Approach to a patient with stroke

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

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.

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

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.

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.

Internal Carotid Artery 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.

Internal Carotid Artery 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

Internal Carotid Artery 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

Internal Carotid Artery 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

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

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

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Approach to a patient with stroke