Pediatric Stroke and Cardiac Disease: Challenges in Recognition and Management

Introduction: Brain Injury in Cardiac Patients

Children with cardiac disease constitute up to 30% of pediatric arterial ischemic strokes (AIS)¹ and have an 8-fold increased risk of hemorrhagic stroke compared with healthy controls.²

Abnormal cerebral hemodynamics in utero contribute to a high incidence of white matter injury, immature brain structure, and lower brain volumes in infants with congenital heart disease (CHD).^3,4. Postnatally, further insults accumulate from chronic hypoxemia, frequent critical illnesses, infections, surgeries, and hospitalizations.⁵ Acquired injury from ischemic stroke or intracranial hemorrhage thus occurs in the background of atypical brain development. Routine preprocedural MRI reveals neurologic injury in up to 41% of infants with CHD before any intervention,^4,6,7 and a further 30% have evidence of injury on post-operative imaging.⁷ Because pre-existing brain injury influences the safety of interventions requiring anticoagulation and post-operative neurologic complications such as seizures,⁸ pre-procedural neuroimaging may be useful.

This review covers the epidemiology, mechanisms of injury, and challenges in the management of stroke in children with cardiac disease.

Predominantly ischemic injuries

The incidence of AIS in children with cardiac disease has been estimated to be as high as 132 per 100,000, with children having single ventricle physiology at the greatest risk (1380/100,000).⁹ Additional risk factors can be grouped into three main categories: (1) Alterations in blood composition (e.g., acquired prothrombotic states due to sepsis or surgery), (2) alterations in blood flow promoting thrombus formation (implanted valves¹⁰), and anatomical flow obstructions or impaired function additionally contributing to impaired cerebral perfusion, and (3) alterations in the endothelium (implanted or intravascular prosthetic materials). Cardiac surgery, catheterization,^10,11 and mechanical circulatory support (MCS) including ventricular assist devices (VAD)^12,13 or extracorporeal membrane oxygenation (ECMO),¹⁴ combine multiple risk factors and are associated with high rates of neurologic injury.

Common patterns of cardioembolic stroke include large vessel occlusion (LVO) and/or multifocal, often bilateral, showers of microemboli affecting multiple vascular territories (Fig 1). Both acquired and congenital cardiac disease are associated with periods of hypotension during critical illness and risk for cardiac arrest. Inadequate global cerebral perfusion can cause hypoperfusion or “watershed” type injuries (Fig 1).

Figure 1. Imaging Patterns in children with cardiac stroke.

(A) CT scan demonstrating hypoattenuation consistent with acute R MCA infarct. (B) MR Angiogram demonstrating acute occlusion of the right M1 artery. (C) MRI demonstrating multifocal areas of restricted diffusion concerning for embolic process. (D) restricted diffusion in the bilateral posterior watershed regions and right anterior watershed region. Images showing (E) restricted diffusion consistent with acute R MCA infarction and (F) susceptibility-weighted imaging demonstrating hemorrhagic transformation from the same patient as panel E.

Predominantly hemorrhagic injuries

Patterns of intracranial hemorrhage (ICH) include both intra-axial and extra-axial bleeding, specifically subdural hematoma (SDH); intraparenchymal hemorrhage (IPH); and subarachnoid hemorrhage. Of these, SDH and IPH are the most common in children.¹⁵ Although intraventricular hemorrhage (IVH) is a common pattern of injury in preterm neonates with CHD,¹⁶ it is still unclear whether cardiac disease is an independent risk factor for IVH in preterm populations.^16–18 IVH can also occur in term neonates with CHD, but it is typically low grade.^16,19 Diagnosis, management, and outcomes of neonatal IVH have been covered in depth in several recent reviews,^20–22 and are beyond the scope of this article.

Hemorrhage associated with anticoagulant therapy is a major contributor to ICH in children with cardiac illness. While significant practice variation remains, common indications for antithrombotic therapy for primary stroke prevention include MCS; presence of mechanical heart valves or other prosthetic material; severely reduced LV function; and some single ventricle physiologies (e.g., Fontan); and for secondary stroke prevention in a child with CHD and stroke.²³

Infected (mycotic) aneurysms due to bacterial endocarditis are prone to spontaneous rupture and hemorrhage.

Neuroprotection and Neurostabilization

The acute management of suspected stroke follows the same principles as non-cardiac patients and entails optimizing cerebral perfusion pressure and oxygenation while considering re-perfusion therapies and anticoagulation to prevent stroke recurrence and monitoring for secondary complications including seizures (Fig 2). Oxygenation and mean arterial pressure and/or cerebral perfusion pressure goals should be tailored to the specific cardiac physiology (e.g., for chronically cyanotic patients or those with chronic heart failure). An interdisciplinary approach is crucial, for example in patients with single ventricle physiology who have undergone palliation with a cavopulmonary shunt. In these children, the superior vena cava drains directly into the pulmonary arteries, which can result in elevated central venous pressure that may impact cerebral venous drainage.

Figure 2. Initial Diagnostic Steps in acute stroke.

Many cardiac patients have implanted devices that are MRI incompatible (pacemakers, implantable cardiac defibrillators (ICDs), post-operative pacing wires, sternal wires, ventricular assist devices (VADs), chest tubes). DWI- diffusion weighted imaging, ADC- apparent diffusion coefficient, FLAIR- fluid attenuated inversion recovery, SWI- susceptibility weighted imaging, LKW- last known well, ACT- activated clotting time, LVO- large vessel occlusion

Post-stroke seizures occur more frequently in young children and are often subclinical.^24–26 In addition to obtaining EEG for clinically concerning symptoms (e.g., altered mental status, abnormal movements, unexplained tachycardia), clinicians should have a low threshold for continuous EEG monitoring in children who are under 2 and those who are receiving postsurgical sedation or paralysis that may mask clinical seizures.⁸

Acute Management of AIS

Antithrombotic therapy

Many children with complex congenital heart disease are receiving antithrombotic therapy at the time of stroke.²⁷ In patients with risk factors for both thromboembolism and hemorrhage, time-critical neuroimaging is crucial to ascertain stroke type (hemorrhagic or ischemic) and inform management. Therapeutic anticoagulation is seldom reversed before imaging given the high risk of thromboembolism associated with most indications for anticoagulation in this population (e.g., mechanical valves, VADs, etc.) but is held until neuroimaging is completed if hemorrhagic stroke is suspected.

Reperfusion therapies

Both tissue plasminogen activator (tPA) and endovascular thrombectomy (EVT) are covered in detail in the “Acute Management” article in this issue, along with limitations in pediatric evidence-based recommendations. For children with cardiac disease, several aspects merit discussion here.

tPA

Identifying a focal neurologic deficit and obtaining neuroimaging that demonstrates an ischemic stroke within the classic tPA window of 4.5 hours is a significant barrier to tPA use since many children are critically ill and heavily sedated at the time of stroke. If a stroke is rapidly identified, the high rate of baseline antithrombotic therapy and frequent surgeries in this population are the source of most clinical uncertainty regarding tPA. Many clinicians apply published inclusion and exclusion criteria from the Thrombolysis in Pediatric Stroke (TIPS) trial²⁸ and current adult guidelines including extended time windows based on advanced neuroimaging,²⁹ though intravenous (IV) tPA remains off-label in children. Any prior ICrH is an absolute contraindication, and a history of stroke within the past 90 days is a relative contraindication. Use of low molecular weight heparin within the preceding 24 hours is also an absolute contraindication. In adults, however, if the aPTT is within normal range, the use of bivalirudin or unfractionated heparin is only a relative contraindication to thrombolysis. Anticoagulation with warfarin is not a contraindication if the INR is <1.4. While therapeutic warfarin may be reversed in adult patients to permit tPA administration, this practice is uncommon and highly controversial in children. Antiplatelet therapy (usually aspirin) is not a contraindication to tPA,²⁹ and it is typically appropriate to resume 24 hours after tPA for patients on antiplatelet agents at baseline.

Cardiac catheterization via a compressible artery is not a contraindication, but recent major surgery (within 10–14 days) and arterial puncture of a noncompressible vessel (within 7 days) are relative contraindications.

Careful consideration of the risk-benefit ratio for the individual patient in a multidisciplinary team discussion is crucial to ensure best practice.

Endovascular Thrombectomy

Adults with cardiac disease have benefited from endovascular thrombectomy (EVT) because many of the conditions that preclude tPA administration in this population do not prohibit EVT. Specifically, recent surgery, concurrent anticoagulation, and MCS are not contraindications to EVT. Moreover, EVT is beneficial up to 24 hours after the last known well in appropriately selected adults with evidence of salvageable tissue,^30,31 rather than the narrow 4.5-hour tPA window. Pediatric case series of EVT for large vessel occlusion (LVO) have reported safety and efficacy.^32–36 These individual case series were corroborated in the Save ChildS Study, a large, multicenter retrospective study of EVT in pediatric stroke.³⁷. Children with cardiac disease comprised up to 30–60% of these patients.^33–38 However, no prospective literature informs the use of recanalization in childhood stroke. The risks of intervention and optimal patient selection should be carefully considered with a multidisciplinary team that ideally includes pediatric vascular neurology, neuro-interventional radiology, critical care physicians, neurointensivists and pediatric anesthesiologists familiar with CHD patients.³⁹ Thrombectomy should be performed by an interventionalist experienced with EVT and pediatric cases, and an understanding of any aberrant anatomy of the heart, aortic arch, or great vessels.^39,40

Supportive Management

Initiation, escalation, and/or change of antithrombotic therapy may be indicated as acute treatment in patients who do not receive tPA or EVT, and/or for secondary prevention in some cases. Early initiation of anticoagulation in adults with stroke was associated with an increased risk of hemorrhage⁴¹. However, retrospective studies in children suggest that antithrombotic therapy within the first week after ischemic stroke does not increase the risk of hemorrhagic transformation,⁴² including in children with cardioembolic stroke.⁴³ Anticoagulation may be preferred over antiplatelet therapy for cardioembolic stroke;^10,27 the strategy and anticoagulant choice are discussed further in the “Acute Management” article in this issue.

Complications of AIS and special management considerations

Hemorrhagic transformation

Hemorrhagic transformation (HT) of ischemic stroke can occur spontaneously; as a complication from acute thrombolytic therapies; or related to antithrombotic therapies initiated for secondary stroke prevention.⁴⁴ HT ranges from asymptomatic petechial hemorrhage to life-threatening hemorrhage with mass effect.⁴⁵ In pediatric case series, the rate of HT ranges from ∼10%−30%; the majority of these are petechial and mild or asymptomatic.^1,42,46 Cardioembolic stroke^1,47 and larger stroke size¹ have been associated with increased risk of HT in children. The risk of HT after IV tPA and/or endovascular intervention is covered in the accompanying article on the acute management of ischemic stroke.

Initiating or resuming antithrombotic therapy after stroke

There are no prospective studies or consensus guidelines on the optimal timing and strategy for initiating or resuming antithrombotic therapy after stroke in children with cardiac disease. Two retrospective studies^43,48 concluded that antithrombotic therapy initiated early after stroke does not increase the risk of clinically significant HT. The multidisciplinary team should weigh the risk of recurrent cerebral or systemic thromboembolism against the likelihood of HT. For example, for children with a large ischemic stroke while on MCS, continuing anticoagulation is reasonable. For those with a lower risk of thromboembolism, anticoagulation may be resumed cautiously within the first week after stroke, with the exact timing and strategy individualized on a case-by-case basis. Repeat neuroimaging is often obtained 2–5 days after initiation of antithrombotic therapy (neurologic changes will necessitate earlier evaluation), but no prospective studies have investigated the optimal timing, modality, or number of follow up scans, hence significant variation in practice exists between institutions.

Periprocedural or “provoked” strokes

Cardiac surgery, catheterization, and mechanical circulatory support (VAD or ECMO) constitute major risk factors for stroke.^11,49. In a large, recent study of children with cardiac disease who had an arterial ischemic stroke, 26% of the strokes occurred within 72 hours of cardiac surgery or catheterization or while on MCS;11 single-center cohorts have reported that up to 50% of ischemic strokes in cardiac patients occur periprocedurally.

Cardiac Catheterization

Single-center cohorts estimate that roughly ∼15%−37% of all strokes in pediatric cardiac patients occur after cardiac catheterization.^50–52 The majority of strokes (up to 95%) occurred during interventional catheterization, with pulmonary vein dilation and trans-septal needle puncture identified as the highest risk.⁵¹ Periprocedural infection and critical illness have also been identified as important risk factors.⁵² Children with stroke during cardiac catheterization have been treated with thrombectomy,⁵¹ but evidence including prospective outcomes supporting tPA or thrombectomy for strokes attributable to cardiac catheterization in children is lacking. In the absence of a cardiac thrombus or other indication for antithrombotic therapy, there is also no consensus on the utility of long-term antithrombotic therapy after peri-procedural stroke.

Stroke during cardiac surgery

A temporal association with cardiac surgery is present in many children, with ischemic stroke occurring at a rate of ∼5 strokes per 1000 children undergoing a cardiac operation.^11,53 Noninvasive neuromonitoring should be considered when post-operative sedation or neuromuscular blockade limits the neurologic exam. Asymmetry, focal or generalized epileptiform discharges or seizures on continuous EEG may reflect periprocedural injury.^54–56 Cerebral near-infrared spectroscopy (NIRS) may show asymmetry in cases of ICrH or ischemia. Neurological examination should be obtained as soon as safe and feasible to lift paralysis and lighten sedation. If sedation and/or paralysis cannot be reduced and clinical suspicion of stroke is high, teams should have a low threshold for neuroimaging with CT/CTA.

Stroke during mechanical circulatory support

The prosthetic surfaces of VADs and ECMO circuits promote thrombus formation. Though this risk is mitigated by anticoagulation,⁵⁷ children on MCS remain at high risk for ischemic stroke. The risk is highest in small children (<10 kg) on pulsatile VADs such as the Berlin EXCOR, where combined ischemic and hemorrhagic stroke rates of up to 33% have been reported.^12,13,58 Older children and those on continuous flow devices have lower stroke rates (6%−12%),⁵⁹ comparable to those on ECMO (7%−11%).^60,61 While the necessity for anticoagulation typically precludes tPA for VAD-associated acute stroke, there are case reports of good neurological outcomes after thrombectomy for LVO in children on MCS.^62,63 In children receiving therapeutic antithrombotic therapy at the time of the stroke, a multidisciplinary decision should be made about whether to change the current regimen. For example, recent registry data found that transitioning to bivalirudin for anticoagulation in Berlin EXCOR patients was associated with a significant decrease in stroke (from 30% to 12%) as compared to historical controls managed on unfractionated heparin.⁶⁴

Infectious Endocarditis

Neurovascular complications of infectious endocarditis (IE) include embolic strokes from valvular vegetations, infected aneurysms, which may rupture and cause ICH, and multifocal microhemorrhages. In patients with IE, angiography to exclude infected aneurysms should be considered, particularly if hemorrhage has occurred. Antithrombotic therapy is not effective for primary or secondary stroke prevention in IE and may increase the risk of clinically significant ICH.^65–67 For children on anticoagulation at baseline, it is important to carefully consider the indication for anticoagulation and whether anticoagulation can safely be held. Surgical repair of damaged valves may require anticoagulation on cardiopulmonary bypass. Current (adult-oriented) literature suggests deferring surgical repair for at least 3–4 weeks in patients with hemorrhage; earlier surgery (1–2 weeks) is acceptable in patients with ischemic stroke and no associated HT if more rapid lifesaving cardiac procedures are necessary.⁶⁸

Secondary Prevention of Acute Ischemic Stroke

Reported rates of stroke recurrence in children with cardiac disease range from 12%−27%, with a higher risk of recurrence in congenital, compared to acquired conditions.^10,57,69 Infants and children with cyanotic CHD (pre-surgery or post-palliation with residual right to left shunting) and those with cardiomyopathy had the highest recurrence rates.¹⁰ Other risk factors include mechanical valve placement, acute infection, and thrombophilia.¹⁰ Consensus-based guidelines recommend antithrombotic therapy for secondary stroke prevention in cardioembolic stroke^27,57,70 However, there is uneven adherence to this recommendation and variation in the timing of initiation and duration of treatment. Even with appropriate therapy, children with cardiac disease remain at risk for recurrent stroke.^10,48 The persistently high incidence of stroke in children with cardiac disease⁹ may therefore reflect a combination of inadequate antithrombotic therapy and drug failure, highlighting the need for ongoing cardiac stroke-specific registry research and clinical trials.^9,10,48

Acute management of hemorrhagic stroke and subdural hematomas

Hemorrhagic stroke should be suspected in any child with heart disease receiving anticoagulation and presenting with acute mental status change, seizures, focal neurological deficits, or signs of increased intracranial pressure.

ICrH is a serious complication of MCS including VAD and ECMO, often with a poor prognosis.^71,72 Large hemorrhage increases the risk of secondary ischemia from mass effect and blood vessel compression, and SAH can lead to vasospasm.⁷³ Additional complications can include hydrocephalus from IVH (either in isolation or associated with IPH).

Acute management

The complexities of ICrH management over the wide spectrum of pediatric cardiopulmonary abnormalities and associated hemodynamic variability have confounded the development of evidence-based recommendations for management. Therefore, current practices are either extrapolated from adult guidelines or based on small, mostly retrospective, pediatric studies and expert opinions.^27,74

Initial management of ICH and SDH includes elevation of the head of the bed to 30 degrees, strict control of arterial CO2 and pH to prevent vasoconstriction and/or vasodilation, initiation of measures to control intracranial pressure, and urgent consultations with hematology and neurosurgery services (Fig 3). Confirmed seizures (including EEG-only) should be treated with antiseizure medications; however, the role of seizure prophylaxis is controversial.²⁷ Blood pressure management goals after intracranial hemorrhage lack evidence in children with cardiac disease. Blood pressure reduction requires a cautious approach to avoid inadvertently reducing cerebral perfusion and causing secondary brain injury.

Figure 3.

Initial Management of Intracranial Hemorrhage in Children with Cardiac Disease

Continuous systemic anticoagulation is required to prevent thrombus formation in the MCS systems, further complicating acute management of intracranial hemorrhage,⁷⁵ but even children not on MCS often receive antiplatelets or anticoagulation for their underlying disease. Despite efforts to monitor anticoagulation levels to prevent ischemic and hemorrhagic stroke, the evidence for a correlation of the levels with neurological outcomes remain poor.⁷⁶ Once a hemorrhage has occurred, whether to continue, stop or reverse anticoagulation requires careful consideration of risks and benefits in the multidisciplinary setting including a neurologist with stroke expertise, cardiologist and/or cardiac intensivist and/or neurointensivist, hematologist and neurosurgeon. In children for whom no neurosurgical intervention is planned, the risk of thromboembolism vs the risk of hemorrhage expansion needs to be carefully considered. Small adult series suggest that continuing anticoagulation with close neurological monitoring and repeated neuroimaging to assess hemorrhage stability may be acceptable in patients with small, nonsurgical IPH,⁷⁷ but pediatric studies are lacking.

Platelet transfusion for ICH occurring while on antiplatelet therapy is controversial outside of traumatic ICH. An adult trial (PATCH) showed worse outcomes in adults who received platelet transfusion for spontaneous ICH in the context of antiplatelet treatment.⁷⁸ However, significant thrombocytopenia may require correction.

A small study including children with ICrH on VAD suggested transfusing both platelets and plasma (for factor inhibitors) and holding anticoagulation for 24–48 hours until ICrH stabilization.⁷⁵ Mayer and colleagues published the largest study of pediatric ICH on VAD to date.⁷⁹ The authors suggest immediately reversing anticoagulation and antiplatelets, with reversal targets depending on the size of the hemorrhage and type of VAD. Compared to EXCOR, HeartMate II contains a fibrin-based biological surface and therefore does not require long-term anticoagulation, only ASA. Therefore, a full reversal of the prothrombin time, activated partial thromboplastin time and platelet count over 100×109/L might not always be required.⁷⁹ This topic is complicated by a limited pathophysiological understanding of coagulation states in critically unwell children as well as the lack of clinically relevant pathology tests to help evaluate hypercoagulopathic vs bleeding states.

In children with ICrH on ECMO support, balancing the risk of ICH progression against the premature withdrawal of ECMO or continuing ECMO without anticoagulation if it cannot be weaned is very challenging and requires multidisciplinary collaboration. Yang and colleagues emphasized the usefulness of combining neuroimaging (CT or HUS) with continuous NIRS to monitor for ICH expansion.⁷¹ The authors terminated ECMO when NIRS declined to >20% from baseline or hematoma diameter was >5 cm; peak procalcitonin level, neonatal age and extracorporeal cardiopulmonary resuscitation were independent risk factors for ECMO-associated ICH.⁷¹

Surgical intervention

Large IPH requires surgical consideration and possibly reversal of anticoagulation. The decision to intervene surgically considers the location of the hemorrhage; duration and severity of neurological deficits; increased intracranial pressure; and child’s ability to tolerate short-term normalization of coagulation followed by gradual reinstitution of anticoagulation.⁷⁵ Emergency surgeries for intracranial hemorrhage are associated with an increased risk of postoperative hemorrhagic events and a high rate of re-operations with poor outcomes, particularly in children on ECMO.⁷⁴ Despite the high surgical risks, evacuation of hemorrhage in selected children with ICH on VAD can be lifesaving and acceptable outcomes have been reported.^75,79

Resuming anticoagulation

After ICrH, the optimal time to resume anticoagulation remains controversial. In children who do not require surgery and have a stable hemorrhage on follow-up imaging, such as those with a thin SDH in the context of MCS, it may be safe to resume anticoagulation with close monitoring of neurological status. However, significant practice variation exists in the timing and number of follow-up neuroimaging studies. Interval imaging will be shorter, 6–12 hours, in children with larger IPH or if mass effect is present. Follow-up imaging to assess bleed stability after resuming anticoagulation is typically obtained once at a therapeutic level for 24 hours. In children on LVAD whose anticoagulation must be held for neurosurgical intervention, device parameters can be adjusted to ensure full ejection to minimize thrombus formation during reduced or no anticoagulation.⁷⁹ Hematologic consultation is recommended to optimize and monitor coagulation parameters in the postoperative period, including monitoring daily lactate dehydrogenase and plasma hemoglobin levels to identify intra-pump thrombus formation and hemolysis.⁷⁹

Timing of subsequent cardiac surgery

Due to concerns about hemorrhage expansion, it is common to delay necessary cardiac surgeries after ICH, particularly those requiring anticoagulation on cardiopulmonary bypass. However, no pediatric prospective data or guidelines address this topic. Instead, many clinicians extrapolate from adult literature on the optimal timing of valve replacement surgery after ICH in infective endocarditis. Current guidelines based on this literature recommend deferring cardiac surgery for at least 4 weeks after ICH; however, this is often challenging.^80,81

Outcomes

Neurological outcomes after stroke in children with complex congenital or acquired heart diseases depend not only on neurological recovery but also on the severity of systemic and cardiovascular illness. For example, in infants with CHD and acquired brain injury, neurologic outcome is also influenced by factors that can reflect non-neurologic illness, such as ICU length of stay and duration of mechanical ventilation.^82,83 In one small population-based study of pediatric cardioembolic stroke, factors associated with poor outcome included headache (P = 0.048), high Pediatric National Institutes of Health Stroke Scale at presentation (P = 0.05) and discharge (P = 0.05), and high Pediatric Stroke Outcome Measure at discharge (P = 0.0008).⁶⁹ Because CHD and associated comorbidities can impair brain growth and development even in the absence of stroke, the impact of stroke on neurodevelopment is difficult to predict. The major driver of adverse neurological outcomes is the location and burden of recurrent strokes and cumulative brain injuries.²⁷ Children with severe congenital cardiac lesions require more surgical interventions, each of which carries a risk for new neurologic injury. The role of MCS in neurological outcomes remains understudied as these children represent a heterogeneous group with unique circumstances and rare comorbidities that cannot be accounted for in a limited sample.⁸⁴ Adverse neurodevelopment and cognitive impairments have been reported in ECMO survivors; however, no studies compare cardiac ECMO survivors to matched patients of similar age undergoing similar cardiac surgery who did not require ECMO support.⁸⁵

Conclusion

We have provided an update on the management of ischemic and hemorrhagic stroke in children with congenital and acquired cardiac disease including children on mechanical cardiopulmonary support. There is an urgent need for pediatric studies guiding acute management in children with ICH, including blood pressure targets, anticoagulation management and surgical timing. Future directions will also include the role of biomarkers in children at high risk of cardioembolic stroke or ICH.

Abbreviations:

AIS

Acute Ischemic stroke

ICH

Intracerebral hemorrhage

ICrH

Intracranial hemorrhage

tPA

Tissue plasminogen activator

MCS

Mechanical circulatory support

CHD

Congenital heart disease

VAD

Ventricular Assist Device

ECMO

Extracorporeal membrane oxygenation

IVH

Intraventricular hemorrhage

IPH

Intraparenchymal hemorrhage

SDH

Subdural hematoma

SAH

Subarachnoid hemorrhage

EVT

Endovascular Thrombectomy

HT

Hemorrhagic transformation