Cerebrovascular Accident

1. HOANG CUONG MS-V
HaNoi Medical University
Cerebrovascular
Accident (Stroke)

2. o Introduction
o Risk Factors
o Pathophysiology
o Recognizing Stroke
o Clinical Features
o Initial Assessment
o Immediate laboratory
o Diagnostic
o Management and Prevention
Contents

3. • A stroke (apoplexy) is a neurological impairment caused by a
disruption in blood supply to a region of the brain, typically
lasting longer than 24 hours with evidence of acute infarction.
• Stroke, also known as cerebrovascular accident (CVA),
cerebrovascular (CVI), or brain attack.
• Transient Ischemic attack (TIA): Clinical syndrome of rapid of
focal deficits of brain function which resolves within 24 hours
• Progressive Stroke (Stroke in evolution): A stroke in which the
focal neurological deficits worsen with time.
• Completed Stroke: A stroke in which the focal neurological
deficits persist and do not worsen with time.
Introduction

4. Type of Stroke
Ischemic (87%) Hemorrhagic (13%)
• Thrombotic
• Embolic
• Systemic hypoperfusion
• Intraparenchymal
• Subarachnoid
• Caused by a blockage in th
e blood vessels to the brain
• Caused by burst or leaking
blood vessels in the brain
• Aneurysms, Arteriovenous
Malformations (AVMs)

5. Risk Factors
Modifiable Risk Factor Non-modifiable Risk Factors
• Hypertension
• Atrial Fibrillation
• Transient Ischemic Attack
• Diabetes
• Hypercholesterolemia
• Cigarette Smoking
• Drug Abuse
• Obesity
• Physical Inactivity
• Age >55
• Gender: Men > Women
• Race:
o African Americans
o Asian-Pacific Islanders
o Hispanics
• Family History

6. • Large artery disease – atherosclerosis of large vessels,
including internal carotid artery, vertebral artery, basilar
artery, and other major branches of the Circle of Willis.
• Small vessel disease (Lacunar infarction)- changes due to
chronic disease, such as diabetes, hypertension,
hyperlipidemia, and smoking
• Cardioembolism – the most common cause of an embolic
stroke is atrial fibrillation
• Stroke of determined etiology – such as inherited diseases,
metabolic disorders, and coagulopathies.
• Stroke of undetermined etiology – after exclusion of all the
above
Cause of Ischemic

7. • Intracerebral hemorrhage – ruptured of a blood vessel
and accumulation of blood within the brain.
→ blood damage from chronic hypertension, vascular
malformations, or the use medications associated with ↑
bleeding rates, such as anticoagulants, thrombolytics ,
and antiplatelet agents.
• Subarachnoid hemorrhage: trauma to the head or
rupture of a cerebral aneurysm.
Cause of hemorrhage

11. Pathophysiology of ischemic Stroke
- Cerebral Autoregulation
• CBF (cerebral blood flow) determined
resistance within cerebral blood vessels
• Smooth muscle contract when CPP increases
and relax when CPP drops
• Nitric oxide also plays a role in
autoregulation
• Occurs within a mean arterial pressure 60-
150 mmHg
• Outside this range, CBF increases or
decreases with CPP
• Ischemia at low and edema at high CPP

12. Pathophysiology of ischemic Stroke
Effects of decreased cerebral blood flow
on vital brain functions
Impaired during ischemic stroke
• As CPP falls, blood vessels dilate to increase
CBF. Reduced CPP beyond compensation
reduces CBF
• The normal CBF ~40 to 60 mL/100g of brain
per minute
• When CBF drops below 15 to 18 mL/100g of
brain per minute
→ several physiologic changes occur
→ loses electrical activity (although
neuronal membrane integrity and function
remain intact)
→ manifest a neurologic deficit
• When CBF below 10mL/100g of brain per minute → membrane failure
→ ↑ extracellular potassium and intracellular calcium → eventual cell death

13. The process of neuronal ischaemia and infarction
Pathophysiology of ischemic Stroke

14. - Mechanisms of ischemic cell injury and death
(1) Reduction of blood flow reduces supply of oxygen and hence ATP
(2) Energy-dependent membrane ionic pumps fail
→ Cytotoxic oedema and membrane depolarisation
→ Calcium entry and releasing glutamate
(3) Calcium enters cells via glutamate-gated channels
(4) Activates destructive intracellular enzymes
(5) Destroying intracellular organelles and cell membrane, with release
of free radicals → Free fatty acid release activates pro-coagulant
pathways → exacerbate local ischaemia
(6) Glial cells take up H+ → can no longer take up extracellular
glutamate and also suffer cell death → liquefactive necrosis of
whole arterial territory
Pathophysiology of ischemic Stroke

16. Ischemic core
Oligemic penumbra
- Concept of ischemic penumbra
• Cerebrovascular tissue undergoing ischemia has two layers:
(1) Inner core of severe ischemia with blood flow below 10-25% →
necrosis of both neuronal as well as supporting glial elements.
(2) Outer layer of less severe ischemia (penumbra), supplied by
collaterals
→ can be retrieved by timely therapeutic intervention
• Following an ischemic even:
 Ischemic core ≤10-12 ml/100g/min
 Ischemic penumbra ≤18-20 ml/100g/min
 Oligemia: 18-50 mL/100g/min
→ Neurons in the penumbra are mostly
dysfunctional, but may recover if reperfused in time.

18. - Cerebral edema and its effects
• Cytotoxic/cellular edema: Evolves within minutes to hours and are
potentially reversible. It is characterized by swelling of all the cellular
elements of the brain, including neurons, glia, and endothelial cells.
(due to failure of ATP-dependent ion transport, as well as release of
oxygen-derived free radicals)
• Vasogenic edema: Occurs over hours and days and are irreversible. It
causes increased permeability of brain capillary endothelial cells to
macromolecular serum proteins (e.g., albumin) → increase in
extracellular fluid volume along with ↑ intracranial pressure (ICP)
→ persistent ischemia, irreversible damage to brain cells; and when
severe may lead to cerebral herniation and potentially death.
• Initially acute hypoxia causes cytotoxic edema → Vasogenic edema
with progression of infarction.

20. - Effects of ischemia on structural integrity of brain
• Hypoxia → release of proteases like matrix metalloproteases (MMP)
→ loss of structural integrity of brain tissue and blood vessels
→ breakdown of the protective blood-brain barrier → cerebral edema,
along with secondary progression of brain injury.
• Angiogenesis: Hypoxia inhibiting degradation of hypoxia-inducible
factor-1 (HIF-1) → stimulates VEGF (essential for angiogenesis)
• Angiogenic growth factor → secreted by inflammation-associated
infiltrates (leucocyte, macrophages, damaged blood platelets).
• Brain ischemia → activate the immune mechanism → exacerbation of
damage and clinical deterioration of the patient.

21. Pathophysiology of Hemorrhage Stroke
• This form of stroke occurs due to rupture of a blood vessel in the
brain.
• First, there is mass effect from the hematoma itself, followed by
activation of the coagulation cascade→ release of inflammatory
cytokines, and blood-brain barrier (BBB) disruption →perihematomal
edema formation and secondary brain injury.
• Finally, continued bleeding, or hematoma expansion
→ Raised ICP, which may further restrict cerebral blood flow

23. Recognizing Stroke: BEFAST

24. Recognizing Stroke: BEFAST
• Numbness or weakness of the face. Without adequate perfusion,
oxygen is also low → facial tissues → not function properly.
• Change in mental status. Due to decreased oxygen, the patient
experiences confusion
• Trouble speaking or understanding speech.
• Visual disturbances.
• Homonymous hemianopsia: loss of half of the visual field
• Loss of peripheral vision: Difficulty seeing at night and is
unaware of objects or the borders of objects.
• Hemiparesis. Weakness of the face, arm, and leg on the same side
due to a lesion in the opposite hemisphere.
• Hemiplegia. Paralysis of the face, arm, and leg on the same side
due to a lesion in the opposite hemisphere.

25. Recognizing Stroke: BEFAST
• Ataxia. Staggering, unsteady gain and inability to keep feet
together.
• Dysarthria. This is the difficulty in forming words.
• Dysphagia. There is difficulty in swallowing.
• Paresthesia. There is numbness and tingling of extremities and
difficulty with proprioception.
• Expressive aphasia. Unable to form words that is understandable
yet can speak in single-word responses.
• Receptive aphasia. Unable to comprehend the spoke word and can
speak but may not make any sense.
• Global aphasia. Combination of both expressive and receptive
aphasia

26. Recognizing Stroke: BEFAST
• Motor Loss:
 Hemiplegia, Hemiparesis
 Flaccid paralysis and loss of or ↓ in deep tendon reflexes (initial
clinical feature) → (after 48 hours) reappearance of deep reflexes
and abnormally ↑ muscle tone (spasticity)
• Communication Loss
 Dysarthria (difficulty speaking); Dysphasia (impair speech) or
aphasia (loss of speech); Apraxia (inability to perform a previously
learned action)
• Perceptual Disturbances and Sensory Loss:
 Visual-perceptual dysfunctions (homonymous hemianopia)
 Sensory losses: slight impairment of touch or more severe with
loss of proprioceptional; difficult in interrupting visual, tactile,
and auditory stimuli

27. Recognizing Stroke: BEFAST
• Impaired Cognitive and Psychological Effects:
 Frontal lobe damage: Learning capacity, memory, or other higher
cortical intellectual functions → impaired.
→ limited attention span, difficulties in comprehension,
forgetfulness, and lack of motivation.
 Depression, other psychological problems: emotional lability,
hostility, frustration, resentment, and lack of cooperation.

28. Arterial Circulation of the brain.

29. Clinical features of the stroke syndromes
- Total anterior circulation syndrome (TACS)
- Common symptoms:
 Hemiparesis
 Higher cerebral dysfunction (e.g. aphasia)
 Hemisensory loss
 Homonymous hemianopia (damage to optic
radiations)
- Common cause:
 Middle cerebral artery occlusion
(Embolism from heart or major vessels)

30. - Partial anterior circulation syndrome
(PACS)
- Common symptoms:
 Isolated motor loss (e.g. leg only, arm
only ,..)
 Isolated higher cerebral dysfunction (e.g.
aphasia, neglect)
 Mixture of higher cerebral dysfunction and
motor loss (e.g. aphasia with right
hemiparesis,..)
- Common cause:
 Occlusion of a branch of the middle cerebral
artery or anterior cerebral artery
(Embolism from heart or major vessels)

31. - Lacunar syndrome (LACS)
- Common symptoms:
 Pure motor stroke – affects two limbs
 Pure sensory stroke
 Sensory-motor stroke
 No higher cerebral dysfunction or
hemianopia
- Common cause:
 Thrombotic occlusion of small perforating
arteries
(Thrombosis in situs)

32. - Posterior circulation stroke (POCS)
- Common symptoms:
 Homonymous hemianopia (damage to
visual cortex)
 Cerebellar syndrome
 Cranial nerve syndromes
- Common cause:
 Occlusion in vertebral, basilar or
posterior cerebral artery territory
(Cardiac embolism or thrombosis in situs)

33. Acute ischemic stroke syndromes
according to vascular territory
Artery involved Syndrome
Anterior cerebral
artery
Motor and/or sensory deficit (leg>face, arm)
Grasp, sucking reflexes
Abulia, paratonic rigidity, gain apraxia
Middle cerebral
artery
Dominant hemisphere: aphasia, motor and
sensory deficit (face, arm >leg> food), may be
complete hemiplegia if internal capsule
involved, homonymous hemianopsia
Non-dominant hemisphere: neglect,
anosognosia, motor and sensory deficit (face,
arm> leg>foot), homonymous hemianopia

34. Artery involved Syndrome
Posterior cerebral
artery
Homonymous hemianopia: Alexia without
agraphia (dominant hemisphere); visual
hallucinations, sensory loss, choreoathetosis,
spontaneous pain (thalamus); III nerve palsy,
paresis of vertical eye movement, motor deficit
(cerebral peduncle, midbrain)
Penetrating
vessels
Pure motor hemiparesis (classic lacunar
syndrome)
Pure sensory deficit ;Pure sensory-motor deficit
Hemiparesis, hemolateral ataxia
Dysarthria/clumsy hand
Internal carotid
artery
Progressive or stuttering onset of MCA
syndrome, occasionally ACA syndrome as well
if insufficient collateral flow

37. Characteristics of stroke subtypes
Stroke type Clinical course Risk Factors Other clues
Intracerebral
Hemorrhage
Gradual progression during
minutes or hours
Hypertension, trauma, bleed
diatheses, illicit drugs, vascular
malformations.
Sex or other
physical activity
Subarachnoid
hemorrhage
Abrupt onset, severe
headache
Focal brain dysfunction less
common than with other
types
Smoking, hypertension, alcohol use,
genetic susceptibility (eg, polycystic
kidney disease, family history of
subarachnoid hemorrhage) and
sympathomimetic drugs
Sex or other
physical activity
Ischemic
(thrombotic)
Stuttering progression with
periods of improvement.
Lacunes develop over hours
or at most a few days; large
artery ischemia may evolve
over longer periods
Atherosclerotic risk factors (age,
smoking, diabetes mellitus, etc.)
Men > women. May have history of
TIA
May have neck bruit
Ischemic
(embolic)
Sudden onset with deficit
maximal at onset.
Clinical findings may
improve quickly
Atherosclerotic risk. Men > women.
History of heart disease (valvular,
atrial fibrillation, endocarditis)
Getting up at night
to urinate, or
sudden coughing or
sneezing.

41. Predictors of neurologic deterioration
included the following:
- Internal carotid artery (ICA) occlusion
- Brainstem infarction
- Middle cerebral artery (MCA) M1 segment
occlusion
- Territorial infarction
- Diabetes mellitus

42. Overview
• Intracerebral hemorrhage:
 Derived from arterioles or small arteries.
 The neurologic symptoms → ↑ gradually over minutes or a few
hours. (in contrast to brain embolism) do not begin abruptly and
are not maximal at onset.
• Subarachnoid hemorrhage:
 Releases blood directly into the cerebrospinal fluid (CSF) under
arterial pressure → rapidly increasing ICP.
 Death or deep coma ensues if the bleeding continues.
 Symptoms of SAH abruptly in contrast to the more gradual onset
of ICH.
 Headache is an invariable symptom
 No important focal neurologic signs unless bleeding → brain, CSF.

43. Overview
Brain ischemia
• Thrombosis:
 Atherosclerosis → most common cause
 Neurologic symptoms → fluctuate, remit, or progress.
• Embolism:
 Abrupt and usually maximal at the start.
 Unlike thrombosis, multiple sites within different vascular
territories may be affected when the source is the heart (eg, left
atrial appendage or left ventricular thrombus) or aorta.
 Systemic hypoperfusion:
 More general circulatory problem → brain and other organs.
 The neurologic signs are typically bilateral, diffuse and nonfocal

44. Initial General Assessment
Sudden loss of focal brain function → Core feature of the onset of
ischemic stroke → serious medical conditions.
→ The initial evaluation requires a rapid but broad assessment.
• Insuring medical stability
• Quickly reversing any conditions → patient’s problem
• Moving toward uncovering the pathophysiologic basic of the
patient’s neurologic symptoms.
• Determining if patients with acute ischemic stroke → candidates
for iv thrombolytic therapy or endovascular thrombectomy
 Time is of the essence in the hyperacute evaluation of stroke patients.
 The history, physical examination, serum glucose, oxygen saturation,
and a noncontrast CT scan → sufficient in most cases.

45. Initial General Assessment
• Airway, breathing and circulation:
o Assessing vital sign and ensuring stabilization of airway, breathing,
an circulation → All patients with critical illness.
Airways, Breathing, and Oxygen COR LOE
1. Airway support and ventilator assistance are
recommended for the treatment of patients with acute
stroke who have decreased consciousness or who have
bulbar dysfunction that causes compromise of the airway
I C-EO
2. Supplement oxygen should be provided to maintain
oxygen saturation >94%
I C-LD
3. Supplemental oxygen is not recommended in nonhypoxic
patients with AIS
III: No
benefit
B-R
4. Hyperbaric oxygen (HBO) is not recommended for
patients with AIS except when caused by air embolization
III: No
benefit
B-NR

46. Blood Pressure COR LOE
1. Hypotension and hypovolemia should be corrected to
maintain systemic perfusion levels necessary to support
organ function
I C-EO
2. Patients who have elevated BP and are otherwise eligible
for treatment with IV alteplase should have their BP
carefully lowered so that their systolic BP is <185 mmHg
and their diastolic BP is <110 mmHg before IV fibrinolytic
therapy is initiated.
I B-NR
3. The usefulness of drug-induced hypertension in patients
with AIS is not well established
IIb C-LD

47. Class IIb, LOE C-EO
Patient otherwise eligible for acute reperfusion therapy except that BP is >185/110 mmHg
Labetalol 10-20 mg IV over 1-2 min, may repeat 1 time; or
Nicardipine 5 mg/h IV, titrate up by 2.5 mg/h every 5-15 min, maximum 15 mg/h;
when desired BP reached, adjust to maintain proper BP limits; or
Clevidipine 1-2mg/h IV, titrate by doubling the dose every 2-5 min until desired BP
reached; maximum 21 mg/h
Other agents (eg, hydralazine, enalaprilat) may also be considered
If BP is not maintained ≤185/110 mmHg, do not administer alteplase
Management of BP during and after alteplase or other acute reperfusion therapy to maintain
BP ≤180/105 mmHg:
Monitor BP every 15 min for 2h from the start of alteplase therapy, then every 30 min
for 6h, and then every hour for 16h
Options to Treat Arterial Hypertension in Patients with AIS Who Are
Candidates for Acute Reperfusion Therapy*

48. Class IIb, LOE C-EO
If systolic BP >180-230 mmHg or diastolic BP >105-120 mmHg:
Labetalol 10 mg IV followed by continuous IV infusion 2-8 mg/min; or
Nicardipine 5mg/h IV; titrate up to desired effect by 2.5 mg/h every 5-15 min,
maximum 15 mg/h; or
Clevidipine 1-2 mg/h IV, titrate by doubling the dose every 2-5 min until desired BP
reached; maximum 21 mg/h
If BP not controlled or diastolic BP>140 mmHg, consider IV sodium nitroprusside
Management of BP during and after alteplase or other acute reperfusion therapy to maintain
BP ≤180/105 mmHg:
Options to Treat Arterial Hypertension in Patients with AIS Who Are
Candidates for Acute Reperfusion Therapy*
*Different treatment options may be appropriate in patients who have comorbid
conditions that may benefit from acute reductions in BP such as acute coronary event,
acute heart failure, aortic dissection, or preeclampsia/eclampsia

49. o Fever
- A primary central nervous system infection such as meningitis,
subdural empyema, brain abscess, and infective endocarditis.
- Common etiologies of fever including aspiration pneumonia and
urinary tract infection should also be excluded.
- Fever → contribute to brain injury:
 Enhanced release of neurotransmitters
 Exaggerated oxygen radical production
 More extensive blood-brain barrier breakdown
 Increased numbers of potentially damaging ischemic
depolarizations of the focal ischemic penumbra
 Impaired recovery of energy metabolism and enhanced inhibition
of protein kinase
 Worsen of cytoskeletal proteolysis

50. Temperature COR LOE
1. Sources of hyperthermia (temperature >38oC) should be
identified and treated, and antipyretic medications should
be administered to lower temperature in hyperthermic
patients with stroke
I C-EO
2. The benefit of induced hypothermia for treating patients
with ischemic stroke is not well established. Hypothermia
should be offered only in the context of ongoing clinical
trials
IIb B-R

51. • History
o Establishing the time of ischemic stroke symptom onset → main
determinant of eligibility for treatment with iv thrombolysis and
endovascular thrombectomy.
o Unable to provide a reliable onset time → defined as the time
patient was last known to be normal or at baseline neurologic status.
o Therapeutic window for iv thrombolysis ≤4.5h or mechanical
thrombectomy ≤24h from symptom onset.
→ need to be accurate but rapid.
o The history and physical examination → distinguish: other
disorders vs brain ischemia. Eg. Seizure, syncope, migraine,
hypoglycemia, hyperglycemia, or drug toxicity etc.
→ ask: take insulin or oral hypoglycemic agents, history of
epilepsy, drug overdose or abuse, or recent trauma.

52. o Diagnosing an ICH or SAH as soon as possible.
o Acute onset headache and vomiting → ICH/SAH > thromboembolic
stroke; abrupt onset of ↓ cerebral function without focal symptoms
→ favor the diagnosis of SAH.
o Ask: take anticoagulant drugs
→ The history → focus upon the time of symptom onset, the course of
symptom over time, possible embolic sources, items in the differential
diagnosis, and concomitant diseases.

53. Differential diagnosis of Stroke and TIA
“Structural” stroke mimics
• Primary cerebral tumours
• Metastatic cerebral tumours
• Subdural haematoma
• Cerebral abscess
• Peripheral nerve lesions
(vascular or compressive)
• Demyelination
“Functional” stroke mimics
• Todd’s paresis (after epileptic
seizure)
• Hypoglycaemia
• Migrainous aura (with or
without headache)
• Focal seizures
• Ménière’s disease or other
vestibular disorder
• Conversion disorder
• Encephalitis

54. Feature Stroke Stroke mimics
Symptom onset Sudden (minutes) Often slower onset
Symptom progression
Rapidly reaches
maximum severity
Often gradual onset
Severity of deficit Unequivocal
May be
variable/uncertain
Pattern of deficit Hemispheric pattern
May be non-specific
with confusion,
memory loss, balance
disturbance
Loss of consciousness Uncommon More common
Characteristic features of stroke and non-stroke syndro
mes (‘Stroke mimics)

55. • Physical examination:
o Careful evaluation of the neck and retroorbital regions → vascular
bruits, and palpation of pulses in the neck, arms, and legs →
absence, asymmetry, or irregular rate?
o Heart: Auscultate → murmurs?
o Lungs → abnormal breath sounds, bronchospasm, fluid overload, or
stridor.
o Skin → signs of endocarditis, cholesterol emboli, purpura,
ecchymoses, or recent surgery or other invasive procedures.
o Funduscopic examination → cholesterol emboli or papilledema.
o Head → Signs of trauma
o Tongue laceration → suggest a seizure
o Extremities → systemic arterial emboli, distal ischemic, cellulitis,
and deep vein thrombosis

56. Neurologic evaluation:
o Ischemia in different vascular territories → specific syndrome.
o Three most predictive examination findings → Facial paresis, arm
drift/weakness, and abnormal speech.
o National Institutes of Health Stroke Scale (NIHSS) → recommended
for all patients with suspected stroke.
o NIHSS score, composed of 11 items, total score of 0 to 42 → cut-
points of NIHSS score <5 for mild, 5 to 9 for moderate, and ≥10 for
severe stroke.
o 11 items: Level of consciousness (3), LOC questions (2), LOC
commands (2), Best gaze (2), Visual (3), Facial palsy (3), Motor arm
left/right (4), Motor leg left/right (4), Limb ataxia (2), Sensory (2),
Best language (3), Dysarthria (2), Extinction and inattention
(formerly neglect) (2)

57. Immediate Laboratory Studies
• Urgent brain imaging with CT or MRI → mandatory in all patients
with sudden neurologic deterioration or acute stroke.
→ All patients with suspected stroke → following studies urgently:
• Noncontrast brain CT or brain MRI
• Finger stick blood glucose
• Oxygen saturation
→ Other immediate tests:
• Electrocardiogram
• Complete blood count including platelets
• Troponin
• Prothrombin time and INR (international normalized ratio)
• Activated partial thromboplastin time,etc

58. Immediate Laboratory Studies
→ Thrombolytic therapy for acute ischemic stroke → not be delayed
while awaiting the results of hematologic studies.
• The only test that is mandatory before initiation of iv alteplase is
blood glucose.
• The following laboratory studies → in selected patients:
o Serum electrolytes, urea nitrogen, creatinine
o Liver function tests; toxicology screen; Blood alcohol level;
Pregnancy test in women of child-bearing potential
o Arterial blood gas if hypoxia is suspected
o Chest radiograph if lung disease is suspected
o Lumbar puncture if SAH is suspected
o Electroencephalogram if seizures are suspected
o Chest radiography, urinalysis and blood culture → if fever

59. Brain Imaging COR LOE
All patients admitted to hospital with suspected acute
stroke should receive brain imaging evaluation on arrival
to hospital. In most cases, noncontrast C (NCCT) will
provide the necessary information to make decisions
about acute management.
I B-NR
• Diagnostic testing → most cost-effect.
• Although diffusion-weighted magnetic resonance imaging (DW-MRI)
is more sensitive than CT for detecting AIS, routine use in all
patients with AIS is not cost-effect.
• NCCT scanning of all patients with acute stroke has been shown to
be cost-effective primarily because of the detection of acute ICH and
the avoidance of antithrombotic treatment in these patients.
AHA/ASA guideline

60. Other Diagnostic Test COR LOE
1. Only the assessment of blood glucose must precede
the initiation of IV alteplase in all patients
I B-R
2. Baseline ECG assessment is recommended in patients
presenting wit AIS, but should not delay initiation of IV
alteplase.
I B-NR
3. Baseline troponin assessment is recommended in
patients presenting with AIS, but should not delay
initiation of alteplase.
I B-NR

61. • Early signs of infarction on noncontrast CT:
o Hypoattenuation involving one-third or more of the middle
cerebral artery (MCA) territory
o Obscuration of the lentiform nucleus
o Cortical sulcal effacement
o Focal parenchymal Hypoattenuation
o Loss of the insular ribbon or obscuration of the Sylvian fissure
o Hyperattenuation of large vessel (eg, “hyperdense MCA sign”)
o Loss of gray-white matter differentiation in the basal ganglia

62. C: Caudate; L: lentiform; IC: internal capsule; I: Insular ribbon

63. Stroke Management Issues
• Fluid:
- Isotonic saline without dextrose → agent of choice for intravascular
fluid repletion and maintenance fluid therapy.
- Hypotonic fluids → exacerbate cerebral edema in acute stroke and
are less useful than isotonic solutions.
- It’s best to avoid fluids containing glucose → exacerbate
hyperglycemia.

64. Stroke Management Issues
• Hypoglycemia:
- Hypoglycemia → cause focal neurologic deficits mimicking stroke
→ Check the blood sugar and rapidly correct low serum glucose
(<60 mg/dL [3.3 mmol/L]) at the first opportunity.
• Hyperglycemia:
- Blood glucose level >126 mg/dL (>7.0 mmol/L)
- Hyperglycemia → augment brain injury: ↑ tissue acidosis from
anaerobic metabolism, free radical generation, and ↑ blood brain
barrier permeability.
- AHA/ASA guidelines → achieve: 140 to 180 mg/dL (7.8 to 10mmol/L)
- ESI guideline → achieve: >180 mg/dL (>10 mmol/L)

65. Stroke Management Issues
Glucose COR LOE
1. Evidence indicates that persistent in-hospital
hyperglycemia during the first 24 hours after AIS is
associated with worse outcomes than normoglycemia, and
thus, it is reasonable to treat hyperglycemia to achieve
blood glucose levels in a range of 140 to 180 mg/dL and
to closely monitor to prevent hypoglycemia
IIa C-LD
2. Hypoglycemia (blood glucose <60mg/dL) should be
treated in patients wit AIS.
I C-LD

66. Stroke Management Issues
• Swallowing assessment
- Dysphagia → common after stroke → risk factor for developing
aspiration pneumonia.
- Assess swallowing function prior to administering oral medication
or food.
• Head and body position:
- During the acute phase of stroke → position head & body→ the risk
of elevated ICP and aspiration, and comorbid cardiopulmonary
disease.
- Recommend keeping the head in neutral alignment with the body
and ↑ head of the bed to 30o for patients → risk:
• ↑ ICP (ie, ICH, cerebral edema,..)
• Aspiration (eg, dysphagia and/or diminished consciousness)

67. Stroke Management Issues
• Head and body position:
• Cardiopulmonary decompensation or oxygen desaturation.
- In the absence of these problems → keeping the head of bed in the
position → most comfortable for the patient.
• Blood pressure management:
- Before thrombolytic therapy is started → SBP ≤185 mmHg and DSP
≤110 mmHg → stabilized and maintained ≤180/150 mmHg for at
least 24 hours after thrombolytic treatment.
- For patients with ischemic stroke → not thrombolytic therapy → Not
be treated acutely unless the hypertension is extreme ( SBP >220 or
DBP >120 mmHg), or patient have active ischemic coronary disease,
heart failure, aortic dissection, hypertensive encephalopathy, or
pre-eclampsia/eclampsia.

68. Stroke Management Issues
• Blood pressure management:
- For patients with acute ICH → SBP 150-220 mmHg → acute lowering
of SBP to 140 mmHg; SBP >220mmHg → aggressive reduction of blood
pressure with a continuous iv infusion of antihypertensive
medication and frequent (every 5 min) BP monitoring → 140 to 160
mmHg is a reasonable target.
- Choice of antihypertensive agent: reversible and titratable
intravenous agents → best suited for precise blood pressure lowering
→ iv labetalol, Nicardipine, and Clevidipine as first-line
antihypertensive agents → rapid and safe titration to the goal blood
pressure.
- Iv Nitroprusside → second-line therapy.