CerebroVascular Accident

CerebroVascular Accident
CVA
Definition:
Sudden loss of brain functions result from disruption of blood supply to part of brain disruption may cause temporary or permanent loss of brain function, movement, sensation, thought, speech and memory.

Risk factors:
Hypertension, heart disease, elevated cholesterol, diabetes mellitus, obesity, carotid stenosis, polycythemia, smoking and alcohol intake à all of this develop atherosclerosis.

Pathophysiology/Etiology
1. Partial or complete occlusion of a cerebral blood vessel resulting from cerebral thrombosis (due to arteriosclerosis) or embolism.
2. Ischemia (penumbra) related to decreased blood flow to an area of the brain secondary to systemic disease, such as cardiac or metabolic disease.
# because of ischemia à brain compensates by vasodilatation to ↑ blood flow à if not enough and there is mismatch between O2 delivery and O2 consumption called (misery perfusion).
If not treat, the underling cause fails compensatory mechanism à cell failure à cell death.
3. Hemorrhage occurring outside the durra (extradural), beneath the dura mater (subdural), the subarachnoid space (subarachnoid), or within the brain substance (intracerebral).

Clinical Manifestations
Clinical manifestations vary depending on the vessel affected and the cerebral territories it perfuses. (Symptoms are usually multiple).
A. Motor loss: loss of voluntary control over motor movement à rang from hemi paresis to paraplegia or quadriplegia.
Early signs of motor loss:
Flaccid paralysis with loss of deep tendon reflexes for 48 hr then Spasticity (abnormal increase in muscle tone) of the extremities on the affected side.
B. Communication loss:
1. Aphasia: unable to read, write, or comprehend.
2. Dysarthia: difficulty in speaking.
3. Apraksia: inability to perform the previously learned action.
C. Cognitive defect: defect in long and short term memory, decrease in attention span, altered judgment process.
D. Sensory loss: less of touch.
E. Perceptual visual changes: inability to interpret the sensation.
F. Emotional defect: loss of emotional control, stress à derision.


Diagnostic Evaluation
1. Carotid ultrasound-to detect carotid stenosis.
2. CT-to determine cause and location of stroke.
3. Cerebral angiography-to determine extent of cerebrovascular insufficiency.
4. MRI may be done to localize ischemic damage.

Management
A. Acute Treatment
1. Support of vital functions-maintain airway, breathing, oxygenation, circulation.
2. Reperfusion and hemodilution with volume expanders (dextran or pentastarch); thrombolytic therapy with tissue plasminogen activator (t-PA, Activase) or urokinase (Abbokinase); vasodilation with nimodipine (Nimotop).
3. Management of increased ICP.
4. Diuretic treatment to reduce cerebral edema, which peaks 3 to 5 days after infarction.
5. Calcium channel blockers to reduce blood pressure and prevent cerebral vasospasm.
B. Subsequent Treatment
1. Anticoagulation after hemorrhage is ruled out.
2. Antiplatelet agents such as ticlopidine (Ticlid) or aspirin.
3. Antispasmodic agents for spastic paralysis.
4. Physical therapy and rehabilitation program.
5. Treatment of poststroke depression with antidepressants.


Complications
1. Aspiration pneumonia
2. Spasticity, contractures: (abnormal increase in muscle tone) of the extremities on the affected side.
3. Deep-vein thrombosis; pulmonary embolism
4. Post stroke depression
5. Brain stem herniation


Nursing process
Nursing Assessment
1. Maintain neurologic flow sheet during acute phase.
2. Assess for voluntary or involuntary movements, tone of muscles, and presence of deep tendon reflexes (reflex return signals end of flaccid period and return of muscle tone).
3. Also assess mental status, cranial nerve function, sensation/proprioception, bladder control.
4. Monitor bowel and bladder function.
5. Monitor effectiveness of anticoagulation therapy.
6. Frequently assess level of function and psychosocial response to condition.

Nursing alert:
Prothrombin time levels are report in international normalized ratios (INR). Anticoagulants are adjusted to maintain an INR at 2.0 to prevent stroke and the associated complication of intracranial and subdural hemorrhage. Report international normalized ratios that are elevated to reduce the risk of bleeding or decreased levels to adjust therapy to be more effective.