Authors

  1. Toufic El Hussein, Mohamed PhD, NP
  2. Green, Tyler

Abstract

Determining the treatment plan and how to successfully manage a patient suffering from an acute ischemic stroke can be challenging for a registered nurse (RN) in the emergency department. Using a mnemonic in the treatment process assists in reducing medical errors and increases the likelihood of making positive clinical outcomes. Mnemonics sum up complex strategies into relevant information that can be comprehensible for users. The authors have created a mnemonic strategy to provide RNs in the emergency department with a structured approach to the pharmacotherapeutic strategies used in treating patients with an acute ischemic stroke. All guidelines used throughout the article are in concurrence.

 

Article Content

MNEMONICAL learning supports higher thinking by encoding information for the purpose of rapid access and use.1 Using a mnemonic helps health care providers recall details needed for developing effective medical management plans.2

 

A pilot study was conducted to assess whether the use of a mnemonic would help nurses recall specific steps in providing care.2 A quasi-experimental research approach was used and focused on nurses giving valuable education to a transplant patient population while utilizing a mnemonical strategy as an aid. A total of 36 participants completed all of the study components. It was concluded that a mnemonical approach to help nurses recall the steps in patient education proved to be an effective way to increase their ability to access their knowledge.2

 

This article provides registered nurses (RNs) with an overview of acute ischemic stroke in an emergency care setting and the treatment plan that follows. The ABCD mnemonic (Table 1) is listed as Antiplatelets and/or Anticoagulants, Blood pressure, Clot extraction and/or dissolution, and Diagnostics. It is listed in alphabetical order to assist in memorizing but is not intended to be followed chronologically. The mnemonic is to be used as an aid memoir and should never replace the clinical judgment of the stroke team (emergency physician, emergency nurse, neurologist, and neurology nurse).

  
Table 1 - Click to enlarge in new windowTable 1. Alphabetical Mnemonic

PATHOPHYSIOLOGY

Stroke is defined as a sudden deficit in neurological functions caused by an impairment of perfusion to the brain.3 Stroke diagnosis is divided into 2 categories: ischemic or hemorrhagic. The lack of blood to the brain results in an ischemic stroke due to either decrease or cessation of blood supply.3 An ischemic stroke can be either embolic or thrombotic. A thrombotic stroke is the less common subtype and occurs when a thrombus is formed locally in either the anterior or posterior circulation of the brain due to an underlying pathology, for example, stenosis or dissection of a brain artery. An embolic stroke is a subset of ischemic stroke and is identified as an occlusion of the brain arteries by a clot that arises from the heart or other sites. While cardioembolic stroke is the most common type of embolic strokes, artery-to-artery embolization is not uncommon.3

 

Anterior and posterior circulations make up the blood circulation of the brain. Both of these circulations are connected by the posterior communicating arteries, which make up the circle of Willis4 (Figure 1). Thrombi are commonly formed proximal to the middle cerebral artery (MCA), due to internal carotid artery plaques or common carotid artery plaques.5 One of the primary risk factors of strokes is atrial fibrillation,6 often caused by atrial fibrosis, and is associated with decline in its contractility. Atrial hypocontractility results in blood flow stasis in the left atrial appendage and activation of platelets and coagulation cascade that promote thrombus formation.7 A clot that develops from atrial fibrillation is likely to go into the anterior circulation in the MCA.4

  
Figure 1 - Click to enlarge in new windowFigure 1. The Circle of Willis.

A hemorrhagic stroke is a life-threatening emergency defined as sudden rupture of cerebral blood vessels where the leaked blood surrounds the brain and compresses its tissue and cells.8

 

A transient ischemic attack (TIA) is similar to a stroke clinically and produces analogous symptoms but tends to last few minutes. TIA is a temporary blockage of blood flow to the brain and is considered as a warning sign for recurrent strokes.9 It has been reported that 5% of TIA patients will develop a stroke within 24 hours, 5% within 48 hours, 10% within 1 a week, 9% within a month, and 10% to 20% within 3 months.10 RNs must be aware of the prognostic clinical scores, such as ABCD2, to risk stratify stroke in patients presenting with TIA in order to intervene early.10 The ABCD2 score depends on age of the patient, blood pressure (BP), clinical manifestations, duration of symptoms, and diabetes history.11 The ABCD2 score can effectively predict early progression of a cerebral infarction from TIA.10

 

MNEMONIC

Antiplatelets and Anticoagulants are drugs used to inhibit clot formation and delay hemostasis. Patients with an acute ischemic stroke, who are not already on antiplatelet therapy, should be given at least 160 mg of acetylsalicylic acid (ASA) as a one-time loading dose after a computed tomographic (CT) scan has excluded intracranial hemorrhage (ICH).12 If patients are eligible for intravenous alteplase, ASA should be delayed until 24 hours postthrombolysis and once a hemorrhagic stroke has been ruled out on repeated CT scan.12 Receiving ASA prior to emergency department (ED) admission is not a contraindication for thrombolytic therapy as long as CT brain scan confirms the absence of acute bleeding.12

 

If the cause of the stroke is determined to be minor noncardioembolic or a high-risk TIA, a combination of clopidogrel and ASA should be given for a duration of 21 to 30 days, followed by antiplatelet monotherapy (such as ASA or clopidogrel alone) indefinitely.12 A loading dose of 300 to 600 mg of clopidogrel and 160 mg of ASA should be given at the initiation of treatment.13 A randomized trial was performed that assigned patients with a minor ischemic stroke or high-risk TIA to receive clopidogrel plus aspirin or to receive aspirin alone.14 Major ischemic events occurred in 121 of 2432 (5.0%) patients receiving clopidogrel and aspirin and in 160 of 2449 (6.5%) patients receiving aspirin alone (P = .02). Therefore, in patients with a minor ischemic stroke or high-risk TIA, dual antiplatelet therapy is recommended with a combination of clopidogrel and ASA. This combination increases the risk of hemorrhage as opposed to those who receive aspirin alone.14

 

In an acute ischemic stroke, the risk of a recurrent stroke event and hemorrhage is at its highest just days after the initial stroke occurs.15 In terms of treatment of patients with atrial fibrillation who have experienced an acute cardioembolic stroke, direct-acting oral anticoagulants (DOACs) have been shown to be effective and superior to warfarin to reduce the risk of another stroke with fewer side effects.16 Using the CHA2DS2-VASc score (https://www.mdcalc.com/cha2ds2-vasc-score-atrial-fibrillation-stroke-risk), which calculates the stroke risk for patients with atrial fibrillation, and the National Institutes of Health Stroke Scale (NIHSS) score (https://www.mdcalc.com/nih-stroke-scale-score-nihss), which helps quantify the severity of the stroke, clinicians can determine which patients need to be anticoagulated.17 Examples of DOACs include direct thrombin inhibitors (eg, dabigatran) and factor Xa inhibitors (eg, apixaban, edoxaban, and rivaroxaban). Licensed independent practitioners should perform a quick review of systems and evaluate patients for bleeding tendencies before prescribing a DOAC.18 Dosing requirements are outlined in Table 1. For patients who are started on anticoagulant therapy, such as a DOAC, bridging is not recommended with an intravenous heparin. The choice or whether to start the DOAC alone or in combination with an unfractionated heparin (bridging) is based on the risk of a thrombus developing compared with the risk of bleeding.17 The risk of ICH is increased with the use of antiplatelets and anticoagulants.17

 

Blood pressure management is a vital aspect of treatment of patients presenting with an acute ischemic stroke. Patients with an acute ischemic stroke often present with elevated arterial BP, which tends to worsen the clinical outcomes.19 A retrospective analysis study was conducted to examine whether increased BP was associated with death after an acute ischemic stroke.20 It was concluded that of 1891 patients, 277 (14.7%) died within 90 days.20 All patients who died had an increase in BP, particularly an elevation in systole (systolic standard deviation for alive vs dead patients = 13.4 vs 15.9 mm Hg; P < .001).20 During an acute ischemic stroke, hypertension should not be aggressively lowered in patients who are not eligible for thrombolytic therapy because brain perfusion is proportional to mean arterial BP. An ideal range of mean arterial pressure (MAP) is between 50 and 150 mm Hg. When the pressure of MAP increases above the regular limits, an increase in cerebral blood flow leads to edema and hemorrhage.21 Excessive lowering of BP, on the other hand, can cause further exacerbation of ischemia.12 Extreme increase in blood (systolic blood pressure [SBP] >220 mm Hg or diastolic blood pressure [DBP] >120 mm Hg) should be treated to reduce the BP by at least 15% in the first hour but not more than 25% in the first 24 hours.22 As seen in Table 2, for patients who are eligible for thrombolytic therapy, very high BP (>185/110 mm Hg) should be treated to reduce the risk of ICH.12 Lowering BP must be individualized to each patient. High SBP must be managed with antihypertensive medications, such as the combination of an angiotensin-converting enzyme (ACE) inhibitor with a thiazide-like diuretic (Table 1). Autoregulating is vital in the first 24 hours after a stroke, and SBP should be kept less than 185/110 mm Hg. After the acute phase has elapsed, the initiation of chronic antihypertensive therapy can be considered.23 As per the Hypertension Canada Guidelines updated as of 2018, the combination of an ACE inhibitor and a thiazide/thiazide-like diuretic is the preferred treatment option poststroke.22

  
Table 2 - Click to enlarge in new windowTable 2. r-tPA in Ischemic Stroke: Indications and Contraindicationsa

In the notable 2001 Perindopril Protection Against Recurrent Stroke Study (PROGRESS), 6105 patients with a history of ischemic stroke and TIA with and without hypertension were randomized into 3 groups that received perindopril alone, in combination with indapamide, or placebo. After a mean of 3.9 years, the treatment group with the combination of perindopril plus indapamide had SBP and DBP decreases of 12 and 5 mm Hg, respectively, and a lower stroke risk than patients who received double placebo.24 As noted in Table 1, the recommended dose as per the PROGRESS trial is 4 mg/d of perindopril in combination with 2.5 mg/d of indapamide to manage hypertension poststroke and decrease the likelihood of recurrent strokes. The American Heart Association/American Stroke Association updated 2019 guidelines recommend that hypertensive patients with BP that is more than 185/110 mm Hg but are otherwise eligible for emergency reperfusion therapy should be treated with labetalol 10 to 20 mg intravenously, nicardipine 5 mg/h intravenously, or clevidipine 1 to 2 mg/h intravenously. Further dosage instructions are outlined in Table 1. If BP is not maintained at 185/110 mm Hg or less, alteplase must not be administered.23 Licensed independent practitioners must be aware of different guidelines regarding pharmacological management in order to treat the patient's hypertension accordingly.

 

Clot dissolution or extraction is the physical or pharmacological removal of a clot from the brain. For clot dissolution, alteplase, or recombinant tissue plasminogen activator (r-tPA), is a thrombolytic drug that breaks down the clot, preventing the blood from reaching the brain.25 As outlined in Tables 1 and 2, all patients with N embolic stroke should be offered intravenous alteplase 0.9 mg/kg, 90-mg total dose, within 4.5 hours of the onset of stroke.12 However, in a randomized controlled trial (RCT) completed, a total of 503 patients with an acute stroke of unknown time of onset were randomly assigned to receive alteplase or placebo after magnetic resonance imaging (MRI) suggested a recent cerebral infarction.26 Of the 503 patients enrolled, 254 patients were randomly assigned to receive alteplase and 249 received placebo. A positive survival outcome was reported in 131 of the 246 patients in the alteplase group (53.3%) and in 102 of 244 patients in the placebo group (41.8%). There were 10 deaths in the alteplase group and 3 in the placebo group. The rate of hemorrhage was 2.0% in the alteplase group and 0.4% in the placebo group. The authors of the study concluded that those who received intravenous alteplase had a functionally better outcome but an increased risk of hemorrhage. Initiation of alteplase is time-dependent and should be started as soon as possible.27 Patients on low-molecular-weight heparin who received a full dose within the last 24 hours must not be given alteplase but immediately considered for endovascular thrombectomy23 (Table 2).

 

Although many research studies have proved that alteplase is a successful treatment option, there are many contraindications that limit its use. Along with the narrow time window, other limitations include an increased rate of ICH and bleeding, a low recanalization rate in large artery occlusion such as the proximal MCA, the internal carotid artery, or the basilar artery, and unresponsiveness to large thrombi.28

 

RNs in the ED should be aware of the potential complications and the exclusion/inclusion criteria that may arise for patients undergoing thrombolytic therapy during the acute phase of an ischemic stroke23 (Table 2).

 

To keep the aforementioned discussion relevant, we link it to a clinical case.

 

Mr Helmi, a 65-year-old recent refugee from Syria, presented to the ED accompanied by his wife with right upper and lower extremity weakness associated with facial drop and slurred speech. Mrs Helmi reported that her husband's symptoms started 2 hours prior to the presentation. Mr Helmi denied visual disturbance, headache, chest pain, palpitations, dyspnea, dysphagia, fever, dizziness, loss of consciousness, bowel or urinary incontinence, or trauma. Mrs Helmi reported that her husband has type 2 diabetes mellitus, hypertension, and hyperlipidemia and only 6 months ago started receiving medical therapy as he could not afford to buy medications before his arrival to the Canada. Mr Helmi was an active smoker who started smoking at the age of 25 years, an average of 1 pack per day (40PYHx). His physical examination was remarkable for right-sided facial droop, dysarthria, and right-sided hemiplegia. His NIHSS score was calculated as 8. Initial CT angiogram of head and neck reported occlusion of the left MCA, with a large perfusion deficit in the complete MCA territory. Mr Helmi's BP was 200/110 mm Hg, so intravenous labetalol 20 mg was given to lower BP to less than 185/110 mm Hg in preparation for tPA administration. The stroke team was activated, and intravenous r-tPA was administered after excluding contraindications. Unfortunately, the neurological deficits were not reversed after administration of r-tPA.

 

For clot extraction, an endovascular thrombectomy approach is used to physically extract the clot.29 There are three3 techniques for mechanical thrombectomy. As shown in Figures 2 and 3, the first technique involves inserting a mesh tube, also known as a stent retriever, into the artery in the lower extremities, moving it up to the brain, and then extracting the clot.29 Another technique is the aspiration technique. The thrombus is passed with the microwire and the microcatheter, and the aspiration catheter is placed in the proximal part of the thrombus (Figure 3). Entrapment of the thrombus is indicated by lack of backflow. The catheter is then retrieved with constant negative pressure to avoid loss of the thrombus.29 Finally, the "Solumbra" technique involves the use of a stent retriever with simultaneous aspiration.30

  
Figure 2 - Click to enlarge in new windowFigure 2. Solitaire revascularization device. (C) Medtronic, Inc. 2020.
 
Figure 3 - Click to enlarge in new windowFigure 3. Thrombectomy.

Eligibility often varies by age, stroke severity, and onset time. Endovascular therapy can be offered to patients irrespective of eligibility for alteplase.12 Many RCTs have concluded that endovascular thrombectomy improves the outcomes of patients with an acute stroke.31 The ideal time window for a patient who is to receive endovascular thrombectomy is within 6 hours of symptom onset.23 Those who have a large-vessel occlusion or discovered symptoms upon awakening may be considered for thrombectomy within 24 hours of symptom onset depending on the extent of brain ischemia on perfusion imaging.12 A 2016 meta-analysis (n = 1287) completed concluded that each 1-hour delay to reperfusion of the brain was correlated with an increase in disability and decrease in functional independence.32

 

Endovascular thrombectomy is available to patients who have received alteplase and those who have not.12 Intravenous alteplase is time sensitive, and patients should be treated with alteplase prior to thrombectomy.12 In a meta-analysis of 13 studies conducted, it was concluded that patients who had received a combination of alteplase with mechanical thrombectomy had better outcomes and lower mortality.31 Patients with a posterior circulation occlusion should be considered for endovascular thrombectomy but must be aware of the risks. Risks or complications include but are not limited to access site problems, device-related complications, and hemorrhage during procedure or postoperatively.33

 

Posterior circulation occlusions have been associated with poorer outcomes than that with anterior circulation. A retrospective study of the database of acute ischemic stroke cases that went under a combined thrombectomy technique called direct aspiration first pass technique (ADAPT) thrombectomy for large-vessel occlusions was completed.34 A total of 436 patients underwent ADAPT thrombectomy, of whom 13% had posterior circulation thrombectomy. Patients with posterior circulation did not show much of a difference in preprocedural variables that included age, NIHSS score, and onset to groin time compared with patients with anterior circulation (P > .05).34 In conclusion, it was discovered that when patients are carefully selected for thrombectomy, those with posterior circulation occlusions can achieve similar outcomes to those with anterior occlusions. ADAPT has proven to be a promising new method that is more effective and less costly than the regular aspiration and stent retrieval technique.35 After the patient and/or the substitute decision maker have confirmed that they want to go forward with endovascular thrombectomy, the patient will need to be sedated. Procedural sedation is preferred over general anesthesia and intubation due to the harmful drop in BP during induction of general anesthesia.12 Similar to intravenous alteplase, time is critical for reperfusion from endovascular thrombectomy. Endovascular treatment requires an experienced team to perform rapid assessment to achieve treatment as soon as possible. The stroke team must work together to help expedite the process of screening patients for endovascular thrombectomy.36

 

Given that Mr Helmi's acute neurological deficits did not improve, the stroke team ordered cerebral MRI, which showed a partial diffusion lesion in the left basal ganglia with a complete perfusion deficit of the left MCA territory and a persistent occlusion of the MCA upon performing magnetic resonance angiography. After consent from Mrs Helmi, the interventional neuroradiologist performed mechanical thrombectomy after giving Mr Helmi conscious sedation. Complete recanalization was accomplished with the Solitaire retriever in one attempt 6 hours after stroke onset. Angiography at the end of the intervention showed a complete reperfusion of the previously occluded left MCA territory.

 

Diagnostics for a patient presenting with an acute ischemic stroke is a time-sensitive process. When the patient arrives to the ED with a suspected stroke, the neurological team will attempt to determine the time the patient was last seen normal and assess stroke severity using a standardized stroke scale, also known as the NIHSS.12 The NIHSS is an assessment tool that provides a quantitative measure of stroke deficits. It gives an evaluation of acuity, appropriate treatment, and patient outcomes.4 After determining severity of the stroke, the patient must receive emergency brain imaging to rule out a hemorrhagic stroke. It is essential to complete imaging within 25 minutes of arrival and complete interpretation of the scan within 45 minutes to exclude a hemorrhagic stroke.36

 

Both noncontrast MRI and noncontrast CT are effective to rule out the risk of an intracerebral hemorrhage.12 Computed tomography angiography allows for rapid identification of suspected large-vessel occlusions. Best practice for large-vessel occlusions has transitioned to primarily thrombectomy (with or without intravenous alteplase), thus establishing a lesion that will allow for neurointervention is critical.37 CT perfusion imaging is used to assess characteristics of blood flow to ascertain stroke completeness.37 Brain and vascular imaging is vital as it determines quickly whether the patient can be started on thrombolytic therapy and who would be eligible for endovascular thrombectomy.12 To prevent the likelihood of recurrent strokes, the use of MRI is appropriate to evaluate secondary stroke prevention methods.23 In addition, MRI after the use of r-tPA is useful in evaluating hemorrhagic transformation.38

 

IMPLICATIONS FOR EMERGENCY NURSES

Emergency nurses play a crucial role in the early recognition and treatment of patients with a stroke. It is vital for emergency nurses to be able to recognize all signs and symptoms of an acute ischemic stroke in order to rapidly activate the stroke team (emergency physician, emergency nurse, neurologist, and neurology nurse). ED nurses also facilitate and coordinate the delivery of care through effective communication with the EMS (emergency medical services) team and the radiology department to expedite the process of promptly transporting the patient to diagnostic imaging for early diagnosis of either an ischemic stroke or a hemorrhagic stroke and the intervention that follows. ED nurses collaborate with the stroke team by triaging the patient, gathering relevant information, and keeping the patient's family and significant others informed and updated. The main finding of this article is that it is critical for all members of the health care team to be aware of the treatment plan that follows the discovery of an acute ischemic stroke. The mnemonic, ABCD, can be easily translated into clinical practice to assist ED nurses in helping develop a treatment plan for patients with an acute ischemic stroke.

 

CONCLUSION

We presented a general overview of the treatment plan for an acute ischemic stroke in the ED. Using the alphabetical mnemonic, Antiplatelet and/or Anticoagulants, Blood pressure, Clot dissolution and/or extraction, and Diagnostics, will help RNs, with support from the stroke team, develop a treatment plan that is effective, easily remembered, and based on current evidence.

 

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cerebrovascular accidents; embolic; endovascular extraction; stroke; thrombolytics