heralding the Roman Empire’s birth.
Under Augustus, the empire experienced the Pax Romana, a 200-year period of relative peace and stability. Augustus reformed the military, established efficient administrative systems, and initiated grand construction projects. The empire's borders expanded, encompassing territories from Britain to Egypt and from Spain to the Euphrates. Roman legions, renowned for their discipline and engineering prowess, secured and maintained these vast territories, building roads, fortifications, and cities that facilitated control and integration.
The Roman Empire’s society was hierarchical, with a rigid class system. At the top were the patricians, wealthy elites who held significant political power. Below them were the plebeians, free citizens with limited political influence, and the vast numbers of slaves who formed the backbone of the economy. The family unit was central, governed by the paterfamilias, the male head who held absolute authority.
Culturally, the Romans were eclectic, absorbing and adapting elements from the civilizations they encountered, particularly the Greeks. Roman art, literature, and philosophy reflected this synthesis, creating a rich cultural tapestry. Latin, the Roman language, became the lingua franca of the Western world, influencing numerous modern languages.
Roman architecture and engineering achievements were monumental. They perfected the arch, vault, and dome, constructing enduring structures like the Colosseum, Pantheon, and aqueducts. These engineering marvels not only showcased Roman ingenuity but also served practical purposes, from public entertainment to water supply.
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June 3, 2024 Anti-Semitism Letter Sent to MIT President Kornbluth and MIT Cor...Levi Shapiro
Letter from the Congress of the United States regarding Anti-Semitism sent June 3rd to MIT President Sally Kornbluth, MIT Corp Chair, Mark Gorenberg
Dear Dr. Kornbluth and Mr. Gorenberg,
The US House of Representatives is deeply concerned by ongoing and pervasive acts of antisemitic
harassment and intimidation at the Massachusetts Institute of Technology (MIT). Failing to act decisively to ensure a safe learning environment for all students would be a grave dereliction of your responsibilities as President of MIT and Chair of the MIT Corporation.
This Congress will not stand idly by and allow an environment hostile to Jewish students to persist. The House believes that your institution is in violation of Title VI of the Civil Rights Act, and the inability or
unwillingness to rectify this violation through action requires accountability.
Postsecondary education is a unique opportunity for students to learn and have their ideas and beliefs challenged. However, universities receiving hundreds of millions of federal funds annually have denied
students that opportunity and have been hijacked to become venues for the promotion of terrorism, antisemitic harassment and intimidation, unlawful encampments, and in some cases, assaults and riots.
The House of Representatives will not countenance the use of federal funds to indoctrinate students into hateful, antisemitic, anti-American supporters of terrorism. Investigations into campus antisemitism by the Committee on Education and the Workforce and the Committee on Ways and Means have been expanded into a Congress-wide probe across all relevant jurisdictions to address this national crisis. The undersigned Committees will conduct oversight into the use of federal funds at MIT and its learning environment under authorities granted to each Committee.
• The Committee on Education and the Workforce has been investigating your institution since December 7, 2023. The Committee has broad jurisdiction over postsecondary education, including its compliance with Title VI of the Civil Rights Act, campus safety concerns over disruptions to the learning environment, and the awarding of federal student aid under the Higher Education Act.
• The Committee on Oversight and Accountability is investigating the sources of funding and other support flowing to groups espousing pro-Hamas propaganda and engaged in antisemitic harassment and intimidation of students. The Committee on Oversight and Accountability is the principal oversight committee of the US House of Representatives and has broad authority to investigate “any matter” at “any time” under House Rule X.
• The Committee on Ways and Means has been investigating several universities since November 15, 2023, when the Committee held a hearing entitled From Ivory Towers to Dark Corners: Investigating the Nexus Between Antisemitism, Tax-Exempt Universities, and Terror Financing. The Committee followed the hearing with letters to those institutions on January 10, 202
2. OUTLINE
Introduction
Types & Risk Factors of Stroke
Pathophysiology of Stroke
Signs & Symptoms of Stroke
Investigations
Poor prognostic factors in Stroke
Primary & Secondary prevention
Acute Management of Stroke
3. INTRODUCTION
o Stroke is defined as
Abrupt onset of neurological deficit
Persists more than 24 hour.
With no apparent case other than that of vascular
origin
5. TIA(Transient ischemic attack):A clinical syndrome of
rapid onset of focal deficits of brain function, which
resolves with in 24 hours,regardless of whether there’s
imaging evidence of new permanent brain injury.
PROGRESSIVE STROKE:A stroke in which focal
neurological deficits worsen with time.
Also called stroke in evolution.
o COMPLETED STROKE:A stroke in which the focal
neurological deficits persists & donot worsen with time.
10. PATHOPHYSIOLOGY OF STROKE
Brain requires constant supply of glucose &
oxygen, delivered by blood.
Brain receives 15% of resting output & accounts for
20% of total body oxygen consumption.
Cerebral blood flow is maintained via auto
regulation. Thus the brain is highly aerobic tissue
where oxygen is limiting factor.
Blood flow
If zero leads to death of brain tissue within 4-10 mins
<16-18ml/100g tissue/min infarction with in an
hour.
<20ml/100gm tissue/min ischemia without infarction
unless prolonged for several hours or day.
11. HEMORRHAGIC STROKE
Two types
Intracerebral hemorrhage(ICH)
Subarachnoid hemorrhage(SAH)
Higher mortality rates when
compared to ischemic stroke
12. PATHOPHYSIOLOGY OF HEMORRHAGIC STROKE
Explosive entry of blood into the brain parenchyma
structurally disrupts neurons.
White matter fibre tracts are split.
Immediate cessation of neuronal function.
Expanding hemorrhage can act as a mass lesion
and cause further progression of neurological
deficits.
Large hemorrhages can cause transtentorial coning
and rapid death.
13. INTRACEREBRAL HEMORRHAGE
o Result of chronic hypertension
o Small arteries are damaged due to hypertension
o In advanced stages vessel wall is disrupted and
leads to leakage
SUBARACHNOID HEMORRHAGE
o Most common cause is rupture of saccular or
Berry aneurysms
o Other causes include arteriovenous
malformations, angiomas, mycotic aneurysmal
rupture etc.
o Associated with extremely severe headache
15. THROMBOTIC STROKE
Atherosclerosis is the most common pathology
leading to thrombotic occlusion of blood vessels
Lacunar stroke
Accounts for 20% of all strokes
Results from occlusion of small deep penetrating
arteries of the brain
Thrombosis leads to small infarcts known as lacunes
Clinically manifested as lacunar syndromes
16. EMBOLIC STROKE
o Cardioembolic stroke
Embolus from the heart gets lodged in intracranial
vessels
MCA most commonly affected
Atrial fibrillation is the most common cause
Others: MI, prosthetic valves, rheumatic heart disease
o Artery to artery embolism
Thrombus formed on atherosclerotic plaques gets
embolized to intracranial vessels
Carotid bifurcation atherosclerosis is the most common
source
Others: aortic arch, vertebral arteries etc.
17. Tissue surrounding the core region of infraction
which is ischemic but reversibly dysfunctional.
Maintained by collaterals.
Can be salvaged if reperfused in time
Primary goal of revascularization therapies.
Ischemic penumbra
19. HISTORY
Ask for onset and progression of neurological
symptoms – completed stroke or stroke in evolution
History of previous TIAs
History of hypertension & diabetes mellitus
History of heart conditions like arrhythmias, RHD &
prosthetic valves
History of seizures & migraine
History of anticoagulant therapy
History of oral contraceptive use
History of any hypercoagulable disorders like sickle
cell anemia & polycythemia vera
Substance abuse: cocaine, amphetamines
20. EXAMINATION OF A STROKE PATIENT
The neurological examination is highly variable and
depends on the location of the vascular lesion.
Skin: look for xanthelasma,rashes,limb ischemia
Eyes:look for diabetic changes,retinal
emboli,hypertensive changes,arcus senilis
CVS: hyper/hypotension, abnormal
rhythm,murmursraised JVP, peripheral pulses and
bruits Respiratory system: pulmonary edema, infection
Abdomen: urinary retention
Locomotor system: injuries sustained during collapse
with stroke, comorbities which influence functional
abilities.
21.
22. LEFT AND RIGHT HEMISPHERE STROKE:
COMMON PATTERNS
Aphasia
Right hemiparesis
Right-sided sensory loss
Right visual field defect
Poor right conjugate gaze
Dysarthria
Difficulty reading, writing,
or calculating
Neglect of left visual field
Extinction of left-sided
stimuli
Left hemiparesis
Left-sided sensory loss
Left visual field defect
Poor left conjugate gaze
Dysarthria
Spatial disorientation
Left (Dominant) Hemisphere
Stroke: Common Pattern
Right (Non-dominant)
Hemisphere Stroke:
Common Pattern
23. CLINICAL LOCALIZATION OF STROKE
SYNDROMES
Prerequisites
Functional anatomy of brain.
Blood supply to the different parts of brain.
30. LOCALIZATION OF STROKE SYNDROMES
Clinical localization of the site of the lesion.
Identifying the vascular territory and the vessel
involved.
Correlating with the imaging findings.
31. CLASSIFICATION
Large vessel stroke within the
anterior circulation
Large vessel stroke within the
posterior circulation
Small vessel disease of either
vascular bed
34. STROKE WITHIN THE ANTERIOR
CIRCULATION
Due to occlusion of Internal carotid
artery and its branches
Middle cerebral artery, Anterior
cerebral artery and Anterior choroidal artery
35.
36.
37. MIDDLE CEREBRAL ARTERY INFARCTION -
SUPERIOR BRANCH
o Clinical features
Contralateral hemiplegia – face and
upper limb more involved than lower
limb.
Contralateral hemisensory loss.
Conjugate gaze paresis(patient looks
towards the side of lesion.
Broca’s dysphasia (if left sided)
38. MIDDLE CEREBRAL ARTERY INFARCTION -
INFERIOR BRANCH
o Clinical features
Contralateral hemianopia.
Wernicke’s dysphasia ( if left sided )
Left spatial neglect ( if right sided )
39. MIDDLE CEREBRAL ARTERY INFARCTION - STEM
OCCLUSION
o Clinical features
Contralateral hemiplegia
Contralateral hemisensory loss
Contralateral gaze palsy
Contralateral hemianopia
Global dysphasia (Left sided lesion)
Anosognosia and amorphosynthesis
(Right sided lesion)
Altered sensorium (due to edema)
40.
41. MIDDLE CEREBRAL ARTERY INFARCTION-
LENTICULOSTRIATAL OCCLUSION
Deep penetrating or lenticulostriate
branches– Internal capsule, caudate
nuclues, putamen and outer pallidus
Occlusion of lenticulostriate branches-
If ischemia of internal capsule produces
pure motor or sensorymotor stroke
contralateral to the side of lesion
If ischemia of putamen, pallidus-
predominantly parkinsonian features
42. ANTERIOR CEREBRAL ARTERY INFARCTION
o Clinical features
Contralateral
a.paralysis of leg and foot with paresis
of arm
b.cortical sensory loss over leg and foot
c.presence of primitive reflexes
Urinary incontinence
Gait apraxia
Mutism, delay and lack of spontaneity of motor acts
Apraxia of left sided limbs(with left sided lesion and
corpus callosum involvement)
43. ANTERIOR CHOROIDAL ARTERY
Supplies posterior limb of internal capsule,
retrolentiform and sublentiform parts
Syndrome comprises
c/l hemiplegia
c/l hemianaesthesia
c/l homonymous hemianopia
49. LATERAL MEDULLARY SYNDROME
A. IPSILATERAL
1.Xth cranial nerve palsy
2.Cerebellar signs
3.Horner’s syndrome
4.Impaired pain, temperature
and touch On the upper half
of face
B. CONTRA LATERAL
1.Impaired pain and temperature
over the body
50. BASILAR ARTERY
Paramedian- wedge of pons in midline.
Short circumerential- lateral two thirds of
pons and middle and superior cerebellar
peduncles.
Long circumferential- Superior and anterior
inferior cerebellar.
51. BASILAR ARTERY SYNDROMES
Occlusion of basilar artery-b/l brainstem signs.
Occlusion of basilar branch artery- unilateral motor,
sensory and cranial nerves.
Complete basilar artery occlusion(Locked in state)-
b/l long tract(sensory/motor) with cranial nerve and
cerebellar dysfunction- preserved consciousness,
quadriplegia and cranial nerve signs.
53. MEDIAL INFERIOR PONTINE SYNDROME
Results from thrombosis of the para median branches of
the basilar artery. Affected structures--
Corticospinal tract
Lesions result in
contralateral spastic hemiparesis.
Medial lemniscus
Lesions result in
contralateral loss of tactile sensation from the trunk
extremities.
Abducent nerve roots
Lesions result in
ipsilateral lateral rectus paralysis.
54. LATERAL INFERIOR PONTINE SYNDROME
anterior inferior cerebellar artery (AICA) syndrome
Affected structures and resultant deficits include--
facial nucleus and intraaxial nerve fibers
Lesions result in:
Ipsilateral facial nerve paralysis
Ipsilateral loss of taste from the ant. 2/3 of tongue
Ipsilateral loss of lacrimation and reduced
salivation
Loss of corneal and stapedial reflexes
(efferent limbs).
55. MEDIAL PONTINE SYNDROMES
Caused due to occlusion of paramedian and
short circumferential branches of basilar
artery
Corticobulbar and corticospinal-c/l face, arm
and leg paralysis
Cerebellar peduncles-ataxia of limb and gait
57. WEBER SYNDROME-OCCLUSION OF PERFORATING
BRANCH OF POSTERIOR CEREBRAL ARTERY
Clinical features
1.Ipsilateral
a.3rd nerve palsy
2.Contralateral
a.hemiplegia
58. BENEDIKT SYNDROME-OCCLUSION OF PERFORATING
BRANCH OF POSTERIOR CEREBRAL
Clinical features
1.Ipsilateral
a.3rd nerve palsy
2.Contralateral
a.cerebellar ataxia
59. DORSAL MIDBRAIN (PARINAUD'S) SYNDROME
-paralysis of upward and
downward gaze
-pupillary disturbances
(Pseudo-
Argyll Robertson pupils)
-absence of convergence
(Convergence-Retraction
nystagmus on Attempts
at upward gaze)
-noncommunicating hydrocephalus
60. DIFFERENTIATING FEATURES BETWEEN ANTERIOR
AND POSTERIOR CIRCULATION STROKE
Clinical features Posterior circulation Anterior circulation
A.History
1.Vertigo Present Absent
2.Unsteadiness Present Absent
B.Physical findings
1.Crossed hemiplegia Present Absent
2.Bilateral deficits Present Absent
3.Cerebellar signs Present Absent
4.Ocular findings(LMN/INO/Gaze deviation to paralysed side) Present Absent
5.Dissociated sensory loss Present Absent
6.Sensory loss over V1 and V2 Present Absent
7.Horners syndrome Present Absent
61. DIFFERENTIAL DIAGNOSIS OF STROKE
Craniocerebral / cervical trauma
Meningitis/encephalitis
Intracranial mass
Tumor
Subdural hematoma
Seizure with persistent neurological signs
Migraine with persistent neurological signs
Metabolic
Hyperglycemia
Hypoglycemia
Post-cardiac arrest ischemia
Drug/narcotic overdose
62. HYPOGLYCEMIA
Cause Hemiplegia and aphasia
The wide use of bedside rapid laboratory testing for
glucose now makes this easily detectable and treatable.
The hemiplegia may resolve immediately with the
administration of intravenous glucose but resolution over a
hours is also reported.
SPACE OCCUPYING LESIONS
Subacute or chronic duration of symptoms, however some
patients may present with acutely probably due to bleeding
into a tumour
Associated with deep seated bursting headache, projectile
vomiting due raised ICT.
MIGRAINE
Migraine may actually precipitate a stroke, but there is also
a variant of migraine, hemiplegic migraine.
63. INVESTIGATION OBJECTIVES
To confirm the vascular nature of the lesion
The pathological type of the vascular lesion
The underlying vascular disease
Risk factors present.
64.
65. GENERAL INVESTIGATIONS
Identify conditions which may predispose towards
premature cerebrovasculardisease.
Full blood count – polycythemia, thrombocytopoenia.
Blood glucose – diabetes mellitus.
Serum lipids – hypercholesterolemia.
Blood cultures – SBE.
HIV screen – AIDS.
Syphilis serology – VDRL.
Clotting Screen.
Thrombophilia Screen – Protein C, Protein S, AT- III.
Anticardolipin antibodies – SLE.
Lumbar Puncture – subarachnoid haemorrhage.
67. CT SCAN
Mandatory initial investigation
Haemorrhage appears instantly as a hyperdense
area
Infarct appears as a hypodense area
Infarct may not appear before 48 hrs
MRI may be done instead but ct scan is more
sensitive for detecting haemorrhage
Diffusion weighted MRI is good for identifying
ischaemic lesion.
77. ASSESSMENT OF A PERSON WITH
SUSPECTED STROKE & EMERGENCY
SUPPORTIVE CARE
EMS should be instructed in the rapid recognition,
evaluation, treatment and transport
Baseline assessment within minutes, CT scan ASAP)
Immediate evaluation of the following:
1. Airway
2. Vital signs
3. General medical assessment (including
evidence of injury, cardiovascular
abnormalities)
4. Neurological assessment (frequent)
Maintenance of adequate tissue oxygenation: protecting
the airway, O2 inhalation
Maintaining optimal blood pressure (autoregulation faulty
or lost in stroke patients)
78. PRIMARY AND SECONDARY PREVENTION
A- antiplatelet and anti coagulants
B- blood pressure lowering medication
C- cholesterol lowering, cessation of
smoking
D- diet
E- exercise
79. MANAGEMENT OF A TRANSIENT
ISCHAEMIC ATTACK (TIA)
MEDICAL MANAGEMENT
(if diffuse atherosclerotic disease or poor operative
candidates)
1. Stop smoking
2. Concurrent medical problems to be addressed:
Emboli from heart and other parts of cardiovascular
system
(a) anti coagulants: Heparin(IV), Warfarin(oral)
(b) anti platelet drugs: Aspirin(oral), Ticlopidine
Diabetes, Hypertension, Hyperlipidemia
80. MANAGEMENT OF A TRANSIENT
ISCHAEMIC ATTACK(TIA) – CONT’D
SURGICAL MANAGEMENT
CAROTID AND CEREBRAL ARTERIOGRAPHY
All above can be done only if there is relatively little
atherosclerosis elsewhere in cerebrovascular system.
STENOSIS
Mild to Moderate
Regular Follow Up
Severe
Carotid Endarterectomy
81. MANAGEMENT OF AN ACUTE
EPISODE OF STROKE
AIRWAY - Maintain airway, prevent aspiration, keep nil per oral
BREATHING - Maintain oxygen saturation > 97%
- Supplementary oxygen
CIRCULATION - Adequacy of pulse and BP
- Fluid, Anti Arrhythmics, Ionotropes
HYDRATION - Prevent dehydration ; give adequate fluids
- Parenteral or via nasogastric tube
NUTRITION - Nutritional supplements and Nasogatric feeding
MEDICATION - Administer medication also by routes other than
oral
82. MANAGEMENT OF AN ACUTE
EPISODE OF STROKE CONT’D
BLOOD PRESSURE - unless indicated (heart or renal
failure,hypertensive encephalopathy or aortic dissection) it
should not be lowered for the fear of expansion of infarct.
Ischaemic stroke - maintain 180/110 mm Hg
Haemorrhagic stroke – keep MAP <115 mm Hg
BLOOD GLUCOSE - INSULIN to treat
hyperglycaemia(can increase infarct size)
- maintain < 200mg%
TEMPERATURE - early use of antipyretics
PRESSURE AREAS – To prevent occurrence of decubitus
ulcers
INCONTINENCE
85. ISCHAEMIC STROKE
THROMBOLYTICS and REVASCULARISATION -
- tPA (alteplase)-0.9mg/kg(max 90mg)
10% of dose – initial IV bolus
remainder infused over one hour
- to be used < 3 hrs of onset of symptoms
(for maximum efficacy)
- haemorrhage to be ruled out
NEUROPROTECTIVE AGENTS.
86. ANTI PLATELET THERAPY
Asprin, Clopidogrel
- act by inhibiting platelet aggregation and
adhesion.
- aspirin 300mg single dose to be given
immediately following diagnosis.
- if alteplase given it can be with held for 24 hrs.
- later aspirin at a dose of 75 mg in combination
with clopidogrel 75 mg daily for about one year
duration.
87. ANTI COAGULANTS
HEPARINS , WARFARIN
-heparins act by accelerating the inhibition of factor II and factor X
of coagulation cascade
-warfarin antagonises vitamin K to prevent activation of clotting
factors
-decrease risk of recurrence and venous thromboembolism
-intra cranial haemorrhage to be excluded before therapy
-more useful if stroke is evolving
HYPEROSMOLAR AGENTS
- reduce cerebral oedema
- 20% mannitol IV – 100ml TID
- oral glycerol if swallow is normal
Concurrent medical problems such as atrial fibrillations to be
tackled
OTHERS:
- PENTOXYPHYLLINE to be used within 12 hrs
-NEUROPROTECTIVE AGENTS
88. HAEMORRHAGIC STROKE
Control of hypertension
Control coagulation abnormalities (esp due to oral
anticoagulants)
Surgical decompression
Surgery for aneurysms and arterio-venous
malformations
Anti platelet and anti coagulants are
contraindicated
89. REHABILITATION
Physiotherapy - as early as possible
Occupational therapy
Speech therapy
Improve quality of life with
motor aids -leg brace, toe
spring , cane , walking stick
93. PROGNOSIS
ISCHAEMIC STROKE
Mortality rate in first 30 days is 8-12%
Can vary depending upon size, location, symptoms of
stroke
Time that elapses from the event to medical intervention
First 3 hrs after stroke - GOLDEN PERIOD
INTRACEREBRAL HAEMORRHAGE
Mortality rate in first 30 days is almost 50%
Site and extent of hematoma also plays a role in
determining the prognosis
Hamorrhagic strokes have a poor prognosis compared
to ischaemic type .
Editor's Notes
ASPIRIN
Antiplatelet agent, irreversible COX inhibitor Prevent adhesion and aggregation of platelets Platelet aggregation inhibitors dose of 81 mg enteric-coated aspirin is usually started
Platelet aggregation inhibitors
Abiciximab, Clopidogrel, Ticlopidine, Dipyridamole
PHYSIOTHERAPY
- initially passive moments, later active movements, in every case early mobilization, prevents contractures, spasticity and atrophy