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Table of Contents
REVIEW ARTICLE
Year : 2022  |  Volume : 10  |  Issue : 3  |  Page : 153-163

Management of acute stroke


Department of Neurology, National Institute of Mental Health and Neurosciences, Bengaluru, Karnataka, India

Date of Submission08-Sep-2020
Date of Decision06-Nov-2020
Date of Acceptance08-Sep-2020
Date of Web Publication12-Jul-2022

Correspondence Address:
Dr. Girish Baburao Kulkarni
National Institute of Mental Health and Neurosciences, Hosur Road, Bengaluru - 560 029, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ajim.ajim_66_20

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  Abstract 


Management of acute stroke has considerably changed over the past 20 years. It has evolved from extreme nihilism to an exciting science where patients can improve to near normal with reperfusion therapies. We have reviewed the recent advances in the management of acute stroke, especially acute ischemic type (AIS). A search was done in pub med with keywords- “Acute Stroke,” “Treatment,” and “Recent advances.” Relevant articles were downloaded, cross-references were reviewed and this article was written. Stroke care requires the organization of the available facilities at the hospital to provide basic to advanced services, with coordination between different centers through the Hub and Spoke model. Recognition of time of onset of stroke, knowledge about options available for AIS patients at 4.5, 6, and 24 h and planning appropriate imaging studies helps in management. Intravenous thrombolysis and endovascular therapies play a key role in the reperfusion in patients with AIS. Patients with transient ischemic attack/minor stroke should be treated with dual anti-platelets, for at least three weeks followed by a single agent. Investigating a stroke patient for modifiable risk factors and classifying them to various subtypes will help in the prevention of recurrence. Management of intracerebral hemorrhage requires evaluation for etiology and supportive care. Cerebral venous thrombosis is a rare but unique type of stroke, which requires knowledge about signs on imaging, risk factor evaluation, and treatment with anticoagulants. Health education plays an important role in prevention and compliance with medications.

Keywords: Endovascular therapy, intravenous thrombolysis, ischemic stroke


How to cite this article:
Taallapalli AV, Mailankody P, Kulkarni GB. Management of acute stroke. APIK J Int Med 2022;10:153-63

How to cite this URL:
Taallapalli AV, Mailankody P, Kulkarni GB. Management of acute stroke. APIK J Int Med [serial online] 2022 [cited 2022 Aug 11];10:153-63. Available from: https://www.ajim.in/text.asp?2022/10/3/153/350748




  Introduction Top


Stroke is a neurological emergency with the major cause of global death and disability.[1] It is divided into ischemic and hemorrhagic, depending on the pathology. Sudden onset of symptoms in the form of weakness of the limbs, sensory disturbances, speech disturbances, loss of vision or imbalance, and rarely loss of consciousness are the typical symptoms of a stroke. Over the last two decades, significant improvements have taken place in acute ischemic stroke treatment in the form of intravenous thrombolysis (IVT) and endovascular therapy (EVT). We aim to highlight the importance of triaging and treating stroke patients as early as possible since the treatment is time-dependent, better organization of stroke care, improve the hospital facilities, and use antiplatelets and anticoagulants appropriately in the secondary prevention in this review.


  Definition, Epidemiology, Pathophysiology of Stroke Top


Stroke is defined by the World Health Organization as “Rapidly developing clinical signs of focal (or global) disturbance of cerebral function, lasting more than 24 h or leading to death, with no apparent cause other than that of vascular origin.”[2] However, the definition of stroke was revised by the American Heart Association/American Stroke Association in 2013[3] to include, any objective evidence of permanent brain, spinal cord, or retinal cell death due to a vascular cause based upon pathological or imaging evidence with or without the presence of clinical symptoms, to include following entities in stroke-central nervous system infarction; ischemic stroke; silent infarction; intracerebral hemorrhage; stroke caused by intracerebral hemorrhage; silent intracerebral hemorrhage; subarachnoid hemorrhage (SAH); subarachnoid hemorrhage causing stroke; thrombosis of cerebral venous sinuses; not otherwise specified.

As per the Global Burden of Disease study, 2016 the lifetime risk of developing a stroke is 24.9% in the world.[4] In India, stroke is the 2nd most common cause of death.[5] The incidence of stroke is 119-145/100,000. The adjusted prevalence rate of stroke is more in the urban (334–424/100,000) than in the rural areas (84-262/100,000). Ischemic stroke is the most common subtype of stroke which contributes to 75%–80%. The incidence of intracranial hemorrhage (ICH) ranges from 20 to 25% among all strokes. The case fatality rate within 28 days of onset is 25%–35%.[5] Pathophysiologically stroke can be of arterial or venous types. Ischemic stroke may be classified into atherosclerotic, cardioembolic, lacunar, stroke due to specific etiology and undetermined.[6] The common risk factors can be classified as modifiable (Hypertension, diabetes, alcoholism, etc.) and nonmodifiable (age, sex, race), and their identification will help in planning treatment and preventing recurrence. Hemorrhagic stroke can be classified into SAH and intracerebral hemorrhage broadly. The venous strokes are rare, constitute about 1% of strokes, and have distinct etiology, presentation, and treatment protocol.[7]


  Clinical Features, Diagnosis and Differential Diagnosis of Stroke Top


The symptoms at presentation depend on the stroke type and area of involvement. If symptoms improve within 24 h, it is called a transient ischemic attack (TIA). A TIA typically lasts less than an hour, more often minutes. In a progressive stroke, the signs and symptoms develop gradually and get worse over time. Completed stroke is defined as the neurologic deficit due to occlusive cerebrovascular disease which may persist for hours or days. It is important to identify the syndrome and localize the neuroaxis since treatment varies according to the site and nature of the pathology.[8] Patients usually present with a combination of acute onset of weakness, speech and language disturbances, sensory, visual disturbances, and rarely loss of consciousness. Presentation depends on the arterial territory, side of the brain, and whether lesions are cortical or subcortical and pressure on the surrounding structures in case edema develops.

The pattern of symptoms and signs help in localizing the stroke. Cortical strokes present with aphasia, apraxia, gaze deviation, field defects. Sub-cortical strokes present with isolated hemiparesis, ataxic hemiparesis, facio-brachial weakness, dysarthria, and hemisensory loss. The blurring of vision in one eye with or without contralateral hemiplegia, limb shaking TIAs occur in internal cerebral artery disease. Acute lower limb weakness, acute akinetic mutism, abulia, and amotivation occur in anterior cerebral artery occlusion. The middle cerebral artery (MCA) disease presents with hemiplegia, hemi-sensory loss, aphasia, apraxia, gaze deviation. Acute-onset vertigo, vomiting, ataxia, diplopia, dysphagia, and hiccups favor posterior circulation stroke. Acute-onset ataxia, eye movement abnormalities, acute coma, and locked-in state favor the diagnosis of basilar artery occlusion. Patients with hemorrhagic stroke have altered sensorium, agitation, headache, gaze deviation, seizure, and mydriatic pupil. SAH presents with an acute severe headache with drowsiness. Cerebral venous thrombosis (CVT) causes acute/sub-acute headache, seizures, focal deficit, encephalopathy, cranial nerve palsies, vision loss, and coma.


  Diagnosis Top


History taking is very crucial in the diagnosis of stroke. The majority of arterial strokes occur in seconds, rarely, symptoms may evolve over a few hours. Seizures may occur in embolic and hemorrhagic strokes. Patients with a known cardiac illness like rheumatic heart disease, atrial fibrillation, ischemic heart disease can present with embolic stroke. Patients with intracranial hemorrhage present with sudden onset of severe headache. Headache, seizures, and focal deficits are the usual manifestations of venous strokes and occur in women more commonly and may be associated with anemia, puerperium, and intake of hormonal pills.

A thorough examination including general physical examination, pulse rate, blood pressure, all peripheral pulses, cardiovascular system, and neurological examination helps in localizing and also predicting the etiology in some cases. The fundus examination helps in ruling out hypertensive changes, diabetic changes in case of arterial strokes, and papilledema in venous strokes. The severity of stroke is assessed by the National Institute of Health Stroke Scale (NIHSS) score (0-42). A score of 0: no symptoms, 1-4: minor stroke, 5-15: moderate stroke, 16-20: moderate to severe stroke, 21-42: severe stroke.[9]


  Differential Diagnosis Top


The nonvascular conditions which present as sudden-onset neurological deficit, [Table 1] similar to acute stroke are called the stroke mimics and they should be differentiated appropriately.[10]
Table 1: Differential diagnosis of stroke and clinical features

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  Investigations Top


The investigations ordered usually are blood, cardiac, and imaging studies (computed tomography [CT] and magnetic resonance imaging [MRI]), and are planned based on the time of onset of symptoms and treatment strategy. The investigations help in confirming the diagnosis, ruling out the mimickers, identifying the risk factors or etiologies, and planning the immediate and long-term treatment.


  Blood Investigations Top


In an acute stroke patient in the window period, random blood sugar is a must before the intervention. Other investigations can be done during admission as a part of the etiological workup [Table 2].
Table 2: Typical investigations for a stroke patient

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  Imaging Top


In acute stroke in window period (0-24 h depending on AIS type), imaging is important to rule out hemorrhage and decide on acute reperfusion therapies: IVT and endovascular therapy (EVT). In sub-acute and chronic strokes, imaging (CT/MRI) is done to confirm the stroke, to study the etiopathogenesis (CT angiography [CTA], neck vessel Doppler, digital subtraction angiography [DSA]) and plan the treatment accordingly (medical/surgical). The CT is the workhorse in any stroke care center and has advantages and disadvantages over MRI [Table 3].[11],[12] There is no role of DSA in the diagnosis of acute stroke. However, it is used to do EVT, evaluation of chronic strokes, dissection, and carotid disease. In acute stroke, CT and CTA form the primary imaging modalities which help in detecting the areas of brain infarcted (CT) and area of occlusion/stenosis of the vessel (CTA).
Table 3: Differences between computerized tomography and magnetic resonance imaging in the evaluation of patients with stroke

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The early ischemic changes in CT are loss of gray and white distinction, obscuration of basal ganglia, insular cortex, sulcal effacement, and hypodensity [Figure 1]. Hyperdense arteries may indicate thrombosis. It can also occur in dehydration and polycythemia, in these conditions all the vessels will be hyperdense in contrary to thrombosis where the involved vessel will be hyperdense.
Figure 1: Patient presented with right sided weakness for seven hours. The computed tomography shows loss of grey-white differentiation in left side (arrow) fronto temporal areas. Also left lentiform nucleus and internal capsule are hypodense suggestive of acute infarct

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  Computed Tomography Angiography Top


The CTA [Figure 2] helps in diagnosing carotid artery diseases like stenosis, occlusion, and dissection. In acute ischemic stroke, the site of occlusion in the large vessels, collateral status can be identified, and EVT can be planned.
Figure 2: The computed tomography angiography images of different patients. (a) Left middle cerebral artery, M1 occlusion. (b) Left internal carotid artery stenosis with calcified plaque (arrow) suggestive of extracranial atherosclerotic disease. (c) Left internal carotid artery cavernous part stenosis with calcified plaque suggestive of intracranial atherosclerotic disease

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  Magnetic Resonance Imaging Top


The MRI includes techniques like diffusion-weighted image (DWI), apparent diffusion coefficient, fluid-attenuation inversion recovery (FLAIR), susceptibility-weighted imaging (SWI), contrast angiography with gadolinium, and perfusion imaging. The diffusion-weighted MRI [Figure 3] is a sensitive tool in identifying ischemia in acute ischemic stroke. The signal changes in the FLAIR sequence develop after 4.5 h. In a wake-up stroke, the DWI-FLAIR mismatch helps us in selecting patients for IVT. The SWI reveals blooming in the areas of hemorrhage/thrombosed sinuses. Perfusion imaging [Figure 4] plays a pivotal role of assessing the blood flow pattern. By comparing the diffusion and perfusion images the window period for MCA stroke has been extended up to 24 h [Figure 4].[13],[14]
Figure 3: Patient is 40-year-old male presented in six hours to casualty with right sided weakness and aphasia. (a) Diffusion weighted image shows restriction in left temporal and frontal area in Middle cerebral artery territory. (b) Apparent diffusion coefficient map shows reversal. (c) The fluid-attenuated inversion recovery shows mild hyperintensities in the same areas. (d) The susceptibility-weighted imaging shows blooming in left middle cerebral artery (M1), suggestive of thrombus

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Figure 4: A 57-year-old lady presented with right sided weakness. Last known to be normal was 16 hrs (wake up stroke). (a) Computed tomography brain plain shows hypodensity in left centrum semi-ovale. (b) The angiography (computed tomography angiography) shows left M1 distal occlusion. (c) Diffusion restriction (diffusion-weighted image) in left posterior putamen. (d) Perfusion-mean transit time shows increased MTT in left middle cerebral artery territory with prolonged time to peak (TTP). (e) showing mismatch with diffusion core. Mechanical thrombectomy was done and patient improved. (f) One day after mechanical thrombectomy, MRI, FLAIR image shows no further extension of infarct

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  Role of Imaging in Intracerebral Hemorrhage Top


The CT has a pivotal role in diagnosing ICH, calculating volume, and also gives a clue about causes like vascular abnormalities causing hemorrhage [Figure 5]. If there is suspicion of aneurysm/abnormal vessels, CTA and DSA are helpful. MRI helps in diagnosing cerebral microbleeds.
Figure 5: Plain CT image of a patient with acute headache and right sided weakness. It shows hyperdensity in left thalamic, internal capsule and lentiform nucleus areas suggestive of hemorrhage

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  Imaging in Cerebral Venous Thrombosis Top


The CT plays a pivotal role in diagnosing CVT and MRI is a complimentary investigation, especially in detecting deep CVT and in cortical-vein thrombosis [Figure 6].[15],[16]
Figure 6: The computed tomography plain image shows (a) String/chord sign. (b) Dense triangle sign. (c) Dense lateral sinus sign. (d) Cashew sign. Contrast enhanced computed tomography reveals. (e) Empty delta sign; T2 magnetic resonance imaging reveals. (f) Hemorrhagic infarct

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The findings in imaging can be direct (where the presence of thrombus is demonstrated) and/or indirect (when evidence of venous infarct is demonstrated) signs. The following are direct signs of CVT [Figure 6] in CT: (1) String/chord sign: Hyperdensity in cortical veins compared to the parenchyma, (2) Dense triangle sign: Hyperdensity in the posterior part of Sagittal sinus, (3) Dense lateral sign: hyperdensity in the lateral sinus, (4) Empty delta sign in contrast imaging: Triangular filling defect in sinus. The indirect signs are: (1) Cashew nut sign: Concave-shaped juxta cortical hemorrhages, (2) Hemorrhagic venous infarcts, (3) Slit ventricles, (4) Contrast enhancement along the gyrus.


  Treatment Modalities in Acute Stroke Top


Primary prevention

It involves the prevention of stroke occurrence in a person before it happens. The approach can be the prevention of the emergence of risk factors, by lifestyle modifications like exercise and diet (primordial prevention). Primary prevention strategies are mainly targeted towards those who are at risk of stroke, because of the presence of the risk factors (like alcohol, smoking, diabetes, hypertension, and deranged lipid profile).[17]

Secondary prevention

It involves the therapies that are targeted to prevent the recurrence of stroke by identifying and managing risk factors.[18] The chief risk factors are hypertension, smoking, diabetes, alcohol overuse, abnormal blood lipids, and hormonal preparations. The antiplatelets and anticoagulants are used for the prevention of further progression of thrombosis and recurrence of stroke. In a noncardio embolic stroke with TIA/minor stroke (NIHSS <4), dual antiplatelet therapy and statin are recommended for 3 weeks, followed by a single antiplatelet. If it is moderate and severe stroke, the single antiplatelet agent is preferred. In patients with ischemic stroke with atrial fibrillation/major cardiac risk factors, anticoagulants can be started in 4–14 days and the target prothrombin time international ratio (PT INR) recommended is 2-3. Anticoagulants have to be continued lifelong. If the patient comes beyond the window period (24 h) or after the acute reperfusion therapies, secondary prevention measures have to be followed in all ischemic stroke patients [Table 4].
Table 4: Drugs used in secondary prevention of stroke

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The patients with carotid stenosis with stroke have to be managed according to the severity of stenosis. Mild stenosis (<50%) is treated with a single antiplatelet drug and statin lifelong. Moderate (50–69) and severe (70%–99%) stenosis must be treated with carotid endarterectomy/stenting. Procedure results vary from center to center based on the expertise of the interventionist. The HMG co A reductase inhibitors (statins) help in reducing stroke recurrence and also have pleiotropic effects.[Table 4] The Atorvastatin (10–80 mg), rosuvastatin (10–20 g) can be used with a target of LDL cholesterol 70–110 mg/dl.[19] Patients with hyperhomocysteinemia and Vitamin B12/folate deficiency has to be treated with parenteral injections. The neuroprotective agents commonly used in stroke are piracetam, citicoline, edaravone, and cerebrolysin. They act as membrane stabilizers and free radical scavengers. They are currently not recommended, can be decided on a case-to-case basis.[7],[11],[20],[21]


  Supportive Treatment Top


Supportive treatment like maintaining the airway, breathing and oxygenation, blood pressure maintenance (<185/110 mm Hg), blood glucose maintenance (140–180 mg/dl), pneumatic compression device to prevent leg-vein thrombosis, prevention of bedsores, swallowing assessment, physiotherapy, and speech therapy play a pivotal role while treating stroke patients.[11]


  Intracranial Hemorrhage Top


The management of ICH is challenging. In the majority of patients, it is due to Hypertensive bleed and therapy is supportive in the form of airway maintenance, temperature control, nutrition, control of hypertension, and oxygenation saturation. The target blood pressure is 140/90 mm Hg. Anti edema measures and anti-hypertensives should be started. In the majority of hypertensive deep ganglionic bleed, decompressive surgery may not be helpful but in cerebellar and lobar ICH it may be indicated.[22]


  Management of Cerebral Venous Thrombosis Top


Heparin 5000 units subcutaneous injection can be administered four times a day for 10 days. Acenocoumarin has to be started on day 6 (4 mg on the 1st day, 3 mg on the 2nd day, and 2 mg on the 3rd day and then continue on 1 mg, target INR 1.5-2.5). Antiedema measures such as mannitol, glycerol, acetazolamide, and antiepileptics can be added accordingly.[7],[23]


  Reperfusion Therapies in Acute Ischemic Stroke Top


In patients presenting in the window to a casualty with ischemic stroke, two types of therapies can be offered: IVT (0–4.5 h) and endovascular therapy (EVT) (usually between 0–6 h, and 6–24 h in highly selected anterior circulation stroke) [Figure 7], [Figure 8], [Figure 9]. The IVT (alteplase/tenecteplase) has been approved since 1995 and EVT since 2015 [Table 5]. They help in restoring the circulation in blocked vessels by chemical lysis (IVT) [Table 6], [Table 7], [Table 8] or evacuation of the clot (EVT). Since brain tissue survival depends on the time they should be planned as early as possible in an eligible patient. The number needed to treat with IVT ranges from 7 to 14 and EVT ranges from 2 to 8 based on the time of onset and intervention.
Figure 7: Flowchart for management of acute stroke

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Figure 8: Flowchart for management of intracranial hemorrhage

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Figure 9: Flow chart for management of cerebral venous thrombosis

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Table 5: Landmark trials in the evolution of intravenous thrombolysis

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Table 6: Indications for intra venous thrombolysis

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Table 7: Contraindications for intra venous thrombolysis

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Table 8: Special considerations for intra venous thrombolysis (3-4.5 h)

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The IVT involves the injection of a specific dose of the fibrinolytic drug [Table 9] into veins that cause lysis of clots and recanalization of the vessel. Monitoring of the side effects like anaphylaxis, ICH, hypertension has to be done during the infusion.[11],[18],[24],[25],[26],[27]
Table 9: Agents used in intravenous thrombolysis

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Manpower requirement

To pursue IVT, a stroke unit is essential, which comprises physicians trained in stroke/neurologist, neurosurgeon, physiotherapist, and social worker, with the availability of nursing staff, CT for 24 h.

Advantages and disadvantages

The IVT is a boon for acute ischemic stroke patients. It improves the course in at least 30% of patients. The disadvantage is that it is costly and if ICH occurs, it is dreadful and may lead to death/morbidity in 5%–8% of patients.[11]


  Post Infusion Monitoring Top


The Glasgow coma scale and blood pressure should be monitored every 15 min for 1 h and every 30 min for 4 h and every 1 h for 18 h. If the patient develops a severe headache, acute hypertension, nausea, vomiting, discontinue the infusion, and obtain an urgent CT head. Systolic BP should be maintained below 180 and diastolic BP below 105 mm of Hg. Administer nitroglycerine infusion or intravenous labetalol if the BP rises above these limits [Table 10].
Table 10: Management of complications of intravenous thrombolysis

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  Endovascular Therapy for Stroke Top


Endovascular therapy is one of the best available treatments for acute stroke with large vessel occlusion with good chances of recovery if treated in time. It includes mechanical thrombectomy in acute stroke presenting within the window period, and carotid stenting which helps in secondary prevention of stroke. Over the last two decades, the field of endovascular stroke intervention has grown exponentially. The landmark trials and conclusions are enlisted in the following [Table 11].
Table 11: Landmark trials in endovascular treatment for stroke

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The following are the pivotal trials in endovascular therapy which paved a way for approval and clinical utility of EVT [Table 11]. Target blood vessel is proximal MCA/ICA occlusion.[13],[14],[28],[29],[30],[31],[32],[33],[34],[35],[36],[37],[38],[39],[40]

Agents used

The Mechanical Embolus Removal in Cerebral Ischemia devise was used initially which did not produce robust evidence of the benefit of EVT. Gradually, the clot retrieval devices, aspiration devices, and stent retrievers evolved, which resulted in a good outcome. The success of EVT depends on the timing of intervention, duration of the procedure, infarct core, and patient factors like diabetes, and hypertension [Table 12] and [Table 13]. Complications like ICH can occur rarely.[13],[14]
Table 12: Indications for endovascular treatment for stroke

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Table 13: Endovascular therapy for patients in 6-24 h window period (DEFUSE and DAWN criteria)

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Manpower

The EVT procedure is technically demanding. It needs an interventionist trained in endovascular therapy. Also, a team of neurologists, neurosurgeons, physiotherapists, speech therapists, and social workers are essential. Nursing staff and CT scan are mandatory.

The advantage is that it has a very low number to treat, a high chance of recovery if recanalization is achieved. Disadvantages are: Technically demanding, costly (2–5 lakh rupees), very few centers in India can do the procedure at present.


  Stroke Unit and How to Make Your Hospital Into a Stroke Ready Hospital Top


A stroke unit is an organized, identified in-hospital facility that entirely is dedicated to treating stroke patients. It is staffed by a multidisciplinary team with special knowledge in stroke care [Table 14]. Stroke units are divided into three types: Advanced stroke services, essential stroke services, and minimal healthcare services. Advanced services are provided chiefly at tertiary care hospitals, minimal health care facilities are available at primary health centers.[41]
Table 14: Health service capacity for stroke care (stroke unit) checklist

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  Conclusion Top


Stroke is the second leading cause of morbidity and mortality worldwide. Ischemic stroke is the most common type. Clinical features at presentation help in localizing the stroke. Imaging reveals the type of stroke. Blood investigations and cardiac evaluation are mandatory in evaluation. Daily exercises, risk factor management help in primary prevention. The recent development in IVT and EVT are the landmark therapies in the management of ischemic stroke in this era. Based on the etiology, anti-platelets/anti-coagulants have to be started for secondary prevention. Hospitals have to prepare the checklist and try to improve the facilities and upgrade according to the guidelines.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
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    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9]
 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7], [Table 8], [Table 9], [Table 10], [Table 11], [Table 12], [Table 13], [Table 14]



 

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  In this article
Abstract
Introduction
Definition, Epid...
Clinical Feature...
Diagnosis
Differential Dia...
Investigations
Blood Investigations
Imaging
Computed Tomogra...
Magnetic Resonan...
Role of Imaging ...
Imaging in Cereb...
Supportive Treatment
Intracranial Hem...
Management of Ce...
Reperfusion Ther...
Post Infusion Mo...
Endovascular The...
Stroke Unit and ...
Conclusion
Treatment Modali...
References
Article Figures
Article Tables

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