Ischaemic stroke is caused by blockage of arteries in the brain and accounts for 87% of all strokes. The main types are thrombosis, embolism, and hypoperfusion. Risk factors include atherosclerosis, small vessel disease, and cardiogenic embolism from conditions like atrial fibrillation. Symptoms depend on the affected brain region and may include weakness, sensory loss, speech problems, and visual issues. Treatment involves stabilizing vital functions, managing blood pressure and glucose, and administering thrombolysis within 4.5 hours or revascularization procedures for selected patients to restore blood flow. Secondary prevention focuses on controlling risk factors and long-term anticoagulation or antiplatelet therapy.
Is characterized by the sudden loss of blood circulation to an area of the brain, resulting in a corresponding loss of neurologic function. Acute ischemic stroke is caused by thrombotic or embolic occlusion of a cerebral artery and is more common than hemorrhagic stroke.
It can occur
in the carotid
artery of the
neck as well as
other arteries.
When an artery is acutely occluded by thrombus or embolus, the area of the CNS supplied by it will undergo infarction if there is no adequate collateral blood supply.
Surrounding a central necrotic zone, an ‘ischemic penumbra’ remains viable for a time, i.e. it may recover function if blood flow is restored.
CNS ischemia may be accompanied by swelling for two reasons:
● cytotoxic oedema – accumulation of water in damaged glial cells and neurones,
● vasogenic oedema – extracellular fluid accumulation as a result of breakdown of the blood–brain barrier.
In the brain, this swelling may be sufficient to produce clinical deterioration in the days following a major stroke, as a result of a rise in intracranial pressure and compression of adjacent structures.
Is characterized by the sudden loss of blood circulation to an area of the brain, resulting in a corresponding loss of neurologic function. Acute ischemic stroke is caused by thrombotic or embolic occlusion of a cerebral artery and is more common than hemorrhagic stroke.
It can occur
in the carotid
artery of the
neck as well as
other arteries.
When an artery is acutely occluded by thrombus or embolus, the area of the CNS supplied by it will undergo infarction if there is no adequate collateral blood supply.
Surrounding a central necrotic zone, an ‘ischemic penumbra’ remains viable for a time, i.e. it may recover function if blood flow is restored.
CNS ischemia may be accompanied by swelling for two reasons:
● cytotoxic oedema – accumulation of water in damaged glial cells and neurones,
● vasogenic oedema – extracellular fluid accumulation as a result of breakdown of the blood–brain barrier.
In the brain, this swelling may be sufficient to produce clinical deterioration in the days following a major stroke, as a result of a rise in intracranial pressure and compression of adjacent structures.
Severe hypertension that is a potentially life-threatening condition refers to a hypertensive crisis.
Severe hypertension is further classified into hypertensive emergencies or hypertensive urgencies.
Hypertensive emergency refers to a severe hypertension that is associated with new or progressive end-organ damage. In these clinical situations, blood pressure should be reduced immediately to prevent or minimize organ dysfunction.
Hypertensive urgency refers to severe hypertension without evidence of new or worsening end-organ injury.
A hypertensive emergency is hypertension with acute impairment of one or more
organ systems that can result in irreversible organ damage. Especially:-
Central nervous system
Cardiovascular system
Renal system.
The term hypertensive emergency is primarily used as a specific term for a hypertensive crisis with a diastolic blood pressure greater than or equal to 120mmHg and/or systolic blood pressure greater than or equal to 180mmHg.
Hypertensive emergency differs from hypertensive crisis in that, in the former, there is evidence of acute organ damage.
This includes scores, prehospital and emergency department management of stroke. it goes into details of stabilisation and general management. definitive management options are thrombolysis or thrombectomy. briefly described complications of stroke and management as well
This is a comprehensive approach to a hypertensive patient presenting to the emergency department.
Discussing:-
- Hypertensive emergency
- Hypertensive Urgency
- Hypertensive Crisis
- Hypertensive encephalopathy and retinopathy
- Accelerated Hypertension
- Malignant hypertension
This talk covers the most important aspects of treatment of acute ischemic stroke, such as thrombolysis, use of antiplatelets, BP and sugar control and general supportive care.
DEFINITION
• Myxedema coma is a rare life-threatening condition.It is the decompensated state of severe hypothyroidism in whichthe patient is hypothermic and unconscious.The condition occurs most often among elderly women in the winter months and appears to be precipitated by cold.
• Myxedema coma, occasionally called myxedema crisis, is a rare life- threatening clinical condition that represents severe hypothyroidism with physiological decompensation. The condition usually occurs in patients with long-standing, undiagnosed hypothyroidism and is usually precipitated by infection, cerebrovascular disease, heart failure, trauma, or drug therapy.
• Myxedema is also used to describe the dermatologic changes that occur in hypothyroidism which refers to deposition of mucopolysaccharides in the dermis, which results in swelling of the affected area.
Severe hypertension that is a potentially life-threatening condition refers to a hypertensive crisis.
Severe hypertension is further classified into hypertensive emergencies or hypertensive urgencies.
Hypertensive emergency refers to a severe hypertension that is associated with new or progressive end-organ damage. In these clinical situations, blood pressure should be reduced immediately to prevent or minimize organ dysfunction.
Hypertensive urgency refers to severe hypertension without evidence of new or worsening end-organ injury.
A hypertensive emergency is hypertension with acute impairment of one or more
organ systems that can result in irreversible organ damage. Especially:-
Central nervous system
Cardiovascular system
Renal system.
The term hypertensive emergency is primarily used as a specific term for a hypertensive crisis with a diastolic blood pressure greater than or equal to 120mmHg and/or systolic blood pressure greater than or equal to 180mmHg.
Hypertensive emergency differs from hypertensive crisis in that, in the former, there is evidence of acute organ damage.
This includes scores, prehospital and emergency department management of stroke. it goes into details of stabilisation and general management. definitive management options are thrombolysis or thrombectomy. briefly described complications of stroke and management as well
This is a comprehensive approach to a hypertensive patient presenting to the emergency department.
Discussing:-
- Hypertensive emergency
- Hypertensive Urgency
- Hypertensive Crisis
- Hypertensive encephalopathy and retinopathy
- Accelerated Hypertension
- Malignant hypertension
This talk covers the most important aspects of treatment of acute ischemic stroke, such as thrombolysis, use of antiplatelets, BP and sugar control and general supportive care.
DEFINITION
• Myxedema coma is a rare life-threatening condition.It is the decompensated state of severe hypothyroidism in whichthe patient is hypothermic and unconscious.The condition occurs most often among elderly women in the winter months and appears to be precipitated by cold.
• Myxedema coma, occasionally called myxedema crisis, is a rare life- threatening clinical condition that represents severe hypothyroidism with physiological decompensation. The condition usually occurs in patients with long-standing, undiagnosed hypothyroidism and is usually precipitated by infection, cerebrovascular disease, heart failure, trauma, or drug therapy.
• Myxedema is also used to describe the dermatologic changes that occur in hypothyroidism which refers to deposition of mucopolysaccharides in the dermis, which results in swelling of the affected area.
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
HOT NEW PRODUCT! BIG SALES FAST SHIPPING NOW FROM CHINA!! EU KU DB BK substit...GL Anaacs
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Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
2. WHO Definition of Stroke
“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[1].”
By this definition ,TIA, which lasts <24 hours, and patients
with stroke symptoms caused by subdural hemorrhage, tumors,
poisoning, or trauma are excluded.
1.WHO MONICA Project Investigators. The World Health Organization MONICA Project (Monitoring trends
and determinants in cardiovascular disease). J Clin Epidemiol 41, 105-114. 1988
3. Classification of Stroke
Ischemic Stroke — three subtypes:
Thrombosis : In situ obstruction of an artery.
Embolism : Particles of debris originating elsewhere
that block arterial access to a particular brain region.
Systemic hypoperfusion : More general circulatory
problem, manifesting itself in the brain and perhaps
other organs.
Hemorrhagic Stroke due to intracerebral hemorrhage
or subarachnoid hemorrhage
Data compiled by AHA show that strokes due to
ischemia, intracerebral hemorrhage and subarachnoid
hemorrhage are 87%, 10%, and 3 %respectively[8]
8. Roger VL, Go AS, Lloyd-Jones DM, et al. Heart disease and stroke statistics--2011 update: a
report from the American Heart Association. Circulation 2011; 123:e18.
7. Causes of Ischaemic stroke
1)Atherothromboembolism (50%)
- atherothrombotic plaque can grow to
obstruct a vessel with intraluminal
propagation of the thrombus to cause
occlusion
2)Intracranial small vessel disease
(25%)
- is due to lipohyalinosis , microatheroma,
or thromboembolism from a larger artery
3)Cardiogenic embolism (20%)
- Most common causes: AF and valvular
heart disease
8. Investigation
FBC- exclude anaemia, thrombocytopenia
RP- hydration status
RBS- exclude hypoglycaemia
FLP & FBS
12 lead ECG
CXR
CT Brain- differentiate haemorrhage or
ischaemic stroke, confirm site of lesion n
extent of brain affected
ECHO- for suspected cardioembolism,
assess cardiac function.
9. Management
Oxygen and airway support: prevent
hypoxia and worsening of neurological injury.
Elective intubation to secure airway meybe
needed.
Observation: V/S monitoring, GCS charting
Mobilisation: limb physiotherapy,
occupational therapy
BP: Mild hypertension is desirable at 160-
180/90-100. BP reduction should not be
drastic. Proposed substance: Labetolol 10-20
mg boluses @ 10min interval up to 150-300
mg, rate of labetolol infusion:1-3mg/min, or T.
Captopril 6.25-12.5mg.
10. Management
Blood Glucose: If hyperglycaemia, to treat with
insulin, if hypoglycaemia, treat with glucose
infusion
Nutrition: perform swallowing test, if fail, to
insert RT.
Raised ICP: IV Mannitol (0.25-0.5g/kg) over
20min, can be given every 6 hr. If hydrocephalus
is present, to drain using intraventricular
catheter. Hemicraniectomy and surgical
decompressive therapy with 48H after symptom
onset is recommended to prevent herniation.
Ventriculostomy & suboccipital craniectomy is
effective in relieving hydrocephalus & brainstem
11. Reperfusion of Ischaemic
Brain
IV thrombolysis with rt-PA: 0.9mg/kg,
max 90mg. 10% of the dose given as
bolus, followed by 60min infusion.
Recommended within 4.5hr of onset of
ischaemic stroke
Aspirin: Start within 48Hr of onset. Use
of aspirin within 24Hr of rt-PA is not
recommended.
Anticoagulant: use of heparins is not
routinely recommended.
Use of streptokinase is contraindicated in
acute ischaemic stroke due to poor
clinical outcome.
12. Primary Prevention
HPT: tx if BP>140/90, target BP for
diabetics <130/80.
DM: maintain tight glycaemic control
Hyperlipidaemia: High risk group: keep
LDL<2.6, if no risk factor LDL<4.2
Aspirin therapy: 100mg OD is useful for
female age >65
Smoking cessation.
13. Secondary Prevention
Aspirin: recommended:75-350mg OD
Clopidogrel: 75mg OD.
Ticlopidine: 250mg BD
Double therapy: combination of aspirin &
clopidogrel.
Anti-hypertensive treatment: ACE-i is
useful to reduce recurrent stroke in
normotensive & hypertensive pt.
Lipid-lowering: should be considered in pt
with previous ischaemic stroke
Diabetic control: good glycaemic control
14. Antiplatelet for acute
cardioembolic stroke
Warfarin: adjusted dose may be
commenced within 2-4 days after patient
is neurologically & medically stable.
Heparin(unfractionated): adjusted dose
may be started if pt at high risk of
embolism.
Anticoalation may be delayed for 1-2
weeks if there has been substantial
haemorrhage. Urgent anticoagulation in
pt with moderate-to-large cerebral infarct
is not recommended as high risk of ICB
complication.
15. Cardiac condition predisposing to
ischaemic stroke:
Atrial fibrillation: assess by CHA2DS2Vasc score.
Aspirin (75-325) is enough for pt<65 yrs with lone AF.
Dabigatran etexilate (110-150) is as effective compare
to warfarin in non-valvular AF.
Prosthetic heart valves: Life-long warfarin, target
INR:2.5-3.5
Bioprosthetic heart valve: if high risk, consider
warfarin 3-12 months or longer. For all other pt, give
warfarin for 3 months then aspirin (75-150) OD
Mitral stenosis: if risk factor present, consider long
term warfarin. All other pt, start aspirin.
MI & LV dysfunction: If LV thrombus is present,
consider 6-12mths warfarin. If LV clot not present but
has risk factor, consider warfarin 3-6 mths then
aspirin. If dilated cardiomyopathy consider life-long
warfarin.
16. Revascularisation Procedure
Carotid endarterectomy: Indicated for
stenosis 70-99% after a recent
ischaemic event.Early intervention within
2 weeks is more beneficial. Not
recommended for stenosis <50%. Pt
should remain on antiplatelet before &
after surgery.
Carotid angioplasty & stenting:
alternative to CEA if surgery is
undesirable, technically difficult or
inaccessible. Use of dual antiplatelet at
least 4 weeks after procedure.
17. Conclusion
Over last few decades, advances has been made in
management of acute ischaemic stroke. This occurred
along with advances of imaging methods as well as
primary and secondary prevention.
General care of stroke patient in ward still plays a vital
role to achieve better outcome. Many complication can
be anticipated and avoided in acute stroke setting.
Management of stroke is to recognise as acute medical
emergency and for therapeutic nihilism is to be
abolished as standard practice.
Education of general population regarding symptoms of
stroke and urgency to arrive in hospital for treatment
early will change the outlook for stroke survivors.