Stroke and TIA: Recognition, Assessment, Emergency Management and Nursing Care

Add a labelled stroke pathway image here.

Learning objectives

• Define stroke, TIA, ischaemic stroke, haemorrhagic stroke, large-vessel occlusion and the ischaemic penumbra.
• Recognise anterior and posterior circulation symptoms using FAST/BE-FAST and identify stroke mimics.
• Perform a structured ABCDE and focused neurological assessment, including glucose and a baseline neurological score.
• Obtain and communicate the last-known-well time, medication history and functional baseline.
• Explain emergency imaging, laboratory tests, reperfusion pathways, haemorrhage care and TIA prevention.
• Provide safe pre-hospital, emergency-department and nursing care while preventing aspiration, hypoxia, fever, pressure injury and deterioration.

1. Definitions and clinical categories

Stroke is sudden focal neurological dysfunction caused by a vascular disturbance of the brain, spinal cord or retina. It may be due to an arterial blockage (ischaemia) or bleeding (haemorrhage). Symptoms can include weakness, numbness, facial droop, speech disturbance, visual loss, incoordination, severe headache, reduced consciousness or neglect.

Transient ischaemic attack (TIA) is a transient episode of neurological dysfunction caused by focal brain, spinal cord or retinal ischaemia without acute infarction on appropriate imaging. Symptoms resolving does not remove the emergency: the patient needs urgent assessment for a preventable future stroke.

2. Pathophysiology

Ischaemic cascade

An arterial occlusion deprives neurons of oxygen and glucose. ATP depletion stops ion pumps, causing membrane depolarisation, glutamate release, calcium influx, cytotoxic oedema and cell death. The central core becomes irreversibly injured quickly. Around it lies the penumbra: dysfunctional but potentially salvageable tissue supplied by collateral vessels. Reperfusion and physiological optimisation aim to preserve this tissue. Hypoxia, fever, hypotension, severe hyperglycaemia and seizures increase secondary injury.

Haemorrhagic injury

Blood directly damages neurons, raises intracranial pressure and may expand during the first hours. Oedema, hydrocephalus, reduced cerebral perfusion and herniation can follow. Blood-pressure surges, anticoagulants, thrombocytopenia and coagulopathy can worsen expansion. A patient may have a relatively normal initial examination and deteriorate rapidly, so repeated observations are essential.

Large-vessel occlusion

Occlusion of the internal carotid, proximal middle cerebral, basilar or selected other arteries can produce a large threatened territory. Severe cortical deficit, gaze deviation, aphasia, neglect, dense hemiplegia or coma should trigger urgent vascular imaging and consideration of endovascular thrombectomy.

3. Causes and risk factors

• Long-standing or uncontrolled hypertension, the leading modifiable risk factor for both ischaemic and haemorrhagic stroke.
• Atrial fibrillation and other cardiac arrhythmias; recent myocardial infarction, cardiomyopathy, valvular disease, endocarditis or intracardiac thrombus.
• Diabetes, dyslipidaemia, obesity, smoking, harmful alcohol use, physical inactivity and sleep apnoea.
• Carotid or intracranial atherosclerosis, arterial dissection, vasculitis and hypercoagulable states.
• Sickle-cell disease, severe anaemia, HIV-related vasculopathy, tuberculosis or other infections where clinically relevant.
• Pregnancy and the postpartum period, pre-eclampsia/eclampsia, cerebral venous thrombosis and hormonal risk factors.
• Cocaine, amphetamines and other sympathomimetic drugs; trauma, aneurysm, vascular malformation and anticoagulant use.
• Previous stroke or TIA, family history, age and social determinants that delay access to emergency care.

4. Recognition and first contact

Ask the witness, family or care worker when the person was last definitely normal, not merely when the abnormality was noticed. For a wake-up stroke, record the time the patient was last seen normal before sleep and the time found abnormal. Record whether symptoms are improving, fluctuating or progressing. Do not allow the patient to drive.

Pre-hospital actions

• Ensure scene safety, use standard precautions and perform a rapid primary survey.
• Call the emergency system, pre-alert the receiving hospital and state suspected stroke, last-known-well time, glucose, airway status and anticoagulant use.
• Position safely: head and trunk slightly elevated if tolerated; lateral recovery position if vomiting or reduced consciousness while protecting the spine when trauma is possible.
• Maintain airway patency, suction secretions and provide oxygen only for hypoxaemia or respiratory compromise according to protocol.
• Check capillary glucose. Treat severe hypoglycaemia promptly; document the value because hypoglycaemia is a common stroke mimic.
• Keep the patient nil by mouth. Do not give aspirin, food, drink or oral medicines before a swallow assessment and brain imaging have excluded haemorrhage.
• Do not aggressively lower blood pressure in the field unless a specific emergency indication and protocol apply; cerebral perfusion may depend on the pressure.
• Bring medication lists, anticoagulant packets, identification and contact information. Minimise scene delay.

5. Emergency assessment: ABCDE

Establish two IV lines if this does not delay imaging, attach ECG and pulse oximetry, and obtain a 12-lead ECG to detect atrial fibrillation or myocardial ischaemia. Correct hypotension and hypoxia. Avoid hypotonic fluids and unnecessary glucose-containing fluids.

6. Focused history

• Onset: exact last-known-well time, progression, wake-up presentation and witnessed collapse.
• Deficit: face, arm, leg, speech, vision, balance, swallowing, headache, seizure, confusion and sensory symptoms.
• Bleeding risk: warfarin, direct oral anticoagulant, heparin, antiplatelet medicines, liver disease, recent operation, gastrointestinal bleeding or intracranial bleeding.
• Medical history: hypertension, diabetes, atrial fibrillation, prior stroke/TIA, sickle cell disease, malignancy, migraine and seizures.
• Baseline function: usual mobility, communication, cognition, activities of daily living and pre-stroke disability; ask about baseline modified Rankin status.
• Potential mimic: hypoglycaemia, seizure with post-ictal weakness, migraine aura, infection, intoxication, electrolyte disturbance, syncope or functional neurological disorder.
• Context: pregnancy/postpartum status, trauma, infection, recent travel, substance use, allergies, last oral intake and goals of care.

7. Examination and stroke severity

Perform a rapid but reproducible examination and document the time. Assess alertness, orientation, speech and comprehension; pupils and eye movements; visual fields; facial symmetry; tongue and palate; arm and leg power and drift; sensation; coordination; gait only when safe; neglect; extinction; dysarthria; aphasia; cerebellar signs and meningism. Look for gaze deviation and a dense deficit suggesting large-vessel occlusion.

The NIH Stroke Scale (NIHSS) quantifies consciousness, orientation, commands, gaze, visual fields, facial movement, arm and leg motor function, ataxia, sensation, language, dysarthria and neglect. It supports communication and treatment selection but can under-score posterior circulation strokes. A low NIHSS does not exclude disabling aphasia, visual loss, ataxia or basilar occlusion.

8. Imaging and investigations

1. Non-contrast CT brain: obtain urgently to exclude haemorrhage and identify early ischaemic change. A normal early CT does not exclude ischaemia.
2. CT angiography: identify carotid, intracranial or basilar large-vessel occlusion, dissection and selected vascular lesions.
3. CT perfusion or MRI diffusion/perfusion: select patients with wake-up stroke, late presentation or uncertain onset for extended-window treatment when available.
4. Blood tests: bedside glucose, full blood count and platelets, electrolytes, renal function, coagulation studies, group and save, pregnancy test when relevant, and other tests directed by the history. Do not delay urgent treatment for routine results when there is no reason to suspect abnormality.
5. Cardiac tests: 12-lead ECG, telemetry, troponin when indicated and later echocardiography or prolonged rhythm monitoring for an embolic source.
6. Additional tests: temperature, urinalysis, toxicology or infection tests only when clinically indicated; do not let a non-essential test delay stroke imaging.

9. Emergency management of ischaemic stroke

Immediate physiological care

• Activate the stroke team and record arrival, imaging, decision and treatment times.
• Maintain a patent airway, oxygenate hypoxaemic patients, treat fever, correct severe glucose abnormalities and use isotonic fluid for dehydration or shock.
• Keep the head midline, avoid tight clothing around the neck, prevent aspiration and perform a swallow screen before oral intake.
• Manage blood pressure according to the intended treatment. Patients not receiving reperfusion are usually not rapidly lowered unless pressure is extreme or another hypertensive emergency exists. Patients eligible for thrombolysis require the treatment-specific threshold in the current protocol.

Intravenous thrombolysis

Eligible patients with disabling acute ischaemic stroke may receive intravenous thrombolysis within the standard time window, commonly up to 4.5 hours from last-known-well, with selected wake-up or extended-window patients considered by advanced imaging and specialist criteria. Alteplase or tenecteplase choice, dose, contraindications, blood-pressure threshold and monitoring must follow the current stroke protocol and senior stroke clinician decision.

Before treatment, confirm CT has excluded haemorrhage, assess recent surgery/bleeding, anticoagulants, platelets and coagulation concerns, and document consent or the emergency decision. During and after treatment perform frequent neurological and blood-pressure checks, watch for headache, vomiting, acute hypertension or deterioration, avoid unnecessary invasive procedures and treat suspected intracranial bleeding as an emergency. Do not give antiplatelet or anticoagulant therapy during the first 24 hours unless a specialist protocol explicitly directs otherwise; obtain follow-up imaging before starting it.

Mechanical thrombectomy

Patients with an eligible large-vessel occlusion may benefit from catheter thrombectomy, usually in an early window and, for selected patients with favourable imaging, in later windows up to 6–24 hours or as defined by current guidance. Notify the endovascular team immediately. If the first facility cannot provide thrombectomy, stabilise without avoidable delay and arrange transfer with imaging, medication history, NIHSS and treatment times.

Antiplatelet and secondary prevention

After haemorrhage is excluded, clinicians may start aspirin according to local protocol when thrombolysis has not been given. Short-course dual antiplatelet therapy may be selected for specific high-risk TIA or minor stroke patients; it is not an automatic treatment for every patient. Identify atrial fibrillation and other embolic sources, manage blood pressure and diabetes, address smoking and alcohol, prescribe statin therapy when indicated, and arrange rehabilitation and follow-up.

10. Emergency management of haemorrhagic stroke

• Stabilise airway, breathing and circulation; intubate with expert help if consciousness or protective reflexes are failing.
• Urgently involve neurology, neurosurgery, anaesthesia and critical-care teams. Repeat neurological observations and prepare for rapid deterioration.
• Control blood pressure smoothly to the target specified by the haemorrhage protocol; avoid sudden hypotension and large oscillations.
• Stop anticoagulants and reverse them urgently with the correct agent for warfarin, dabigatran, factor Xa inhibitors or heparin under specialist direction. Do not give empiric reversal without knowing the drug and timing where this could cause harm.
• Manage raised intracranial pressure: head elevation and midline positioning, analgesia and antiemesis, normoxia, normocapnia, fever control, treatment of seizures and neurosurgical measures such as ventricular drainage or evacuation when indicated.
• Do not give aspirin or thrombolytic therapy. Correct severe hypoglycaemia, avoid fever and maintain adequate cerebral perfusion.
• Provide family communication, goals-of-care discussion and transfer to a monitored neurocritical environment.

11. TIA pathway

Even when symptoms have resolved, document the exact deficit and timing. Perform glucose, neurological examination, brain imaging and vascular imaging where available; obtain ECG and assess for atrial fibrillation. Look for carotid disease and other embolic sources. After haemorrhage is excluded, a clinician may begin antiplatelet therapy promptly and arrange urgent specialist review. Anticoagulation for atrial fibrillation is timed to infarct size, bleeding risk and imaging. Give explicit return precautions for recurrent weakness, speech difficulty, visual loss, severe headache, collapse or imbalance.

12. Complications and prevention

13. Nursing and EMT responsibilities

• Use a time-stamped stroke checklist and communicate using a structured handover: last-known-well, deficit, glucose, anticoagulant, NIHSS, CT/CTA result, treatment and response.
• Maintain airway equipment and suction at the bedside; position safely and keep oral intake withheld until swallow screening.
• Perform prescribed neurological observations: consciousness, pupils, speech, limb power, gaze, vital signs, glucose and temperature. Escalate any change immediately.
• Measure blood pressure correctly with an appropriate cuff, repeat manually when unexpected and avoid unnecessary arm compression on a weak or vascular-access limb.
• Protect the affected shoulder, support the arm, avoid pulling during transfers and use safe mobilisation techniques.
• Prevent hypoglycaemia, fever, dehydration, constipation, urinary retention, pressure injury, falls and venous thromboembolism.
• Provide calm explanations; aphasia is not the same as confusion. Use short sentences, yes/no questions, writing or pictures and allow extra response time.
• Document assessment, consent, relatives contacted, investigations, medication administration, adverse effects, referrals and transfer times.
• Teach the patient and family about FAST, medication adherence, blood-pressure checks, diabetes control, smoking cessation, safe diet, rehabilitation and when to return urgently.

14. Special presentations and mimics

• Wake-up stroke: use last-known-well and advanced imaging criteria; do not assume the patient is outside treatment.
• Pregnancy/postpartum: consider eclampsia, cerebral venous thrombosis, dissection and haemorrhage; involve obstetric and stroke specialists.
• Sickle-cell disease: assess for anaemia, acute chest syndrome, infection and previous stroke; follow the sickle-cell transfusion protocol.
• Anticoagulant use: identify exact agent and last dose; this affects thrombolysis and reversal decisions.
• Seizure at onset: persistent focal deficit after a seizure can still be stroke; re-assess when post-ictal features improve.
• Common mimics: hypoglycaemia, hyperglycaemia, migraine, seizure, sepsis, encephalopathy, intoxication, vestibular disease, tumour and functional neurological symptoms.

15. Applied emergency scenarios

Scenario 1: FAST-positive patient at 90 minutes

A 67-year-old suddenly develops aphasia and right-arm weakness 90 minutes after being seen normal. Check glucose, ABCDE and anticoagulant history, pre-alert the stroke team, obtain urgent CT/CTA and prepare for protocol-based reperfusion. Do not delay for a meal, routine paperwork or non-essential investigations.

Scenario 2: Wake-up stroke with large deficit

A patient wakes with gaze deviation and dense hemiplegia. Record last-known-well before sleep, activate the stroke pathway, perform CT/CTA and consider advanced imaging for thrombolysis or thrombectomy eligibility. Arrange transfer early if endovascular treatment is unavailable.

Scenario 3: Intracerebral haemorrhage on anticoagulant

A patient has severe headache, vomiting and reduced consciousness. Protect the airway, obtain immediate CT, stop anticoagulant, identify the exact agent and urgently involve critical care, neurosurgery and the reversal service. Avoid aspirin and thrombolysis.

Scenario 4: Resolved TIA

A patient had 15 minutes of unilateral weakness that resolved. Treat this as urgent: record the episode, check glucose and ECG, image the brain and vessels, assess atrial fibrillation and arrange rapid secondary prevention. Give clear return precautions.

16. Revision questions

1. Why is last-known-well time more useful than the time symptoms were noticed?
2. List five stroke mimics that must be checked during the primary assessment.
3. Why must oral intake be withheld until a swallow screen?
4. What findings suggest posterior circulation stroke or large-vessel occlusion?
5. Which observations are required after thrombolysis, and why is follow-up imaging important before antithrombotics?
6. Outline the immediate actions for haemorrhagic stroke in a patient taking an anticoagulant.

Key takeaways

• Stroke and TIA are emergencies even when symptoms improve.
• Time, glucose, airway, oxygenation, CT and vascular imaging drive safe decisions.
• Never give food, drink, aspirin or thrombolysis before the appropriate assessment and imaging pathway.
• Thrombolysis, thrombectomy, blood-pressure targets and anticoagulant reversal require current specialist protocols.
• Repeated neurological observations and careful nursing prevention reduce avoidable secondary injury.