Stroke Flashcards
Define stroke
Rapidly developing clinical signs of focal (or global) disturbance of cerebral function, lasting more than 24 hours or leading to death, with no apparent cause other than that of vascular origin
TRANSIENT ISCHAEMIC ATTACK
Transient ischemic attacks are episodes of temporary and focal dysfunction of vascular origin, which are variable in duration, commonly lasting from 2 to 15 minutes, but occasionally lasting as long as a day (24 hours). They leave no persistent neurological deficit.
What is an Ischaemic stroke?
An episode of neurological dysfunction caused by focal cerebral, spinal, or retinal infarction
What is a Stroke caused by ICH (Intracerebral hemorrhage)?
Rapidly developing clinical signs of neurological dysfunction attributable to a focal collection of blood within the brain parenchyma or ventricular system that is not caused by trauma
What is a Stroke caused by subarachnoid hemorrhage?
Rapidly developing signs of neurological dysfunction and/or headache because of bleeding into the subarachnoid space (the space between the arachnoid membrane and the pia mater of the brain or spinal cord), which is not caused by trauma.
What is a Stroke caused by cerebral venous thrombosis?
Infarction or hemorrhage in the brain, spinal cord, or retina because of thrombosis of a cerebral venous structure.
What is a Stroke not otherwise specified?
An episode of acute neurological dysfunction presumed to be caused by ischemia or hemorrhage, persisting ≥24 hours or until death, but without sufficient evidence to be classified as one of the above.
Classification of Stroke
1. Ischemic stroke (80%)
i) Thrombotic (50%): These are caused by a blood clot (thromus) that develops in the brain’s blood vessels (usually seen in older persons, especially those with high cholesterol and atherosclerosis, or diabetes.
They can be further divided into:
1. Large vessel thrombosis 2. Small vessel thrombosis
ii) Embolic (30%): These are caused by a blood clot or plaque debris that develops elsewhere in the body and then travels to one of the blood vessels in the brain through the bloodstream
Types:
a. Cardioembolic eg. Due to atrial fibrillation
b. Artery- artery embolic
- Haemorrhagic Stroke (20%): Hemorrhagic strokes occur when an artery supplying the brain ruptures and bleeds. It can be divided into:
i) Intracerebral haemorrhage (15%): Bleeding is from the arteries within the brain.
ii) Subarachnoid haemorrhage (5%): Bleeding is in the subarachnoid space usually due to a ruptured cerebral aneurysm
Clinical classification of stroke
1- Completed stroke: Complete focal neurological deficit at onset and lasting > 24hrs.
2- Progressive stroke/Stroke in evolution: symptoms worsening gradually or in stepwise fashion over hrs or days with symptoms lasting >24 hrs
3- Transient ischemic attack (TIA): symptoms lasting < 24hrs
Difference between haemorrhagic and ischaemic stroke
In a hemorrhagic stroke, blood leaks into brain tissue
In an ischaemic stroke, the clot stops blood supply to an area of the brain
What are 5 Non-modifiable risk factors of stroke?
Age
Race
Male gender
Previous stroke
Family hx
What are modifiable risk factors of stroke?
Hypertension
Diabetes mellitus
Alcohol
Cigarette smoking
Dyslipidemia
Physical inactivity
Cardiac risk factors
Hemoglobinopathies
Vasculitis – HIV, syphilis,
Connective tissue diseases
Causes of Hemorrhagic Stroke (7 A’s of hemorrhagic stroke)
What is the most common cause?
- Chronic hypertension (rupture of Charcot-Bouchard aneurysms, Saccular aneurysms)
- AV malformations
- Amyloid angiopathy,
- Anticoagulant therapy (Warfarin, Heparin)
- Antiplatelets
- Angioma (Cavernous hemangioma)
- Amphetamines and other Drugs-cocaine, sympathomimetics
Most common cause is HYPERTENSION
What are the areas of infarction in the brain?
Core area: infarct with irreversible damage (dead area) <10% cerebral bloos flow
Penumbra: tissue at risk, sustains reversible damage (dying area) < 20% cerebral blood flow
Oligemia: viable tissue, no infarct or risk
PATHOPHYSIOLOGY ISCHAEMIC STROKE
- Lack of oxygen supply to ischaemic neurones
- ATP depletion
- Membrane ions system stops functioning
- Depolarisation of neurones
- Influx of calcium
- Release of neurotransmitters, including glutamate, activation of N-methyl-D-aspartate and other excitatory receptors at the membrane of neurones
- Further depolarisation of cells
- Further calcium influx
Pathophysiology of Hemorrhagic Stroke
Explosive entry of blood into the brain parenchyma structurally disrupts neuronal activity by:
- Compression of neurons and vessels leading to additional ischemic damage
- Cerebral oedema
- Splitting neuronal planes
- Vasospasm from Direct neurotoxicity of blood
The above 4 mechanisms leading to severely elevated Intracranial pressure leading to brain herniation and death
What are the Clinical Features of Ischemic stroke & Intracerebral hemorrhage?
(a) General features
(b) MCA distribution
(c) PCA distribution
(d) Internal Capsule
(a) General features – LOC (loss of consciousness), vomiting, seizures, HA (headache)
(b) MCA distribution
– contralateral weakness (face & arm > leg)
+ aphasia (R)(difficulty communicating/speaking) because the left MCA supplies Broca’s areas
+ sensory neglect (L) (they neglect sensations on the opposite side of the body)
(c) PCA distribution – Homonymous hemianopia (loss of vision in the same half of both eyes) + other motor deficits
(d) Internal capsule – sensorimotor loss (face=arm=leg), marked dysarthria (slurred speech), no cortical deficits eg aphasia
ACA distribution
- contractural weakness of lower extremities > face and upper extremities and sensory loss
abulia: decrease motivation or desire to participate in activities, akinetic mutism
What are Lacunar Syndromes = Small vessel syndromes?
What’s are they usually associated with?
Lacunar syndromes are clinical manifestations of lacunar infarcts, which are small (<15 mm) subcortical ischemic strokes affecting the deep penetrating arteries of the brain. These infarcts occur due to occlusion of small branches of larger cerebral arteries.
Lacunar strokes do not involve the cerebral cortex, so they lack cortical signs (no aphasia, agnosia, neglect, or visual field deficits).
Indicate occlusion of perforating arteries in the subcortex, brainstem, or cerebellum,
often associated with chronic hypertension and diabetes mellitus
may be clinically silent, (only seen on imaging), or result in stroke syndromes involving densely packed white matter tracts with specific localization patterns.
The most commonly described small vessel syndromes include:
- pure motor: Contralesional hemiparesis
- pure sensory: Contralesional hemisensory loss
- sensorimotor: Contralesional
weakness and numbness - ataxic hemiparesis: Contralesional
(mild to moderate) hemiparesis and limb ataxia out of proportion to the degree of weakness - dysarthria-clumsy hand syndrome; Slurred speech and (typically fine motor)
weakness of contralesional hand
A less common, but striking, small vessel syndrome manifests as hemiballism from infarction in the subthalamic nucleus: Contralesional limb flailing or dyskinesia
INVESTIGATIONS for lacunae syndromes
Imaging – non-enhanced CT Brain
Blood workup – FBC, ESR, Glucose, lipid profile, E & U, Cr, (± HIV, VDRL, Clotting profile, autoantibodies for individual cases), lipid profile
ECG, ECHO
± Carotid Doppler (ischaemic stroke)
CXR,
Principles of Acute Ischaemic Stroke Care
(1) achieve timely recanalization of the occluded artery and reperfusion of the ischemic tissue
(2) optimize collateral flow
(3) avoid secondary brain injury.
Management of stroke; General measures
- Stabilise; ABCs
- If applicable care of the unconscious patient (HDU/ICU, careful nursing, attention to airway and vital signs, regular turning & skin care, oral hygiene via suctioning, irrigation of the eyes ± taping, sphincter care, feed – IV, NG, PEG)
- Monitor blood pressure
- Assess swallowing (gag reflex ± swallow test); NPO for the 1st 24 hours post stroke
ISOTONIC IVFs ONLY - Early physiotherapy
- Insulin for elevated blood glucose (Known DM or not)
MANAGEMENT; Indications for antihypertensive use in acute ischemic stroke
BP > 220/120mmHg on more than 2 occasions or MAP > 140 (EXCLUDE pain, raised ICP,)
Associated hypertensive emergencies
Acute pulmonary edema
Acute kidney dysfunction
Hypertensive encephalopathy
Aortic dissection
DO NOT CRASH/RAPIDLY LOWER THE BP
Which arteries supply the:
- Lateral potions of the Frontal, Parietal and Temporal lobes
- Medial portion of the Frontal and Parietal lobes
- Cerebellum and Brain Stem
- Occipital lobe
- Lateral potions of the Frontal, Parietal and Temporal lobes: Middle Cerebral Arteries
- Medial portion of the Frontal and Parietal lobes: Anterior Cerebral Arteries
- Cerebellum and Brain Stem:
branches of the Vertebral (supplies medulla, posterior and inferior cerebellum)
and Basilar artery (supplies pons, superior, anterior and inferior cerebellum) - Occipital lobe: Posterior Cerebral Artery (which also supplies the temporal lobe, thalamus and midbrain)
The parts of the primary motor cortex in the frontal lobe that control the legs and arms & face are supplied by which major arteries?
Name the parts and the arteries
Primary motor cortex controls voluntary movement of skeletal muscles
Legs and personality: controlled by the medial portion of the primary motor cortex and this is supplied by the ACA
Arms, face and speech: controlled by the lateral portion of the primary motor cortex and this is supplied by the MCA
The parts of the somatosesory cortex in the parietal lobe that control the legs and arms & face are supplied by which major arteries?
Name the parts and the arteries
The somatosensory cortex, located in the postcentral gyrus of the parietal lobe, is responsible for processing sensory information from the body.
Legs: controlled by the medial portion of the somatosensory cortex and this is supplied by the ACA
Arms & face: controlled by the lateral portion of the somatosensory cortex and this is supplied by the MCA
Cause of stroke in the young
Congenital heart defect
Hypercoaguability
Current trends in management of AIS (investigations and treatment)
Emergency triage & initial evaluation; (including immediate stabilization of ABCs).
Evaluation also rule out stroke mimics
INVESTIGATIONS; ALL patients
* non-contrast neuroimaging (CT still standard of care): It rules out hemorrhagic stroke by detecting hyperdense (bright) areas that indicate blood.
* RBS: excludes hypoglycemia which can mimic stroke symptoms
* SPO2: detects hypoxia which worsens brain injury
* serum E, U, Cr (helps check the renal status)
* FBC (+ platelets) to check for anemia
* ECG: Detect atrial fibrillation (AF), MI, or other cardiac causes of embolism
* ECHO: Identify cardiac sources of emboli
* Carotid Doppler (to check for occlusion in carotid artery) (not emergent)
Selected patients (eg stroke in the young <45years – toxicology screen; CXR;
Definitive AIS TREATMENT:
* Thrombolysis (rtPa) within a specific time-frame (4.5 hours)
* For patients out of therapeutic window & those with contraindications to thrombolysis , commence ASA 300mg (aspirin inhibits platelet aggregation therefore it is CONTRAINDICATED for hemorrhagic stroke).
- General measures – adequate positioning, avoid hypoxia, manage fever/hyperthermia
- BP management; no intervention in 1st 24 hours unless BP > 220/120mmHg, or presence of medical emergency that warrants antihypertensive Rx (acute kidney injury, myocardial infarction, heart failure, aortic dissection)
DO NOT CRASH THE BP!!!!
Aim for gradual reduction using titratable parenteral antihypertensives; 15% - 25% reduction in SBP or MAP over 1st 24 hours
Thrombolysis-eligible patients must have BP < 180/110mmHG
- Maintain euvolemia using isotonic fluids
- Blood glucose management – avoid hypoglycemia. Treat hyperglycemia; Target 140 – 180mg/dl (7.8 – 10mmol/L)
- Monitor and manage complications; cerebral edema with ↑ICP, DVT, contractures, pressure ulcers
Rehabilitation and secondary prevention
What is the most common location for hypertensive bleeding?
Putamen
Contradictions to thrombolysis
BP above 180/100mmHg
Why shouldn’t you give a stroke patient dextrose-containing fluid?
It can worsen their cerebral oedema
What should you give a stroke patient in an acute emergency
Only insulin do not give an oral hypoglycemic agent eg. metformin
Cardioembolic strokes are most commonly caused by what?
Atrial fibrillation
Difference in onset of embolic and thrombotic stroke
E: maximal in onset
T: gradual
Management of Ischemic
THROMBOLYSIS; within 3 – 4.5 hours of stroke onset (standard of care)
Tab ASA 300mg daily
Statin therapy: reduce factor if there is hyperlipidemia
Maintain cerebral perfusion (euvolemia) (IVFs 3L/24hours)
DVT prophylaxis (SC LMWH/heparin)
Anticipate and Rx complications
CURRENT TRENDS IN MANAGEMENT OF ICH (investigation
- Rapid triage and ER evaluation
- Emergency non-contrast brain imaging (CT scan)
- Blood workup - RBS, serum chemistry, clotting profile, PT_INR , platelet count , TT, toxicology
- Evaluate for other causes of ICH especially if elderly, atypical location of bleed (lobar), absence of risk factors
- Attention to euvolemia, oxygen saturation, euglycemia, treat hyperthermia (>38⁰C)
- Monitor for and manage complications – early neurologic deterioration (hematoma expansion, edema),
- Treat clinical seizures; no room for prophylactic anticonvulsants
MANAGEMENT; INTRACEREBRAL HAEMORRHAGE
Maintain cerebral perfusion
Manage raised ICP
Rx of elevated BP to prevent hematoma expansion
Intermittent pneumatic compression stockings for DVT prophylaxis
NO NSAIDS/ASA
Prophylactic anticoagulation in the acute phase (individualized basis)
NEUROSURGERY IN SELECTED CASES
DVT prophylaxis – Avoid anticoagulants in the 1st 48 – 72 hours post-ICH
-Use of anticoagulants in ICH should be on a case by case basis;
-also based on availability of non-pharmacologic (mechanical) alternatives (pneumatic compression stockings)
Blood pressure management – High BP associated with early neurologic deterioration, hematoma expansion, dependency, death.
-For SBP 160 - 220mmHg lowering to 140mmHg considered safe
-For SBP > 220mmHg ; aggressive reduction (must be with a titratable agent with facilities for intensive monitoring)
What is a CARDIOEMBOLIC STROKE?
A cardioembolic stroke is an ischemic stroke caused by a blood clot (embolus) originating from the heart, which travels through the bloodstream and blocks a cerebral artery.
- Most commonly caused by atrial fibrillation (responsible for ~50% of all cardioembolic strokes)
- Secondary stroke prevention differs in cardioembolic strokes especially that due to atrial fibrillation
- Variability in the estimated risk of stroke in Afib depending on presence of other risk factors
Presentation Of Cardioembolic Stroke
- Neurologic symptoms that are maximal at onset: Since cardioembolic strokes occur due to sudden arterial occlusion by an embolus, symptoms appear abruptly and at full severity from the beginning (unlike thrombotic strokes, which may progress gradually over hours).
- A stroke syndrome that localizes to a large artery territory, particularly when there is clinical evidence of cortical involvement, also suggests a cardioembolic source: Cardioemboli typically lodge in major arteries like the middle cerebral artery (MCA), posterior cerebral artery (PCA), or basilar artery, affecting large areas of the brain.
- Evidence of multiple foci of concurrent or sequential ischemia, particularly in multiple cerebrovascular or systemic vascular beds, is also strongly suggestive of cardioembolism: Cardioembolism can result in shower emboli, affecting multiple territories in the brain or other organs. Imaging may show infarcts in different vascular distributions (e.g., MCA + PCA involvement).
Use of risk stratification scores
IN CARDIOEMBOLIC STROKE
Use of risk stratification scores in Afib
CHADS2
- Congestive cardiac failure - 1
- HTN- 1
- Age > 75yrs - 1
- DM -1
- previous stroke/TIA -1
If the Tscore ≥ 2: anticoagulants are recommended
CHA2DS2- VASc [CCF – 1, HTN – 1, Age ≥ 75yrs – 2, DM – 1, previous stroke, TIA/ thromboembolism – 2,Vascular Dx (previous M.I., P.A.Dx, aortic plaque – 1, Age 65 – 74yrs - 1 Sex category (female) – 1]. Tscore ≥ 2 (anticoag)
CHA₂DS₂-VASc Scoring System: is more refined and includes other risk factors
C – Congestive heart failure (CCF) → 1 point
H – Hypertension → 1 point
A₂ – Age ≥ 75 years → 2 points
D – Diabetes mellitus → 1 point
S₂ – Previous stroke, TIA, or thromboembolism → 2 points
V – Vascular disease (previous MI, PAD, aortic plaque) → 1 point
A – Age 65–74 years → 1 point
S – Sex category (Female) → 1 point
Tscore ≥ 2 (anticoagulant recommended)
Target – INR of 2 – 3
Treatment of stroke with Afib includes rate control (eg, beta blockers, ccb, digoxin) +/- rhythm control (antiarrhythmics)
RISK OF BLEEDING DURING ANTICOAGULATION IN CARDIOEMBOLIC STROKE
HAS-BLED score (HTN SBP > 160mmHG – 1, Abnormal renal or liver fxn – 1 each, Stroke – 1, History of bleeding predisposition – 1, Labile INR – 1, Elderly Age > 65yrs – 1, Drugs esp NSAIDS +/- antiplatelets, excess alcohol – 1each,). Tscore ≥ 3 (cautious)
Complications of stroke
- CNS – repeat stroke, hematoma growth (ICH), hemorrhagic conversion, cerebral edema, raised ICP (± herniation), hydrocephalus, seizures
- RS - Aspiration, aspiration pneumonia, hypostatic pneumonia, pulmonary edema, pulmonary embolism
- CVS - Arrhythmias, cardiogenic shock,
- Endocrine - ↑RBS, disturbance of salt & water homeostasis
- UGS – UTI
- GIT - Stress (Cushing’s) ulcers, GI bleeding, paralytic ileus, malnutrition
- Limb – DVT, contractures, adhesive capsulitis
- Skin – decubitus ulcers
- Psychology – Depression
REHABILITATION & SECONDARY PREVENTION of stroke
- Lifestyle modifications
- Rx of risk factors (HTN, DM, infections, prophylaxis in Afib),
- ASA (or other antiplatelet) for life if ischemic
- Statin (regardless of lipid levels) if ischemic
- Physiotherapy
- Occupational therapy
- Speech therapy
- Assisted living/ adaptation of home to deficits
Risk stratification in TIA
- Historically regarded as benign …no longer so
- Decision on evaluation following a TIA - admit or not to admit for evaluation
- Neuroimaging for TIA – MRI
- Depends on the calculated future risk of stroke
The ABCD2:
* age ≥ 60 years (1 point)
* BP ≥ 140/90 mm Hg at presentation (1 point)
* clinical features: unilateral weakness (2 points) or speech/language impairment without weakness (1 point)
* duration ≥60 minutes (2 points) or 10 to 59 minutes (1 point)
* DM (1 point).
ABCD2 score can vary from 0 to 7
< 3 low risk
4-5 moderate risk
6-7 high risk
Therefore we aim to reduce risk factors
What is a SUBARACHNOID HEMORRHAGE; Nontraumatic/aneurysmal?
Neurologic emergency
Accounts for ~5% of all strokes
Occurs at a younger age than other types of stroke
High mortality
Intracranial aneurysms
Risk of rupture dependent on other factors
Risk factors for SAH
Non-modifiable:
Age
Female gender
Previous hx of SAH
FHx of SAH
Hx of aneurysm in 1st degree relatives
Modifiable;
Hypertension
Cigarette smoking
Heavy alcohol use
Sympathomimetic drug ab(use)
Clinical features of SAH
- Sudden severe headache (thunderclap)+/- L.O.C and neck stiffness, nausea and vomiting
- Focal features may suggest cause or complication
6th cranial nerve palsy – Raised ICP
3rd cranial nerve palsy – posterior communicating /PCA/superior cerebellar artery - Paraparesis & abulia (a state of apathy/ diminished motivation); anterior communicating artery
- Hemiparesis + aphasia/neglect; MCA aneurysm
- Impaired L.O.C & impaired upgaze; Hydrocephalus
- Unilateral visual loss & bi-temporal hemianopia (Loss of temporal (outer) vision in both eyes); ICA aneurysm
Diagnosis of SAH (investigations)
Non-contrast enhanced CT
Lumber puncture (if CT is negative)
CT/MR angiography
Management of SAH
General measures as for other strokes
Prevent rebleeding (Tx aneurysm)
Prevent vasospasm; Nimodipine 60mg 4 hourly * 21days
Anticipate and Rx complications; hydrocephalus
Bedrest (including no bathroom privileges) & supportive management; control HTN, analgesics for headaches, DVT prophylaxis, laxatives
Complications of SAH
Rebleed
Vasospasm and delayed cerebral infarction
Hydrocephalus
Cardiopulmonary; arrhythmias, neurogenic pulmonary edema
Hyponatremia ; SIADH or cerebral salt wasting
DVT
Seizures
