Precise discussion about stroke subtypes

1. STROKE SYNDROMES
By Mekonnen.A (ECCMR1)
Advisor
Dr.Feven(Ass.proff.ECCM)
Modulator
Dr.Ebsa(ECCMR3)
10/20/2021 1

2. Outlines
• Introduction
• Definition
• Epidemiology
• Classification
• Pathophysiology
• Diagnosis
• Pre hospital management
• ED management of Acute Stroke
• General stroke treatment
• Specific treatment
• Primary prevention & Secondary prevention
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3. Specific objectives
▪Define stroke
▪Explain pathophysiology of stroke
▪Classify stroke syndromes
▪Identify risk factors
▪ Describe acute stroke management
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4. CASE PRESENTATION
• A 70-year-old man is brought to the ED by EMS.
The man’s wife noted that when she awoke this
morning her husband was unable to get out of
bed. He had slurred speech and could not move
the right side of his body, including his face, arm,
and leg, prior to this he was complaining of chest
pain. He describes the pain as heavy and
retrosternal, his BP is 190/100mmhg
• ED, 12-Lead revels anterior STEMI
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5. INTRODUCTION AND EPIDEMIOLOGY
• One stroke every 40 seconds
• One death from stroke every 4 minutes)
•77% are primary strokes, whereas 23% represent
recurrent strokes
• Stroke patients have an in-hospital mortality rate of
- 5 % to 10 % for ischemic stroke and
- 40% to 60% for intracerebral hemorrhage (ICH)
• Only 10% of stroke survivors will recover completely
• leading cause of adult disability.
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6. EPIDEMIOLOGY, Ethiopia
• According to WHO data published in 2017
stroke death reached 6.23 % of total deaths
In-hospital mortality -18%
• SPHMMC( sept 1ST , 2015 – August 30th ,2016 )
▪ Most common stroke - Hemorrhagic stroke -61.3%
▪ Most common risk factor-hypertension – 60.7%
▪ Structural heart disease –18.4%
▪ A-Fib–14.7%
▪ Diabetes –11%
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7. Definition
• Stroke is defined as any disease process that
interrupts blood flow to the brain.
• Acute episode of neurological dysfunction
caused by vascular lesions
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8. Mechanisms of stroke
1 - Ischemic strokes( 87% of all strokes ) -
categorized by cause:
▪ thrombotic
▪ embolic
▪ hypoperfusion related
2 – Hemorrhagic , subdivided into
▪ intracerebral (10% of all strokes)
▪ nontraumatic subarachnoid hemorrhage ( 3%
of all strokes)
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9. Ischemic Stroke Classification
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10. Vascular Supply & Neuroanatomy
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12. Anterior and Posterior Circulation of
the Brain
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13. HISTORY
▪The timing of symptom onset
▪The presence of associated symptoms
▪The medical history may point toward a particular
mechanism of stroke.
– sudden onset of symptoms - embolic or
hemorrhagic stroke
– waxing and waning deficit suggests a thrombotic
or hypo perfusion-related stroke
•Quickly exclude as many stroke mimics as possible
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14. Stroke Mimics
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16. Selected Stroke Symptoms
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17. Cont.
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18. INITIAL DIAGNOSTIC EVALUATION
Brain imaging -NCCT
•Most acute ischemic strokes are not visualized by a
noncontrast brain CT in the early hours of a stroke.
•NCCT is primarily to exclude
- intracranial bleeding
- abscess
- tumor
- other stroke mimics
- to detect current contraindications to thrombolytics
(extensive regions of clear hypoattenuation)
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19. Cont.
• Diffusion-weighted MRI is superior to
noncontrast-enhanced CT or other types of
MRI (T1/T2 weighted, fluid-attenuated
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20. Five early signs of ischemic stroke on
CT head
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21. VASCULAR IMAGING
• Guides endovascular therapies of
—Intracranial large-vessel stenosis or
occlusion
• CT angiography or magnetic resonance
angiography can detect these lesions.
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22. ISCHEMIC STROKE SYNDROMES
ACA INFARCTION
• Uncommon (0.5% to 3% of all strokes)
• Contralateral sensory and motor symptoms in the
lower extremity with sparing of the hands and
face.
A left-sided lesion
- akinetic mutism
- nonfluent aphasia with greatly reduced
spontaneous speech
-retained auditory comprehension
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23. Cont.
• A right-sided infarction
-confusion and motor hemineglect.
• Bilateral occlusion - can cause
- combination of the above symptoms
- poor outcome
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24. MCA INFARCTION
•The vessel most commonly involved in stroke
•Motor and sensory loss contralateral to the
affected cortex.
•These deficits variably affect the face and
upper extremity more than the lower extremity
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25. Cont.
• If the dominant hemisphere is involved
- aphasia (receptive, expressive, or both) is often
present.
• If the nondominant hemisphere is involved
- inattention
- neglect
- extinction on double-simultaneous stimulation
- dysarthria without aphasia
- constructional apraxia (difficulty in drawing
complex two-dimensional figures) may occur
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26. POSTERIOR CIRCULATION
•The classic symptoms and signs
- ataxia
- nystagmus
- altered mental status
- vertigo
- visual field loss
- cranial nerve VII signs
- sensory deficit
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27. Basilar artery occlusion
Locked-in syndrome
• bilateral pyramidal tract lesions in the ventral
pons
• complete muscle paralysis except for upward
gaze and blinking.
• High risk of death and poor outcomes
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28. CEREBELLAR INFARCTION
• Nonspecific symptoms
- dizziness (with or without vertigo)
- nausea and vomiting
- gait instability/ ataxia
- dysarthria
- hearing loss
▫Mental status may vary from alert to comatose
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29. Cont.
• Up to 25% of non contrasted head CTs can be
normal in cerebellar infarction.
– emergent DWI
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30. LACUNAR INFARCTION
• Pure motor or sensory deficits caused by
infarction of small penetrating arteries.
– chronic hypertension
– increasing age
• Favorable prognosis than other stroke
syndromes
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31. HEMORRHAGIC STROKE SYNDROMES
• 15% of all strokes
- 1/3 are the subarachnoid type
- 2/3 are from intracerebral hemorrhage
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32. Cont.
SAH - leakage of blood into the subarachnoid
space
• classically – sudden onset severe headache.
ICH - bleeding into the brain parenchyma itself
• typically – acute neurologic deficit often
accompanied by headache.
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33. SUBARACHNOID HEMORRHAGE
• 75% of atraumatic SAH are caused by a ruptured
aneurysm.
• 20% of cases a cause is not identified.
• The remaining causes are miscellaneous
conditions
- arteriovenous malformations
- sympathomimetic drugs
• 20% of patients with one aneurysm will have an
additional aneurysm.
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34. CLINICAL FEATURES
• severe headache of acute onset
(“thunderclap” headache) that reaches
maximal intensity within seconds.
- loss of consciousness
- Seizure
- nuchal rigidity
- nausea and vomiting
- Photophobia
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35. Cont.
• Approximately 20% of patients develop their
symptoms while engaged in activities that cause
increased blood pressure such as
-Exercise
- sexual intercourse
- defecation
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36. Risk Factors for Subarachnoid
Hemorrhage
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37. Diagnosis of Subarachnoid
Hemorrhage
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38. Ottawa Subarachnoid Hemorrhage
Rule
A–Age >40
N–Neck pain or stiffness
T–Thunderclap headache
L–LOC-witnessed
E–Exertion during onset( defecation, sexual
intercourse )
F–Flexion( limited neck during exam)
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39. Cont.
Inclusion criteria
• Glasgow coma scale score = 15 of 15 ( patient was alert
and oriented)
• No history of fall or head trauma in the past 7 days
• Presentation within 14 days of headache onset
Exclusion criteria
• A previously established history of headache syndrome
• Returning for reassessment of a headache that was
previously evaluated with computed tomography (CT)
and lumbar puncture
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40. Diagnosis SAH…
• Imaging
-The initial diagnostic modality of choice is a
noncontrast CT
– CT angiography and MRI or magnetic
resonance angiography are options after a
negative head CT
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41. Cont.
LUMBAR PUNCTURE
▪Normal findings on head CT + absence of
xanthochromia + zero or few RBCs (<5 × 106
RBCs/L) in tube 4 exclude subarachnoid
hemorrhage.
▪A normal head CT + positive finding of
xanthochromia or elevated RBC count in tube 4
should be considered diagnostic of
subarachnoid hemorrhage.
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42. Grading Scales for Subarachnoid
Hemorrhage
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43. INTRACEREBRAL HEMORRHAGE
•Spontaneous ICH - 8% to 11% of all acute
strokes
▫ 3% to 9% of patients treated with tissue
plasminogen activator for acute ischemic stroke
▫ 0.3% to 0.6% in those taking OAC.
≈ 6% to 16% of all cases of ICH.
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44. ICH (Continued)
▫ Seven-day mortality is approximately 30%
▫30-day mortality rate of up to 50%
≈ one half of patients dying in the first 2
days
▫1-year mortality about 55%
▫10-year mortality approximately 80%.
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45. ICH -Risk factors
▪ Long-standing hypertension
– basal ganglia
– thalamus
– pons
▪Amyloid angiopathy
– lobar hemorrhage
– common in the elderly
▪ Arteriovenous malformations (AVMs)
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46. Cont.
▪Anticoagulants
▪Drugs(cocaine , amphetamines)
▪Tumors
▪Hemorrhagic transformations of AIS
▪Vacuities
▪Cerebral venous sinus thrombosis(CVST) -
ischemic infarcts/hemorrhage
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48. 10/20/2021 48

49. MOST COMMON SITES FOR
HYPERTENSIVE INTRACRANIAL
HEMORRHAGE
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50. Prehospital Stroke Management
• Recognition of stroke symptoms
• Emergency medical service
- Support ABC
- Perform pre-hospital assessment of stroke
- Establish time (LKN).
- Transport to a hospital with stroke unit
-Take a witness and caregiver
- Notification to the receiving hospital
- Check blood sugar if possible
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51. Prehospital Stroke Scales
Cincinnati Prehospital Stroke Scale (If any
of the three items are abnormal,
sensitivity = 66%, specificity = 87% for
acute stroke.)
1. Facial droop (abnormal: one side of
face does not move as well as other
side)
2. Arm drift (abnormal: one arm does
not move or one arm drifts down
compared with the other)
3. Speech (abnormal: slurred,
inappropriate words or mute)
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52. Cont.
Los Angeles Prehospital Stroke Screen (If
answers to all items 1–6 are “Yes” or
“Unknown,” sensitivity = 91% specificity
= 97% for acute stroke.)
1. Age >45 y
2. No history of seizure disorder
3. New onset of neurologic symptoms in
last 24 h
4. Patient ambulatory at baseline (prior
to event)
5. Blood glucose level of 60–400
milligrams/d
6. Obvious asymmetry in any of the
following examinations: facial
smile/grimace, grip, arm strength
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53. Cont.
Melbourne Ambulance Stroke Screen (If
answers to all items 1–4 are “Yes” PLUS
at least one of 5–8 is present, sensitivity
= 90% , specificity = 74% for acute
stroke.)
1. Age >45 y
2. No history of seizure/epilepsy
3. Not wheelchair-bound/bedridden at
baseline
4. Blood glucose 50–400 milligrams/dL
5. Unilateral facial droop
6. Unilateral hand grip weakness
7. Unilateral arm drift
8. Abnormal speech
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54. National institute of health stroke
scale
▪Determine the severity / prognosis
▪ possible location of the stroke
▪Strongly associated with degree of injury
/infarction
▪Guide reperfusion therapies
▪complications from the stroke and reperfusion
strategies.
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55. National Institution of Health Stroke
Scale (NIHSS)
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56. (continued)
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57. 10/20/2021 57
Time goals for
management of
patients with suspected
stroke algorithm after
arrival to ED

58. • Immediate general assessment and stabilization
- Assess ABC and vital signs
- provide oxygen if hypoxic , spo2 >94%
- Obtain IV access
- Obtain blood samples
- Check blood sugar, treat if needed
- Perform neurologic screening assessment
- Activate stroke team
- Order Immediate brain CT scan
- Obtain 12-lead ECG
Arrival to Emergency department:
10min
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59. After arrival to Emergency
department: 25min
▪ The CT scan should be completed
▪Immediate neurological assessment by stroke
team or specialist of stroke
- Review patient history
- Establish symptoms onset(LKN)
- Perform neurologic examination , assess by
the NIHSS
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60. After arrival to Emergency
department: 45min
Does CT scan show any Hemorrhage?
Establish neurological and CT diagnosis
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61. Does CT scan show any Hemorrhage?
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62. NINDS Targets for Potential
Thrombolytic Candidates
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63. TREATMENT OF ACUTE ISCHEMIC
STROKE
▪IV thrombolytics /Alteplase
▪Anti platelets
▪Blood Pressure
▪Anticoagulants
▪Mechanical Thrombectomy
▪Emergency CEA– carotid angioplasty and
stenting
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64. Inclusion and Exclusion Criteria for tPA
for Acute Ischemic Stroke
tPA Inclusion Criteria
1. Age ≥18 yr
2. Diagnosis of ischemic stroke / disabling
3. Onset of stroke symptoms < 4h30
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66. Relative Exclusion Criteria
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67. Dosage of rtPA
▪ The standard total dose of alteplase is 0.9
milligram/kg IV
▪Maximum dose is 90 milligrams
▪ Administer 10% of the dose as a bolus over 1
minute, with the remaining amount infused over
60 minutes.
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68. Cont.
• The dose of tenecteplase is weight-based
▫<60 kg, 30 milligrams
▫60-70 kg, 40 milligrams
▫80-90 kg, 45 milligrams;
▫For>90 kg, 50 milligrams .
• The maximum dose is 50 milligrams.
•Tenecteplase is given as a single IV bolus over
5-10 seconds
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69. Antiplatelet
• ASA is typically given at an initial dose of 325
mg within 24–48 hours of stroke onset.
• The dose may be reduced to 81 mg in the
post–acute stroke
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70. Dual antiplatelet therapy
• Minor stroke =NIHSS score of ≤3
• High / moderate risk TIA =ABCD2 score ≥ 4
• A- Fib patients who cannot receive warfarin.
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71. Cont.
• ASA 160 -325 mg loading, followed by 50 -
100mg daily plus clopidogrel 300 mg loading
and 75mg daily for 21 days
• DAPT reduces risk of recurrent stroke
compared to ASA alone ( 6.3 % VS 4.4 %)
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72. Acute Anticoagulant Therapy
• Anticoagulation for acute ischemic stroke has
never been shown to be effective.
• Even among those with atrial fibrillation, the
stroke recurrence rate is only ~5–8% in the
first 14 days, which is not reduced by early
acute anticoagulation.
• Anticoagulation is mostly used for long-term
secondary prevention
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73. Cont.
Acute anticoagulation with heparin can be used with
cases.
• Cardio embolic conditions at high risk for recurrence
- thrombus on valves
- metallic prosthetic valves or mural thrombus
- documented large-artery(ICA,MCA,or basilar
artery)occlusive clot at risk for distal embolism
- arterial dissection (carotid and vertebral artery
dissection)
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74. Cont.
• Anticoagulation with heparin/LMWH followed
by warfarin is indicated for venous sinus
thrombosis both with and without
hemorrhagic infarcts.
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75. A-Fib and cardioembolic stroke
• In the setting of acute atrial fibrillation,
Anticoagulation/ warfarin is indicated to
prevent recurrent embolic strokes.
• Initiate between 4-14 days
• Target INR for warfarin therapy is 2–3
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76. Cont.
Withholding anticoagulation for two weeks is
generally recommended for those pts
• large infarctions
•hemorrhagic transformation
• poorly controlled hypertension
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77. Criteria for large infarcts
▪NIHSS >15
▪ >1/3 of MCA territory involved
▪ >1/2 of PCA territory involved
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78. ENDOVASCULAR THERAPY
• Intra-arterial thrombolysis
• Mechanical clot disruption/extraction.
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79. AHA/ASA Indications for Endovascular
Therapy With a Stent
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80. ASPECTS Score
on the CT Imaging
C—Caudate
I—Insular Ribbon
C—Internal Capsule
L—Lentiform nucleus
M1—Anterior MCA cortex
M2—MCA cortex lateral to the insular ribbon
M3—Posterior MCA cortex
M4—Anterior MCA superior territory
M5—Lateral MCA superior territory
M6—Posterior MCA superior territory
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81. AIS WITH CONCURRENT AMI
▪Problematic/ delay a time-dependent
procedure for the one other.
▪Therapies for acute myocardial infarction (e.g,
heparin) that are contraindicated in acute stroke
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82. Cont.
• Treatment with IV alteplase followed by
percutaneous coronary angioplasty and
stenting if indicated is reasonable.
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83. Blood Pressure
• BP should not be lowered acutely unless
necessary for treatment of
▫ acute coronary syndrome
▫ aortic dissection
▫ CHF
▫ SBP >220 mm Hg or DBP >120 mm Hg.
• BP lowering should proceed cautiously with
the goal of 15% during the first 24 hours.
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84. RX of HTN During and After
Thrombolytics Therapy
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85. TIA
• A transient episode of neurological
dysfunction caused by focal brain, spinal cord,
or retinal ischemia, without acute infarction.
• About 33% of TIAs have signs of infarction on
MRI.
• 10% of the patients who experience a TIA will
experience a stroke within 3 months
- one-half of these occur within the first 2
days.
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86. TIA…admission criteria
• Crescendo TIAs
• Duration of symptoms >1 hour
• Symptomatic internal carotid artery stenosis >50
percent
• Known cardiac source of embolus such as atrial
fibrillation
• Known hypercoagulable state
• High risk of early stroke after TIA ( ≥6 )
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87. ABCD2 Score for Assessing Stroke Risk
in Patients With a TIA
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88. Treatment of acute ICH
High blood pressure
▪Labetalol 10–20 milligrams IV over 1–2 min; may repeat
once
▪Nicardipine 5 milligrams/h IV infusion, titrate up by 2.5
milligrams/h every 5–15 min until desired BP is reached;
maximum 15 milligrams
▪Esmolol IV bolus, 500 µg/kg as a load; maintenance use,
50– 200 µg/kg/min
▪Nitroprusside 0.5–10 µg/kg/min
▪Hydralazine 10–20 mg Q 4–6 h
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89. Recommendations for Surgical
Treatment of ICH
1. Cerebellar hemorrhage >3 cm
2. Brain stem compression and hydrocephalus
from ventricular obstruction.
2. ICH associated with a structural lesions
▪ aneurysm
▪ arteriovenous malformation
▪ cavernous angioma
3. Young patients with large lobar hemorrhage ≥50
мl)
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90. ICH Volume Estimation
▪VOL (CM3 ) = A X B X C/2
–A = Maximal diameter in cm (axial)
–B =Maximal diameter in cm perpendicular to
“A” (axial)
–C =Maximal length in cm (coronal) or no, of CT
slices multiplied by CT slice thickness(0.5-1cm)
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91. Reversal of Anticoagulation for
Intracerebral Hemorrhage
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92. Treatment of aneurysmal
subarachnoid hemorrhage
▪Anticoagulants and antiplatelet
discontinuation and reversal
▪Intracranial pressure and blood pressure
▪Prevention & treatment of vasospasm
▪Surgery
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93. Prevention & treatment of vasospasm
▪Triple-H therapy
- hemodilution
- induced hypertension (with pressor
agents such as phenylephrine or dopamine)
-hypervolemia
▪ Statins
▪ Nimodipine
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94. Management of Raised ICP
and Hydrocephalus
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95. • Osmotherapy
- Mannitol 20% (0.25–0.5 g/kg
- Hypertonic saline solutions (NaCL 23.4%,
30ml)
• External ventricular drainage (EVD)
•Lumbar drainage
• Decompressive craniectomy
Raised ICP and Hydrocephalus…
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96. Investigational approaches
-Antifibrinolytic therapy
-Glucocorticoid therapy
-Seizure prophylaxis
- Endothelin (ET) receptor antagonists
-Magnesium sulfate
-Nicardipine
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97. In-hospital Managements
General Supportive Care
▪ Positioning
▪Supplemental Oxygen
▪Blood Pressure
▪Continues cardiac monitor
▪Temperature
▪Glucose
▪Dysphagia
▪Oral care
▪Nutrition
▪Deep Vein Thrombosis Prophylaxis
▪Rehabilitation
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98. Secondary Stroke Prevention
(“BLASTED”)
• Blood pressure
• LDL
• ASA (antiplatelet)
• A1C
• Stroke rehabilitation
• smoking cessation counseling
• cardiac follow up
• Echocardiography
• Doppler for carotid stenosis, diabetes (A1C,
diabetes educator)
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99. References
©Tintinalli’s Emergency Medicine,9th edd.
©ROSEN’S EMERGENCY MEDICINE,9th edd
©AHA/ASA GUIDELINES FOR MANAGEMENTS
OF AIS,2019
©Uptodate 21.6
©The Washington Manual of Medical
Therapeutics, 36th Edd
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THANKS