Stroke Lecture Flashcards
STROKE: Defined
Destruction of a portion of brain tissue as a result of circulatory failure in the distribution of a specific arterial vessel
Ischemic Stroke (84%) - Thrombotic (53%): Cause, Onset, Risk factors
Thrombotic (53%)
Cause: Platelet Aggregation/Vessel Occlusion
Onset: During Sleep when BP is lowest
Risk Factors: - Large Vessel Disease - Atherosclerosis - Dissection - Arteritis Small Vessel Disease - Chronic Hypertension - Lacunar : small subcortical infarcts
Hemorrhagic Strokes (16%)
Bleeding around brain
SAH (Subarachnoid Hemorrhage) (6%)
Ruptured Aneurysm
Bleeding inside brain (10%) ICH (Intracerebral Hemorrhage) Hypertension Cocaine Many other IVH (Intraventricular Hemorrhage) Usually an extension of ICH Rarely isolated
Stroke Symptoms
Sudden onset of weakness / numbness of face, arm, leg Sudden decrease in level of consciousness Facial droop Confusion Aphasia Dysarthria Visual field deficit (difficulty seeing with one or both eyes) Hemisensory deficits Ataxia Difficult walking Dizziness Severe headache and vertigo Nausea or vomiting
Acute Management of
Ischaemic Stroke
Accurate diagnosis of stroke Definition of stroke type Acute general medical care Re-perfusion Neuroprotection
Pathology
Ischemia energy deficit
Na+/K+ channel failure in the cell
Cause cytotoxic edema: shift of water into intracellular compartment
Leads to a narrowing of the extracellular matrix
Restricted diffusion of water within the cell
Increase signal which can be measured with DWI
Core and Penumbra
• In the absence of blood flow, available energy can maintain neuronal viability for 2-3 minutes
• In the brain, ischemia is incomplete, with collateral supply
• Cerebral ischemia = central irreversibly infarcted tissue core surrounded by peripheral region of stunned cells, the ‘penumbra’
• The penumbra is potentially salvageable with early
recannalization
Penumbra
When a cerebral artery is occluded, a core of brain tissue dies rapidly (irreversible)
Surrounding this infarct core is an area of brain that is hypoperfused but does not die quickly, because of collateral blood flow,
This surrounding area is penumbra (salvageable)
Its fate depend on the reperfusion of the ischemic brain
Will also die unless early recanalization is present
Thrombolysis via tPA, thrombus removal, etc.
Coagulation
Coagulation Factors
Fibrinogen
Fibrin
Fibrinolysis
Tissue Plasminogen Activator
Plasminogen
Plasmin
Fibrinolysis
Recombinant Tissue Plasminogen Activator (rt-PA)
- Structure. Naturally occurring plasminogen activator present in most normal and neoplastic cells, Mr = 68,000 daltons. Preferentially activates plasminogen bound to fibrin.
- Mechanism of action. Converts plasminogen to plasmin, which lyses fibrin clots.
- NIND study (1995); European Cooperative Acute Stroke Study (ECASS I, ECASS III); Alteplase Thrombolysis for Acute Noninterventional Therapy in Ischemic Stroke (ATLANTIS trial)
- Approved in US in 1996; Approval in Canada in 1999
- Indications. Alteplase is FDA approved for MI and acute ischemic stroke
- Method of administration. I.V. or I.A. injection
- Major side effects. Bleeding.
Thrombolysis
Alteplase (0.9mg/kg) - Within 4.5 hours of the stroke.
The efficacy of thrombolytic drugs depends on the age of the clot. Older clots have more fibrin cross-linking and are more compacted or in plain English older clots are more difficult to dissolve.
Beyond that time, the efficacy diminishes and higher doses are generally required to achieve desired lysis and the great the risk of unwanted complications.
10% of total dose bolus 2-3 mins
90% of total dose infuse over 60 mins
Risks: Hemorrhagic Transformation
Occurs in ~ 3% patients with ischemic stroke ~ 4% patients who received tPA (within 36 hrs of infusion)
Cause:
Ischemic brain and damaged blood vessels
Injured blood vessels become “leaky”
Restored blood flow results in hemorrhage
Occurrence influenced by:
Size and location of infarct; Degree collateral circulation;
Use of anticoagulants and interventions;
Increased thrombolytic dose; Treatment initiated > 3h;
Elevated blood pressure; NIHSS > 20;
Acute hypodensity or mass effect.
Hemorrhagic Transformation - symptoms
Neurological worsening
Increased BP
Respiratory changes
Hemorrhagic Transformation - management
CT
Control BP
Avoid use of anticoagulants
Possible surgery