NOTE on this recommendation
Time is Brain! The goal of emergency department management is rapid assessment of all patients with a suspected acute stroke. For patients who may be eligible for intravenous tissue plasminogen activator, the target is to complete rapid assessment and initiate treatment within 90 minutes of stroke symptom onset.
All patients presenting to an emergency department with suspected stroke or transient ischemic attack must have an immediate clinical evaluation and investigations to establish the diagnosis, rule out stroke mimics, determine eligibility for thrombolytic therapy, and develop a plan for further management.
Patients presenting with stroke or transient ischemic attack should not be discharged from the ED without diagnostic evaluations, consideration of functional impairments, initiation or modification of secondary prevention therapy, and a plan for ongoing management.
3.3.1 Initial Evaluation
- Patients with suspected acute stroke should have a rapid initial evaluation for airway, breathing and circulation [Evidence Level B].
- A neurological examination should be conducted to determine focal neurological deficits and assess stroke severity [Evidence Level B]. A standardized stroke scale should be used.
- Monitoring in the acute phase should include heart rate and rhythm, blood pressure, temperature, oxygen saturation, hydration, swallowing ability, and presence of seizure activity [Evidence Level B].
Acute blood work, including routine chemistry, electrolytes, hematology and coagulation should be conducted as part of the initial evaluation [Evidence Level B]. Refer to Box 3.3 for additional information. - Electrocardiogram and chest X-ray should be completed, especially where the patient has a clinical history or evidence of heart disease or pulmonary disease [Evidence Level B].
3.3.2 Neurovascular Imaging
All patients with suspected acute stroke or transient ischemic attack should undergo brain imaging (MRI or CT) immediately [Evidence Level A], and vascular imaging of the brain and neck arteries as soon as possible [Evidence Level B].
- If MRI is performed, it should include diffusion-weighted sequences to detect recent ischemia and gradient echo and fluid-attenuated inversion recovery (FLAIR) sequences to determine extent of infarct or presence of hemorrhage [Evidence Level B].
- If MRI is not possible as the initial imaging, a non-contrast CT scan of the brain should be performed [Evidence Level B].
- Vascular imaging of the carotid and vertebral arteries by duplex ultrasonography, CT angiography (CTA), magnetic resonance angiography (MRA) or catheter angiography should be performed within 24 hours of a transient ischemic attack or ischemic stroke unless the patient is clearly not a candidate for revascularization [Evidence Level B]. Ideally CTA or MRA is performed at the time of the initial CT or MRI.
- If not done as part of the original assessment in the emergency department, extracranial vascular imaging should be done as soon as possible to better understand the cause of the stroke event and guide management decisions. Imaging of the intracranial vessels might be warranted in some cases. Duplex ultrasonography, CT angiography (CTA), or magnetic resonance angiography (MRA) of the extracranial and intracranial vessels may be considered. In some circumstances catheter angiography of the extracranial and intracranial vessels should be considered [Evidence Level B].
3.3.3 Cardiovascular Investigations
- Following an initial electrocardiogram, serial electrocardiograms (i.e., daily) should be done over the first 72 hours post-stroke to detect atrial fibrillation and other acute arrhythmias [Evidence Level B].
- Serial electrocardiograms in the first 72 hours combined with a Holter monitor during hospitalization may be considered in order to increase detection of atrial fibrillation [Evidence Level C]. 215
- Echocardiography, either 2-D or transesophageal, should be considered for patients with suspected embolic stroke and normal vascular imaging in whom there are no contraindications to coagulation [Evidence Level B].
3.3.4 Acute Blood Pressure Management
There is a lack of clear evidence from randomized controlled trials to guide the emergent and urgent treatment of elevated blood pressure in the setting of acute ischemic or hemorrhagic stroke. Pharmacological agents and routes of administration should be chosen to avoid
precipitous falls in blood pressure [Evidence Level C]. The following recommendations reflect the paucity of evidence in this area and indicate the need for further research.
- Ischemic stroke eligible for thrombolytic therapy: Very high BP (>185/110mmHg) should be treated concurrently in patients receiving thrombolytic therapy for acute ischemic stroke in order to reduce the risk of secondary intracranial hemorrhage. [Evidence Level B].
- Ischemic stroke patients not eligible for thrombolytic therapy: Treatment of hypertension in the setting of acute ischemic stroke should not be routinely undertaken [Evidence Level C]. Extreme blood pressure elevation (e.g. systolic > 220 or diastolic > 120mmHg) may be treated to reduce the blood pressure by ~15 percent, and not more than 25%, over the first 24h with gradual reduction thereafter [Evidence Level C]. Avoid excessive lowering of blood pressure as this may exacerbate existing ischemia or may induce ischemia, particularly in the setting of intracranial arterial occlusion or extracranial carotid or vertebral artery occlusion [Evidence Level C].
3.3.5 Blood Glucose Abnormalities
- patients with suspected acute stroke should have their blood glucose concentration checked immediately [Evidence Level B].
- Blood glucose measurement should be repeated if the first random glucose value is elevated greater than 10 mmol/L. The repeat measures should include a fasting glucose and an A1c[Evidence Level B].
- Hypoglycemia should be corrected immediately [Evidence Level B].
- If the repeat glucose levels and the A1c are elevated (fasting glucose greater than 7 mmol/L; A1c greater than 7percent), the use of anti-hyperglycemic agents should be considered [Evidence level C], and in the longer term, education on lifestyle changes and diabetes [Evidence level A].18
Refer to recommendation 2.4 for additional information
3.3.6 Other Investigations that may be required in the Emergency Department
- Blood cultures if endocarditis is suspected [Evidence level B].
- Fasting lipid profile [Evidence level A].
- Investigations for hypercoagulability and vasculitis (Evidence Level C).
Refer to Box 3.3 for list of common coagulopathy investigations
All suspected stroke patients: complete blood count (CBC), electrolytes, creatinine, urea, glucose, international normalized ratio (INR), partial thromboplastin time (PTT),thyroid-stimulating hormone (TSH), fasting lipid profile, creatine kinase (CK), troponin test
Arterial coagulopathy screen: anticardiolipin (Antiphospholipid) antibody, Lupus anticoagulant
Venous coagulopathy: protein S, protein C, antithrombin III, prothrombin gene mutation, factor V Leiden mutation
Vasculitis: erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), antinuclear antibody (ANA), syphilis screen
Patients who present to hospital with suspected stroke often also have significant physiological abnormalities and comorbidities. These can complicate management of stroke. Signs and symptoms that may explain etiology or predict later complications such as space-occupying infarction, bleeding, or recurrent stroke, and medical conditions such as hypertension and the presence of a coagulopathy will have an impact on treatment decisions. An efficient and focused assessment is required to understand the complex needs of each patient.
It is impossible to differentiate infarct from hemorrhage by clinical examination alone. Brain imaging is required to guide management, including the selection of time-sensitive interventions. A CT scan or MRI is important since clinicians may disagree on the clinical diagnosis of stroke (versus not stroke) in about 20 percent of patients.
Initial management of elevated blood pressure in acute stroke patients remains controversial due to the lack of evidence to clearly guide practice. At the same time, this is an area where clinicians often seek guidance from stroke specialists. The recommendations for this area emphasize caution and diligence in monitoring and treating extremely high blood pressure in the first hours after stroke onset.
Diabetes is a major modifiable risk factor for vascular disease that may be first diagnosed at the time of a stroke. Severe hyperglycemia (blood glucose greater than 22 mmol/L) is a relative contraindication to the administration of intravenous alteplase. Hyperglycemia at the time acute stroke increases size of the damaged area in experimental animals and is associated with poor clinical outcomes in epidemiological studies.
- Protocols and standing orders to guide initial blood work and other clinical investigations.
- Local protocols for prioritizing stroke patients for rapid access to appropriate diagnostics such as CT scans and duplex ultrasound, communicated to all relevant personnel such as emergency department, imaging, and stroke teams.
- Agreements to ensure patients initially managed in rural hospitals without neurovascular imaging capability have timely access to CT scans within 24 hours at partnering facilities.
- Local protocols, especially in rural and remote locations, for rapid access to clinicians experienced in interpretation of diagnostic images, including access through telemedicine technology.
- Proportion of stroke patients who receive a brain CT/MRI within 24 hours of hospital arrival (core).
- Proportion of patients who do not undergo carotid imaging in emergency who have an appointment booked before discharge for carotid imaging as an outpatient.
- Median time from time INR drawn to results available.
- Proportion of patients with blood glucose levels documented during assessment in the emergency department.
- Proportion of stroke patients who receive a brain CT/MRI within 60 minutes of hospital arrival.
- Median time from stroke symptom onset to carotid imaging.
- Proportion of patients with known diabetes who have blood glucose levels in therapeutic range for that patient.
Measurement Notes
- Data may be obtained from laboratory reports or patient chart.
- Stratify analysis for patients who arrive within 3.5 hours of stroke symptom onset and those who arrive beyond 3.5 hours.
- Performance measure 1: apply to patients who may be candidates for acute thrombolysis (i.e. who arrive at hospital within 3.5 hours of stroke onset) and for patients who may be eligible for other time-sensitive interventions.
- Performance measures 1 and 2: Time interval measurements for CT and MRI should be calculated from the time the patient is triaged in the emergency department until the time noted on the actual brain imaging scan. Documentation of triage time is recorded on the emergency department chart.
- Performance measure 3: For out-patient carotid imaging, a notation should appear in the discharge summary, or in nursing notes, with an indication that the test has actually been booked prior to the patient leaving the hospital.
- Performance measure 5: Use medical history to determine whether patient was known to have diabetes prior to the stroke event.
- Canadian Stroke Strategy emergency medical services education package
- Canadian Neurological Scale (CNS) pocket cards (order online)
- National Stroke Nurses Council: Best Practice Nursing Care Across the Acute Stroke Continuum: Modules 1&2
An initial assessment of all suspected stroke patients is critical to facilitate rapid access to time-sensitive treatments and to minimize potential negative outcomes of stroke. Neurovascular imaging is considered one of the most important diagnostic tests to perform immediately after patient arrival at hospital, as many management decisions follow the differential diagnosis resulting from imaging.216
Clinical protocols, pathways and algorithms have been reported in the literature and have been found to have a moderate benefit in efficiencies of early assessments and patient course in hospital. Stroke response protocols are commonly implemented to increase efficiency for emergency medical services and emergency departments receiving stroke patients. These also include the use of tools such as standing order sets, stroke code protocols and prenotification (as described in Recommendation 3.1).
Neurovascular Imaging: Despite the absence of randomized trials, there is uniform agreement that non-contrast Computed Tomography (CT) should be the initial imaging study of patients who present with acute ischemic stroke. The primary purpose of the head CT is to exclude intracranial hemorrhage although other important information may be obtained. A head CT should be obtained emergently in those patients potentially eligible for thrombolytic therapy. Strict goals of 25 minutes from presentation to the emergency room to completion of the scan and 45 minutes until interpretation have been recommended based on randomized controlled trials of thrombolytic therapy. Although magnetic resonance imaging may provide more information in specific cases, it is not generally recommended as the initial brain imaging study in patients with an acute stroke. In a decision-analysis model, a policy of ‘scan all immediately’ was more cost-effective than ‘scan all within 48 hours’ or ‘scan patients on anticoagulants or in a life-threatening condition immediately and the rest within 14 days’. Up to 15 percent of children and young adults with stroke have arterial dissections; vascular imaging is required to refine the diagnosis and management decisions.217
Eight clinical practice guidelines have recommended head CT as the initial imaging study for patients with acute ischemic stroke. Whereas all guidelines recommend obtaining the CT scan promptly, more recent guidelines concerning patients eligible for thrombolytic therapy have established target times of 25 minutes for completion of the CT scan following presentation to the emergency room and 45 minutes for interpretation of the CT scan. Most importantly, CT scanning allows the early detection of intracranial hemorrhage, an absolute contraindication to thrombolytic therapy. CT images also provide information regarding early ischemic changes in the brain, mass effect from edema, middle cerebral artery embolic material (hyperdense MCA sign), other vascular lesions, and prior cerebral infarctions.
Members of the Stroke Council of the American Heart Association have issued specific guidelines for the use of imaging in transient ischemic attacks and acute stroke.7 The authors strongly recommend CT of the head without contrast enhancement as the initial brain imaging procedure in patients with acute stroke. The authors classified this recommendation as a “strong positive recommendation” resulting from evidence based on one or more well-designed studies of a diverse population using a gold standard reference test in a blinded evaluation appropriate for the proposed diagnostic application.
Wardlaw et al. conducted a cost-effectiveness analysis of the use of CT and tested 13 strategies.218 The study indicates that of 13 possible imaging strategies, a policy of “CT scan all patients immediately” is dominant. Although the costs of CT scanning are highest for this strategy because of more scanning occurring after hours, these higher costs are offset by savings in the length of inpatient stay because many management decisions and better outcomes depend on accurate early diagnosis of stroke. The costs of after-hours scanning would have to rise markedly (well above the current maximum costs) to outweigh the cost savings in length of stay on current bed occupancy cost figures. The results were sensitive to a fall in the cost of inpatient days. The unusual sensitivity of the incremental cost effectiveness estimates is largely a product of the very small difference in outcome between a strategy of “scan all immediately” and one of “scan all within 48 hours of admission to hospital.” Because the majority of patients have cerebral infarction, the main treatment is aspirin, and there is no good evidence of a time dependency of the effect of aspirin up to 48 hours after stroke.
About 15 to 20 percent of ischemic strokes are caused by symptomatic extracranial carotid artery disease. Rapid identification of patients with symptomatic carotid artery disease who would be candidates for carotid revascularization is a management priority. Since patients with carotid territory transient ischemic attack or minor stroke and high-grade ipsilateral carotid artery stenosis are at very high risk of early stroke recurrence, and because the absolute benefit derived from carotid endarterectomy is highly time-dependent, there is a need to quickly rule in or rule out the presence of significant carotid artery disease in appropriate patients. Of all the diagnostic tests, carotid imaging is arguably the most important study to be performed early. Outdated guidelines recommend that it be performed within one week of the presenting event, but more recent expert opinion recommends that it be performed within 24 hours. The opportunity for stroke prevention may be missed if there are delays in diagnosis and treatment of symptomatic carotid disease.205
While brain imaging is essential for diagnosis, referral and management of suspected paediatric stroke patients, the wide differential diagnosis for stroke-like presentations in children requires more specific initial imaging, namely magnetic resonance imaging (MRI) compared with adults. MRI can also screen for the site of arterial or venous occlusion (AHA) and is less invasive for infants and young children than other types of imaging. However conventional angiography may be required to diagnose specific arteriopathies requiring specific treatments (anticoagulation for dissection, immunosuppressants for vasculitis). 219-221 One population-based cohort study investigated cases of arterial ischemic stroke.219Of 97 children having experienced a later childhood stroke, 52 received cerebrovascular imaging and it was found that children with a vascular abnormality had a 5-year cumulative recurrence rate of 66 percent. High-risk patients can be rapidly identified with the use of cerebrovascular imaging. In children, arterial dissection is common (14 percent of childhood stroke) and clinical indicators unreliable. Neck pain is rarely found and 50 percent of cases are non-traumatic.
Cardiac Investigations: Detection of atrial fibrillation and treatment to minimize the risk of first or recurrent stroke is not well managed. In a recent study by Douen and colleagues, One hundred forty-four patients with ischemic stroke admitted to a stroke unit were followed with serial ECGs. These were performed in 143
patients with a baseline of 10 (7%) patients having a history of AF. Serial ECGs detected 15 new AF cases in P_0.011). Holter was also completed in 12 of 15 new cases of AF but surprisingly identified AF in only 50 percent (6 of 12). Holter monitoring was performed in 126 cases and in this subgroup, there was no statistically significant difference in the rate of AF detection with ECG or Holter.215Other studies have also reported the lower sensitivity of Holter monitoring in detecting atrial fibrillation in stroke and TIA patients, although procedures and techniques for both Holter and serial ECGs will impact outcomes.222
Acute Blood Pressure Management:
Blood pressure is frequently elevated during acute stroke but then returns to pre-stroke levels within a few days after the event. There is a U-shaped relationship between acute blood pressure and outcome after stroke.223 Elevated blood pressure is a risk factor for intracranial hemorrhage in patients with acute ischemic stroke who are treated with intravenous alteplase. 224Elevated blood pressure may also increase the risk of hematoma expansion in patients with acute intracerebral hemorrhage. 225
Despite this observational evidence, there is uncertainty about the optimal management of blood pressure in the hours and days after acute ischemic and hemorrhagic stroke. 226,227 The data from the trials included in a Cochrane review [Cochrane 1] were too limited to provide reliable guidance on the indications for the use of drugs to lower or raise blood pressure in acute stroke, or precise estimates on the likely effects of these drugs on blood pressure. Concerns persist that excessive blood pressure lowering may be harmful, as demonstrated by several trials that studied vasoactive drugs for their putative neuroprotective properties.227
Several ongoing clinical trials are evaluating blood pressure lowering in acute stroke (refer to the Clinical Trials Registry www.stroketrials.org)
Blood Glucose: Elevated blood sugar (hyperglycemia) in the acute phase of stroke is common, documented in up to 40 percent of patients. Several large clinical studies have now demonstrated a positive association between post-stroke hyperglycemia and poor outcome from stroke, infarct progression, greater mortality, and reduced functional recovery.228 Hyperglycemia is clearly shown to have deleterious effects on brain tissue in animal models of cerebral ischemia, increasing the size of the damaged brain tissue and surrounding edema in the brain.7, 229-231 It remains unclear as to what extent post-stroke hyperglycemia is a “normal” physiological response, or whether hyperglycemia per se increases cerebral damage in the acute phase. There are accumulating clinical data to suggest that much of this response is associated with impaired glucose metabolism, with the prevalence of previously unrecognized diabetes, or impaired glucose tolerance preceding stroke as high as 42 percent. Although a direct causal relationship has not yet been established, it is probable that an important relationship exists between hyperglycemia and stroke outcome. Patients with hyperglycemia have worse functional outcomes at hospital discharge and are less likely to be living independently at six months and one year post-stroke. Mortality in stroke patients with early hyperglycemia is also significantly higher. To date, no strong evidence exists for a specific strategy for treating hyperglycemia in stroke to improve stroke outcomes; however, practice guidelines uniformly recommend treating elevated glucose levels.
The Glucose in Stroke Trial (GIST-UK), a randomized, controlled trial of glucose treatment with intravenous glucose-potassium-insulin over 24 hours, compared to a normal saline infusion control group, enrolled a total of 933 patients.228 The primary outcome measure, 90-day mortality, was not significant when the groups were compared. Several factors may have contributed to the negative study result: poor recruitment so this could possibly be an underpowered study. Patients had only modestly elevated glucose levels on study entry and glucose spontaneously decreased in the saline control arm.
Fuentes et al (2009) studied the effect of capillary glucose levels on outcomes in patients with acute stroke.230 In a multicenter, prospective, and observational cohort study of 476 patients with ischemic stroke within less than 24 hours from stroke onset, capillary finger-prick glucose and stroke severity were determined on admission and three times a day during the first 48 hours. Poor outcome (modified Rankin Scale >2) was evaluated at 3 months. The receiver operating characteristic curves showed the predictive value of maximum capillary glucose at any time within the first 48 hours with an area under the curve of 0.656 (95% CI, 0.592 to 0.720; P





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