10/11 - CVA Pathology and Medical Management Flashcards
More common side for CVA
Left (possibly due to fluid dynamics of L vs R branch from aortic arch); MCA most common
Transient Ischemic Attack (TIA)
Transient episode of neurological dysfunction
Temporary disturbance in blood supply to the brain spinal cord or retina without permanent death of tissue.
Symptoms usually last ? 1 hour.
3-17% 90-day risk of a completed stroke.
Up to 50% occur within 48 hours of the TIA
Stroke
Disruption of the vascular supply to the brain brainstem or spinal cord that leads to infarction (death) of CNS tissue.
Symptomatic or silent.
Symptomatic strokes manifest by cerebral or spinal dysfunction caused by CNS infarction.
Silent strokes are documented CNS infarction that was asymptomatic
Stroke epidemiology
?795 000 strokes per year in the United States
?610 000 are first strokes
> 5 000 000 stroke survivors in the US
#1 cause of disability in the US
4th leading cause of death in the US (#2 worldwide)
4-8% recurrence in 1st 3 months
Overall 7-10% recurrence/year
Highest in first year
Survival*
~50% at 3 years
~33% at 10 years
*comorbidities common
Ischemic stroke
61-87%; Thrombotic Vs Embolic; Large Vs Small vessel; Arterial Vs Venous
Hemorrhagic
Intraparenchymal Vs Subarachnoid
Primary Vs Secondary (conversion)
Higher proportion of hemorrhage in children
Large vessel thrombotic stroke
Slow stuttering onset due to gradual occlusion +/- collateral circulation
Possibly preceded by TIA
Small vessel thrombotic ?lacunar? stroke
Associated with longstanding hypertension and diabetes
Basal ganglia internal capsule and brainstem
Cardioembolic Etiologies in Ischemic Stroke
Valvular atrial fibrillation Nonvalvular atrial fibrillation Acute myocardial infarction Bacterial endocarditis DVT with a patent foramen ovale Mitral valve prolapse Prosthetic mechanical heart valves Possible injury in multiple vascular distributions
Cerebral venous thrombosis
Relatively rare
Higher risk in peripartum period OCPs + smoking coagulopathies
Hemorrhagic Stroke facts
Intraparenchymal (75%) vs. subarachnoid (25%) Fast large volumes of blood Increased mortality If survived decreased morbidity BP and ICP control MAP = 1/3 (SBP-DBP) + DBP MAP-ICP=CPP Vomiting systolic BP >220 mm HG severe headache coma decreased level of consciousness and progression over minutes-hours suggest hemorrhage.
Rapid deterioration in neurological status is common
Intraparenchymal Hemorrhagic Stroke
75% of hemorrhagic strokes
Hypertensive hemorrhages
Rupture of micro-aneurysms
Putamen»thalamus pons cerebellum and cerebral hemispheres.
Non-hypertensive hemorrhages
Sympathomimetic agents
Cavernous angiomas amyloid angiopathy intracranial tumors bleeding disorders trauma vasculitis hemorrhagic conversion infection
Subarachnoid Hemorrhagic Stroke
25% of hemorrhagic strokes Progressive deficits over minutes to hours Headache and decreasing consciousness Etiologies: Saccular aneurysms Most common cause of SAH 45 % risk of death in the 1st 30 days Most within a few days Arteriovenous malformations (AVMs)
EMS Management of stroke
Airway breathing and circulation (ABC) Cardiac monitoring Intravenous access Oxygen if needed Rapid identification of stroke/time of onset Rule out (and treat) stroke mimics Keep NPO (no food or drink) Alert receiving ED Rapid transport to closest appropriate facility
ED Evaluation
General medical examination Identify contributing factors: Drug exposures trauma cardiac conditions NIH Stroke Scale Glasgow Coma Scale Dysphagia screen Airway breathing and circulation (ABC) Adequate hydration Treat elevated temperatures Glucose control Cardiac monitoring for 1st 24 hours Cautious initial approach to HTN
Non-enhanced brain CT scan (NECT) (Medical Diagnosis)
The acute study of choice
Quick and affordable
Blood and bone visible
Radiation exposure
Does not show brain tissue changes such as hypoxia/anoxia
Helps identify nonvascular etiologies
E.g. brain tumor
Certain findings may predict hemorrhage with TPA
Early infarct signs including edema and mass effect
Poor visualization of small cortical and subcortical acute infarcts
Not as useful for imaging the ?posterior fossa? because of bone artifacts
Vascular Evaluation
Conventional angiogram Still appears to be gold standard Magnetic Resonance Angiogram (MRA) CT angiogram Carotid ultrasound Transcranial doppler ultrasound
Magnetic Resonance Imaging
Better than CT Identifies: Acute small cortical strokes Posterior fossa lesions Acute vs. chronic lesions Subclinical satellite lesions May be preferable when TPA is not considered No radiation exposure
Considerations: More time consuming and less available Patient contraindications Claustrophobia Internal devices Metal implants
AHA/ASA Guidelines for Ischemic Stroke - Medical Treatment
Airway breathing and circulation (ABC) Airway protection in dysphagia or decreased LOC/NPO Adequate hydration Treat elevated temperatures Glucose control Cardiac monitoring for 1st 24 hours Cautious initial approach to HTN Oxygen only if hypoxic Identify etiology of hypovolemia or hypotension
AHA/ASA Guidelines for Ischemic Stroke - Medical Treatment
Intravenous (IV) TPA given in ? 3 hours of stroke onset in appropriate patients
Possible expansion of window to 4.5 hours in selected patients
SBP <120
PT implications?
AHA/ASA Guidelines for Hemorrhagic Stroke ? Medical Treatment
ABCs Rapid transport Immediate imaging Careful blood pressure management Normalize fluid balance and electrolytes Control seizures Normalize body temperature Correct any bleeding disorders (specific to the problem) DVT prophylaxis Clot evacuation and ventricular drainage as required
Pressure Monitors
Control intracranial pressure (ICP)
Elevate head osmotherapy (mannitol) hyperventilation barbiturate coma sedatives ventricular monitors lasix
Risk of decreasing cerebral perfusion pressure
Cerebral perfusion pressure = mean arterial pressure ? intracerebral pressure (CPP=MAP-ICP)
