Intravenous thrombolysis and mechanical thrombectomy

01Purpose and principlesWhat the treatment does and how it fits into care.

Intravenous thrombolysis dissolves thrombus pharmacologically and is most effective when given early. Eligibility is not a checklist detached from clinical judgement: the treating stroke physician weighs whether the neurological deficit is disabling, whether imaging shows haemorrhage or extensive irreversible injury, whether haemostasis is impaired and whether recent events create an unacceptable bleeding hazard. The team should clarify last-known-well, anticoagulant type and last dose, blood pressure, glucose, premorbid function, recent surgery, trauma, stroke and bleeding while CT is being acquired.

Mechanical thrombectomy physically retrieves an occluding clot from a large intracranial artery. CTA identifies the target; perfusion or MRI helps select some patients in later or unknown windows. A patient presenting to a primary stroke centre may need immediate discussion and transfer to a comprehensive centre. The referring team should send images electronically, continue eligible thrombolysis, maintain safe physiology and avoid waiting for investigations that will not change transfer. Posterior circulation thrombectomy, including basilar occlusion, is a specialist network decision informed by contemporary evidence and local commissioning.

Complications differ but overlap. Alteplase and tenecteplase can cause symptomatic intracranial haemorrhage, systemic bleeding and orolingual angioedema. Thrombectomy can cause arterial perforation, dissection, embolisation into a new territory, contrast-related problems and access-site bleeding. Both treatments may be followed by reperfusion injury, cerebral oedema or haemorrhagic transformation. Protocolised neurological and blood-pressure observation, rapid repeat CT for deterioration and clear handover are therefore part of the treatment rather than optional aftercare.

Key points

Reperfusion decisions are made by an acute stroke service using disabling deficit, last-known-well, imaging, premorbid function, bleeding risk and patient wishes; age or NIHSS alone should not become an automatic exclusion.
NICE recommends tenecteplase or alteplase as intravenous thrombolysis options for selected acute ischaemic stroke within 4.5 hours when intracranial haemorrhage has been excluded and contraindications are addressed; use the locally commissioned stroke protocol.
Wake-up or later-presenting stroke may be thrombolysed when MRI or perfusion imaging demonstrates a favourable tissue pattern under current specialist protocols; clock time is not the only modern selection tool.
Mechanical thrombectomy is offered rapidly for eligible proximal intracranial large-vessel occlusion, commonly within 6 hours and in selected patients up to 24 hours using clinical and advanced-imaging criteria.
Do not withhold intravenous thrombolysis from an otherwise eligible patient merely because thrombectomy is planned; bridging treatment and transfer should proceed in parallel unless a specialist contraindication applies.
Before thrombolysis, blood pressure must be reduced to 185/110 mmHg or lower and glucose, anticoagulant exposure, recent bleeding or surgery and platelet or coagulation concerns must be evaluated without unnecessary testing delays.
After intravenous thrombolysis, maintain blood pressure below 180/105 mmHg for the first 24 hours under the stroke protocol, avoid antiplatelet and anticoagulant treatment for 24 hours, perform follow-up imaging before starting it, and investigate any neurological decline, headache, vomiting or hypertension immediately.
Thrombectomy care includes anaesthetic strategy, arterial access, reperfusion assessment and post-procedure blood-pressure planning at a specialist centre; successful recanalisation does not guarantee completed tissue recovery.

02Indications, selection and cautionsWho may benefit, who needs urgent treatment and important alternatives.

Disabling acute deficit

Aphasia, hemianopia, neglect, gait-preventing ataxia or dominant-hand weakness may be disabling even with a modest NIHSS and merits explicit reperfusion review.

Large-vessel phenotype

Gaze deviation, cortical signs, dense hemiplegia, neglect or a high NIHSS increases suspicion for proximal occlusion, but CTA rather than the bedside phenotype confirms the target.

Late-window opportunity

Wake-up or 6–24-hour presentations may retain salvageable tissue when core size, collaterals and clinical deficit are favourable on network-approved advanced imaging.

Post-lysis haemorrhage

New headache, vomiting, acute hypertension, neurological worsening or reduced consciousness after thrombolysis demands immediate cessation of any infusion and emergency imaging.

Orolingual angioedema

Tongue or lip swelling, often asymmetric and more frequent with ACE-inhibitor exposure, may develop during or shortly after intravenous thrombolysis and threaten the airway.

Re-occlusion or oedema

Deterioration despite initial improvement may reflect re-occlusion, incomplete reperfusion, haemorrhagic transformation, seizure or malignant cerebral swelling.

Red flags requiring action

Suspected intracranial haemorrhage, active major bleeding or a known severe haemostatic abnormality requires immediate specialist review and usually precludes thrombolysis.
A direct oral anticoagulant taken recently, an elevated relevant drug level or uncertain exposure cannot be dismissed by a normal INR; use the local anticoagulant-specific pathway.
Blood pressure remaining above the treatment threshold despite careful protocol therapy prevents safe intravenous thrombolysis at that moment.
Basilar occlusion can deteriorate to coma or locked-in syndrome despite initially fluctuating symptoms and requires immediate thrombectomy-centre contact.
Airway swelling, haemodynamic instability, access-site expansion or any post-treatment neurological decline needs emergency senior and critical-care support.

03Assessment before treatmentTests and checks that guide safe selection.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Non-contrast CT brainFirst step
Why
Exclude intracranial haemorrhage and assess the extent of established infarction before either reperfusion treatment.
Interpretation and limitations
Small early changes do not automatically prohibit treatment, while extensive irreversible injury increases haemorrhage risk and reduces expected benefit; expert imaging review is essential.
02
CT angiography
Why
Identify the location of a treatable large-vessel occlusion and define cervical vessels and access anatomy.
Interpretation and limitations
A proximal anterior circulation or basilar target should trigger immediate network discussion; collateral and tandem-lesion information helps procedure planning.
03
Perfusion CT or MRI selection
Why
Estimate infarct core and threatened tissue for extended-window thrombectomy or imaging-selected thrombolysis.
Interpretation and limitations
Mismatch thresholds are treatment- and pathway-specific; motion, delay and poor cardiac output can distort automated results, so images require expert correlation.
04
Coagulation and anticoagulant assessment
Why
Identify clinically important impaired haemostasis when history or medicine exposure makes it relevant.
Interpretation and limitations
INR is useful for warfarin but does not exclude significant DOAC activity; specialist assays, timing, renal function and local policy guide decisions without delaying patients who have no reason for abnormality.
05
Full blood count and glucose
Why
Identify severe thrombocytopenia, anaemia or a glucose disturbance that changes safety or diagnosis.
Interpretation and limitations
Do not wait for a platelet result when there is no suspicion of thrombocytopenia under the local protocol, but obtain urgent data when history suggests marrow disease, chemotherapy or bleeding.
06
Follow-up brain CT
Why
Exclude post-reperfusion haemorrhage before antithrombotic treatment or urgently investigate deterioration.
Interpretation and limitations
Routine imaging is commonly performed around 24 hours after thrombolysis, while symptoms mandate immediate imaging rather than waiting for the scheduled scan.

04Treatment approachPreparation, options, escalation and aftercare.

01LYSEIntravenous thrombolysis decisionFirst stepA patient has a disabling acute ischaemic stroke within a standard or imaging-selected treatment window.

1Confirm last-known-well, deficit and premorbid function, exclude haemorrhage on imaging and review anticoagulants, bleeding, procedures, blood pressure and glucose with the stroke physician.
2Correct a treatable pressure excess carefully to the protocol threshold and obtain only laboratory results that are clinically necessary before treatment.
3Discuss material benefit, symptomatic haemorrhage and uncertainty with the patient or appropriate representative without creating disproportionate delay.
4Administer the approved thrombolytic using the exact weight-based local protocol, document timestamps and begin protocolised post-treatment observations.

02RETRIEVEMechanical thrombectomy pathwayCTA demonstrates a potentially treatable intracranial large-vessel occlusion with compatible disability.

1Send clinical details and imaging immediately to the thrombectomy centre, including onset, NIHSS, ASPECTS or core information, baseline function and anticoagulant exposure.
2Give intravenous thrombolysis promptly when independently eligible and do not wait to see whether it works before arranging transfer.
3Maintain oxygenation, glucose, temperature and appropriate blood pressure, keep the patient nil by mouth and use the fastest agreed transfer route.
4At the specialist centre, confirm clinical and imaging eligibility, obtain consent where possible and select anaesthetic and endovascular strategy through the multidisciplinary team.

03BLEEDDeterioration after reperfusionNeurology, consciousness, headache, vomiting or blood pressure worsens during or after treatment.

1Stop a running thrombolytic infusion, perform ABC assessment and seek immediate stroke, neuroradiology, haematology and critical-care support as indicated.
2Obtain urgent non-contrast CT and send full blood count, coagulation, fibrinogen and treatment-relevant tests without delaying emergency stabilisation.
3If haemorrhage is confirmed, follow the local thrombolytic-associated or anticoagulant-associated reversal protocol and manage pressure, airway and neurosurgical questions.
4EscalationContinue close neurological observation and communicate prognosis and escalation limits after the cause and available interventions are defined.

04AIRWAYThrombolysis-associated angioedemaLip, tongue, oropharyngeal or facial swelling develops during or shortly after thrombolytic administration.

1Stop the infusion, call anaesthetic and critical-care help early and assess voice, stridor, tongue progression and oxygenation continuously.
2Treat according to the local emergency angioedema protocol while preparing for a potentially difficult airway before obstruction becomes complete.
3Withhold the suspected contributing ACE inhibitor and distinguish isolated swelling from anaphylaxis, haemorrhage or trauma.
4Document the reaction and future medicine implications clearly, and monitor in an appropriately staffed environment until progression risk has passed.

05Regimens, contraindications and interactionsTreatment details and the circumstances that modify them.

Restores perfusion by fibrinolysis when given promptly to a specialist-selected patient with disabling acute ischaemic stroke.

Alteplase

For eligible acute ischaemic stroke, give 0.9 mg/kg intravenously to a maximum 90 mg, with 10% as an initial bolus and the remainder infused over 60 minutes.

Use the complete stroke protocol for bleeding exclusions, anticoagulants, blood pressure and imaging; stop immediately for suspected intracranial bleeding or significant angioedema.

Provides a NICE-recommended, single-bolus alternative to alteplase for thrombolysis within 4.5 hours after intracranial haemorrhage has been excluded.

Tenecteplase

For eligible adult acute ischaemic stroke, give 0.25 mg/kg intravenously to a maximum 25 mg as a single bolus, using the dedicated stroke presentation and exact local weight-band protocol.

Apply the full stroke thrombolysis exclusions and monitoring pathway; do not confuse the 25 mg stroke presentation or dose with higher-dose tenecteplase regimens used for myocardial infarction.

Permits safer thrombolysis when pressure is just above the accepted threshold and treats severe hypertension around reperfusion.

Labetalol

Use intravenous bolus dosing or infusion specified by the local hyperacute stroke protocol to bring pressure below the thrombolysis threshold without abrupt hypotension.

Avoid aggressive normalisation; consider bradycardia, heart block, heart failure, bronchospasm and the risk of reducing collateral cerebral perfusion.

Begins early antiplatelet secondary prevention after the immediate thrombolysis bleeding window has safely passed.

Aspirin after reperfusion

Withhold for the first 24 hours after intravenous thrombolysis, then give 300 mg daily only after follow-up imaging excludes significant haemorrhage and the stroke team approves.

Do not combine prematurely with thrombolysis or start after haemorrhagic transformation; swallowing route and any planned anticoagulation require specialist coordination.

06Complications, monitoring and follow-upAdverse effects, response and longer-term review.

Record treatment metrics including arrival, imaging, needle, arterial puncture and reperfusion times so avoidable pathway delay can be reviewed.
Perform neurological and blood-pressure observations at the frequency specified after thrombolysis or thrombectomy, escalating any decline immediately.
Inspect tongue, lips and airway during and after intravenous thrombolysis, particularly in a patient taking an ACE inhibitor or with evolving facial swelling.
Check arterial access sites, distal pulses and haemoglobin when bleeding is suspected after thrombectomy, alongside neurological surveillance.
Obtain follow-up brain imaging before antiplatelet or anticoagulant initiation and sooner for headache, vomiting, hypertension or reduced consciousness.
Reassess infarct mechanism, cardiac rhythm, carotid disease and long-term antithrombotic timing after the acute haemorrhage risk is defined.

07Special situationsVariants, exceptions and circumstances that change the usual approach.

Two treatments can complement

Intravenous thrombolysis may begin while transfer for clot retrieval proceeds; planning thrombectomy is not itself a reason to lose the pharmacological window.

Low NIHSS can conceal disability

Language, vision, gait and skilled hand function should be discussed explicitly because a number alone may understate personal and occupational impact.

DOAC tests differ

A normal INR cannot reassure for apixaban, rivaroxaban, edoxaban or dabigatran; drug timing, renal function and assay availability matter.

Transfer is treatment

Image sharing, accepting-centre contact and ambulance activation should occur as one process because each administrative pause consumes salvageable tissue.

Recanalisation is not recovery

Final outcome also depends on infarct core, collaterals, complications and rehabilitation, so a technically successful procedure still requires rigorous stroke-unit care.

Posterior evidence evolves

Basilar thrombectomy decisions should follow current network criteria because trial evidence, imaging thresholds and commissioning continue to develop.

08Common pitfallsFrequent interpretation and management errors.

01
Do not exclude treatment solely because the patient is very old, has a low NIHSS or cannot provide immediate consent; obtain specialist individualised review.
02
Do not wait for thrombectomy transfer before giving thrombolysis to an otherwise eligible patient unless the treating stroke physician identifies a reason.
03
Do not rely on INR to assess recent direct oral anticoagulant activity or guess eligibility without the anticoagulant-specific protocol.
04
Do not give aspirin, heparin or another antithrombotic during the first 24 hours after intravenous thrombolysis before follow-up imaging.
05
Do not normalise blood pressure aggressively, because sudden reduction can reduce collateral flow to threatened brain.
06
Do not wait for the routine 24-hour scan when a treated patient develops headache, vomiting, hypertension or neurological decline.