Approach to a patient with stroke epic win

Ashwin Haridas Asem Ali Ashraf Adam Ebrahim

Definitions
Stroke
Clinical syndrome of rapid onset of focal deficits of brain function lasting more than 24 hours or leading to death
Transient Ischemic attack (TIA)
Clinical syndrome of rapid onset of focal deficits of brain function which resolves within 24 hours
Amaurosis fugax

Definitions
Progressive Stroke
A stroke in which the focal neurological deficits worsen with time
Also called stroke in evolution
Completed Stroke
A stroke in which the focal neurological deficits persist and do not worsen with time

Epidemiology
Third most common cause of death after cancer and ischeamic heart disease
Most common cause of severe physical disability
Prevalence of stroke in India is about 1.54 per 1000
Death rate is about 0.6 per 1000
Incidence and prevalence of stroke is on the rise due to increasing adoption of unhealthy lifestyle & an increasing life expectancy

Stroke Risk Factors
Fixed
Age
Gender (Male>Female)
Race (Afro-Caribbean>Asian>European)
Heredity
Previous vascular event eg. MI, peripheral embolism
High fibinogen
Modifiable
Hypertension
Heart disease (Atrial fibrillation, endocarditis)
Diabetes mellitus
Hyperlipidaemia
Smoking
Excess alcohol consumption
Oral contraceptives

Anterior Circulation Posterior Circulation

Middle Cerebral Artery

Anterior Cerebral Artery

Posterior Cerebral Artery

Types of Stroke
Ischemic
Hemorrhagic

Ischemic Stroke
80% of strokes
Arterial occlusion of an intracranial vessel leads to hypoperfusion of the brain region it supplies
Two etiological types
Thrombotic
Embolic

Etiology of ischemic stroke
Thrombotic
Lacunar stroke
Large vessel thrombosis
Hypercoagulable disorders
Embolic
Artery to artery
Carotid bifurcation
Aortic arch
Cardioembolic
Atrial fibrillation
Myocardial infarction
Mural thrombus
Bacterial endocarditis
Mitral stenosis
Paradoxical embolus

Thrombotic Stroke
Atherosclerosis is the most common pathology leading to thrombotic occlusion of blood vessels
Hypercoagulable disorders – uncommon cause
Antiphospholipid syndrome
Sickle cell anemia
Polycythemia vera
Homocysteinemia
Vasculitis: PAN, Wegener’s granulomatosis, giant cell arteritis

Lacunar stroke
Accounts for 20% of all strokes
Results from occlusion of small deep penetrating arteries of the brain
Pathology: lipohyalinosis & microatheroma
Thrombosis leads to small infarcts known as lacunes
Clinically manifested as lacunar syndromes
Thrombotic Stroke

Embolic Stroke
Cardioembolic stroke
Embolus from the heart gets lodged in intracranial vessels
MCA most commonly affected
Atrial fibrillation is the most common cause
Others: MI, prosthetic valves, rheumatic heart disease
Artery to artery embolism
Thrombus formed on atherosclerotic plaques gets embolized to intracranial vessels
Carotid bifurcation atherosclerosis is the most common source
Others: aortic arch, vertebral arteries etc.

Etiology of ischemic stroke

Blood supply to the brain is autoregulated
Blood flow
If zero leads to death of brain tissue within 4-10min
<16-18ml/100g tissue/min infarction within an hour
Ischemia leads to development of an ischemic core and an ischemic penumbra
Pathophysiology of Ischemic Stroke

Ischemic Penumbra
Tissue surrounding the core region of infarction which is ischemic but reversibly dysfunctional
Maintained by collaterals
Can be salvaged if reperfused in time
Primary goal of revascuralization therapies

ATP depletion Hypoperfusion Failure of Na + /K + ATPase membrane ionic pump Calcium entry Glutamate release Activation of lipid peroxidases, proteases & NO synthase Destruction of intracellular organelles, cell membrane & release of free radicals Free fatty acid release Activation of pro-coagulant pathways Liquefactive necrosis Thrombus/embolus Membrane depolarization & cytotoxic cellular edema

Hemorrhagic Stroke
Two types
Intracerebral hemorrhage(ICH)
Subarachnoid hemorrhage(SAH)
Higher mortality rates when compared to ischemic stroke

Intracerebral Hemorrhage
Result of chronic hypertension
Small arteries are damaged due to hypertension
In advanced stages vessel wall is disrupted and leads to leakage
Other causes: amyloid angiopathy, anticoagulant therapy, cavernous hemangioma, cocaine, amphetamines

Subarachnoid Hemorrhage
Most common cause is rupture of saccular or Berry aneurysms
Other causes include arteriovenous malformations, angiomas, mycotic aneurysmal rupture etc.
Associated with extremely severe headache

Pathophysiology Of Hemorrhagic Stroke
Explosive entry of blood into the brain parenchyma structurally disrupts neurons
White matter fibre tracts are split
Immediate cessation of neuronal function
Expanding hemorrhage can act as a mass lesion and cause further progression of neurological deficits
Large hemorrhages can cause transtentorial coning and rapid death

CLINICAL FEATURES

History
Ask for onset and progression of neurological symptoms – completed stroke or stroke in evolution
History of previous TIAs & amaurosis fugax
History of hypertension & diabetes mellitus
History of heart conditions like arrhythmias, RHD & prosthetic valves

History of seizures & migraine
History of anticoagulant therapy
History of oral contraceptive use
History of any hypercoagulable disorders like sickle cell anemia & polycythemia vera
Substance abuse: cocaine, amphetamines
History

Examination of a stroke patient
The neurological examination is highly variable and depends on the location of the vascular lesion.
Skin: look for xanthelasma,rashes (arteritis,splinter haemorrhages,livedo reticularis),limb ischemia(DVT)
Eyes:look for diabetic changes,retinal emboli,hypertensive changes,arcus senilis(refer to ophthalmologist)

Examination of a stroke patient
CVS: hyper/hypotension, abnormal rhythm(atrial fibrillation),murmurs(valvular anomaly),raised JVP(heart failure),peripheral pulses and bruits(generalised arteriopathy)
Respiratory system: pulmonary edema, infection
Abdomen: urinary retention
Locomotor system: injuries sustained during collapse with stroke, comorbities which influence functional abilities.

General feature
Most cerebrovascular diseases are manifest by the abrupt onset of a focal neurologic deficit, as if the patient was "struck by the hand of God.”
The clinical manifestations of stroke are highly variable because of the complex anatomy of the brain and its vasculature.

‘ HAND OF GOD’

CLINICAL CLASSIFICATION

Stroke Syndromes
Stroke syndromes are divided into: (1) large-vessel stroke within the anterior circulation
(2) large-vessel stroke within the posterior circulation,and
(3) small-vessel disease of either vascular bed.

Stroke Within the Anterior Circulation
The internal carotid artery and its branches comprise the anterior circulation of the brain i.e the anterior and middle cerebral arteries

Middle cerebral artery
Signs and symptoms: Structures involved
Paralysis of the contralateral face, arm, and leg; sensory impairment over the same area: Somatic motor area
Motor aphasia: Motor speech area of the dominant hemisphere
Central aphasia: Central, suprasylvian speech area and parietooccipital cortex of the dominant hemisphere
Conduction aphasia: Central speech area (parietal operculum)

Cont….
Homonymous hemianopia (often homonymous inferior quadrantanopia): Optic radiation deep to second temporal convolution
Paralysis of conjugate gaze to the opposite side: Frontal contraversive eye field or projecting fibers
Central aphasia: Central, suprasylvian speech area and parietooccipital cortex of the dominant hemisphere
Conduction aphasia: Central speech area (parietal operculum)
Homonymous hemianopia (often homonymous inferior quadrantanopia): Optic radiation deep to second temporal convolution

Cont..
Apractognosia(agnosia +apraxia) of the nondominant hemisphere: Nondominant parietal lobe (area corresponding to speech area in dominant hemisphere); loss of topographic memory is usually due to a nondominant lesion, occasionally to a dominant one.
Apraxia is a neurological disorder characterized by loss of the ability to execute or carry out learned purposeful movements, despite having the desire and the physical ability to perform the movements. It is a disorder of motor planning.
Agnosia ( a-gnosis , "non-knowledge", or loss of knowledge) is a loss of ability to recognize objects, persons, sounds, shapes, or smells while the specific sense is not defective nor is there any significant memory loss

Deficits Due To ACA Occlussion
Occlusion of the anterior cerebral artery may result in the following defects:
If stroke occurs prior to the anterior communicating artery it is usually well tolerated secondary to collateral circulation
Paralysis of the contralateral foot and leg
Sensory loss in the contralateral foot and leg
Left sided strokes may develop transcortical motor aphasia
Gait apraxia
Urinary incontinence which usually occurs with bilateral damage in the acute phase

Internal Carotid Artery
The clinical picture of internal carotid occlusion varies depending on whether the cause of ischemia is propagated thrombus, embolism, or low flow. The cortex supplied by the MCA territory is affected most often. With a competent circle of Willis, occlusion may go unnoticed.

If the thrombus propagates up the internal carotid artery into the MCA or embolizes it, symptoms are identical to proximal MCA occlusion.
Sometimes there is massive infarction of the entire deep white matter and cortical surface.

When the origins of both the ACA and MCA are occluded at the top of the carotid artery, abulia or stupor occurs with hemiplegia, hemianesthesia, and aphasia or anosognosia. When the PCA arises from the internal carotid artery (a configuration called a fetal posterior cerebral artery ), it may also become occluded and give rise to symptoms referable to its peripheral territory

In addition to supplying the ipsilateral brain, the internal carotid artery perfuses the optic nerve and retina via the ophthalmic artery. In ~25% of symptomatic internal carotid disease, recurrent transient monocular blindness (amaurosis fugax) warns of the lesion. Patients typically describe a horizontal shade that sweeps down or up across the field of vision

A high-pitched prolonged carotid bruit fading into diastole is often associated with tightly stenotic lesions. As the stenosis grows tighter and flow distal to the stenosis becomes reduced, the bruit becomes fainter and may disappear when occlusion is imminent.

Posterior Circulation
DYSARTHRIA & FACIAL NUMBNESS
ATAXIA & HORNER’S SYNDROME
FACIAL WEAKNESS(LMN)
HEMIPARESIS
HEMISENSORY LOSS
HEMIANOPIA
LOSS OF CONSCIOSNESS
DIPLOPIA, VERTIGO, VOMITING

CLASSICAL PRESENTATIONS
THROMBOTIC
H/O TIA
STROKE IN EVOLUTION
USUALLY HAPPENS EARLY MORNING
EMBOLIC
PATIENTS WITH KNOWN HEART DISEASE LIKE IHD, VALVULAR HEART DISEASE
RAPID RECOVERY
HAEMORRHAGIC
STROKE IN HYPERTENSIVE PATIENTS
ASSOCIATED WITH EMOTIONAL EXCITEMENT
HEADACHE & VOMITING

DIFFERENTIAL DIAGNOSIS
SPACE OCCUPYING LESION(TUMOR)
SEIZURE
MIGRAINE
SUBDURAL HAEMATOMA
METABOLIC DISTURBANCE LIKE HYPOGLYCAEMIA

Hypoglycemia
That transient hypoglycemia may produce a stroke like picture with hemiplegia and aphasia has been known for years.
The wide use of bedside rapid laboratory testing for glucose now makes this easily detectable and treatable. The hemiplegia may resolve immediately with the administration of intravenous glucose but resolution over a hours is also reported

Space Occupying Lesions
Subacute or chronic duration of symptoms, however some patients may present with acutely probably due to bleeding into a tumour
Associated with deep seated bursting headache, projectile vomiting due raised ICT

SEIZURES AND POST ICTAL STATES
Traditional thought is that these postictal symptoms are manifestations of seizure-induced alterations in neuronal function that are reversible; structural neuronal alterations are not present. The postictal weakness or Todd’s paralysis usually follows partial motor seizures but may follow generalized seizures as well. Duration is usually brief but may last 48 hours

MIGRAINE
Migraine may actually precipitate a stroke, but there is also a variant of migraine, hemiplegic migraine, where unilateral hemiparesis outlasts the headache. This is difficult if not impossible to diagnose correctly at first presentation when it must be regarded as a diagnosis of exclusion; only with recurrent, stereotypic attacks can this be suspected. Cases with alternating hemiplegia have been reported. At times this disorder has been shown to be familial.

SUMMARY
Rapid onset focal deficit of brain function confirms stroke
Onset and progression will decide the aetiology
Precise history of deficit will decide the site of lesion

INVESTIGATION OBJECTIVES
To confirm the vascular nature of the lesion
The pathological type of the vascular lesion
The underlying vascular disease
Risk factors present

INVESTIGATION MODALITIES: BRAIN
NON-INVASIVE
CT Scan
MRI Scan
MR Angiography
Doppler Ultrasound
EEG
PET
SPECT
INVASIVE
Lumbar Puncture
Contrast Angiography
(Cerebral Arteriography)
CT Angiography

PATHOLOGICAL TYPES STROKE HAEMORRHAGIC ISCHAEMIC

CT SCAN
Mandatory initial investigation
Haemorrhage appears instantly as a hyperdense area
Infarct appears as a hypodense area
Infarct may not appear before 48 hrs
MRI may be done instead but ct scan is more sensitive for detecting haemorrhage
Diffusion weighted MRI is good for identifying ischaemic lesion

ISCHAEMIC LESION

CT SCAN/MRI VASCULAR NATURE CONFIRMED HAEMORRHAGE ISCHAEMIA Cont’d… STROKE PATIENT

SEARCH FOR SOURCE Cont’d… SEARCH FOR SOURCE CEREBRAL ARTERIOGRAPHY MRA/CTA DOPPLER PET/SPECT

Carotid Artery Ultrasound Showing a Completely Calcified Atherosclerotic Plaque

3-D reconstruction of CT angiogram showing stenosis at the carotid bifurcation

Intra-arterial angiography showing arteriovenous malformation

MR angiogram showing giant aneurysm at the middle cerebral artery bifurcation

HAEMORRHAGE CONFIRMED NORMAL CT SCAN HAEMORRHAGE SUSPECTED LUMBAR PUNCTURE CSF WITH BLOOD/ XANTHOCHROMIA

UNDERLYING DISEASE
Cerebral vasculature
Abnormalities like aneurysms or
AV malformations
Cerebral angiography
Vascular imaging – MRA/CTA or doppler (non invasive)

CARDIOVASCULAR
Like MI, atrial fibrillation, valvular diseases etc.
Electrocardiogram
Chest X-Ray
Echocardiography
Transesophageal ultrasound
Holter monitoring(paroxysmal nocturnal arrhythmia)
Blood cultures
UNDERLYING DISEASE

UNDERLYING DISEASE
Serum lipids for hyperlipidemia
ANA for SLE
MR Angiography for arterial dissection
Lupus anticoagulant for antiphospholipid antibody syndrome
ESR, CRP, ANCA for vasculitis
PT, aPTT, Platelet count for bleeding disorders
Proteins C & S for hypercoagulability

TREATMENT OBJECTIVES
1. MINIMIZE VOLUME OF BRAIN IRREVERSIBLY DAMAGED
2. PREVENT COMPLICATIONS
3. REHABILITATION
4. REDUCE RISK OF RECCURENCE

MANAGEMENT OF A TRANSIENT ISCHAEMIC ATTACK (TIA)
MEDICAL MANAGEMENT
(if diffuse atherosclerotic disease or poor operative candidates)
Stop smoking
Concurrent medical problems to be addressed:
Emboli from heart and other parts of cardiovascular system
(a) anti coagulants: Heparin(IV), Warfarin(oral)
(b) anti platelet drugs: Aspirin(oral), Ticlopidine
Diabetes, Hypertension, Hyperlipidemia

MANAGEMENT OF A TRANSIENT ISCHAEMIC ATTACK(TIA) – Cont’d
SURGICAL MANAGEMENT
CAROTID AND CEREBRAL ARTERIOGRAPHY
STENOSIS
Mild to Moderate Severe
Regular Follow Up
Carotid Endarterectomy
All above can be done only if there is relatively little atherosclerosis elsewhere in cerebrovascular system.

MANAGEMENT OF AN ACUTE EPISODE OF STROKE
AIRWAY - Maintain airway, prevent aspiration, keep nil per oral
BREATHING - Maintain oxygen saturation > 97%
- Supplementary oxygen
CIRCULATION - Adequacy of pulse and BP
- Fluid, Anti Arrhythmics, Ionotropes
HYDRATION - Prevent dehydration ; give adequate fluids
- Parenteral or via nasogastric tube
NUTRITION - Nutritional supplements and Nasogatric feeding
MEDICATION - Administer medication also by routes other than oral

MANAGEMENT OF AN ACUTE EPISODE OF STROKE Cont’d
BLOOD PRESSURE - unless indicated (heart or renal failure,hypertensive encephalopathy or aortic dissection) it should not be lowered for the fear of expansion of infarct.
Ischaemic stroke - maintain 180/110 mm Hg
Haemorrhagic stroke – keep MAP <115 mm Hg
BLOOD GLUCOSE - INSULIN to treat hyperglycaemia(can increase infarct size)
- maintain < 200mg%
TEMPERATURE - early use of antipyretics
PRESSURE AREAS – To prevent occurrence of decubitus ulcers
INCONTINENCE

EARLY MANAGEMENT

ISCHAEMIC STROKE
THROMBOLYTICS and REVASCULARISATION -
- tPA (alteplase)-0.9mg/kg(max 90mg)
10% of dose – initial IV bolus
remainder infused over one hour
- to be used < 3 hrs of onset of symptoms
(for maximum efficacy)
- haemorrhage to be ruled out
NEUROPROTECTIVE AGENTS

ANTI PLATELET THERAPY
Asprin, Clopidogrel
- act by inhibiting platelet aggregation and adhesion.
- aspirin 300mg single dose to be given immediately following diagnosis.
- if alteplase given it can be with held for 24 hrs.
- later aspirin at a dose of 75 mg in combination with clopidogrel 75 mg daily for about one year duration.

ANTI COAGULANTS
HEPARINS , WARFARIN
- heparins act by accelerating the inhibition of factor II and factor X of coagulation cascade
- warfarin antagonises vitamin K to prevent activation of clotting factors
-decrease risk of recurrence and venous thromboembolism
-intra cranial haemorrhage to be excluded before therapy
-more useful if stroke is evolving

ANTI COAGULANTS - Cont’d
HYPEROSMOLAR AGENTS
- reduce cerebral oedema
- 20% mannitol IV – 100ml TID
- oral glycerol if swallow is normal
Concurrent medical problems such as atrial fibrillations to be tackled
OTHERS:
- PENTOXYPHYLLINE (hemorrheology modifier)
to be used within 12 hrs
-NEUROPROTECTIVE AGENTS

HAEMORRHAGIC STROKE
Control of hypertension
Control coagulation abnormalities (esp due to oral anticoagulants)
Surgical decompression
Surgery for aneurysms and arterio-venous malformations
Anti platelet and anti coagulants are contraindicated

REHABILITATION
PHYSIOTHERAPY - as early as possible
- initially passive moments
- later active movements
- in every case early mobilization
- prevents contractures, spasticity and atrophy
OCCUPATIONAL THERAPY

REHABILITATION - Cont’d
SPEECH THERAPY
IMPROVE QUALITY OF LIFE WITH MOTOR AIDS -leg brace, toe spring , cane , walking stick

STROKE UNITS – A MULTIDISCIPLINARY APPROACH
Immediate resuscitation , prevent complications and recurrence
Emergency 24 hr evaluation and comprehensive care
Improves neurological outcome
Reduces mortality
1000 patients admitted to stroke units saves the lives of atleast 5o patients at end of 6 months

SECONDARY PREVENTION
Blood pressure control
Diabetes Management
Lipid Management
Smoking Cessation
Alcohol Moderation
Weight Reduction/Physical Activity
Carotid Artery Interventions
Anti platelet agents / Anti coagulants
Statins
Diuretics +/- ACE inhibitors

COMPLICATIONS
Due to cortical brain injury(immediate)
- Epilepsy/seizures
- Cerebral oedema
Residual deficits from stroke
- Paralysis
- Aphasia

COMPLICATIONS – Cont’d
Due to immobility
- Chest infections
- Pressure sores
- Deep vein thrombosis /
pulmonary embolism
- Painful shoulder
- Urinary infection/constipation
- Depression and anxiety

PROGNOSIS
ISCHAEMIC STROKE
Mortality rate in first 30 days is 8-12%
Can vary depending upon size, location, symptoms of stroke
Time that elapses from the event to medical intervention
First 3 hrs after stroke - GOLDEN PERIOD

PROGNOSIS – Cont’d
INTRACEREBRAL HAEMORRHAGE
Mortality rate in first 30 days is almost 50%
Site and extent of hematoma also plays a role in determining the prognosis
Hamorrhagic strokes have a poor prognosis compared to ischaemic type .

Approach to a patient with stroke epic win

by Ashwin Haridas on May 07, 2010

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