Pediatric arterial ischaemic stroke: monitoring

1. Bedside vignettes: why this matters in the PICU#

Vignette A. The 8-year-old with sudden right-sided weakness#

An 8-year-old presents to the ED 2 hours after sudden onset right-arm weakness and dysarthria. PedNIHSS 12. Non-contrast CT excludes haemorrhage; CT angio shows left M1 occlusion. The pediatric stroke team is activated. The decision to pursue IV-tPA is made in conjunction with the pediatric neurology and stroke service; the decision to also consider mechanical thrombectomy is made jointly with interventional radiology. During the post-arrival workup, the team begins continuous bedside TCD over the right MCA (the unaffected side, as a global haemodynamic monitor), pulses oximetry NIRS over the at-risk hemisphere, and prepares cEEG for the post-recanalisation window. After successful MT with TICI 2b at 4.5 h, post-procedure rSO2 over the recanalised hemisphere rises from 52% to 78% within minutes (hyperperfusion). The team lowers MAP by 15% with a careful esmolol infusion to prevent hyperperfusion bleed; rSO2 settles to 68%; the child does well. 1 2

Vignette B. The 18-month-old after cardiac surgery, the silent stroke#

An 18-month-old is on day 3 after a complex cardiac repair (Norwood stage 1). NIRS over the right cerebral cortex has been trending down over the last 6 hours from 68% to 51%, despite stable systemic haemodynamics. The bedside aEEG shows new asymmetry: the right hemisphere amplitude has fallen 30%. Pupillary exam is symmetric. The team escalates: head CT shows a new right MCA infarct, presumed cardio-embolic from the post-operative state. Anticoagulation is started after multidisciplinary input; continuous NIRS and cEEG remain in place to monitor for malignant oedema in the days ahead. In a non-verbal, sedated post-cardiac-surgery infant, the bedside MNM signals (asymmetric NIRS and aEEG) were the only early markers of the stroke. 1 3

Vignette C. The 12-year-old with sickle cell disease and abnormal STOP TCD#

A 12-year-old with HbSS sickle cell disease is in the annual screening clinic. The STOP-protocol TCD shows TAMMV 215 cm/s in the right MCA (abnormal: ≥ 200 cm/s). The child is asymptomatic. Per the STOP-1 trial, chronic monthly transfusion is initiated to reduce stroke risk from 10% per year (untreated) to 1% per year (transfused). The TCD is repeated in 6 weeks to confirm trend and again at 6 months to assess transfusion response. This is the only modality on this page where a TCD number triggers a multi-year therapy in an asymptomatic child. 4 5

2. What pediatric AIS monitoring is, and what it is not#

Pediatric AIS is a focal arterial occlusion in a child causing acute neurological deficit. It is distinct from:

• Cerebral sinovenous thrombosis (CSVT): venous occlusion presenting with headache, seizures, raised ICP, often more insidious onset.
• Haemorrhagic stroke: intracerebral or subarachnoid bleed; diagnostic imaging and management entirely different.
• Stroke mimics: post-ictal Todd's paresis, complex migraine, conversion disorder, metabolic / encephalopathic syndromes, brain tumours.

The diagnostic burden in children is delayed recognition, not difficult imaging. Children with focal deficits often present several hours late, are misdiagnosed as post-ictal or migrainous, and miss the time window for thrombolysis. The 2019 AHA pediatric stroke guidelines emphasise rapid imaging (MRI with diffusion + MR angiography preferred; CT + CT angio acceptable when MRI is not immediately available) within 6 hours of presentation.

Multimodal monitoring is supportive, not diagnostic. No combination of TCD, NIRS, NPi, ONSD, or cEEG diagnoses stroke. They:

1. Detect early evolution: a falling NIRS rSO2 unilaterally in a sedated child is the bedside signal of a new ischaemic insult.
2. Track peri-interventional: continuous TCD during MT detects re-occlusion or hyperperfusion.
3. Monitor post-recanalisation: NIRS, cEEG, NPi, ONSD all track the evolving oedema and any haemorrhagic transformation.
4. Inform secondary prevention: TCD STOP screening in SCD; serial TCD in moyamoya.

3. Anatomy of pediatric stroke and the relevant monitors#

The relevant arterial anatomy:

• Anterior circulation: ICA → M1-MCA, A1-ACA. The vast majority of large-vessel pediatric AIS.
• Posterior circulation: vertebral arteries → basilar → P1-PCA. Less common; often missed because exam findings are non-localising.
• Circle of Willis collaterals: ACOM and PCOM are the natural bypass routes; collateral status determines penumbra size and prognosis.
• Moyamoya disease: progressive bilateral terminal ICA / M1 stenosis with leptomeningeal "puff of smoke" collaterals; carries a high recurrent stroke risk and is monitored serially with TCD and clinical exam.

Where to place each monitor.

4. The signal: what each modality tells you peri-stroke#

4.1 Bedside TCD#

In the post-recanalisation period, continuous bedside TCD over both MCAs provides three pieces of information:

1. Reocclusion detection: a sudden fall in MFV in the recanalised vessel signals re-thrombosis.
2. Hyperperfusion detection: a rise in MFV on the recanalised side relative to baseline or to contralateral (often > 30%) is the bedside signal of hyperperfusion. 3
3. Embolic monitoring: high-intensity transient signals (HITS) on the TCD spectrum indicate microemboli passing the insonated vessel.

4.2 NIRS#

NIRS rSO2 over the at-risk hemisphere falls with acute ischaemia and rises (often sharply) after recanalisation. The "post-recanalisation rSO2 overshoot" is the bedside hyperperfusion signal. Asymmetric rSO2 (Δ > 10 to 15%) is the bedside detector of evolving stroke in a sedated child whose clinical exam is uninformative. 7 8

4.3 cEEG / qEEG#

After acute stroke, the affected hemisphere shows slowing and reduced fast activity; the qEEG ADR drops; asymmetry rises. In the days after stroke, electrographic seizures (often non-convulsive) occur in 5 to 15% of pediatric AIS, especially with cortical infarcts. cEEG is the surveillance tool. 9 10

4.4 NPi#

Catches evolving malignant oedema with CN III compression earlier than the pen-torch. A new asymmetry > 0.7 or a falling NPi in the days post-stroke triggers urgent imaging and consideration of decompressive surgery. 11 12

4.5 ONSD#

Distends with rising ICP from malignant oedema. Age-banded cut-offs apply (~4.5 mm in 1 to 15 y). Serial ONSD over the post-stroke days is one of the bedside triage signals for decompressive surgery consideration. 13

5. The numbers: what to record peri-stroke#

The peri-recanalisation bedside chart should show all of these on a single 24 h view. The pediatric stroke unit / PICU rounds twice daily.

6. What is normal? Age-banded reference for the monitors in question#

7. What is abnormal? Pattern library#

Decision tree: peri-recanalisation monitoring#

flowchart TD
  Recan[Post-recanalisation] --> NIRS{rSO2 trend}
  NIRS -->|Stable| OK[Continue]
  NIRS -->|Overshoot > 15%| Hyper[Hyperperfusion; lower MAP]
  NIRS -->|Falling on recanalised side| Reocc[Suspect re-occlusion; image]
  Recan --> NPi{NPi asymmetry}
  NPi -->|Falling| Edema[Suspect oedema; image]
  Recan --> EEG{cEEG seizures?}
  EEG -->|Yes| Treat[Anticonvulsant escalation]

8. Try it: interactive widgets#

9. Management decisions in pediatric AIS#

9.1 Acute hyperacute window#

1. Activate the stroke pathway: door-to-imaging within 60 minutes per AHA pediatric stroke guidelines.
2. Imaging: MRI + MRA preferred; CT + CT angio acceptable.
3. Confirm AIS and exclude haemorrhage / mimic.
4. Candidacy assessment for IV-tPA (NIHSS ≥ 6, within 4.5 h of last seen well, no haemorrhage on imaging, no contraindication).
5. Candidacy assessment for MT (proximal large-vessel occlusion, favourable imaging, age and centre considerations).
6. Multidisciplinary decision (pediatric neurology, pediatric stroke team, interventional radiology, PICU, family input).

9.2 Peri-intervention monitoring#

1. Arterial line for continuous BP.
2. Bedside TCD over both MCAs (or contralateral MCA as reference).
3. Bilateral NIRS pads.
4. cEEG initiated for the post-procedure 24 to 48 h.
5. Continuous pulse oximetry, capnography, temperature as standard.

9.3 Post-recanalisation BP management#

The risk of hyperperfusion bleed peaks in the first 24 h post-recanalisation. AHA pediatric stroke guidelines suggest MAP targets in the lower half of the age-appropriate range after successful recanalisation. Bedside NIRS rSO2 overshoot (> 15% above pre-procedure or > 20% asymmetric) prompts gentle MAP lowering (10 to 15%) with esmolol or labetalol. 1 2

9.4 Anticoagulation / antiplatelet for secondary prevention#

Cardio-embolic AIS: anticoagulation (LMWH or warfarin) typically started after 24 to 72 h, depending on infarct size and bleed risk. Arteriopathic AIS: antiplatelet (aspirin 1 to 5 mg/kg/day) usually started after 24 h. Multidisciplinary discussion with pediatric haematology.

9.5 Malignant oedema and decompressive craniectomy#

Large MCA infarct with midline shift > 5 mm, falling NPi, expanding ONSD, and deteriorating exam: decompressive hemicraniectomy reduces mortality in adult MCA infarct and is increasingly used in pediatric MCA infarct in selected centres. Timing is the operative decision: too early may be unnecessary, too late may be futile. 1

9.6 Sickle cell disease (STOP-screening protocol)#

Annual TCD TAMMV screening in children with HbSS or HbSβ-thalassemia, ages 2 to 16 years. TAMMV ≥ 200 cm/s = abnormal, chronic monthly transfusion initiated (STOP-1 / STOP-2). TAMMV 170 to 199 = conditional, re-screen sooner. TAMMV < 170 = normal, annual repeat. 4 5

9.7 Moyamoya progression monitoring#

Serial TCD detects progression of terminal ICA stenosis: rising MCA MFV in the absence of vasospasm + clinical context of known moyamoya disease. Combined with serial MRA, drives the decision about surgical revascularisation (encephalo-duro-arterio-synangiosis or related). 3

10. Clinical contexts: stroke MNM in different scenarios#

10.1 Pediatric AIS in school-age children#

The classic 8 to 12 year old with sudden-onset hemiparesis. Bedside MNM during peri-intervention and the first 48 h post-recanalisation: TCD, NIRS, cEEG, NPi. Decompressive craniectomy if malignant oedema. The TIPS study and 2019 AHA pediatric stroke guidelines provide the framework. 6 1

10.2 Pediatric AIS in toddlers and infants#

Diagnosis is harder (focal signs are subtle, exam-difficult), so MNM (asymmetric NIRS, asymmetric aEEG / cEEG) often raises the first alarm in a sedated post-cardiac-surgery infant or a neonate. Decision-making about thrombolysis in this age group is largely centre-experience-dependent; thrombectomy is rare under age 2. 2

10.3 Cerebral sinovenous thrombosis (CSVT)#

Different physiology (venous outflow obstruction) and different management (anticoagulation, hydration, raised ICP support). MNM role: cEEG for seizures (common in CSVT), ONSD for raised ICP, NIRS for tissue oxygenation. Imaging-driven decisions (MR venography + diffusion). 1

10.4 Stroke in sickle cell disease#

The STOP screening pathway is the central preventive intervention. Acute SCD AIS: emergent transfusion exchange to HbS < 30%; multidisciplinary management with paediatric haematology, neurology, and PICU. MNM during the acute window adds NIRS, cEEG, NPi. 4 5

10.5 Stroke complicating congenital heart disease#

Post-op cardiac patients have stroke rates of 3 to 10%. Bedside MNM (especially asymmetric NIRS) is the early warning. The Norwood, arterial switch, and Glenn / Fontan patients are highest risk. 18

10.6 Stroke during pediatric ECMO#

VA-ECMO has 5 to 15% acute stroke risk. The ELSO neurological surveillance bundle includes daily NIRS, NPi, and selective neuroimaging. Continuous TCD is informative but technically harder on the non-pulsatile ECMO patient. 19 20

10.7 Stroke after meningitis or encephalitis#

Bacterial meningitis (especially pneumococcal) can cause vasculitic stroke. Herpes simplex encephalitis classically affects temporal lobes and causes focal seizures and stroke. MNM role: cEEG (seizures), ONSD (oedema), NIRS (tissue oxygenation). 21 22

10.8 Stroke as a complication of trauma (dissection)#

Cervical artery dissection from blunt or twisting neck trauma can cause AIS hours to days later. The dissection itself may not be obvious on initial CT. MNM role: clinical surveillance, cEEG if obtundation develops, surgical / endovascular decisions through neurosurgery and interventional radiology. 23

10.9 Stroke after cardiac arrest (anoxic, embolic, or both)#

Post-arrest patients can have both diffuse HIE injury and focal embolic stroke. MNM role: cEEG and aEEG for seizures, NIRS for asymmetric desaturation that might indicate focal stroke on top of HIE, NPi for brainstem function. Multimodal prognostication framework applies. 24 18

11. Multimodal integration: stroke MNM stack#

12. Setup and technique#

12.1 Imaging pathway#

1. Activate the pediatric stroke pathway at any sudden focal deficit, dysarthria, or focal seizure with persistent deficit.
2. First imaging: MRI with diffusion + MRA preferred. CT with CT angio acceptable when MRI is delayed.
3. Hyperacute decision about IV-tPA and MT candidacy in a multidisciplinary huddle including pediatric neurology, PICU, interventional radiology, anaesthesia, family.
4. Repeat imaging at 24 h to assess infarct evolution and rule out haemorrhagic transformation.

12.2 MNM bundle at the bedside#

1. Arterial line for continuous BP and arterial sampling.
2. Bilateral NIRS pads (frontal cortex) placed at admission; trend baseline asymmetry.
3. cEEG initiated as soon as practical; full 10-20 montage if available, reduced montage if not.
4. TCD baseline scan: bilateral MCA, ACA, PCA; document MFV, PI on both sides. Continuous (fixed headframe) if available and recanalisation is planned.
5. Pupillometer (NPi) at admission and Q4 hourly during the surveillance window.
6. ONSD at admission and Q12 to Q24 hourly during the malignant-oedema window.
7. Document all MNM values on a unified bedside chart with PedNIHSS, MAP, glucose, temperature.

12.3 Peri-intervention setup#

1. Anaesthesia consult for thrombectomy logistics.
2. Continuous TCD during MT: monitor for re-occlusion, hyperperfusion, embolic signals.
3. NIRS continuous: any asymmetry > 15% during the procedure flagged to the team.
4. Post-procedure: bedside MNM for 48 h minimum; longer if any concern.

12.4 Decompressive craniectomy decision#

The bedside MNM signals that support decompression:

• Midline shift > 5 mm on CT.
• Falling NPi, especially with asymmetry > 0.7.
• Expanding ONSD above age-banded cut-off.
• Falling GCS or PedNIHSS deterioration.
• Failure to respond to maximal medical therapy (hyperosmolar, sedation, normothermia).

The decision is multidisciplinary (neurosurgery, PICU, neurology, family) and centre-experience-dependent. The pediatric outcome data after decompression are evolving but generally favourable when timing is appropriate.

12.5 STOP-protocol TCD in SCD#

1. Annual TCD in HbSS or HbSβ-thalassemia, ages 2 to 16 years.
2. Non-imaging (blind) TCD or non-angle-corrected TCCD: angle correction systematically over-reads TAMMV.
3. TAMMV in MCA (and basilar, in some protocols): time-averaged maximum mean velocity.
4. Interpret per STOP-1 / STOP-2: < 170 normal, 170 to 199 conditional, ≥ 200 abnormal.
5. Abnormal: confirm with second scan within 6 weeks; if confirmed, initiate chronic monthly transfusion to maintain HbS < 30%.

12.6 Moyamoya monitoring#

Serial TCD every 6 to 12 months; pair with serial MRA. Rising MFV in the MCA or new collateral signals indicate progression. Surgical revascularisation (EDAS or related) is the definitive treatment in symptomatic disease. 3

13. Pitfalls#

• Delayed recognition of pediatric stroke: the median time from symptom onset to diagnosis is 24 hours; high index of suspicion is the first step.
• Stroke mimics: post-ictal Todd's paresis, complex migraine, conversion disorder; imaging is the differentiator.
• Adult MFV thresholds in children would miss vasospasm or over-call hyperperfusion; use age-banded reference.
• STOP TAMMV with angle-corrected TCCD: angle correction over-reads; use non-angle-corrected for STOP screening.
• Single-modality decisions: never decide on decompressive craniectomy or IV-tPA on one MNM signal alone; multimodal + clinical + imaging concordance.
• Hyperperfusion bleed: the rSO2 overshoot is the warning; lower MAP gently, not aggressively.
• Cardio-embolic stroke missed in sedated post-cardiac-surgery infants: asymmetric NIRS and aEEG are often the only early markers.
• CSVT diagnosed late: presentation is non-specific; MR venography is the gold standard.
• Pediatric thrombectomy evidence is C-level: outcomes appear favourable but RCT data are limited; centre experience matters.
• Moyamoya progression is silent: serial TCD between annual visits catches it.

14. Combine with…#

• TCD: the central modality for peri-intervention monitoring and STOP screening.
• NIRS: bilateral asymmetry as the early stroke signal.
• qEEG / cEEG: seizure surveillance and hemispheric asymmetry.
• Pupillometry: malignant oedema early warning.
• ONSD: bedside ICP surrogate for oedema progression.
• Clinical exam: the diagnostic gate; PedNIHSS is the structured exam tool.
• Foundations: autoregulation: the physiology behind post-recanalisation hyperperfusion.

15. Evidence summary#

16. Recent literature (2022 to 2025)#

• Sun 2020 pediatric thrombectomy meta-analysis: aggregate of small series suggesting favourable recanalisation rates and functional outcomes in selected children with large-vessel occlusion. 2
• LaRovere 2022 pediatric TCD primer: updated guidance including stroke and moyamoya monitoring. 16
• Naim 2023 pediatric post-arrest brain injury: framework that overlaps with peri-stroke MNM (multimodal prognostication, NPi, cEEG). 18
• Figaji 2025 pediatric MMM consensus: stroke and brain-injury MNM as a single overlapping framework. 25
• Helbok 2024 pediatric MMM: NIRS, cEEG, NPi as the practical bedside stroke MNM bundle. 26
• Tasker 2023 PCCM review: stroke as a pediatric neurocritical care entity with overlapping MNM strategy. 29

17. Self-check#