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Acute Management of Stroke

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Acute Management of Stroke

Author: Edward C Jauch, MD, MS, FAHA, FACEP; Chief Editor: Helmi L Lutsep, MD more... Updated: Jul 10, 2012

Initial Treatment
The goal for the acute management of patients with stroke is to stabilize the patient and to complete initial evaluation and assessment, including imaging and laboratory studies, within 60 minutes of patient arrival.[1] (See Table 1, below.) Critical decisions focus on the need for intubation, blood pressure control, and determination of risk/benefit for thrombolytic intervention. Table 1. NINDS* and ACLS** Recommended Stroke Evaluation Time Benchmarks for Potential Thrombolysis Candidate (Open Table in a new window) Time Interval Door to doctor Access to neurologic expertise Door to CT scan completion Door to CT scan interpretation Door to treatment Admission to stroke unit or ICU Time Target 10 min 15 min 25 min 45 min 60 min 3h

*National Institute of Neurologic Disorders and Stroke

**Advanced Cardiac Life Support guidelines

Hypoglycemia and hyperglycemia need to be identified and treated early in the evaluation. Not only can both produce symptoms that mimic ischemic stroke, but they can also aggravate ongoing neuronal ischemia. Administration of glucose in hypoglycemia produces profound and prompt improvement, while insulin should be started for patients with stroke and hyperglycemia. Ongoing studies will help to determine the optimal level of glycemic control.[2] 1/9


Acute Management of Stroke

Hyperthermia is infrequently associated with stroke but can increase morbidity. Administration of acetaminophen, by mouth or per rectum, is indicated in the presence of fever (temperature >100.4 F [38 C]). Supplemental oxygen is recommended when the patient has a documented oxygen requirement. To date, there is conflicting evidence whether supernormal oxygenation improves outcome. Optimal blood pressure targets remain to be determined. Many patients are hypertensive on arrival. American Stroke Association guidelines have reinforced the need for caution in lowering blood pressures acutely. In the small proportion of patients with stroke who are relatively hypotensive, pharmacologically increasing blood pressure may improve flow through critical stenoses. Serial monitoring and interventions when necessary early in the clinical course and eventual stroke rehabilitation and physical and occupational therapy are the ideals of management. (See Table 2, below.) In patients with transient ischemic attacks (TIAs), failure to recognize the potential for near- term stroke, failure to perform a timely assessment for stroke risk factors, and failure to initiate primary and secondary stroke prevention exposes the patient to undue risk of stroke and exposes clinicians to potential litigation. TIAs confer a 10% risk of stroke within 30 days, and one half of the strokes occurring after a TIA, occurred within 48 hours.[3] Table 2. General Management of Patients With Acute Stroke[1, 4] (Open Table in a new window) Treat hypoglycemia with D50

Blood glucose

Treat hyperglycemia with insulin if serum glucose >200 mg/dL

Blood pressure Cardiac monitor

See recommendations for thrombolysis candidates and noncandidates (Table 3) Continuous monitoring for ischemic changes or atrial fibrillation

Intravenous fluids Avoid D5W and excessive fluid administration

IV isotonic sodium chloride solution at 50 mL/h unless otherwise indicated

Oral intake Oxygen Temperature

NPO initially; aspiration risk is great, avoid oral intake until swallowing assessed Supplement if indicated (Sa02 < 94%) Avoid hyperthermia; use oral or rectal acetaminophen and cooling blankets as needed

Thrombolytic Therapy
Current treatments for acute ischemic stroke include IV thrombolytic therapy with tissue-type plasminogen activator (t-PA) and endovascular therapies, including intra-arterial thrombolytic therapy and the use of clot retrieval devices.[5] Surgical management with hemispheric decompression in patients with middle cerebral artery territory infarction and associated life-threatening parenchymal edema has also been supported.[6, 7] Newer stroke trials have shown the benefit of using neuroimaging to select patients who are most likely to benefit from thrombolytic therapy and the potential benefits of extending the window for thrombolytic therapy beyond the guideline of 3 hours with t-PA and newer agents. CT angiography may demonstrate the location of vascular occlusion. CT perfusion studies are capable of producing perfusion images and together with CT angiography are becoming more available and utilized in the acute evaluation of stroke patients.[8] The Diffusion and Perfusion Imaging Evaluation for Understanding Stroke Evolution (DEFUSE) trial demonstrated the benefit of administering IV t-PA within 3-6 hours of stroke onset in patients with small ischemic cores on 2/9


Acute Management of Stroke

diffusion-weighted magnetic resonance imaging (MRI) and larger perfusion abnormalities (large ischemic penumbras).[9] The Desmoteplase In Acute Ischemic Stroke (DIAS) trial similarly demonstrated the benefit of administering desmoteplase in patients within 3-9 hours of onset of acute stroke in patients with a significant mismatch (>20%) between perfusion abnormalities and ischemic core on diffusion-weighted MRI.[10] A study by Jovin et al showed successful endovascular therapy beyond 8 hours from time last seen well in patients selected for treatment based on MRI or CT perfusion imaging. Revascularization was successful in about 73% of patients.[11] Advanced neuroimaging with diffusion and perfusion imaging may then serve an important role in identifying potentially salvageable tissue at risk and guiding clinical decision making regarding therapy.[10, 12, 13, 14, 15] The iScore may also be used in patients with an acute ischemic stroke to predict clinical response and risk of hemorrhagic complications following IV thrombolytic therapy.[16]

Stabilization of Airway and Breathing

Patients presenting with Glasgow Coma Scale scores of 8 or less, rapidly decreasing Glasgow Coma Scale scores, or inadequate airway protection or ventilation require emergent airway control via rapid sequence intubation. When increased intracranial pressure (ICP) is suspected, rapid sequence induction should be directed at minimizing the potentially adverse effects of intubation. In unusual cases of potential imminent brain herniation, where the goal of mechanical ventilation is hyperventilation to decrease ICP by decreasing cerebral blood flow, the recommended endpoint is an arterial pCO2 of 32-36 mm Hg. IV mannitol can be considered as well. Supplemental oxygen use should be guided by pulse oximetry. Patients should receive supplemental oxygen if their pulse oximetry reading or arterial blood gas measurement reveals that they are hypoxic (SaO 2 < 94%). The most common causes of hypoxia in the patient with acute stroke are partial airway obstruction, hypoventilation, atelectasis, or aspiration of stomach or oropharyngeal contents.[17, 18]

Intravenous Access and Cardiac Monitoring

Patients with acute stroke require IV access and cardiac monitoring in the emergency department (ED). Patients with acute stroke are at risk for cardiac arrhythmias. In addition, atrial fibrillation may be associated with acute stroke as either the cause (embolic disease) or as a complication.

Blood Glucose Control

Severe hyperglycemia appears to be independently associated with poor outcome and reduced reperfusion in thrombolysis, as well as extension of the infarcted territory.[19, 20, 21] Additionally, normoglycemic patients should not be given excessive glucose-containing IV fluids, as this may lead to hyperglycemia and may exacerbate ischemic cerebral injury. Blood sugar control should be tightly maintained with insulin therapy, with the goal of establishing normoglycemia (90-140 mg/dL). Additionally, close monitoring of blood sugar level should continue throughout hospitalization to avoid hypoglycemia.[1]

Patient Positioning
Studies have shown that cerebral perfusion pressure is maximized when patients are maintained in a supine position. However, lying flat may serve to increase ICP and thus is not recommended in cases of subarachnoid or other intracranial hemorrhage. Because prolonged immobilization may lead to its own complications, including deep venous thrombosis, pressure ulcer aspiration, and pneumonia, patients should not be kept flat for longer than 24 hours.[22] 3/9


Acute Management of Stroke

Blood Pressure Control

In poor flow stateswhich occur with thrombotic and embolic ischemic stroke, as well as with increased ICP due to cerebral edemathe cerebral vasculature loses vasoregulatory capability and thus relies directly on mean arterial pressure (MAP) and cardiac output for maintenance of cerebral blood flow. Therefore, aggressive efforts to lower blood pressure may decrease perfusion pressure and may prolong or worsen ischemia. Rapid reduction of blood pressure, no matter the degree of hypertension, may in fact be harmful. Both elevated and low blood pressures are associated with poor outcomes in patients with acute stroke.[23] (See Table 3, below.) Studies have demonstrated that blood pressure typically drops in the first 24 hours after acute stroke, whether or not antihypertensives are administered. Furthermore, studies have revealed poorer outcomes in patients with lower blood pressures, with these outcomes correlating with the degree of pressure decline.[23, 24] The consensus recommendation is to lower blood pressure only if systolic pressure is in excess of 220 mm Hg or if diastolic pressure is greater than 120 mm Hg.[18] However, a systolic blood pressure greater than 185 mm Hg or a diastolic pressure greater than 110 mm Hg is a contraindication to the use of thrombolytics. Therefore, the management of elevated blood pressure in acute ischemic stroke may vary, depending on whether the patient is a candidate for thrombolytic therapy.

Hypertension control in nonrt-PA candidates

For patients who are not candidates for thrombolysis with recombinant t-PA (rt-PA) and who have a systolic blood pressure of less than 220 mm Hg and a diastolic blood pressure of less than 120 mm Hg in the absence of evidence of end-organ involvement (ie, pulmonary edema, aortic dissection, hypertensive encephalopathy), blood pressure should be monitored (without acute intervention) and stroke symptoms and complications (eg, increased ICP, seizures) should be treated. For patients with a systolic blood pressure above 220 mm Hg or a diastolic blood pressure greater than 120 mm Hg, labetalol (10-20 mg IV for 1-2 min) should be the initial drug of choice, unless a contraindication to its use exists. Dosing may be repeated or doubled every 10 minutes to a maximum dose of 300 mg. Alternatively, nicardipine may be used for blood pressure control. Nicardipine is given intravenously at an initial rate of 5 mg/h and titrated to effect by increasing the infusion rate 2.5 mg/h every 5 minutes, to a maximum of 15 mg/h. Lastly, nitroprusside at 0.5 mcg/kg/min IV infusion may be used in the setting of continuous blood pressure monitoring. The goal of intervention is a reduction in blood pressure of 10-15%.

Hypertension control in rt-PA candidates

For patients who will be receiving rt-PA, systolic blood pressure greater than 185 mm Hg and diastolic blood pressure greater than 110 mm Hg require intervention. Monitoring and control of blood pressure during and after thrombolytic administration are vital, because uncontrolled hypertension is associated with hemorrhagic complication.[25] The initial drug of choice, labetalol (10-20 mg IV for 1-2 min), may be repeated (maximum dose 300 mg). One to 2 inches of transdermal nitropaste may also be used. As an alternative to these choices, nicardipine infusion at 5 mg/h, titrated up to a maximum dose of 15 mg/h, can be used.[18] Monitoring of blood pressure is crucial; for the first 2 hours, blood pressure should be checked every 15 minutes, then every 30 minutes for 6 hours, and finally, every hour for 16 hours. The goal of therapy should be to reduce blood pressure by 15-25% in the first day, with continued blood pressure control during hospitalization. For patients with systolic blood pressure of 185-230 mm Hg or diastolic blood pressure of 110-120 mm Hg, labetalol is given at a dose of 10-20 mg IV over 1-2 minutes; the dose may be repeated every 10-20 minutes, up to 300 mg total, or an infusion rate of up to 2-8 mg/min may be used.[1] For systolic blood pressure of greater than 230 mm Hg or diastolic blood pressure of 121-140 mm Hg, labetalol at the above doses can be considered. However, nicardipine infusion administered at a rate of 5 mg/h, to a maximum of 15 mg/h, might be a better first choice. For difficult-to-control blood pressure, sodium nitroprusside can be considered.[1] The use of sublingual nifedipine to lower blood pressure in the ED is discouraged, since extreme hypotension may result. Trials of nimodipine, initially thought to be beneficial given its vasodilatory effect as a calcium-channel 4/9


Acute Management of Stroke

blocker, have failed to demonstrate any beneficial outcome in comparison with placebo.[17] Consensus agreement is that these blood pressure guidelines should be maintained in the face of other interventions to restore perfusion, such as intra-arterial thrombolysis.[1] Table 3. Blood Pressure Management in Patients With Stroke* (Open Table in a new window) Blood Pressure Candidates for Pretreatment: fibrinolysis Treatment Labetalol 10-20 mg IVP repeated every 10-20 minutes

SBP >185 or DBP >110 mm Hg


Nicardipine 5 mg/h, titrate by 2.5 mg/h every 5-15 min, maximum 15 mg/h; when desired blood pressure reached, lower to 3 mg/h or

Enalapril 1.25 mg IVP


Sodium nitroprusside (0.5 mcg/kg/min)

DBP >140 mm Hg

Labetalol 10-20 mg IVP and consider labetalol infusion at 1-2 mg/min or nicardipine 5 mg/h IV infusion and titrate

SBP >230 mm Hg or or

DBP 121-140 mm Hg Nicardipine 5 mg/h, titrate by 2.5 mg/h every 5-15 min, maximum 15 mg/h; when desired blood pressure reached, lower to 3 mg/h or SBP 180-230 mm Hg or DBP 105-120 mm Hg Labetalol 10 mg IVP, may repeat and double every 10 min up to maximum dose of 300 mg

Noncandidates DBP >140 mm Hg for fibrinolysis

Sodium nitroprusside 0.5 mcg/kg/min; may reduce approximately 1020%

SBP >220 or Labetalol 10-20 mg IVP over 1-2 min; may repeat and double every 10 min up to maximum dose of 150 mg or nicardipine 5 mg/h IV infusion and titrate DBP 121-140 mm Hg or or 5/9


Acute Management of Stroke

MAP >130 mm Hg Nicardipine 5 mg/h, titrate by 2.5 mg/h every 5-15 min, maximum 15 mg/h; when desired blood pressure reached, lower to 3 mg/h SBP < 220 mm Hg or

Antihypertensive therapy indicated only if acute myocardial infarction, DBP 105-120 mm Hg aortic dissection, severe CHF, or hypertensive encephalopathy present or

MAP < 130 mm Hg

*Adapted from 2005 Advanced Cardiac Life Support (ACLS) guidelines and 2007 American Stroke Association Scientific Statement

Abbreviations: SBP - systolic blood pressure; DBP - diastolic blood pressure; IVP - IV push; MAP - mean arterial pressure

Control of hypotension
Given the need to maintain adequate cerebral blood flow, severe hypotension should be managed in standard fashion with aggressive fluid resuscitation, a search for the etiology of hypotension, and, if necessary, vasopressor support. Evidence suggests that baseline systolic blood pressure below 100 mg Hg and diastolic blood pressure below 70 mm Hg correlate with a worse outcome.[23]

Further Outpatient Care

Poststroke outpatient care largely focuses on rehabilitation and prevention of recurrent stroke. Rehabilitation planning and initiation begins within the first day of the acute stroke. Recent research has demonstrated the benefits of early and aggressive mobilization.[26]

Additional Care
Referral to a physician with a special interest in stroke is ideal. Stroke care units with specially trained personnel exist and are said to show improved outcomes Comorbid medical problems need to be addressed. Assessments of swallow function prior to the reinstitution of oral feeding is recommended.[1] Patients should receive deep venous thrombosis prophylaxis, although the timing of institution of this therapy is unknown.

Medical/Legal Pitfalls
In patients with transient ischemic attacks, failure to recognize the potential for near term stroke, failure to perform a timely assessment for stroke risk factors, and failure to initiate primary and secondary stroke prevention exposes the patient to undue risk of stroke and exposes clinicians to potential litigation.[3]



Acute Management of Stroke

Contributor Information and Disclosures

Author Edward C Jauch, MD, MS, FAHA, FACEP Professor, Division Director, Division of Emergency Medicine and Department of Neurosciences, Medical University of South Carolina College of Medicine Edward C Jauch, MD, MS, FAHA, FACEP is a member of the following medical societies: American College of Emergency Physicians, American Heart Association, American Medical Association, National Stroke Association, Society for Academic Emergency Medicine, and South Carolina Medical Association Disclosure: Nothing to disclose. Coauthor(s) Brett Kissela, MD MS, Professor, Co-Director of the Neurology Residency Program, Vice-Chair of Education and Clinical Services, Department of Neurology, University of Cincinnati Brett Kissela, MD is a member of the following medical societies: American Academy of Neurology, American Heart Association, and Phi Beta Kappa Disclosure: Allergan Consulting fee Consulting; Allergan Honoraria Speaking and teaching Brian Stettler, MD Assistant Professor, Program Director, Emergency Medicine Residency Program, Department of Emergency Medicine, and Faculty Greater Cincinnati/Northern Kentucky Stroke Team, University of Cincinnati Disclosure: Nothing to disclose. Specialty Editor Board Thomas A Kent, MD Professor and Director of Stroke Research and Education, Department of Neurology, Baylor College of Medicine; Chief of Neurology, Michael E DeBakey Veterans Affairs Medical Center Thomas A Kent, MD is a member of the following medical societies: American Academy of Neurology, American Neurological Association, New York Academy of Sciences, Royal Society of Medicine, Sigma Xi, and Stroke Council of the American Heart Association Disclosure: Nothing to disclose. Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference Disclosure: Medscape Salary Employment Howard S Kirshner, MD Professor of Neurology, Psychiatry and Hearing and Speech Sciences, Vice Chairman, Department of Neurology, Vanderbilt University School of Medicine; Director, Vanderbilt Stroke Center; Program Director, Stroke Service, Vanderbilt Stallworth Rehabilitation Hospital; Consulting Staff, Department of Neurology, Nashville Veterans Affairs Medical Center Howard S Kirshner, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, American Heart Association, American Medical Association, American Neurological Association, American Society of Neurorehabilitation, National Stroke Association, Phi Beta Kappa, and Tennessee Medical Association Disclosure: Nothing to disclose. Chief Editor Helmi L Lutsep, MD Professor and Vice Chair, Department of Neurology, Oregon Health and Science University School of Medicine; Associate Director, Oregon Stroke Center Helmi L Lutsep, MD is a member of the following medical societies: American Academy of Neurology and American Stroke Association Disclosure: Co-Axia Consulting fee Review panel membership; AGA Medical Consulting fee Review panel membership; Concentric Medical Consulting fee Review panel membership



Acute Management of Stroke

membership; Concentric Medical Consulting fee Review panel membership Additional Contributors The authors would like to thank Dr. Jennifer Franklin for her assistance with this update.

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Acute Management of Stroke

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