A17. Diagnostic procedures in cerebrovascular disorders Flashcards

(48 cards)

1
Q

Cerebrovascular disorders epidemiology

A

are the third most common causes of death in the western world, after heart disease and cancer.

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2
Q

Cerebrovascular disorders include

A
  • all disorders in which an area of the brain is temporarily or permanently affected by ischemia or hemorrhage , and
  • one or more of the cerebral blood vessels are involved in the pathological process
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3
Q

Stroke types

A

Ischemic stroke (85%)
● Thrombotic (atherosclerotic)
● Embolic
● Haemodynamic
● Lacunar

Hemorrhagic stroke (15%)
● Subarachnoid (SAH)
● Intracerebral (ICH)

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4
Q

which stroke is more common

A

85% of strokes are ischemic, and
only 15% are hemorrhagic

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5
Q

List ischemic strokes

A

● Thrombotic (atherosclerotic)
● Embolic
● Haemodynamic
● Lacunar

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6
Q

List Hemorrhagic strokes

A

● Subarachnoid (SAH)
● Intracerebral (ICH)

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7
Q

Diagnostic procedures done in all patients suspected of cerebrovascular disorders

A

● Neuroimaging (CT or MRI)

● ECG (should not delay imaging or thrombolysis)

● Lab tests:
blood count,
INR,
serum electrolytes,
blood glucose,
CRP,
hepatic and renal functions

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8
Q

Neuroimaging incase of suspected cerebrovascular disorders.

A

(CT or MRI

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9
Q

Stroke protocol
what to do If suspected stroke patient

A
  1. ABCDE (remember glucose - hypoglycemia can mimic acute stroke!)
  2. Blood samples (urgent: Glucose, INR) and blood pressure is taken
  3. GCS, NIHSS: neurological screening assessment
  4. ECG (should not delay CT/MRI)
    (Point 1-4 is usually performed simultaneously (nurses, doctors, neurologist work at same time)
  5. CT or MRI (should be interpreted within 45 minutes)
  6. Thrombolysis (rtPA) considered if within therapeutic window (e-learning: 6 hours, internet: 4,5
    hours) and no contraindications
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10
Q

why do we check glucose in suspected stroke patient

A

hypoglycemia can mimic acute stroke

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11
Q

what do CT or MRI exclude

A
  • Primarily to exclude hemorrhage, but
  • also to visualize intracranial large vessel occlusion
  • and extent of irreversible damage

○ Hemorrhage: consult neurosurgeon
○ Ischemia: candidate for thrombolysis (exclude contraindications)

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12
Q

what to do incase patient who has hemorrhage stroke

A

consult neurosurgeon

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13
Q

what to do incase patient who has ischemic stroke

A

candidate for thrombolysis (exclude contraindications

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14
Q

therapeutic window of stroke thrombolysis (rtPA)

A

e-learning: 6 hours, internet: 4,5
hours)

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15
Q

rtPA stands for

A

Recombinant tissue plasminogen activators

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16
Q

what is mandatory to image within the therapeutic time window

A

■ Brain parenchyma (non-contrast CT or MRI)

■ Extra- and intracranial vessels ( CT- or MR angiography)

● If CTA or MRA cannot be performed, Doppler US might be a solution in order to detect intracranial vessel occlusion

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17
Q

brain parenchyma can be imaged by

A

■ Brain parenchyma
(non-contrast CT or MRI)

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18
Q

Extra- and intracranial vessels can be imaged by

A

( CT- or MR angiography)

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19
Q

what imaging can be used to detect intracranial vessel occlusion
If CTA or MRA cannot be performed

A

Doppler US might be a solution in order to detect intracranial vessel occlusion

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20
Q

what to do If unsure about therapeutic window - e.g in wake-up-strokes

A

DWI-FLAIR mismatch: if ischemia is seen on DWI, but not on FLAIR, it means that the stroke still is in the therapeutic window and can receive thrombolytic
therapy.
DWI-PWI mismatch: DWI shows infarct core, while PWI shows hypoperfused
tissue, and hence this mismatch shows the salvageable tissue (penumbra)

21
Q

In DWI-FLAIR mismatch what does it mean if ischemia is seen on DWI, but NOT on FLAIR,

A

it means that the stroke still is in the therapeutic window and can receive thrombolytic therapy.

Fluid attenuated inversion recovery

22
Q

In DWI-PWI mismatch: what does it mean when DWI shows infarct core, while PWI shows hypoperfused
tissue

A

hence this mismatch shows the salvageable tissue (penumbra)

23
Q

what is mandatory before thrombolysis

A

Hypoglycemia (glucose): can mimic acute stroke
Coagulopathies (INR): CI of thrombolysis (should be under 1,7 to perform)
Blood pressure (BP): hypertension increase hemorrhagic risk of thrombolysis
Hemorrhagic stroke: should be under 140 mmHg
Ischemic stroke:
■ Hyperacute phase: treat only if above 220 mmHg
■ If thrombolysis performed: treat if above 185 mmHg

24
Q

before thrombolysis in hemorrhagic stroke blood pressure should be

A

under 140 mmHg

25
when do we treat hypertension in ischemic stroke
■ Hyperacute phase: treat only if above 220 mmHg ■ If thrombolysis performed: treat if above 185 mmHg
26
what should be done Urgently, but should not delay thrombolysis
● ECG ● Blood count with plt (severe thrombocytopenia/anemia are CI for thrombolysis) ● Electrolytes
27
Diagnostic considerations in cerebrovascular diseases
● Presence of clinical signs (WHO) ● Hemorrhagic vs. ischemic (CT, MRI) ● Pathomechanism (thrombotic, embolic, hemodynamic, small vessel disease) ● Duration of signs ● Brain region (hemisphere, cerebellum, brainstem; territorial-borderzone) ● Anterior-Posterior ● Supplying vessel (carotid artery, vertebrobasilar, lacunar, ACA, MCA, PCA) ● Prognostic by signs (Bamford – OCSP) ○ TACI, PACI, POCI, LACI ● Etiology - TOAST ○ Large vessel atherosclerosis ○ Small vessel occlusion (lacuna) ○ Cardioembolism ○ Other determined cause ○ Unknown cause
28
4 questions to think/ask about in cerebrovascular diseases
1. Is it a neurological disease? 2. If yes, where is the lesion? 3. What pathological conditions may cause a lesion at this site? 4. In this patient, which of these conditions are most likely to be present?
29
list examination done incase of suspected Hemorrhagic stroke
● CT and possibly CT angio ● CSF examination if strong suspicion, but normal CT ● TCD (transcranial doppler) can detect and monitor vasospasms in SAH ● Test for coagulopathies (must be corrected with antidotes) and blood pressure (must be kept under 140 mmHg)
30
TCD (transcranial doppler) what is it used for
can detect and monitor vasospasms in SAH
31
diagnostics In TIA patients or patients with fast recovery
● Diagnostic work-up, especially urgent vascular imaging ● Ultrasound ● CTA or MR
32
Etiology of ischemic strokes
* Cerebral embolism * Thrombus * Small vessel occlusion (lipohyalinosis) * Systemic hypoperfusion
33
etiology of intracerebral hemorhage
* Ruptured cerebral artery or microaneurysm * Trauma * Reperfusion injury after ischemic stroke
34
etiology of SAH
* Ruptured berry aneurysm * Arteriovenous malformation Trauma (see “Traumatic brain injury”)
35
Ischemic stroke risk factors
Age > 65 years Hypertension Atrial fibrillation Diabetes mellitus Carotid artery stenosis
36
Intracerebral hemorrhage risk factors
Age > 65 years Hypertension Vasculitis Malignancy Ischemic stroke
37
risk factors of Subarachnoid hemorrhage
Hypertension Tobacco use Family history
38
Ischemic stroke clinical features
Sudden onset of focal neurologic deficits Embolic stroke: possibly, spectacular shrinking deficit
39
Intracerebral hemorrhage clinical features
Headache, confusion, nausea Sudden onset of focal neurologic deficits
40
Subarachnoid hemorrhage clinical signs
Rapid onset of severe headache Meningeal signs Sudden onset of focal neurologic deficits
41
when is Lumbar puncture done and in which type of stroke
Subarachnoid hemorrhage If imaging is negative but suspicion for SAH remains high. CSF may show xanthochromia. (the yellow discoloration of cerebrospinal fluid (CSF) caused by hemoglobin catabolism)
42
treatment of ischemic stroke
* tPA (if within < 4.5 hours of onset of symptoms) * Intra-arterial thrombolysis * Thrombectomy * Aspirin or clopidogrel for secondary prevention
43
treatment of intracerebral hemorrhage
* Reversal of coagulopathy * Blood pressure management * Surgical intervention if there are signs of herniation or increased ICP
44
treatment of SAH
* Reversal of coagulopathy * Blood pressure management * Prevention of vasospasm * Surgical clipping * Endovascular coiling
45
when is Surgical intervention done in intracerebral hemorrhage
if there are signs of herniation or increased ICP
46
pathology of ischemic stroke
Pale infarct → liquefactive necrosis and glial scarring
47
pathology of hemorrhagic stroke
Hematoma surrounded by pale infarct and edema → hemosiderin-lined cavity with glial scarring
48
For both ischemic and hemorrhagic strokes: * most important **nonmodifiable risk factor** and * the most important **modifiable risk factor.**
nonmodifiable risk factor: **age** the most important modifiable risk factor: **arterial hypertension**