Acute Stroke

Acute ischemic stroke is a sudden focal neurologic deficit caused by occlusion of a cerebral artery, accounting for the large majority of all strokes; the remainder are hemorrhagic (intracerebral or subarachnoid hemorrhage). Once a vessel occludes, tissue in the ischemic core dies quickly, while a surrounding rim of at-risk but still-salvageable tissue — the ischemic penumbra — survives only until blood flow is restored. The guiding principle of hyperacute stroke care is therefore time is brain: every minute of delay to reperfusion narrows the chance of a good functional outcome. This chapter covers the hyperacute, emergency-department phase of ischemic stroke — thrombolysis, mechanical thrombectomy, and the acute-phase supportive-care decisions (blood pressure, glucose, temperature, and antithrombotic timing) that follow reperfusion therapy — and is distinct from long-term secondary-prevention pharmacotherapy. Hemorrhagic stroke is addressed only briefly toward the end of this chapter, since its pharmacotherapy is largely reversal-agent-focused rather than a parallel reperfusion pathway.^[1]

F.A.S.T. — the public and first-responder warning-sign check

Transient ischemic attack (TIA)

A TIA produces stroke-like symptoms that fully resolve without infarction on imaging. A TIA is not a benign event — it substantially raises the risk of a disabling stroke in the near term, most steeply in the first days afterward. Manage a suspected TIA with the same urgency as an evolving stroke: same-day assessment, same-day imaging, and same-day initiation of secondary prevention, since the window to prevent a disabling stroke is narrow.^[1]

• Hypertension — the single most important modifiable risk factor for stroke.
• Atrial fibrillation or another cardioembolic source (recent MI with LV thrombus, valvular disease, cardiomyopathy).
• Diabetes mellitus.
• Dyslipidemia.
• Current smoking.
• Excessive alcohol intake.
• High body mass index and low physical activity.
• Known vascular disease — coronary artery disease, peripheral arterial disease, prior MI, heart failure, renal vascular disease.
• Prior stroke or TIA.
• Carotid, vertebral, or basilar artery stenosis.
• Migraine with aura.
• Obstructive sleep apnea.
• Family history of premature vascular disease or a known hemostatic/thrombophilic disorder.
• Illicit stimulant use (cocaine, amphetamines) — can precipitate stroke through vasospasm, hypertension, or cardioembolism, including in young patients without traditional risk factors.

Stroke mimics — screen for these before committing to a stroke work-up

History

• Time last known well, time of symptom onset, and whether symptoms were first noted on waking from sleep.
• Symptoms at onset and whether they have worsened or improved since.
• Medications — especially the time of the last dose of any anticoagulant or antiplatelet drug, and any anticonvulsant, diabetes medication, chemotherapy agent, or steroid that might point to an alternative diagnosis.
• Antecedent trauma, illness, or a previous neurovascular event.
• Vascular comorbidity (angina, MI, heart failure, peripheral or renal vascular disease) or atrial fibrillation.
• Vascular risk factors (see Risk Factors).
• Pre-stroke cognitive and functional status, place of residence, occupation, and social supports — these shape both treatment decisions and disposition planning.

Physical examination

• Rapid evaluation of airway, breathing, and circulation; obtain vital signs including blood pressure.
• Localize the lesion and grade stroke severity using the NIH Stroke Scale (NIHSS — see below).
• Assess for comorbid conditions and a possible underlying cause.

Emergency laboratory and imaging

• CBC, INR, PTT, albumin, electrolytes, glucose (to exclude hypoglycemia as a mimic), HbA1c, urea, creatinine, troponin, liver function tests, lipid profile, and TSH.
• Immediate neurovascular imaging to confirm the diagnosis and plan treatment — noncontrast CT head plus CT angiography (CTA) of the head and neck is the preferred hyperacute imaging strategy. Noncontrast CT head demonstrates changes of ischemic stroke, hemorrhagic stroke, or a mimic such as tumor. CTA head shows intracranial occlusions or stenosis; multiphase CTA provides information about collateral circulation and helps guide acute management. CTA neck can show occlusion, stenosis, dissection, or fibromuscular dysplasia of the carotid, vertebral, or basilar arteries.
• CT perfusion is sometimes used to improve diagnostic yield for small infarcts, exclude mimics, and inform extended-window treatment decisions. MRI brain is occasionally used for extended-window thrombolysis decisions, though emergency MRI access in Canada is limited. Carotid dopplers remain a useful screening tool for carotid stenosis when CTA is unavailable.
• ECG to look for atrial fibrillation, MI, or left ventricular hypertrophy.

Additional investigations if indicated

• Chest x-ray.
• Prolonged cardiac monitoring (minimum 24-hour Holter, though 2 weeks is preferred) and echocardiography (transthoracic, with a bubble study if under 60 years old, plus transesophageal if needed) to search for atrial fibrillation or another cardiac embolic source.
• Brain MRI with diffusion-weighted imaging if the cause of stroke is uncertain, particularly in a young patient.
• Antiphospholipid antibodies, factor V Leiden, and prothrombin gene mutation if an arterial hypercoagulable state is suspected; protein C, protein S, and antithrombin III if venous embolism is suspected together with a patent foramen ovale in a younger patient.
• Inflammatory markers (ESR, CRP, ANA) as a screen for vasculitis.
• Blood cultures and an urgent echocardiogram if infectious endocarditis is suspected.
• MRA with vessel wall imaging, with or without catheter cerebral angiography, if vasculitis or a vascular anomaly is suspected.
• Lumbar puncture if vasculitis, syphilis, or another CNS infection is suspected, or if the CT is negative for blood but subarachnoid hemorrhage is still suspected.
• Malignancy work-up (CT chest, abdomen, pelvis), pregnancy test, and syphilis/HIV serology as indicated.

NIH Stroke Scale (NIHSS) — quantifying severity

The NIHSS is the standard tool for quantifying stroke severity, localizing the lesion, and tracking neurologic change, and it directly drives thrombolysis and thrombectomy eligibility decisions.

The total score ranges from 0 (no deficit) to a maximum of 42. As a rough severity guide: 0 equals no stroke symptoms, 1-4 is a minor stroke, 5-15 is a moderate stroke, 16-20 is a moderate-to-severe stroke, and 21-42 is a severe stroke — these bands inform, but do not alone determine, reperfusion-therapy eligibility (see Choose Initial Treatment).

Unlike the point-sum risk scores used elsewhere in this reference library (for example, the TIMI score in Acute Coronary Syndromes, where every criterion contributes exactly one point), the NIHSS is not a simple binary checklist: each of its 15 items is independently graded across its own point range (0-2, 0-3, or 0-4) based on the severity found on a structured bedside neurologic exam, and several items require the examiner to actually observe a specific finding (visual fields, limb drift, articulation, extinction) rather than tick a present-or-absent box. This graded, exam-driven structure does not fit a simple interactive checkbox calculator the way a uniform one-point-per-criterion score does, and a miscoded severity grade could silently produce a wrong total in a tool meant for real clinical use. This chapter therefore provides the teaching table above rather than a live calculator — score the NIHSS using a validated bedside instrument or certified training module, not by estimation.

• Reperfuse the occluded vessel as fast as possible — target a door-to-needle time of 30 minutes or less for thrombolysis, and the fastest achievable door-to-groin-puncture time for thrombectomy.
• Limit infarct growth by keeping blood pressure, glucose, temperature, and oxygenation within their acute-phase targets.
• Prevent early complications — aspiration pneumonia, venous thromboembolism, hemorrhagic transformation, and malignant cerebral edema.
• Prevent early recurrent stroke through appropriately timed antiplatelet or anticoagulant therapy once it is safe to start.
• Preserve the option of endovascular thrombectomy — do not let thrombolysis, or the work-up for it, delay transfer to a thrombectomy-capable centre.
• Begin the transition to secondary-prevention pharmacotherapy and rehabilitation before transfer or discharge.

• Admit to a dedicated stroke unit with a coordinated interdisciplinary team — this alone improves outcomes independent of drug therapy.
• Continuous cardiac and neurologic monitoring per the post-thrombolysis protocol (see Monitoring and Follow-up) even when thrombolysis was not given.
• Give supplemental oxygen only to correct documented hypoxemia (target SpO2 above 90%) — routine oxygen in a normoxic patient is not beneficial.
• Perform a bedside dysphagia screen before any oral intake, ideally by a trained team; keep the patient nil by mouth if there is reduced consciousness, suspected brainstem stroke, severe dysarthria, a wet voice, a weak cough, impaired palatal sensation, inability to sit upright, or suspected aspiration.
• Use a videofluoroscopic (modified barium swallow) study when the bedside screen is ambiguous and significant aspiration needs to be excluded.
• Start a texture-modified diet for a dysphagic patient at lower aspiration risk, with additional IV fluids as needed; place a nasogastric tube if significant aspiration is demonstrated or suspected and this fits the patient's goals of care. Do not initiate early percutaneous endoscopic gastrostomy (PEG) feeding — delay the PEG discussion until swallowing has had adequate time to recover.
• Mobilize as early as possible once medically stable, and maintain adequate hydration.
• Apply intermittent pneumatic compression stockings within the first 24 hours for venous thromboembolism prevention — they do not cause bleeding and can be used even after intracerebral hemorrhage. Do not rely on graduated compression stockings alone; they lack efficacy for this indication.
• Delay placement of nasogastric tubes, indwelling urinary catheters, and intra-arterial pressure catheters during and shortly after thrombolytic infusion to minimize bleeding risk at puncture or insertion sites.
• Involve family or next of kin as early as possible to provide collateral history (especially time last known well) and consent, since the patient is often unable to communicate.
• Begin rehabilitation as soon as the patient is medically stable, and engage family and community supports early for social reintegration planning.

Pregnancy

Manage suspected stroke in pregnancy or within 6 weeks postpartum with the same urgency and the same initial investigations as a non-pregnant patient, using a combined obstetric, maternal-fetal-medicine, and stroke team. A noncontrast CT head exposes the fetus to a negligible radiation dose; CT contrast has no known harm but limited evidence; MRI is not associated with fetal risk, but avoid gadolinium enhancement.^[1]

Alteplase and tenecteplase do not cross the placenta and are considered a reasonable treatment option in pregnancy despite the absence of trial data (pregnant patients were excluded from the founding trials) — the main patient-specific consideration is an increased risk of postpartum hemorrhage and of bleeding after epidural/spinal anesthesia or cesarean delivery, which should be discussed with obstetrics before treatment where time allows.^[1]

Offer thrombectomy to a pregnant patient with a confirmed large-vessel occlusion using the same criteria as a non-pregnant patient; depending on the clinical scenario, it may be reasonable to forgo thrombolysis and proceed directly to thrombectomy.

ASA at usual doses is safe in pregnancy. Clopidogrel is the preferred P2Y12 inhibitor if dual antiplatelet therapy is needed (ticagrelor is not well studied in pregnancy). UFH and LMWH can be used for anticoagulation, with awareness of increased maternal bleeding risk; warfarin is potentially teratogenic (especially at 6 to 12 weeks' gestation) and should be avoided, and direct oral anticoagulants have insufficient safety data in pregnancy.

Breastfeeding

Continuation of breastfeeding after CT contrast exposure poses no known risk to the infant. Any thrombolytic drug is expected to be destroyed in the infant's gastrointestinal tract, and no hazard has been identified from thrombolysis during breastfeeding, though thrombolysis itself may still raise maternal postpartum or procedural bleeding risk as above. Low-dose ASA is considered compatible with breastfeeding. If anticoagulation is required, LMWH and warfarin are both considered safe during breastfeeding; direct oral anticoagulant safety in breastfeeding has not been established.

Older adults

Age alone should not exclude a patient from thrombolysis or thrombectomy — both remain guideline-endorsed at advanced age, though the eligibility criteria above already account for the higher hemorrhage and futility risk that comes with a large established infarct core, which becomes more common with age. Review comorbidities and pre-stroke functional status carefully, since these — not chronological age by itself — drive the realistic benefit of reperfusion therapy.

Renal impairment

Enoxaparin requires dose reduction, or a switch to unfractionated heparin, at a creatinine clearance of 30 mL/min or less. Consider contrast-induced nephropathy risk before CT angiography, and ensure adequate hydration where feasible without delaying emergency imaging.

A patient taking a direct oral anticoagulant

DOAC use is a relative thrombolysis exclusion requiring clinical judgment, not an automatic one. For a patient on dabigatran, idarucizumab can reverse the anticoagulant effect and may bring the patient back into an eligible window for thrombolysis where the clinical urgency supports it. Reversal of a factor Xa inhibitor (apixaban, edoxaban, rivaroxaban) with andexanet alfa specifically to enable thrombolysis is far less established, and andexanet alfa has limited availability in Canada — in a DOAC-anticoagulated patient with a large-vessel occlusion, proceeding directly to thrombectomy, which does not carry the same systemic bleeding profile, is often the more practical pathway than pursuing thrombolysis-enabling reversal.^[7]

Post-thrombolysis monitoring protocol

For every ischemic stroke patient, regardless of reperfusion therapy: reassess swallowing status at each shift change until it has stabilized; monitor temperature and treat fever promptly; monitor and correct both hyperglycemia and hypoglycemia; and reassess functional status daily to guide rehabilitation and disposition planning. Before transfer or discharge, confirm secondary-prevention pharmacotherapy has been initiated (antiplatelet or anticoagulant therapy, a high-intensity statin, and blood-pressure management as appropriate), and arrange follow-up with a stroke prevention clinic.^[1]

1. Neurologic deterioration during or shortly after thrombolytic infusion: stop the infusion immediately, obtain a STAT noncontrast CT to rule out hemorrhage, and send a fibrinogen level. If intracranial hemorrhage is confirmed, treat empirically with cryoprecipitate (targeting a fibrinogen concentration of 150 mg/dL or higher), consider an antifibrinolytic (tranexamic acid) as an adjunct, and obtain an urgent neurosurgical consultation even though evidence for surgical intervention specifically is limited — manage supportively according to the patient's goals of care.^[7]
2. Orolingual angioedema during or after thrombolysis in a patient taking an ACE inhibitor: manage the airway first (this can progress to obstruction), give IV corticosteroid and antihistamine, and hold the ACE inhibitor.
3. Blood pressure will not come down below 185/110 mmHg despite an appropriate dose of IV labetalol or hydralazine: do not give the thrombolytic — treat as a thrombolysis exclusion and, if a large-vessel occlusion is present, proceed to the thrombectomy pathway instead.
4. Declining consciousness or a new fixed, dilated pupil 1 to 4 days after a large middle cerebral artery infarct (malignant cerebral edema): obtain emergent imaging, start osmotic therapy (mannitol 1 g/kg IV, may repeat every 4 to 6 hours, or hypertonic saline per institutional protocol), and obtain an urgent neurosurgical consultation for possible decompressive hemicraniectomy — this reduces mortality in patients under 60 years of age, though survivors may have significant residual disability, a trade-off that should be discussed explicitly with the patient's substitute decision-maker.^[8]
5. Thrombectomy achieves incomplete or no reperfusion: continue best medical management (antiplatelet/anticoagulant timing per the 24-hour rule if thrombolysis was also given, and BP and glucose targets as above), and monitor closely for malignant edema given the larger residual infarct.
6. Recurrent stroke symptoms after starting dual antiplatelet therapy for a minor stroke or TIA: confirm adherence, re-image to distinguish a new event from a fluctuating deficit related to the index stroke, and reassess for a missed large-vessel or high-grade stenotic source needing a different approach (for example, urgent carotid revascularization).

• Delaying CT imaging or the thrombolysis decision to wait for coagulation results in a patient with no history suggesting a bleeding diathesis and no anticoagulant use — this wastes time a low-risk patient did not need to spend.
• Giving ASA or any other antiplatelet/anticoagulant within 24 hours of thrombolysis, or before the 24-hour CT has excluded hemorrhagic transformation.
• Withholding or delaying thrombectomy because thrombolysis was given first, or withholding thrombolysis because thrombectomy is also planned — give both when both are indicated (bridging therapy), without either one delaying the other.
• Intensively lowering blood pressure to a systolic target below 140 mmHg after thrombolysis — no demonstrated functional benefit, and the current guideline recommends against it.
• Missing a history of direct oral anticoagulant use before giving thrombolysis — always ask specifically about the timing of the last dose of any anticoagulant or antiplatelet drug.
• Starting an oral medication, including ASA, before a bedside dysphagia screen has been completed.
• Using an aggressive IV insulin regimen to tightly control glucose — targets in the 4.4 to 7.2 mmol/L range increase hypoglycemia without improving outcomes; use a subcutaneous regimen targeting 7.8 to 10 mmol/L instead.
• Giving routine supplemental oxygen to a patient with a normal oxygen saturation.
• Using prophylactic osmotic therapy before any sign of mass effect has appeared, or continuing osmotic therapy indefinitely once started — both risk rebound cerebral edema; reserve it for actual signs of mass effect and treat it as a bridge to definitive management.
• Missing the window for malignant cerebral edema by not watching closely enough for declining consciousness in the first several days after a large middle cerebral artery infarct.
• Treating asymptomatic, mild-to-moderate hypertension aggressively in a non-thrombolysis-candidate ischemic stroke patient — permissive hypertension is standard in this group.

How to use this table: Doses are adult doses and require patient-specific confirmation, including renal/hepatic adjustment. Select any drug name to open its complete Pharmasist Drug Database page.

Thrombolytics

Antiplatelet agents

Anticoagulants — cardioembolic (AF-associated) stroke

Timing of the first dose follows the stroke-severity-based initiation guidance in Choose Initial Treatment.

VTE prophylaxis

For a patient who cannot mobilize one or both lower limbs independently and has no contraindication; stop once therapeutic anticoagulation starts.

Acute blood-pressure-lowering agents

Glucose management

Antipyretic/analgesic

Cerebral edema

Anticoagulant reversal (hemorrhagic transformation / anticoagulant-associated ICH)