Stroke: Pathology and medical management Flashcards
Stroke
Sudden loss of neurological function caused
by an interruption of blood flow to the brain
Due to clot (ischemic stroke)
Due to rupture of blood vessel (hemorrhagic
stroke)
Neurological disturbance lasts > 24 hours
Symptoms resolve within 24 hours =TIA
Transient ischemic attack, “mini stroke”
Prevalence of Stroke
2.7% men, 2.5% women≥18 yrs have history of stroke
Incidence of stroke
~795,000 each year
610,000 first attacks
185,000 recurrent attacks
Someone in the US has a stroke every 40 sec
Mortality of Stroke
Someone dies of stroke every 3‐4 mins
1/17 deaths inUS (2005)
53% deaths out of hospital
3rd leading cause of death
Types of Stroke
- ) Ischemic stroke (infarct)
- 87% all strokes
- Blockage in blood vessel - ) Hemorrhagic stroke
- Intracerebral hemorrhage (10%)
- Subarachnoid hemorrhage (3%)
Ischemic Stroke
Most common type (87% all strokes)
Blood clot blocks blood flow
Prolonged ischemia produces infarction
Atherosclerosis common cause of clots
“Thrombotic stroke”
Embolus can also cause occlusion in brain
“Embolic stroke”
Abrupt onset
AF (cardioembolic stroke)
~20% ischemic strokes are cardioembolic
Typically have worse prognosis; greater disability
Etiology of Ischemic Stroke
Atherothromboemolism (50%)
Small vessel disease (25%)
Cardiac embolism (20%)
Rare causes (5%)
General Risk Factors for Ischemic Stroke
Hypertension BP<120/80 have half lifetime risk of stroke of people with HT Heart disease, especiallyAF AF increases risk ~5‐fold % of strokes attributable to AF increases with age Diabetes 65% die from heart disease or stroke
Modifiable Risk Factors of Ischemic Stroke
Hypertension Heart disease Diabetes Smoking Obesity High cholesterol
Un-treatable Risk Factors of Ischemic Stroke
Age Sex Race Prior stroke Family history
Ischemic Penumbra
• Rapid intervention is critical • Ischemic core – cell death, infarction • Ischemic penumbra Restoring blood flow to the ischemic penumbra can minimize neurological deficit
Infarct Medical Management
t‐PA Tissue plasminogen activator Thrombolytic agent breaks up clot 3‐hour window “Time is brain” NIH Stroke Scale (NIHSS) Quantifies severity ▪ 0‐7mild ▪ 8‐16 moderate ▪ >16severe Nature of deficits Medical team, acute Used in decision making
Early warning Signs of Stroke
Sudden numbness or weakness of face, arm, leg,
especially on one side of body
Sudden confusion, trouble speaking or
understanding
Sudden trouble seeing in one or both eyes
Sudden trouble walking, dizziness, loss of balance
or coordination
Sudden severe headache with no known cause
Hemorrhagic Transformation
A possible complication of thrombolytic therapy with t‐PA Can occur naturally in the evolution of cerebral infarction Most common after embolic stroke
Cerebral Edema
Begins within minutes of infarction Can increase intracranial pressure (ICP) Signs of increased ICP: consciousness; coma HR Irregular respirations Unreacting pupils Vomiting Major problem with large infarcts Frequent cause of death in acute stroke
Hemorrhagic Stroke
< 20% all strokes
Abnormal bleeding in the brain
Caused by head injury or burst aneurysm
Intracerebral hemorrhage (ICH)
Bleeding into brain tissue
Subarachnoid hemorrhage (SAH)
Blood vessel rupture on brain surface, bleeds into
subarachnoid space
Loss of blood supply affects brain cell
function
Accumulated blood puts pressure on brain
tissue
Increased pressure on brain can cause death
Higher mortality rate than ischemic stroke
e.g. 38%vs.8‐12%
Despite greater mortality, recovery among
survivors is often better
Recovery pattern: slow for first 6 weeks, then
improve rapidly
Rehab!
Etiology of Hemorrhagic Stroke
Intracerebral hemorrhage (ICH) High blood pressure Aneurysm Illicit drugs (e.g. cocaine) Subarachnoid hemorrhage (SAH) Head injuries** (SAH due to head injury is not considered a stroke) Spontaneous SAH usually due to burst aneurysm Rupture of arteriovenous malformation
Symptoms of ICH
Sudden rise in ICP (both ICH and SAH) Begins abruptly Severe headache Signs of brain dysfunction Confusion, trouble speaking Impaired / loss of vision Large pupils Nausea, vomiting, seizures, loss of consciousness
Symptoms of SAH
Sudden rise in ICP
“Thunderclap headache”
Facial / eye pain, double vision, loss of peripheral
vision
Loss of consciousness
Sleepy and confused, unresponsive, difficult to
arouse
May feel restless
Stiff neck, headaches, vomiting, dizziness, low
back pain
Fever common first 5‐10 days
Complications of SAH
Hydrocephalus
Vasospasm
A second rupture
Hemorrhage Medical Management
CT or MRI ± spinal tap Very high ICPs are often fatal if prolonged Anticoagulants, thrombolytics, and antiplatelet drugs are NOT given Treatments to promote clotting e.g. in people taking anticoagulants
Cerebral Stroke Syndromes
Ischemic stroke Predict pattern of deficits when blood vessels become blocked Left and right hemisphere differences Clinically identifiable subtypes: Oxfordshire Community Stroke Project Classification Cerebral artery syndromes
Left Cerebral Hemisphere
Dominant hemisphere Speech and language Aphasia Slow and cautious Memory
Right Cerebral Hemisphere
Non‐dominant Spatial and perceptual Unilateral neglect Impulsive, poor judgment Short term memory