1. Stroke is the third leading cause of death globally and its incidence is increasing in India due to risk factors like aging, smoking, and dietary habits.
2. The majority of strokes are ischemic (87%) with atrial fibrillation being the leading cause, and the rest are hemorrhagic.
3. Timely management following the stroke chain of survival - detection, dispatch, delivery, door, data, decision, drug, and disposition - can help improve outcomes. This includes administration of intravenous thrombolysis within 4.5 hours.
Liver transplantation indications, contraindications, types of donors and recipients, types of transplants, surgical options, and post transplant management.
Liver transplantation indications, contraindications, types of donors and recipients, types of transplants, surgical options, and post transplant management.
explaining the presently available criteria to define futility in liver transplantation and prposing future trends in the definition of futility in liver transplantation
History of liver transplant.
Why and When liver need to be transplant ?
What at basic requirements in LT.
Success and Failure %age
Global statistics of organ donation
Liver transplantation current status, controversies and mythsAbhishek Yadav
Details the present status, indications, techniques about liver transplantation. Also dispels some common myths surrounding liver transplantation. #liver transplantation # living donor liver transplantation #liver cirrhosis #liver failure#transplantation#live donor#drabhishekyadav.com#liversurgeon#myths#livedonorlivertransplantation#organtransplantation#alcohololiverdisease
an updated account on management of TIA, Ischemic and hemorrhagic stroke in Sri Lanka. This is based on American Stroke Association and NICE guidelines.
explaining the presently available criteria to define futility in liver transplantation and prposing future trends in the definition of futility in liver transplantation
History of liver transplant.
Why and When liver need to be transplant ?
What at basic requirements in LT.
Success and Failure %age
Global statistics of organ donation
Liver transplantation current status, controversies and mythsAbhishek Yadav
Details the present status, indications, techniques about liver transplantation. Also dispels some common myths surrounding liver transplantation. #liver transplantation # living donor liver transplantation #liver cirrhosis #liver failure#transplantation#live donor#drabhishekyadav.com#liversurgeon#myths#livedonorlivertransplantation#organtransplantation#alcohololiverdisease
an updated account on management of TIA, Ischemic and hemorrhagic stroke in Sri Lanka. This is based on American Stroke Association and NICE guidelines.
Acute stroke management
IV thrombolysis guidelines
IV thrombolysis side effects
Early CT changes in stroke
ASPECTS scoring
AHA stroke guidelines
Thrombolysis controversies
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Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
Title: Sense of Smell
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 primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
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Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
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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.
2. STROKE
• Third leading cause of death globally
• Incidence in INDIA-73/100000
• Likely to increase with risk factors- aging,
smoking, dietary habits
• DEFINED AS FOCAL NEUROLOGICAL DEFICIT
OF PRESUMED VASCULAR ONSET LASTING 24
HRS OR LONGER AS OPPOSED TO TIA(<24hrs)
3. Causes of stroke
• 87% strokes – Ischemic
• ETIOLOGY- 29% Cardioembolic (AF)
16% Large vessel stenosis
16% Lacunar
3% Migraine, malignancy,
hypercoagulable states
• 13% of them- ICH OR SAH
Petty GW, Brown RDJ, Whisnant JP et al (1999) Ischemic stroke subtypes: a
population-based study of incidence and risk factors. Stroke 30:2513–2516
4. OXFORD/BAMFORD CLASSIFICATION
• TOTAL ANTERIOR CIRCULATION(TACS)
• PARTIAL ANTERIOR CIRCULATION(PACS)
• POSTERIOR CIRCULATION(POCS)
• LACUNAR (LACS)
Bamford J, Sandercock P, Dennis M et al (1991) Classification and natural history of
clinically identifiable subtypes of cerebral infarction. Lancet 337:1521–1526
8. Stroke chain of survival
• Detection - early recognition of s/s
• Dispatch - activation of 9-1-1,EMS dispatch
• Delivery - triage and transport
• Door - ED triage to high acuity area
• Data - ED evaluation, labs , imaging
• Decision - appropriate t/t, discussion with family
• Drug - appropriate drugs or other interventions
• Disposition- timely admission to stroke unit/ICU/Transf
9. ED BASED CARE
• DOOR TO PHYSICIAN ≤10 minutes
• DOOR TO STROKE TEAM ≤15 minutes
• DOOR TO CT INITIATION ≤25 minutes
• DOOR TO CT INTERPRETATION ≤45 minutes
• DOOR TO DRUG ≤60 minutes
• DOOR TO STROKE UNIT ADM ≤3 hours
11. • FOUR INTERVENTIONS IN AIS SUPPORTED BY
CLASS I EVIDENCE:
1. Care on a stroke unit
2. Intravenous tissue plasminogen activator within
4.5 h of stroke onset
3. Aspirin within 48 h of stroke onset
4. Decompressive craniectomy for Supratentorial
malignant hemispheric cerebral infarction
13. Patient history
• Time of symptom onset
• Defined as when the patient was at his or her
previous baseline or symptom-free state.
• For patients unable to provide this information or
who awaken with stroke symptoms, the time of
onset is defined as when the patient was last awake
and symptom-free or known to be “normal”
• Risk factors for arteriosclerosis and cardiac disease
• History of drug abuse, migraine, seizure, infection, trauma, or
pregnancy
• Historical data related to eligibility for therapeutic
interventions in acute ischemic stroke
14. EXAMINATION
• VITAL SIGNS- HR,BP,TEMP,O2 SATURATION
• Detailed physical examination head to toe
• Head and face- signs of trauma or seizure activity.
• Auscultation of the neck may reveal carotid bruits
• Signs of congestive heart failure.
• Chest exam - cardiac murmurs, arrhythmias, and
rales
• Skin -stigmata of coagulopathies, platelet
disorders, signs of trauma, or embolic lesions
(Janeway lesions, Osler nodes)
19. Score grading
SCORE STROKE SEVERITY
0 NO STROKE
1-4 MILD STROKE
5-15 MODERATE STROKE
16-20 MODERATE TO SEVERE
21-42 SEVERE STROKE
20.
21. Immediate evaluation
ALL PATIENTS
• Noncontrast brain CT or
brain MRI
• Blood glucose
• Oxygen saturation
• Serum electrolytes
• Renal function tests
• Complete blood count
• Platelet count
• Markers of cardiac ischemia
• Prothrombin time/INR
• APTT
• ECG
SELECTED PATIENTS
• TT and/or ECT if it is suspected the
patient is taking direct thrombin
inhibitors or direct factor Xa
inhibitors
• Hepatic function tests
• Toxicology screen
• Blood alcohol level
• Pregnancy test
• Arterial blood gas tests (if hypoxia is
suspected)
• CXR (if lung disease is suspected)
• Lumbar puncture (if SAH is
suspected and CT negative for
blood
• EEG(if seizures are suspected)
22. Early Diagnosis - Imaging
• NCCT - most common modality used in acute
ischemic stroke imaging.
• NCCT excludes parenchymal hemorrhage
• NCCT may demonstrate subtle visible
parenchymal damage within 3 hours.
23. EARLY SIGNS ON CT
• Loss of gray-white differentiation
• Lenticular obscuration-loss of distinction
among the nuclei of the basal ganglia
• Insular ribbon sign-blending of the densities of
the cortex and underlying white matter in the
insula and over the convexities -Cortical
ribbon sign
• Sulcal effacement
24.
25. CT ANGIOGRAPHY
• CT angio head and neck to assess intracranial and cervical
circulation for stenoses and occlusions
• Useful
1. patients who present just outside the treatment window for I/V
thrombolysis but may be candidates for intraarterial clot lysis
(provides information as to the location and extent of the clot)
2.patients who cannot undergo MRI
• Perfusion CT measures absolute cerebral blood flow to help
identify the degree of reversibility of brain injury, but not all
vascular territories can be imaged completely
• Diff. between regions of brain infarction and ischemic penumbra
• A complete CT examination including NCCT, CT angio &perfusion
CT can be performed in approximately 10 minutes
26. MRI BRAIN
• Standard MRI sequences (T1 weighted, T2 weighted,
fluid- attenuated inversion recovery [FLAIR]) are
relatively insensitive
• Diffusion-weighted imaging (DWI) most sensitive(88%
to 100%) and specific(95% to 100%) for detecting
infarcted regions, even at very early time points, within
minutes of symptom onset
• DWI allows identification of the lesion size, site, and
age
• DWI can detect relatively small cortical lesions and
small deep or subcortical lesions, including those in the
brain stem or cerebellum, areas often poorly or not
visualized with standard MRI sequences and CT scan
27. • MR angiography evaluates the blood vessels
of the brain and neck
• MRI perfusion-weighted imaging (PWI)
measures relative blood flow in the brain
• Perfusion maps may take 5 to 40 minutes of
postprocessing time
• The use of PWI and DWI may identify patients
who would benefit from recanalization
therapy outside the established 3-hour time
window for intravenous tPA
28.
29. REPERFUSION THERAPY
• Intention of reperfusion therapy is to restore
impaired blood flow to the ischemic penumbra
before irreversible neuronal death occurs.
• Use of intravenous rt-PA as soon as possible but
within 4.5 h of stroke onset, following exclusion
of a hemorrhagic stroke by NCCT
• Intraarterial thrombolysis can be done within 6 h
and mechanical embolectomy within 8 h of
symptom onset in those who are not candidates
for rt-PA or who fail to improve after full rt-PA
therapy
30. I/V Thrombolysis
• NINDS rtPA STROKE study- 1996
• Two parts- part 1 – rate of neurogical recovery
at 24 hrs- no sig diff observed
• Part 2 – rate of complete recovery at 90 days
and the results were significant
• ECASS, ECASSII , ATLANTIS- No benefit
• Diff between NINDS AND these studies was
time of intervention and dose used
31. CRITERIA(0-3hrs)
INCLUSION CRITERIA
• Ischemic stroke with clearly defined time of onset
• Onset of symptoms<3hrs before start of t/t
• Neurologic deficit measurable using the NIH
stroke scale
• Age >18yrs
• CT scan of the brain without evidence of ICH
32. Exclusion criteria(Absolute C/I)
• Head trauma or prior stroke within past 3 mths
• Symptoms s/o SAH
• Prior H/O Intracranial hemorrhage
• BP>185/110 not responding to antihypertensive t/t
• Arterial puncture at non compressible site within last 7 days
• Evidence of active internal bleeding
• Intracranial neoplasm, aneurysm, AV malformation
• Recent intracranial/intraspinal surgery
• Blood glucose <50 mg/dl
• CT – MULTILOBAR infarction(>1/3rd)
• Acute bleeding diathesis
plat count<100000
Heparin received within 48hrs- Elevated APTT
Current use of anticoagulant with INR>1.7
Current use of DTI or Direct factor Xa inhibitors with elevated
tests
33. Relative exclusion criteria
• Only minor or rapidly improving stroke symptoms
• Pregnancy
• Seizure at onset with postictal residual
neurological impairments
• Major surgery or serious trauma within previous
14 days
• GI or Urinary tract hemorrhage within previous
21 days
• Acute MI within previous 3 months
34. CRITERIA FOR EXTENDED PERIOD
(UPTO4.5HRS)
Inclusion criteria
• Age 18-80yrs
• Diagnosis of ischemic stroke causing measurable
neurological deficit(sym for atleast 30 mins)
• Onset within3-4.5hrs
Relative exclusion criteria
• Age>80yrs
• Severe stroke(NIHSS>25)
• Taking anticoagulant regardless of INR
• H/O both DM and prior ischemic stroke
35. • FDA approved dose of rtPA-0.9mg/kg(max 90mg)
• Bolus of 10%dose over 1 min with rest over 60 mins
• Close monitoring of patients for first 24 hrs
• BP every 15 mins for first 2 hrs, every 30 mins for next 6hrs
and then every hour for 16hrs
• Should be maintained below 185/110mmHg
• Neurological assessment using NIHSS – If change noted
stop infusion and do CT SCAN .
• Arterial punctures, nasogastric tubes, and catheterization
avoided in order to minimize the risk of bleeding.
• Subjects who have been on antiplatelet agents before their
event may receive t-PA
• NO Anticoagulant/antiplatelet for first 24 hrs
• CT at 24hrs –no hemorrhage- start antithrombotic
37. INTRA ARTERIAL THROMBOLYSIS
• Direct administration of intra-arterial thrombolytic
agents into the clot –
• ADV- lower tPA dose and a decreased risk of
systemic hemorrhagic complications.
• DISADV- time and expertise required for
catheterization.
38. Inclusion criteria
• Patient must be between 18 and 85 years of age
• National Institutes of Health stroke scale score between 11 and 30
• Angiographic complete occlusion (TIMI 0) or penetration with
minimal perfusion (TIMI 1) of the apparent symptom-related M1 or
M2 segment of the MCA or of the basilar artery
• Diagnosis of ischemic stroke causing measurable neurological deficit
characterized by the sudden onset of acute focal neurologic deficit
presumed to be due to cerebral ischemia after exclusion of
hemorrhage by CT scan.
• Onset of symptoms within 6 hours of IA t-PA administration.
(Consider if patient presents within 4.5 hours of stroke.) In event of
basilar thrombosis, the time window is 12 hours.
39. Mechanical clot disruption/extraction
• Considered as both primary perfusion therapy
and in conjunction with pharmacological
fibrinolysis for recanalization
• 4 devices have FDA approval
1. MERCI RETRIEVAL SYSTEM(2004)
2. THE PENUMBRA SYSTEM(2007)
3. SOLITAIRE FLOW RESTORATION DEVICE(2012)
4. TREVO RETREIVER(2012)
40. MECHANICAL THROMBOLYSIS
• Patients who are ineligible for or who failed I/V
rtPA treatment
• The Mechanical Embolus Removal in Cerebral
Ischemia (MERCI) retrieval device has been
studied most extensively (FDA approved)
• The Multi-MERCI trial tested a newer device (L5)
and allowed pretreatment with intravenous tPA
• Further studies of the MERCI device are
forthcoming in the MR- Rescue and the IMS III
trials.
41.
42.
43. STUDY DESIGN
• Phase 3 multicentre clinical trial
• randomized clinical group assignment
• open label treatment
• blinded end point evaluation
44.
45. MR CLEAN STUDY CONCLUSION
• In patients with acute ischemic stroke caused by a
large arterial occlusion of anterior circulation,
intra arterial treatment within six hours were
effective and safe
• IA treatment leads to a clinically significant
increase in the functional independence in daily
life by 3 months, without any increase in
mortality
• Triggered stoppage of mutilpe other trials:
ESCAPE, SWIFT, PRIME, EXTEND1A and REVASCAT
46.
47.
48.
49.
50.
51. Management in ICU
• Airway and ventilation management
• Hemodynamic and fluid optimization
• Fever and Glycemic control
• Anticoagulation, Antiplatelet and
thromboprophylaxis therapy
• Control of seizures
• Surgical interventions for malignant middle
cerebral artery and cerebellar infarction
52. Airway and Ventilation
• Causes of hypoxemia following stroke
Respiratory infections
Aspiration
ARDS
Pulmonary embolus
Pulmonary edema (neurogenic or cardiogenic)
Respiratory muscle weakness
• All patients should undergo swallow assessment on admission
• Continuous monitoring of oxygenation with pulse oximetry
• Oxygen supplementation reserved for those with SpO2 <94 %.
• Regular ABG monitoring - to maintain normocapnea-target PaCO2
35–45 mmHg (higher in those with COPD and CO2 retention).
53. INDICATIONS FOR INTUBATION AND MECHANICAL VENTILATION
• Decreased conscious level (GCS <8)
• evidence of brainstem dysfunction
• To prevent aspiration pneumonia
• Adjuvant therapy for intracranial hypertension or significant
cerebral edema
Acute respiratory failure,
• Generalized tonic–clonic seizures or status epilepticus
If endotracheal intubation required-RAPID SEQUENCE
INTUBATION
• Short-acting sedatives should be used
• Minimise hemodynamic changes
• Tracheostomy should be considered after 1 week of
mechanical ventilation if a reasonable outcome is predicted
54. Hemodynamics and fluid management
• 80 % - hypertensive at presentation (chronic hypertension,
stress, raised ICP or neuroendocrine response)
• Severe hypertension contributes to cardiorespiratory
complications and promotes cytotoxic edema and hemorrhagic
transformation within infarcted tissue
• Conversely, severe hypotension will compromise cerebral
perfusion and potentially increase infarct volume
• Regular noninvasive BP monitoring in all AIS patients on the ICU
& continuous BP monitoring in patients with cardiovascular
instability and those who are mechanically ventilated
• Fluid balance should be carefully monitored and managed to
maintain euvolemia
• 0.9 % saline to be used for fluid replacement and dextrose-
containing fluids should always be avoided
55. Approach to elevated BP
A.NOT ELIGIBLE FOR THROMBOLYTIC THERAPY
1.SBP<220 mmHg or DBP<120
• Observe unless other end-organ involvement (e.g., aortic dissection, acute
myocardial infarction, pulmonary edema, hypertensive encephalopathy)
• Treat other symptoms of stroke (e.g., headache, pain, agitation, nausea,
vomiting)
2.SBP>220 or DBP>121-140
• Labetalol 10-20 mg IV over 1-2 min
May repeat or double every 10 min (maximum dose 300 mg)
OR
• Nicardipine 5 mg/hr IV infusion as initial dose; titrate to desired effect by
increasing 2.5 mg/hr every 5 min to maximum of 15 mg/hr
Aim for a 10-15% reduction
3.DBP>140
• Nitroprusside 0.5 μg/kg/min IV
• Aim for 10-15% reduction
56. B. ELIGIBLE for thrombolytic therapy
Pretreatment
• Systolic >185 mm Hg OR diastolic >110 mm Hg
• Labetalol 10 to 20 mg IV over 1 to 2 min, may repeat OR
• Nicardipine infusion 5 mg/hr, titrate up by 2.5 mg/hr at 5- 15min
intervals
• If BP does not decline and remains >185/110 mm Hg, do not
administer rtPA
During/after Treatment
1. Diastolic >140 mm Hg
Sodium nitroprusside 0.5 μg/kg/min IV infusion as initial dose and
titrate to desired blood pressure
2. Systolic >230 mm Hg OR diastolic 121-140 mm Hg
• Labetalol 10 mg IV over 1-2 min (UPTO300MG) or give initial
labetalol dose, then start labetalol drip at 2-8 mg/min OR
• Nicardipine 5 mg/hr IV infusion as initial dose and titrate to desired
effect if not controlled , consider sodium nitroprusside
3. Systolic 180-230 mm Hg OR diastolic 105-120 mm Hg
• Labetalol 10 mg IV over 1-2 min May repeat or double labetalol
every 10-20 min
57. • Cardiac problems commonly coexist with AIS, either as
a trigger for the disease (e.g., cardioembolic stroke) or
as a result of the stroke itself
• Dysrhythmias ( 57 % ) elevated cardiac troponin levels (
17.5 %) and at least 12 % have abnormal left
ventricular function on ECHO
• All AIS patients on ICU should undergo continous ECG
monitoring
• ECHO at least once during the course of their
admission (repeated if abnormal ventricular function
identified).
• Cardiac troponin should be measured in patients with
ECG changes and echocardiographic evidence of
impaired ventricular function.
58. Hyperglycemia
• Hyperglycemia occurs in more than 40 % of AIS patients
• Marker of illness severity, associated with deleterious
effects, including increased cortical toxicity, larger infarct
volumes and susceptibility to infection.
• Poststroke hyperglycemia is independently associated with
increased mortality and morbidity at 90 days and
postthrombolysis ICH
• Regular blood glucose monitoring is essential.
• Treatment with continuous insulin infusion to maintain
serum glucose between 140 and 180 mg/dl is preferred in
the ICU.
59. FEVER
• Pyrexia affects up to 50 % of patients after AIS and
is independently associated with poor outcome
• Avoid pyrexia (T >37.5 °C).
• Investigate for and treat infectious causes of fever
• Regular paracetamol (acetaminophen) therapy as
a first- line therapy in those with temperatures
>37.5 °C,
• Second-line therapy includes intravenous
metamizole, rapid infusion of cold saline (4 °C) and
the use of automatic cooling systems.
• Role of therapeutic hypothermia is controversial
60. Antiplatelet agents
• For patients who are not eligible for tPA, aspirin is
the only antiplatelet drug that has been
evaluated in the acute treatment of stroke.
• Oral administration of aspirin (initial dose is 325
mg) within 48 hours after stroke onset is
recommended (Class I A).
• In patients who receive tPA, antiplatelet therapy
should start 24 hours after thrombolytic therapy
• The usefulness of clopidogrel for the treatment of
acute ischemic stroke is not well established
(Class IIb C).
61. Anticoagulation
• Use of anticoagulation in the first 24 h following
I/V rt-PA is currently contraindicated.
• Urgent anticoagulation for the management of
noncerebrovascular conditions not
recommended for patients with moderate-to-
severe strokes because of an increased risk of
serious intracranial hemorrhagic complications
(Class IIIA)
62. INDICATIONS FOR
ANTICOAGULATION
Atrial fibrillation with or without
RHD
Prosthetic heart valve
DVT
Hypercoagulable state
Venous sinus thrombosis
Arterial dissection
CHADS2 SCORE
• CONGESSTIVE HEART FAILURE
• HYPERTENSION(>140/90)
• AGE>75YRS
• DIABETES MELLITUS
• PRIOR STROKE OR TIA
• NOACS
• Dabigatran,Rivaroxaban,Api
xaban
• Efficacy equivalent to
warfarin in preventing
stroke and less likely to
produce ICH but higher
chances of GI bleed
Anticoagulants
63. Thromboprophylaxis
• Early mobilization reduces the risk of
thromboembolic complications of AIS.
• All immobilized AIS patients on ICU should be
treated with prophylactic-dose subcutaneous
LMWH to prevent DVT and mechanical
intermittent calf compression.
• Treatment should be started early, but LMWH
should not be started until 24 h following
thrombolysis.
64. Seizures
• Convulsive and nonconvulsive seizures are
uncommon after AIS
• No role for prophylactic anticonvulsants
• Seizures should be treated aggressively and a
long-acting anticonvulsant considered
• First-line anticonvulsant is phenytoin
• LEVETIRACETAM being used widely nowadays
65. NEUROPROTECTIVE AGENTS
• Among patients already taking statins at the time of
onset of ischemic stroke, continuation of statin therapy
during the acute period is reasonable (Class IIaB)
• The utility of induced hypothermia for the treatment of
patients with ischemic stroke is not well
established(Class IIbB)
• At present, transcranial near-infrared laser therapy is
not well established for the treatment of acute
ischemic stroke (Class IIbB)
• At present, no pharmacological agents with putative
neuroprotective actions have demonstrated efficacy in
improving outcomes after ischemic stroke, and
therefore, other neuroprotective agents are not
recommended (Class IIIA)
66. Complications of stroke
• Hemorrhagic transformation
• Cerebral edema
• Hyperthermia
• Hyperglycemia
• Deep venous thrombosis
67. HEMORRHAGIC TRANSFORMATION
Symptomatic intracerebral hemorrhage occurs in about 6% of patients
receiving intravenous rtPA & has been associated with high morbidity
and mortality
Risk factors include
• symptom severity
• early infarct signs on admission brain CT
• older age, elevated systolic blood pressure,
• low platelet count
• elevated serum glucose
• history of diabetes
Most tPA-related intracranial hemorrhages occur in the first few hours
after treatment.
• Hemorrhagic transformation can also occur in the absence of
reperfusion therapy
68. ICH-S/S
• New neurological deficit
• worsening of existing neurological deficits
• Headache
• Nausea, vomiting
• Decreased level of consciousness
• Marked hypertension
• Bradycardia
69. T/T-
• Discontinue infusion
• Obtain CT stat
• Order PT, APTT, fibrinogen
• Type and cross match blood
• Neurosurgery opinion
• Administer FFP OR Cryoppt
• The role of surgery is unclear, but decompressive
surgery/hematoma evacuation may be indicated
in large superficial hematomas and/or those
causing significant mass effect.
70. NEUROMONITORING
• Clinical and radiological monitoring are the
cornerstones of identifying deterioration after AIS.
• Routine ICP monitoring is not recommended but can
be considered in those with large infarct volumes or
hemorrhagic conversion with mass effect.
• However, ICP values are often normal even in the
presence of large infarct volumes.
• Optic nerve ultrasonography
• Transcranial Doppler (TCD) ultrasonography is a
noninvasive monitor that is able to assess cerebral
blood flow velocity in basal cerebral vessels and is
perhaps the most promising neuromonitor after AIS.
71. CEREBRAL EDEMA
• Patients with ischemic stroke with cerebral
edema and mass effect are at risk for brain
herniation, brainstem compression, coma, and
death.
• Mass effect caused by ischemic infarcts typically
peaks 3 to 5 days after symptom onset.
• Clinical examination more sensitive in detecting
worsening cerebral edema than ICP monitoring
72. • If suspected elevated ICP maintain ABC
• Keep head end elevated to 30 degrees
• Hyperosmolar therapy- Mannitol/hypertonic
saline
• MANNITOL-0.5 to 1 g/kg loading dose and can be
followed by boluses of 0.25 g/kg every 6 hours
• Monitor serum osm. <320 mosm
• Hypertonic saline(3%/7.5%) can be used
• 2ml/kg bolus can be given and then repeated
• Monitor serum osm and serum sodium
73. SURGERY
• Decompressive craniectomy is a controversial therapy
for malignant middle cerebral artery (MCA) stroke
Malignant MCA stroke is indicated by:
• MCA territory stroke of >50% on CT
• Perfusion deficit of >66% on CT
• Infarct volume >82 mL within 6 hours of onset (on MRI)
• Infarct volume of >145mL within 14 hours of onset (on
MRI)
• National Institutes of Health Stroke Scale score is often
>20 with dominant hemispheric infarction and >15
with nondominant hemispheric infarction
74. • There are 3 important trials that have studied
decompressive hemicraniectomy for malignant
MCA strokes in patients <60 years of age
• DESTINY trial (2007)
• Prospective, MC RCT from Germany
• Outcome: 88% vs 47% survival in favour of
decompressive craniectomy
• DECIMAL trial (2007)
• Prospective, MC RCT from France
• Outcome: ARR 52.8% in mortality favouring the
decompressive craniectomy group (75% vs 22%
survival)
75.
76. • HAMLET trial (2009)
• Prospective, MC RCT from the Netherlands
• Outcome: ARR 38% in mortality favouring the
decompressive craniectomy group
• Pooled analysis of DESTINY, DECIMAL and HAMLET
• Patients aged <60y with supratentorial infarctions treated
with decompressive craniectomy, usually within 48 hours of
stroke onset
• Hemicraniectomy compared with medical management
• Reduced mortality (22% versus 71%)
• No individual study showed an improvement in the
percentage of survivors with good outcomes (mRS score, 0–
3)
– Only shown in a pooled analysis (43% versus 21%).
– Only 14% of surgical survivors could look after their own affairs
without assistance (mRS score, 2)
•
77.
78. • Subsequently, the DESTINY II Trial (2014) studied
patients aged >60 years:
• n = 112 patients >60 years of age (median age was 70)
• Primary outcome measure was survival without severe
disability
• 38% in the hemicraniectomy group vs 18% in the
control group
• Secondary outcomes:
• Overall mortality was lower in the surgery group (33%
vs 70%)
• Almost none of the survivors has an outcome as good
as an mRS score of 3; almost all post-operative
survivors were severely disabled
79. END OF LIFE
• Despite early aggressive treatment some patients
do not have a satisfactory degree of clinical
recovery, and withdrawal of life-sustaining
therapies and a shift to end- of-life care is
appropriate.
• Documented early discussion with patients and
relatives to ascertain previous wishes is vital.
• An outcome that is acceptable to an individual
patient, rather than to the clinical team, should
drive decision-making regarding ‘‘do not attempt
resuscitation’’ orders and other limitations of
care.
80.
81. Long term airway management
Close fluid status monitoring
Monitor cardiac function
Blood glucose Monitoring
Control temperature
Anticoagulant and antiplatelet
use
82. TAKE HOME MESSAGES
• Intravenous tPA should be administered to all
patients of AIS who present within 3 hours of
stroke onset and meet the NINDS inclusion and
exclusion criteria.
• The risk of symptomatic intracranial hemorrhage
with intravenous tPA is approximately 6%.
• Intra-arterial tPA and mechanical thrombectomy
are alternative treatment strategies for acute
stroke patients who are ineligible for or fail
intravenous tPA treatment .
83. • Patients with acute ischemic stroke should be
maintained euglycemic, euvolemic, and
normothermic.
• Permissive hypertension may be beneficial,
but in patients receiving tPA blood pressures
should be maintained at or less than 185/110
mm Hg.
• Patients with life-threatening cerebral edema
from hemispheric infarctions require
hyperosmolar therapy and may benefit from
early surgical decompression
Rest of undiagnosed one third – may have underlying undiagnosed paroxysmal AF
Both cortical and subcortical –total
Predominant cortical- partial
Vertebrobasilar artery–posterior
Deep perforating arteries- lacunar
Vertebrobasilar territory – cerebellum, brainstem, medial aspect of occipital lobe, thalamus, inferomedial temporal lobe
Locked in syndrome – basilar occlusion secondary to pontine infarction- only eye blinking response
NEGLECT-involves sensory association areas in parietal lobe(stimulus is felt when it is alone and not in presence of competing stimulus
Aphasia-perisylvian fissures
NINDS
A thorough examination to identify acute comorbidities and conditions that may impact treatment selection is important
Severity grades to be added
NECT is relatively insensitive in detecting acute and small cortical or subcortical infarctions, especially in the posterior fossa. Despite these limitations, its widespread immediate availability, relative ease of interpretation, and acquisition speed make NECT the most common
Detection is influenced by the size of the infarct, severity of ischemia, and the time between symptom onset and imagng.
Ability of observers to detect these early infarct signs on NCCT is quite variable and occurs in ≤67% of cases imaged within 3 hours
Increased density within the occluded artery, such as the hyperdense middle cerebral artery (MCA) sign, indicative of large-vessel occlusion
MRI has better resolution of the brain parenchyma and, in particular, evaluates the brainstem and cerebellum with higher resolution than CT
Unfortunately, MRI is less immediately available than CT, requires more time and cooperation from the patient, and may not be feasible in the face of claustrophobia or of ferromagnetic implants/fragments within the body.
When used without a contrast agent, MRA creates vessel images by taking advantage of the flow voids caused by moving blood in the magnetic field.
MR ANGIO May overestimate the degree of arterial stenosis or give the impression of an arterial occlusion when a complete occlusion may not exist
Assess risk benefit ratio if these present
MINOR COMPLICATIONS
MAJOR COMPLICATION-ICH
MINOR-Angioedema of tongue, lips, face or neck in 1-5% pts
Usually mild symptoms and resolve
Glucocorticoids and antihistaminincs
Neurological recovery was better at 90 days, recanalization rate was stat sig(p=0.0001)No mortality benefit
The trial enrolled 151 patients who had stroke symptom dura- tion of 3 to 8 hours or less than 3 hours with a contraindication for tPA. Patients also had a substantial neurologic deficit (NIHSS R8) and an oc- clusion of a treatable vessel. Partial or complete recanalization was achieved in 46% of patients on intention-to-treat analysis, and almost half (46%) of these had good neurologic outcomes at 90 days (modified Rankin score of 0–2). Clinically significant procedural complications were reported in 7% of patients.
both high and low BP having adverse effects on outcom
DONOT USE HYPOTONIC FLUIDS
A recent study, the INSULINFARCT trial, concluded that continuous intravenous insulin infusion provided superior glucose control to subcutaneous insulin therapy but also resulted in larger infarct growth [48]. The rates of serious adverse events and death at 3 months were similar in the subcutaneous and intravenous insulin groups, but the study was not powered to detect clinical changes.
SOME HAVE RECOMMENDED DOSE UPTO 6G/DAY OF PCM-PAIS trial
definitive evidence for benefit is currently lacking, and this might be related to heterogeneous study design including differences in temperature targets, hypothermia induction methods, time windows for initi- ation of TH and duration of treatment, and the variable use of adjuvant treatments. e (ICTuS2/ and eurohyp2
The presence of one or more of these risk factors should not be considered a contraindication to tPA treatment, however, in a patient who otherwise qualifies based on the NINDS criteria
The pathophysiology involves matrix metalloproteinases (MMP-9), inflammatory mediators, reactive oxygen species, and sequelae from thrombolytic agents or other anticoagulants such as low-molecular-weight heparin injections or intravenous heparin
Complications associated with mannitol use are hypovolemia, hypotension, and electrolyte disturbances resulting from osmotic diuresis,renal injury