1. Management of Ischemic Stroke
-Dr Bhadresh Mangukiya
D.M Neurology
504 ,Param Doc House Lal Darwaja,Surat

2. Brain Attack! Acute stroke = ‘brain attack’
Every minute matters: ‘time is brain’
Combat therapeutic nihilism

3. Time is Brain…why. The typical patient loses 1
Time is Brain…why? The typical patient loses 1.9 million neurons each minute in which stroke is untreated The ischaemic penumbra

4. WHO DEFINITION OF STROKE
A NEUROLOGICAL DEFICIT OF
Sudden onset
With focal rather than global dysfunction
In which, after adequate investigations, symptoms are presumed to be of non-traumatic vascular origin
and last for >24 hours
Sudden:
Sudden onset out of full health DD post MI, endocarditis, vasculitis, mets
Focal: intoxication, vasculitis, encephalitis, hysteria,
>24 hrs: TIA, Todd’s, migraine
Presumed non-traumatic vascular origin: exclude head trauma, neck trauma, whiplash, systemic vascultitis, cardiac source of emboli AF, but also endocarditis, post MI, hypotension

5. New definition of TIA
A brief episode of neurological dysfunction caused by focal brain or retinal ischaemia with clinical symptoms lasting less than one hour without evidence of infarction

8. Types of Stroke
85% Ischemic
15 %
hemorrhagic

9. Is it stroke?
Which territory?
What is pathophysiology?
Risk factors?
Etiology?
Treatment?

10. Left MCA Syndrome Language loss (aphasia) Right hemiparesis
Right hemisensory loss
Right visual field cut
Left gaze preference

11. Right MCA Syndrome Left hemi-neglect Left hemiparesis
visual,spatial,
Left hemiparesis
Left hemisensory loss
Left visual field cut
Neglect of deficits
“anasgnosia”

12. Stroke is due to sudden vascular occlusion
ACA
MCA

13. Vascular occlusion causes stroke symptoms
50-70% of all stroke is due to embolism (cardiogenic and artery-to-artery)
80 % of acute strokes are due to MCA territory ischemia
Arterial occlusion is seen in 80-90% within 6-24° of symptom onset
Spontaneous recanalization seen in ~ 20% within 6 ° of symptoms

14. Stroke Risk Factors Non-modifiable
AGE
Gender -male
Race – Blacks > Asians or Hispanics> Whites
Family Hx.
Coagulation Disorders
Cardiac Disease
Each year, 40,000 more women than men have strokes.
Stroke or heart disease in parents younger than 60 years of age.
Cardiac Disease – A fib, CHF, Cardiomyopathy, Valve disease, Cardiac procedures CCL

15. Stroke Risk Factors Modifiable
Hypertension
Diabetes mellitus
Hypercholesterolemia
Elevated LDL or Low HDL
Elevated homocystein
Smoking
Drug abuse
Alcohol Abuse
Oral Contraceptives
Pregnancy
Migraine Headaches
Obesity
Sleep apnea
Carotid stenosis
A combination of these risk factors will increase risk of stroke!
Homocysteine is an amino acid in the blood. Too much of it is related to a higher risk of coronary heart disease, stroke and peripheral vascular disease (fatty deposits in peripheral arteries).
Evidence suggests that homocysteine may promote atherosclerosis (fatty deposits in blood vessels) by damaging the inner lining of arteries and promoting blood clots. However, a causal link hasn't been established.
Folic acid and other B vitamins help break down homocysteine in the body.

17. Many Causes of Stroke

18. THE BURDEN OF STROKE
Anually more than 15 million people world wide suffer a stroke, 5.5 million die and 5 million are left with permanent disability.
Stroke is 2nd most common cause of death(9.7%).
Incidence of stroke is on the increase in India and other developing countries.
More than 80% of stroke occurs in underdeveloped and developing countries.
Cruide annual incidence rate for first ever stroke (FES) is 145 per 100,000 Persons.

19. Stroke is a treatable condition.
IV tPA is approved for use within 3 hours ( 4.5 hours) .(NINDS)
Intra-arterial therapy has proven to be safe and effective within 6 hours (PROACT II)
Combined IV/IA may be more effective than IV t-PA (Interventional Management of Stroke - IMS)
Mechanical and laser catheter technologies are showing great promise (Angio-Jet)

20. Stroke: The Challenge
Only 1-3% of all stroke victims receive treatment with tPA in the US .
25% of Acute MI patients receive treatment (lytics or PTCA) in the US .
Mean time to presentation
AMI: 3hrs
Acute Stroke: 4-10hrs.

21. Reasons for lack of treatment:
Patient’s inability to recognize stroke symptoms
40% of stroke patients can’t name a single sign or symptom of stroke or stroke risk factor.
75% of stroke patients misinterpret their symptoms
86% of patients believe that their symptoms aren’t serious enough to seek urgent care
Physician’s lack of experience with stroke treatment and therefore reluctance to “risk” treatment
Lack of organized delivery of care in many medical centers throughout the country.

22. 5 sudden

23. Hemiparesis sensory or motor
Vision loss
Gait difficulty
Speech disturbance(understand or speak)
Sudden severe headache

24. Current Status of Specific Treatment for Acute Ischemic Stroke
Yes
1. Tissue plasminogen activator within hrs.
2. Aspirin within 48 hrs.
3. Management in SCU
May Be
1. Neuroprotection
No ?
1. Heparin, Heparinoids
2. Hemodilution
3. Steroids

26. Pre of hospital recognition of stoke. FAST
Facial Weakness
Can person smile
Has mouth dropped
Arm Weakness
Can person raise both arms
Speech problems
Can person speak clearly and understand what you say
Test all three symptoms
Stroke Association campaign to raise awareness
Practice staff should be trained to inform doctor immediately if patient calls with symptoms identifiable
Ambulance crews now trained to use FAST score to prioritise Calls and dispatch.
Act FAST call 108 ambulance.

27. Onset to Entry (By referral method) Section 1 Slide 30 10 20 30 40 5010 20 30 40 50 60 70
0-<1
1-<2
2-<3
3-<4
4-<5
5-<6
6-<9
9-<12
12-<24
>=24
Hours
Pt Numbers
999 GP
Other
GP+999
ASIST data 1999

28. Pre Hospital care
Ambulance services ,health care professionals and general public should receive education concerning the importance of early recognition of stroke, emphasing stroke is a medical emergency.
Stroke patients should be given a high priority by ambulance service.
Ambulance services should be trained to identify stroke by various tools and protocols.
Ambulance services should transfer suspected patients to hospital with stoke unit care.

29. EMS response to 108 call: WILL QUESTION:
Time of onset of stroke symptoms.
Determine nature of neurological symptoms (F.A.S.T.).
NIH Stroke Scale or Glasgow Coma Scale (language/motor response/eye movement).
Hx: recent illness, surgery or trauma.
Recent use of medication/illicit drugs.
Notify receiving hospital that patient appears to be an acute stroke and gives time window.

30. Guidelines for EMS management of patients with suspected stroke
Recommended
Manage ABCs
Cardiac monitoring
Intravenous access
O2(if spo2,92%)
Assess for hypoglycemia
NBM
Alert receiving ED
Rapid transfer to closest stroke centre
Not recommended
Dextrose containg fluid in non hypoglycemic patients
Hypotension/excessive BP reduction
Excess IV fluids

33. Stroke units: State of the Art
Admission to a unit that is dedicated to the care of stroke patients helps to reduce mortality and morbidity.

38. Stroke: Differential Diagnosis
Syncope
Partial epileptic seizure with Todd’s paresis
Migraine attack (aura)
Hypoglycaemia
Hysteria
Intoxication
Subarachnoid haemorrhage
Neuroinfection
Neoplasm
Brain injury
Multiple sclerosis
Peripheral vertigo
ER Procedure: Differential Diagnosis
In stroke patients, clinical features are usually sufficient to enable at least preliminary diagnosis. CT scanning is instrumental in documenting cerebral haemorrhage, neuroinfection or brain injury, but does not help to exclude possibilities such as syncope, partial epileptic seizure with Todd’s paresis, migraine attack with aura, hypoglycaemia, hysteria, intoxication, meningitis or multiple sclerosis. In this context, it is important to remain aware that confirmatory tests should supplement – rather than replace – conventional clinical skills.
In practice, the most important distinction is between ischaemic stroke and intracranial haemorrhage. The clinical features of these conditions may overlap, but their treatment is markedly different.1 Early distinction between the various subtypes of ischaemic stroke is also becoming important (i.e. lacunar vs large artery or cardioembolic stroke), as there is evidence that these may respond differently to different treatments. This is a situation in which neuroimaging techniques such as CT scanning can be invaluable, although clinical scoring systems based on the presence or absence of specific clinical features can also be strongly predictive. One such system – the Allen score – has been found to be 90% accurate in the identification of haemorrhage. 2–4
References
1. European Ad Hoc Consensus Group. European strategies for early intervention in stroke: a report of an Ad Hoc Consensus Group meeting. Cerebrovasc Dis 1996; 6: 315–24.
2. Allen CMC. Clinical diagnosis of the acute stroke syndrome. Q J Med 1984; 208: 515–23.
3. Sandercock PAG, Allen CMC, Corston RN et al. Clinical diagnosis of intracranial haemorrhage using Guy’s hospital score. Br Med J 1985; 291: 1675–7.
4. Celani MG, Righetti E, Migliacci R et al. Comparability and validity of two clinical scores in the early differential diagnosis of acute stroke. Br Med J 1994; 308: 1674–6 27

39. PHYSICAL EXAM GPE,ABCs, Pulse Oximetry,temp.
Carotid Bruits, JVP, Irregular Rhythm
Head and Neck, Chest, Abdomen
Skin –Jaundice, Purpura, Petechia

42. Early diagnostic tests
ALL PATIENTS
Non contrast brain CT or brain MRI
Blood glucose
RFT,S. electrolytes
ECG
Markers of cardiac ischemia
CBC, Plat count*
PT,INR,*APTT*
O2 Saturation
SELECTED PATIENTS
LFT
Toxicology screen
Blood alcohol level
Pregnancy test
ABG
Chest radiography
LP-if SAH is suspected and CT is negative
EEG –if seizures are suspected.

43. EARLY DIAGNOSIS: NON CONTRAST CT SCAN OF BRAIN
Initial imaging modality in hyper ac stroke
Widely available, quick, easy to perform
Accurately identifies ICH,SAH
EARLY SIGNS OF CEREBRAL ISCHAEMIA
Hyper dense MCA artery sign
Hyper dense dot sign
Hypo density of insular ribbon
Hypoensity of basal ganglia
loss of grey white matter differentiation in cortical ribbon
sulcal effacement
EARLY SIGNS ARE ASSOCIATED WITH POORER OUTCOMES

44. Early Hypodensity
Hypodensity

45. Hyperdense middle cerebral artery

46. CT Known time of symptoms <4 hours NIHSS score No haemorrhage
No contraindications
Consent
Age

47. Thrombolysis Alteplase rTPA 0.9mg /Kg
10% of total dose –Bolus 2-3 mins
90% of total dose –Infuse over 60 mins

48. rTPA Alteplase Do not mix t-PA with any other medications.
Do not use IV tubing with infusion filters.
All patients must be on a cardiac monitor
When infusion is complete, saline flush with Normal saline
t-PA must be used within 8 hours of mixing when stored at room temperature or within 24 hours if refrigerated

49. Complications of Thrombolysis
Intra -cerebral haemorrhage-1.7%
(1 in 77 patients) 0.28% fatal
SITS MOST 2007
Bleeding-minor bleeding is common (IV site)
Anaphylaxis- 1%
Ace inhibitors Frontal & insular lesions
Angiodoema 1.3% Canadian study 1,135 pts
Major Heamorrhage 0.4%

51. Angioedema

52. First 24 hours
30% of all stroke patients will deteriorate in the first 24hours
Stroke 2009

53. Monitor GCS Ability to engage with immediate surroundings
Standardised stimuli
E1-E4
V1-V5
M1-M6

54. Best and Worst Score GCS 15- E4 V5 M6
Awake, alert and fully responsive
GCS 3-E1 V1 M1
No cerebrally mediated response to stimulus

55. NIHSS - A Research Tool Fifteen item impairment scale
Neurological outcome
Degree of recovery

56. Physiological Monitoring
Hypoxia
Respirations
Saturations <92%
Associated with neurological deterioration
Temperature
>38C must be treated.
-associated with infarct volume
Arrhythmias
Continuous ECG
Early detection and treatment of AF
Right hemisphere /insular lesions

57. Physiological Monitoring contd
4.Blood pressure
Non thrombolysed patients
BP Not treated unless:
Systolic >220mmHg or
Diastolic >120mmHg with 2 consecutive readings
Thrombolysed patients
BP is treated if:
Systolic >185mmHg or
Diastolic >110mmHg with 2 consecutive readings
Abrupt fall in BP may affect cerebral perfusion pressure

58. Physiological Monitoring contd
5.Blood Sugar
Hyperglycaemia BM>10 treat & monitor
Hypoglycaemia –immediate treatment with glucose
Hyperglycaemia is associated with poor clinical outcome

59. Physiological Monitoring Contd
Anuria
Polyuria
Circulatory failure
Hydration
Glucose
Cerebral perfusion

60. Complications of Stroke
Aspiration Pneumonia
Urinary infection
DVT
Pulmonary Embolus
Shoulder subluxation
Depression
Malnourishment
Pressure sores
Falls
Seizures

61. Swallow Complications (Dysphagia)
Chest Infection
Aspiration Pneumonias
50% are silent
Swallow screen
Nil by mouth first 24hours
Guided eating & drinking regime
Encourage to cough
Sitting out of bed
Mobilisation

62. Mouth Care Increased risk of infection Pain and discomfort
Effects swallow
Gentle mouth care
Adequate hydration
Gentle tooth brushing

63. Head Position Controversial Head in a neutral position
Flat if tolerated.
Or 30 –40 degrees
Aids venous drainage & improves cerebral perfusion

64. Bladder &Bowels Urinary incontinence Urinary infection Avoid catheters
Early plan of care
Adequate hydration
Bowels
Privacy & dignity

65. Psychological Support
Assess mood
Recognise grief/loss
Talk
Engage with family
Interests
Timely realistic goals
Refer

66. Pressure Sores Air mattress Two hourly turns Nutrition Hydration
Personal hygiene

67. Deep Vein Thrombosis Early mobilisation Low molecular weight heparin
Compression devices
TED stockings not beneficial in stroke patients
Clots Trial 2009

68. Positioning Loss of sensation Loss of power Subluxation Supportive
IV lines and BP cuffs avoided on affected limb
Assess moving and handling
Good technique

69. Nutrition Weight MUST assessment Naso gastric tube
Malnourishment associated with poor outcome
Weight
MUST assessment
Naso gastric tube
History of patients eating habits
Controversial
When to commence invasive feeding regime

72. Without thrombolysis
2hrs

74. Thnak You