Stroke

Stroke

Causes
1. Atherothrombosis (23%)
  1. 30 to 50% are preceded by a TIA
  2. Preferential location for atheromas
    1. Aortic arch
    2. Bifurcation of the carotid artery
      1. Easily picked by doppler US
        For the other vessels you can do CT angiography or MRI angiography
    3. Carotid syphon
    4. Bifurcation of the middle cerebral artery and the anterior communicating artery
2. Cardioembolic stroke (15%)
3. Pathologies of small vessels (lacunar stroke) (18%)
  1. Basal ganglia and thalamus
  2. Brainstem (particularly the pons)
4. Cryptogenic stroke (27%)
5. Haemorrhagic stroke (15%)
6. Causes of hemorrhagic stroke
  1. Atherothromboembolism
    1. Embolus
    2. Occlusion
    3. Reduced perfusion
    4. Dolicoectasy
  2. Inflammatory cerebrovascular pathologies
    1. Vasculitis-arteritis
      1. Major causes
        In old people giant cell arteritis
        Takayasu arteritis
      2. Minor causes
    2. Secondary vasculitis associated to other pathologies
  3. Congenital
  4. Arterial dissection
  5. Traumatic injuries
  6. Metabolic diseases
  7. Coagulopathies
  8. Cerebral hypoperfusion
7. The major origins of embolism are
  1. Arterial atherothrombosis
  2. Cardiogenic sources
  3. Paradoxical embolism from DVT
8. Conditions affecting small vessels
  1. Major
    1. Simple diseases of the small vessels (hyaline atherosclerosis)
    2. Complex diseases of the small vessels
  2. Minor
    1. Cerebral amyloid angiopathy
    2. CADASIL
Dissection
1. 2 major consequences
  1. Intramural hematoma
  2. The wall may break and the blood may go internally or externally
2. Natural history
  1. If risk of an aneurism (sub-adventitial dissection), better not to give anticoagulants
  2. If risk of subintimal dissection, better to give anticoagulants
3. Epidemiology
  1. ICA dissection: 2.5-3/100000
  2. Vertebral A. dissection: 1.4/100000
4. Classification
5. Risk factors
  1. Intrinsic
    1. Fibromuscular dysplasia, Marfan’s S
    2. Associated to other pathologies
    3. Connective tissue pathologies
    4. Arterits
  2. Extrinsic
    1. Minor traumatic injuries
    2. Recent upper airways infection that produce some local inflammatory reaction
6. Local clinical manifestations
  1. ICA
    1. Headache
    2. Partial Horner's syndrome
    3. IX, X, XI e XII cranial nerves involvement by compression
  2. Vertebral artery
    1. Headache and cervical pain
  3. The main symptom that informs you that you are facing a dissection is pain: headache
7. Ischemic clinical manifestations
  1. ICA (49-84%)
  2. Vertebral artery (77-96%)
8. Classification
  1. Traumatic/spontaneous
    1. Sudden turning of the head
    2. Strong neck massage
    3. Hyperextension of the head
    4. Helmet closure
  2. Symptomatic/Asymptomatic
  3. Single/Multiple
  4. Intracranial/Extracranial
Warning signs that a stroke is taking place
1. Sudden weakness
  1. But not all strokes produce weakness
  2. It is contralateral
2. Contralateral hemiparesis and contralateral hemiplegia
3. Hemianesthesia
4. Aphasia or neglect, plus decrease in speech production or dysarthria
5. Loss of vision
  1. If the whole MCA is affected
  2. If only a part is affected, we have quadrantanopsia
6. Unexplained dizziness, unsteadiness or sudden fall
  1. The cerebellum or cerebello-vestibular system are involved
Diagnosis
1. Imaging
  1. Not possible (with few exceptions) to perform an angiography because by injecting contrast in a stroke patient you will further damage the site of the lesion due to the breakdown of the BBB in stroke
2. Other exams
  1. EEG
    1. Distinguish between a real phenomenon and a hysteric seizure
  2. Electrocardiogram
  3. Chest x-ray
  4. Hematological studies
  5. Serum electrolytes, blood glucose, renal and hepatic chemical analysis
Prevention
1. Anticoagulation
  1. Heparin (initially) + oral anticoagulants (chronic therapy)
  2. When we believe the stroke is of embolic origin
    1. We know patient is in AF or evidence from CT studies
    2. If not, don't do it
  3. Usually we wait 7 -10 days after the acute event before starting a secondary prevention with anticoagulants
  4. The risk of transformation is extremely high in the first 36 hours and then it gradually decreases
2. 3 strategies
  1. Mass strategy to try to prevent it in all those who are at risk
  2. High risk strategy to prevent stroke only in the patients who are at a very high risk of an event
  3. Concentrate instead on those who already had a primary event thus to prevent recurrences (form of secondary prevention)
3. Control the risk factors
  1. Apply an antiplatelet or anticoagulant treatment
    1. Antiplatelet drugs are to be used only in case of atherothrombotic stroke (no effect on hemorrhagic or lacunar stroke)
  2. In case of hypertension, secondary prevention by ACE-I therapy
  3. Modify life style risk factors
4. Carotid stenosis treatment
  1. If the stenosis is >70%
    1. Not indicated if <50%
  2. If the patient has a symptomatic stenosis
  3. Either surgically or by stenting
5. Patent foramen ovale
  1. in selected cases when there is clear evidence that its patency may be a source of emboli, the closure of the foramen is absolutely indicated
6. Aspirin (antiplatelet) therapy
  1. Antiplatelet drugs
    1. Dipiridamol + aspirin
      1. Treatment of choice
    2. Clopidogrel
  2. Reasonable if we cannot perform fibrinolysis because it is too late
  3. Better not to perform it immediately except if the stroke was of a huge entity
7. Antihypertensive secondary prophylaxis
  1. No evidence that it is beneficial in patients with stroke
  2. Indicated in patients with stroke who have aortic dissection, acute myocardial infarction, heart failure, ARF, hypertensive encephalopathy
  3. ACE-I therapy
8. Anticoagulation in stroke is mandatory only when we have a TIA
  1. Prevent second wave of embolization
  2. Mandatory, start as soon as possible when: TIA or ischemic stroke with complete recovery within 1-2 days due to atrial fibrillation
  3. Mandatory, best time to start unclear: Non-disabling ischemic stroke due to atrial fibrillation, non hemorrhagic transformation
9. Emergency administration of Abciximab
Treatment
1. Acute stroke treatment
  1. 1 - Draw blood
  2. 2 - Perform EKG
  3. 3 - Head CT
  4. If it is more than 6 hours before then you cannot do any appropriate intervention because it becomes too dangerous
  5. If it is less than 4.5 hours, we can do something
  6. The main factors determining the risk of hemorrhagic transformation upon reperfusion are
    1. Time
    2. Extension
    3. Blood pressure
  7. Perform thrombolysis
2. Stem cell therapy
3. Rehabilitation
  1. 25% of patients die, but 40% remain alive with disabilities
4. Thrombolysis
  1. Pharmacological
    1. recombinant tissue plasminogen activator
      1. The injected amount has to be 0.9 mg/kg but we cannot exceed 90 mg as a global dose
    2. They digest fibrinogen, so less fibrin is available to form the fibrin component of the thrombus
  2. Mechanical
  3. Mandatory when major vessels are hit
  4. To be effective it has to be performed within 3 hours from beginning of stroke, but about 25% of strokes happen during night
    1. Possible to understand when it happened with MRI diffusion technique
  5. If we do nothing, ~40% of the vessels will reopen spontaneously
  6. Easier to destroy an embolus than a thrombus
  7. Must be avoided when the patient is under anticoagulation therapy or had recent surgery
  8. Better if it is intravenous (but if you are in a good center, also intra-arterial
    1. Disadvantages of arterial
      1. More time consuming
      2. More invasive (->more risk)
    2. Intra-arterial is indicated in case of vertebra-basilar artery occlusion
  9. Ultrasound thrombolysis is last strategy
5. Reduce the amount of edema
  1. Steroids
  2. Osmotic treatment (the most important one)
  3. Decrease in blood pressure
  4. Opening the brain
  5. Immediate carotid endoartectomy or int.radiology
6. Mandatory to perform CXR, because pulmonary infection is very frequent

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	Created by LewisLewis over 10 years ago