Stroke Management Guidelines
Adabella Frierdich
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. [3] While trials have shown no clear benefit from intensive glucose control in acute stroke patients, it is reasonable to target a glucose level of 140-180 mg/dL. [3, 4]
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]).
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. [3]
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. [5]
Current treatments for acute ischemic stroke include IV thrombolytic therapy with tissue-type plasminogen activator (t-PA) or tenecteplase (tNK) and endovascular thrombectomy. [3] Current American Heart Association/American Stroke Association guidelines for the early management of patients with acute ischemic stroke recommend that patients eligible for intravenous tthrombolysis should receive thrombolysis with tPA or tNK even if endovascular thrombectomy is being considered. [3]
Newer stroke trials have explored 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 4.5 hours. 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. [6]
The Diffusion and Perfusion Imaging Evaluation for Understanding Stroke Evolution (DEFUSE) trial suggested that there might be benefit of administering IV t-PA within 3-6 hours of stroke onset in patients with small ischemic cores on diffusion-weighted magnetic resonance imaging (MRI) and larger perfusion abnormalities (large ischemic penumbras). [7]
The Desmoteplase In Acute Ischemic Stroke (DIAS) trial sought to show the benefit of administering desmoteplase in patients within 3-9 hours of onset of acute stroke with a significant mismatch (>20%) between perfusion abnormalities and ischemic core on diffusion-weighted MRI [8] . Larger randomized trials of desmoteplase were negative. [9]
Muchada et al performed a study on 581 consecutive patients treated with alteplase to identify the impact of time-to-treatment according to stroke severity on functional outcome in patients with acute ischemic stroke. They found that the window for favorable outcome was 120 minutes or less for moderate strokes, but time-to-treatment seemed unrelated to functional outcome in mild and severe stroke. [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. [12]
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. [8, 13, 14, 15, 16]
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.
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. [18, 19]
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.
Severe hyperglycemia appears to be independently associated with poor outcome and reduced reperfusion in thrombolysis, as well as extension of the infarcted territory. [20, 21, 22] 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 closely monitored in acute stroke patients to achieve a goal between 140 and 180 mg/dL. Additionally, close monitoring of blood sugar level should continue throughout hospitalization to avoid hypoglycemia. [1]
Studies have previously shown that cerebral perfusion pressure is maximized when patients are maintained in a supine position. However, lying flat may serve to increase ICP. A cluster-randomized crossover trial in patients with acute stroke (85% ischemic) showed that disability outcomes after acute stroke did not differ significantly between patients assigned to a lying-flat position for 24 hours and patients assigned to a sitting-up position with the head elevated to at least 30 degrees for 24 hours. [23] 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. [24]
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. [25, 26]
In a 2012 analysis of data from The Scandinavian Candesartan Acute Stroke Trial, acute stroke patients with a large decrease or increase or no change in systolic blood pressure experienced an increased risk of early adverse events compared with patients with a small decrease, and patients with an increase or no change in systolic blood pressure had an increased risk of poor neurological outcome compared with other patients. Routine attempts to lower blood pressure in the acute phase of stroke should probably be avoided. [27]
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. [19] 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.
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%.
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. [28]
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 (see nitroglycerin topical) 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. [19]
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.
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