Acute stroke and thrombolysis: quick reference

About this quick reference

This is a practical quick reference for emergency physicians in suspected acute ischaemic stroke. It covers time windows, indications and contraindications for intravenous thrombolysis, weight-based tenecteplase dosing, blood pressure thresholds, monitoring, complications and when thrombectomy should be considered.

The doses and Swedish thresholds below are based on the national guideline for the management of reperfusion treatment in ischaemic stroke, Nationell arbetsgrupp Stroke (the national stroke working group), version 4 of 27 February 2024. The local stroke protocol and immediate contact with the on-call stroke consultant or the thrombectomy centre take precedence where there is a discrepancy or uncertainty.

Intravenous thrombolysis within 4.5 hours improves functional outcome in properly selected patients. Tenecteplase 0.25 mg/kg is a safe and effective alternative to alteplase and is simpler to administer, since the whole dose is given as a bolus [1,2]. In a meta-analysis of three phase 3 trials, tenecteplase was non-inferior to alteplase with respect to an excellent functional outcome, without an increased risk of symptomatic intracerebral haemorrhage or death [3].

Acute overview

1. Activate the stroke call.
2. Establish the time of symptom onset or the time last known to be well.
3. Assess airway, breathing and circulation.
4. Measure the plasma glucose immediately.
5. Perform the NIHSS and document which symptoms are disabling.
6. Measure the blood pressure, initially in both arms if this can be done without losing time.
7. Perform urgent CT of the brain and CT angiography from the aortic arch to the vertex.
8. Contact the thrombectomy centre immediately where large vessel occlusion is possible. Do not wait for the definitive radiology report if the clinical picture and the preliminary images suggest occlusion.
9. Give thrombolysis as soon as haemorrhage and contraindications have been excluded. CT angiography or transport planning must not delay treatment unnecessarily.
10. In unknown time of onset, wake-up stroke or a late time window: perform advanced imaging according to the local protocol.
11. Document weight, agent, dose, time of the bolus and the blood pressure before administration.
12. Prepare for the monitoring and management of intracranial haemorrhage and angioedema.

First of all

The plasma glucose is normally the only test result that must always be known before thrombolysis is started. A full blood count, electrolytes, creatinine, coagulation tests and troponin are taken in parallel but must not delay treatment in a patient without suspected coagulopathy or anticoagulant treatment. An ECG should be recorded but does not have to precede thrombolysis [4].

Test results must, however, be awaited when the history gives reasonable suspicion of:

• warfarin treatment
• recent intake of a direct oral anticoagulant
• heparin treatment
• marked thrombocytopenia
• hepatic insufficiency with coagulopathy
• another known or suspected bleeding disorder

Stroke is a clinical diagnosis. A normal early CT does not exclude ischaemic stroke. Suspicion of a stroke mimic must be weighed against the risk of delaying treatment of a genuine stroke. Thrombolysis of stroke mimics has in meta-analyses carried a low risk of symptomatic intracerebral haemorrhage, about 0.5 percent, but treatment should of course not be given once an alternative diagnosis has become clear [5].

Time windows

Known time of onset

Intravenous thrombolysis can be given when treatment can be started no later than 4.5 hours after symptom onset. Time to treatment is decisive. A patient should therefore not be kept waiting until the end of the time window for additional investigations that do not affect the treatment decision [1].

Where there is transient improvement, the residual symptoms must be assessed. Rapid improvement is not in itself a reason to withhold treatment if a disabling neurological deficit persists.

Wake-up stroke or unknown time of onset

Waking with stroke symptoms does not exclude reperfusion treatment. The patient may be a candidate for:

• intravenous thrombolysis after selection with CT perfusion or MRI
• thrombectomy for a treatable vessel occlusion
• both treatments, if the criteria are met

In an individual patient data meta-analysis of four randomised trials, 47 percent of imaging-selected patients had an excellent functional outcome after alteplase, compared with 39 percent in the control group. Symptomatic intracranial haemorrhage occurred in 3 percent and less than 1 percent respectively [6]. A Cochrane review also found better functional outcome after reperfusion treatment of selected wake-up stroke [7].

CT perfusion is thus not the only possible method. MRI with DWI-FLAIR mismatch is an established alternative. The choice is governed by local resources and must not cause unnecessary delay.

Indication for intravenous thrombolysis

All of the following criteria should normally be met:

• A clinical diagnosis of ischaemic stroke.
• A measurable neurological deficit.
• The deficit is judged to be disabling or potentially disabling.
• Age at least 16 years according to the Swedish protocol.
• For patients under 18, an individual decision together with paediatric emergency specialist services and stroke expertise is required.
• Thrombolysis can be started within the approved time window, or the patient has been selected by advanced imaging where the time of onset is unknown.
• Intracranial haemorrhage has been excluded.
• The blood pressure can be kept below the treatment threshold.
• No contraindication outweighs the expected benefit.

A low NIHSS

The NIHSS is a measure of severity, not a stand-alone treatment criterion. A low NIHSS can conceal a markedly disabling deficit. Examples are:

• isolated aphasia
• hemianopia
• marked dysarthria
• hand paresis
• inability to walk
• swallowing difficulty
• neglect
• an oculomotor disturbance or ataxia in posterior circulation stroke

In mild, clearly non-disabling stroke the benefit of thrombolysis is uncertain and the bleeding risk remains. The assessment must therefore describe the actual deficit, not merely the NIHSS.

Lacunar stroke

Suspected lacunar stroke is not a contraindication. European guidelines recommend that acute lacunar ischaemic stroke be managed according to the usual principles of thrombolysis, even though the direct evidence for this subgroup is limited [8].

Contraindications and situations of risk

Contraindications should be assessed together with the on-call stroke consultant. Several classic exclusion criteria rest on limited evidence and may need to be individualised. In large vessel occlusion, a contraindication to thrombolysis must not automatically lead to thrombectomy being ruled out.

Absolute contraindications according to the Swedish emergency protocol

• Blood pressure of at least 185/110 mmHg despite acute intravenous antihypertensive treatment.
• Intracranial haemorrhage on acute imaging.
• Clinical or radiological suspicion of subarachnoid haemorrhage.
• Strong suspicion of aortic dissection.
• Ongoing non-compressible or clinically significant bleeding.
• Clear suspicion of septic embolisation, for example in infective endocarditis.
• A malignant intracerebral tumour or metastasis with a significant bleeding risk.
• An extensive, already established infarct according to current radiological criteria.
• Ongoing anticoagulation with a relevant residual anticoagulant effect.
• Uncorrected severe coagulopathy.

The older formulation about an infarct involving more than one third of the vascular territory should not be applied mechanically to thrombectomy decisions. Modern trials show that selected patients with a large infarct core can derive substantial benefit from thrombectomy, even though the prognosis is often still serious.

Previous intracerebral haemorrhage

Previous spontaneous intracerebral haemorrhage is regarded as a contraindication in the Swedish emergency protocol. International guidelines are more individualising, since the risk is affected by, among other things:

• the cause of the haemorrhage
• the time since the haemorrhage
• a persisting structural lesion
• the current MRI appearance with microbleeds or suspected cerebral amyloid angiopathy
• the severity of the current stroke
• the possibility of thrombectomy

The decision must be made by a stroke specialist.

An untreated intracranial aneurysm or vascular malformation

A known untreated arteriovenous malformation is an important situation of risk. A small, unruptured aneurysm is by contrast not necessarily an absolute contraindication. A meta-analysis found no documented aneurysm-related intracerebral haemorrhage after thrombolysis among the patients included, but the evidence base was observational and limited [9]. The size, shape, location and previous symptoms of the aneurysm must be taken into account.

Important relative contraindications

• Strong suspicion of another diagnosis, for example hypoglycaemia, migraine, functional symptoms or postictal paresis.
• No residual symptoms.
• Reduced consciousness with a GCS below 12 or an RLS above 2 not explained by basilar artery occlusion.
• Ischaemic stroke, intracranial surgery or severe head trauma within the past 6 weeks.
• A known untreated intracranial arteriovenous malformation.
• Gastrointestinal or urinary tract bleeding within the past 3 weeks.
• Active gastrointestinal malignancy.
• Lumbar puncture within the past 7 days.
• Cardiopulmonary resuscitation within the past 10 days.
• Major surgery within the past 2 weeks.
• Recent biopsy or puncture of a non-compressible vessel.
• A known uncorrected bleeding disorder.
• A platelet count below 100 x 10⁹/L.
• Pregnancy or recent delivery.
• Very extensive early ischaemic changes.
• Suspected pericarditis or an intracardiac thrombus with a high risk of embolisation.
• Another individually assessed high bleeding risk.

Seizure at onset

A seizure at symptom onset is not an automatic contraindication. The question is whether the residual deficit is likely to be caused by ischaemic stroke or by a postictal state. CT angiography, perfusion imaging and the clinical course can be helpful. Treat if ischaemic stroke is still the most likely explanation and the other criteria are met.

Anticoagulants

Always establish:

• the agent
• the dose
• the time of the last intake
• renal function
• the indication for treatment
• any missed doses
• the drug-specific assays available

For apixaban, rivaroxaban and dabigatran, renal function, the dose and the time since the last intake all determine how long the effect persists. A normal INR or APTT does not exclude a clinically relevant effect of a factor Xa inhibitor. Use a drug-specific assay where one is available, according to the local laboratory protocol.

More recent observational data suggest that thrombolysis after recent intake of a direct oral anticoagulant may be safer than previously assumed, but randomised data are lacking. In a small target trial emulation with 98 patients, no symptomatic intracranial haemorrhage occurred among the 49 who received thrombolysis [10]. This is not sufficient to depart routinely from the Swedish guideline.

Dabigatran and idarucizumab

Idarucizumab reverses dabigatran rapidly. International experience and observational data are more extensive than earlier guidelines suggested, but randomised trials of idarucizumab followed by thrombolysis are lacking [11]. The early systematic review comprised only 21 patients and reported one fatal symptomatic intracerebral haemorrhage [12].

Reversal before thrombolysis should therefore:

• be decided by a stroke specialist
• follow the current national and local protocol
• not delay thrombectomy for a treatable vessel occlusion
• be followed by careful assessment of coagulation and by monitoring

Andexanet alfa is not recommended routinely in order to enable thrombolysis after a factor Xa inhibitor.

Before thrombolysis

Blood pressure

The blood pressure must be lower than 185/110 mmHg before thrombolysis is started and thereafter kept below 180/105 mmHg according to many international protocols. The Swedish monitoring protocol may specify a target below 185/110 mmHg during the first 24 hours. Follow the stricter local threshold.

Avoid glyceryl trinitrate for isolated raised blood pressure in acute ischaemic stroke. An abrupt or excessive fall in blood pressure can impair perfusion of the penumbra [4].

Other measures

Choice of thrombolytic agent

Tenecteplase 0.25 mg/kg can be used as an alternative to alteplase within 4.5 hours. European guidelines prefer tenecteplase over alteplase in large vessel occlusion in a patient who is also to undergo thrombectomy [2]. A more recent meta-analysis of 13 randomised trials supports 0.25 mg/kg as the best documented tenecteplase dose [13].

Tenecteplase 0.40 mg/kg must not be used in ischaemic stroke. High-dose treatment has been associated with worse safety, particularly in moderate or severe stroke [2,3].

With an unknown time of onset or in wake-up stroke, the choice of agent should follow the local imaging protocol. The evidence for alteplase after advanced imaging selection is better established than that for tenecteplase [1,6].

Thrombolysis dosing

Tenecteplase

Tenecteplase (Metalyse) is given as an intravenous bolus injection at a dose of 0.25 mg/kg, to a maximum of 25 mg, corresponding to a maximum of 5,000 units. The bolus is given over about 5 to 10 seconds.

The reconstituted solution contains 5 mg/mL.

Check in particular:

• the measured or credibly estimated weight
• the concentration of the reconstituted solution
• that the stroke prescription is 0.25 mg/kg
• that the maximum dose of 25 mg is not exceeded
• that the myocardial infarction dosing is not used by mistake

Alteplase

Alteplase (Actilyse) is given at a dose of 0.9 mg/kg, to a maximum of 90 mg.

• 10 percent of the total dose is given as an intravenous bolus over 1 to 2 minutes.
• The remaining 90 percent is given as an infusion over 60 minutes.

If a serious complication arises during the infusion, the infusion must be stopped immediately. A tenecteplase bolus that has already been given cannot be interrupted, which makes preparedness for complications particularly important.

Thrombectomy

Basic indication

Thrombectomy should be considered when the following are present:

• acute ischaemic stroke
• a clinically significant neurological deficit
• a treatable intracranial vessel occlusion
• no intracranial haemorrhage
• a radiologically and clinically plausible prospect of an improved outcome
• the possibility of starting the procedure within the relevant time window

In anterior circulation stroke this applies above all to occlusion of:

• the intracranial internal carotid artery
• the M1 segment of the middle cerebral artery
• selected M2 occlusions
• tandem occlusions, after individual assessment

The NIHSS is usually at least 6, but patients with an NIHSS of 2 to 5 may have a treatable occlusion and a markedly disabling deficit. A low NIHSS should therefore not prevent CT angiography or contact with the thrombectomy centre.

Randomised trials have shown a large treatment effect in proximal large vessel occlusion, with an estimated number needed to treat of between 3 and 10 depending on selection and outcome measure [14].

Time windows

• Within 6 hours, CT of the brain and CT angiography form the basis.
• Between 6 and 24 hours, extended radiological selection according to the local protocol is usually required.
• An unknown time of onset or wake-up stroke does not exclude thrombectomy.
• Time is normally counted from the time last known to be well when the actual onset is unknown.

Give thrombolysis before thrombectomy when the patient is eligible

Intravenous thrombolysis must not delay transport or thrombectomy. At the same time, a patient eligible for thrombolysis should normally receive intravenous thrombolysis even when thrombectomy is planned.

A Cochrane review of six randomised trials found no clear difference in functional outcome or mortality between direct thrombectomy and thrombectomy after intravenous thrombolysis, but thrombolysis increased the proportion with successful and complete reperfusion [15]. European guidelines therefore continue to recommend so-called bridging thrombolysis when there are no contraindications [2].

Tenecteplase may be particularly practical before transfer, since it is given as a single bolus. A meta-analysis found higher early recanalisation with tenecteplase than with alteplase before thrombectomy, without an increase in symptomatic intracerebral haemorrhage [16].

A large infarct core

A large infarct core is no longer an automatic contraindication to thrombectomy. In a meta-analysis of six randomised trials with 1,870 patients, thrombectomy increased functional independence from 7.4 to 19.5 percent. The number needed to treat for one additional functionally independent outcome was 9. Thrombectomy also reduced the risk of being completely dependent on care or dead [17].

The benefit is, however, on average smaller than with a small infarct core, and the decision must take into account:

• the functional level before the stroke
• age and biological reserve
• the size and location of the infarct
• the level of the vessel occlusion
• the time to possible reperfusion
• collaterals
• comorbidity
• the patient's previously expressed wishes

Basilar artery occlusion

Basilar artery occlusion can produce:

• fluctuating symptoms
• dysarthria and dysphagia
• diplopia and disturbance of eye movement
• ataxia
• tetraparesis
• sudden reduction in consciousness
• coma

Reduced consciousness is not a relative contraindication when basilar artery occlusion is suspected. CT angiography must be performed urgently.

European guidelines support thrombectomy plus best medical treatment for selected patients with basilar artery occlusion and a significant neurological deficit, particularly an NIHSS of at least 10, in both early and late time windows. The evidence is weaker with mild symptoms and with extensive bilateral or brainstem-dominated ischaemic changes [18].

Distal or medium vessel occlusion

Routine thrombectomy for distal medium vessel occlusion is not recommended on the basis of the current randomised evidence. A meta-analysis of three trials with 1,246 patients found no improvement in functional outcome but a higher risk of symptomatic intracranial haemorrhage, 6.4 percent after thrombectomy compared with 3.0 percent after medical treatment [19]. Individual exceptions may arise after assessment at a thrombectomy centre.

Transport

• Transfer to the thrombectomy centre at highest priority.
• Do not wait for a clinical response to thrombolysis.
• Give the tenecteplase bolus before departure if the decision has been made and transport is not delayed.
• An alteplase infusion can continue during ambulance transfer if monitoring, security of the line and preparedness for complications are adequate.
• Send exact times, the NIHSS, the images, the medication list, weight, blood pressure, the agent and the dose given.

Monitoring after thrombolysis

The patient must be cared for on a stroke unit, or an equivalent unit with the expertise to detect and treat intracranial haemorrhage, angioedema and acute neurological deterioration.

After thrombolysis the following should be avoided where possible during the first 24 hours:

• arterial puncture
• central venous catheter
• intramuscular injections
• urinary catheter
• nasogastric tube
• other traumatic or invasive procedures

If such a procedure is medically necessary it must not be withheld, but the bleeding risk should be taken into account.

Anticoagulants, antiplatelet agents and pharmacological thromboprophylaxis should normally not be given during the first 24 hours and may be started only after follow-up imaging has excluded clinically significant bleeding. Precise exceptions after thrombectomy, stenting or another endovascular procedure are decided by the stroke team.

Acute neurological deterioration

Neurological deterioration after reperfusion treatment can be caused by:

• intracranial haemorrhage
• infarct progression
• reocclusion
• a new embolic stroke
• cerebral oedema
• seizures
• hypoglycaemia or hyperglycaemia
• hypotension
• hypoxia
• aspiration
• infection
• dissection or another vascular complication

Do the following immediately:

1. Stop any ongoing alteplase infusion.
2. Check airway, breathing and circulation.
3. Measure the plasma glucose and the blood pressure.
4. Perform urgent CT of the brain, often with CT angiography as well.
5. Take a full blood count, INR, APTT, fibrinogen, blood group and crossmatch.
6. Contact the on-call stroke consultant, the on-call haemostasis service, a neurosurgeon and neurointervention according to the findings.

Complications

Suspected intracranial haemorrhage

Warning symptoms are:

• new or increasing headache
• nausea and vomiting
• an acute rise in blood pressure
• reduced consciousness
• new or increasing focal neurology
• seizures

Symptomatic intracerebral haemorrhage is strongly associated with a poor outcome. The evidence for specific reversal treatment is limited, but fibrinogen replacement and antifibrinolytic treatment are used because alteplase and tenecteplase affect fibrinolysis [20].

Orolingual angioedema

Inspect the mouth and tongue towards the end of the alteplase infusion and after the tenecteplase bolus, particularly in patients taking an ACE inhibitor. The swelling is often asymmetrical and can progress rapidly.

Thrombolysis-related angioedema is often bradykinin mediated. Antihistamines, corticosteroids and adrenaline then have an uncertain or limited effect [21]. Treatment with an ACE inhibitor is an important risk factor [22]. Angioedema can also occur after tenecteplase, and there is no single treatment with robustly documented efficacy [23].

The most important thing is repeated assessment of the airway. Do not wait for complete obstruction before anaesthetics and ENT are contacted.

Documentation

Always document:

• the time of symptom onset or the time last known to be well
• the time of arrival
• the time of the first medical assessment
• the time of CT and CT angiography
• the NIHSS before treatment
• the blood pressure before treatment
• the plasma glucose
• body weight and how it was established
• anticoagulants and the last dose
• the thrombolytic agent and the total dose
• the exact time of the bolus
• the start and stop times of the alteplase infusion
• contact with the on-call stroke consultant and the thrombectomy centre
• the transfer decision
• the clinical response and any complications

Structured care pathways are important, since variation in the implementation of guidelines is still considerable even though thrombolysis, vascular imaging and care on a stroke unit are well established interventions [24]. Protocols that integrate diagnosis, treatment and monitoring can facilitate rapid and reproducible care [25].

Red flags and pitfalls

• Not measuring the plasma glucose.
• Using the NIHSS as the sole measure of the need for treatment. Aphasia, hemianopia or hand paresis can be seriously disabling despite a low NIHSS.
• Withholding treatment merely because the symptoms are improving. Always assess the residual functional deficit.
• Missing basilar artery occlusion. Fluctuating symptoms or reduced consciousness may be the only clear warning.
• Assuming that wake-up stroke cannot be treated. Advanced imaging can identify candidates for thrombolysis or thrombectomy.
• Delaying thrombolysis for an ECG or routine blood tests.
• Delaying contact with the thrombectomy service until thrombolysis has finished.
• Not performing CT angiography with mild symptoms. A low NIHSS does not exclude large vessel occlusion.
• Using tenecteplase 0.40 mg/kg. The stroke dose is 0.25 mg/kg, to a maximum of 25 mg.
• Confusing the tenecteplase dose for stroke with the dose for myocardial infarction.
• Giving antiplatelet agents or anticoagulants before follow-up imaging after thrombolysis.
• Regarding a large infarct core as an automatic contraindication to thrombectomy.
• Routinely performing thrombectomy for distal vessel occlusions without specialist assessment.
• Interpreting a normal INR or APTT as proof that a factor Xa inhibitor has no effect.
• Missing angioedema after tenecteplase because no infusion is running.
• Treating progressive angioedema pharmacologically without simultaneously ensuring airway preparedness.
• Lowering the blood pressure rapidly and steeply. The ischaemic penumbra may be pressure dependent.
• Giving oxygen routinely to a normoxic patient.
• Forgetting aortic dissection with a large difference in blood pressure, chest pain, back pain or absent pulses.

References

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3. Xiong et al. Tenecteplase versus alteplase for acute ischaemic stroke: a meta-analysis of phase III randomised trials. Stroke and Vascular Neurology 2024. PMID: 37640500
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11. Frol et al. Idarucizumab in dabigatran-treated patients with acute stroke: a review and clinical update. Frontiers in Neurology 2024. PMID: 38817549
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20. Charbonnier et al. Intracranial Bleeding After Reperfusion Therapy in Acute Ischemic Stroke. Frontiers in Neurology 2021. PMID: 33633661
21. Suffritti et al. Bradykinin-Mediated Angioedema Induced by Drugs. Journal of Clinical Medicine 2025. PMID: 40869540
22. Qi et al. Alteplase associated Orolingual angioedema: A case report and literature review. Medicine 2022. PMID: 36596071
23. Pitts et al. Tenecteplase-associated orolingual angioedema: A case report and literature review. American Journal of Health-System Pharmacy 2024. PMID: 38270186
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