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Review

Periprocedural Stroke: Stroke Mechanisms, Risks, Outcomes, Prevention, and Treatment

by
Kasim Qureshi
1,*,
Jason Schick
1,
Ahmedyar Hasan
2,
Muhammad U. Farooq
1 and
Philip B. Gorelick
3
1
Trinity Health Hauenstein Neurosciences, 220 Cherry St. SE, Hauenstein 1, Grand Rapids, MI 49503, USA
2
Department of Neurology, University of Minnesota, 12-100 Phillips Wangensteen Building, 516 Delaware St. SE, Minneapolis, MN 55455, USA
3
Simpson Querrey Center for Neurovascular Sciences, Division of Stroke and Vascular Neurology, Davee Department of Neurology, Northwestern University Feinberg School of Medicine, 633 N. St. Clair Street, 19th Floor, Chicago, IL 60611, USA
*
Author to whom correspondence should be addressed.
Anesth. Res. 2026, 3(1), 7; https://doi.org/10.3390/anesthres3010007
Submission received: 16 December 2025 / Revised: 2 February 2026 / Accepted: 7 February 2026 / Published: 17 March 2026
Versions Notes

Abstract

The growth of brain health initiatives in the United States and worldwide has led to a movement to protect the brain from avoidable injury across the lifespan. With the advancement of our armamentarium of neurologic treatments and preventives during the past several decades, the field of preventive neurology has spawned. Under the umbrella of preventive neurology is perioperative brain health, an under-addressed but important topic in the field of neurology. Perioperative brain health is important because perioperative mortality may be relatively high, and morbidity as quantified by brain injury biomarkers (e.g., MRI brain) and clinical phenotypic manifestations related to stroke can be common. In this perspective, in relation to periprocedural stroke, we review the stroke mechanisms, epidemiology and risk factors, risk stratification measures and long-term outcomes, and potential mitigation and treatment opportunities. As perioperative brain health crosses many medical disciplines, multidisciplinary action is needed to bridge the knowledge gaps and reduce brain injury and attendant neurologic complications. Anesthesiologists and other healthcare professionals working in the surgical and procedural field are well-positioned to make important contributions to this growing discipline of the prevention of brain injury in the perioperative period.

1. Introduction

Recent advances in the armamentarium of neurologic treatments and preventatives have paved the way for the establishment of the field of preventive neurology [1,2]. Preventive neurology is a relatively new discipline designed to identify people with a high risk of neurologic conditions and strategies to prevent subsequent brain injury. During the past several decades, there has been a growth in the development and utilization of surgical and endovascular procedures [3]. Whereas the application of the surgeries and procedures provide benefits and new therapeutic options, they may be complicated by adverse neurologic events leading to brain injury and death. In fact, and not well-known to many clinicians, by some estimates, perioperative 30-day death rates may rank as high as the third leading cause of death worldwide [3]. These rates are often driven by cerebrovascular or cardiac surgeries and endovascular interventions, making the brain a key target of injury. Thus, perioperative brain health is an important component of preventive neurology and brain health.
The topic of perioperative brain health is broad, encompassing surgical, minimally invasive, and endovascular approaches. Perioperative stroke, for example, may be defined as any ischemic or hemorrhagic cerebrovascular-induced brain injury lasting at least 24 h and occurring either intraoperatively or within 30 days after the procedure [4]. Although the incidence of perioperative stroke is low across all surgeries, there is an increased risk associated with cardiac and neurological interventions. Furthermore, the absolute burden of brain injury may be high due to a high global volume of surgeries and interventions. In non-cardiac and non-neurologic surgeries, perioperative stroke incidence rates range from 0.2% to 1% based on age and type of surgery and are associated with an eight-fold increase in perioperative mortality [5,6].
The traditional conceptualization of perioperative stroke has been through the lens of clinically recognizable intraoperative or postoperative neurological dysfunction. However, such an approach fails to detect subtle manifestations and long-term consequences incurred from covert or so-called ‘silent’ infarcts. Covert infarcts occur more frequently than clinically manifest infarcts in patients undergoing non-cardiac surgery and are associated with an increased risk of perioperative delirium and, by one-year after surgery, long-term cognitive decline [7]. In the non-operative setting, covert infarcts are shown to be predictors of dementia and cognitive decline [8].
In this article, we provide an overview of the following topics related to perioperative stroke: mechanisms, epidemiology and risk factors, risk stratification and mitigation strategies, and opportunities for treatment and prevention. In the context of our review, we use the term “perioperative” to refer to the entire surgical experience (e.g., before, during, and after surgery), and the term “periprocedural” to refer to a more restricted time frame connoted by the time more immediately around a diagnostic or invasive procedure.

2. Methods

The overview is based on expert opinion and the author’s familiarity with the perioperative stroke literature. Foundational studies were identified through authors’ personal reference libraries that have been developed through prior work in this area. Informal forward tracking citation was performed to identify notable follow-on publications. Pertinent recent guidelines were also reviewed and incorporated. Additional articles were selected based on informal literature searches of specific topics such as pathophysiology and epidemiology to allow additional breadth of coverage. The literature reviews were not systematic and, as an opinion piece, were not designed to utilize methods of systematic reviews or meta-analyses.

2.1. Mechanisms of Perioperative Stroke

Patient-based Factors. Perioperative ischemic and hemorrhagic strokes may occur via mechanisms similar to those causing non-operative stroke; however, there may be unique principles pertaining both to patient vulnerability and precipitating mechanisms [5,9]. Patients who may be vulnerable to perioperative stroke are those with a prior history of stroke including recent stroke or traditional cerebrovascular risk factors such as cardiac disease, hypertension, hyperlipidemia, or other such factors. Furthermore, some people who are receiving antithrombotic therapy for primary or secondary stroke prevention may have these therapies temporarily discontinued leading up to the surgical intervention, thereby potentially rendering them at higher risk of brain infarction. Other patients may be vulnerable to perioperative brain infarction due to poor cerebrovascular reserve, such as those with pre-existing severe intracranial or extracranial atherosclerotic disease [10]. People who undergo procedures requiring traversal through an aortic arch harboring a significant degree of atherosclerosis also may be at higher risk during endovascular procedures as atheromatous material from the aorta may be dislodged to create downstream embolism to the brain.
General Mechanisms and Cardioembolic Sources. Mechanisms of ischemic stroke may include those based on the following: thromboembolism, hypoperfusion, hypoxia, anemia, and large-artery atherosclerosis. Of these mechanisms, thromboembolism accounts for upwards of 50% of all cases [5]. In addition, cardioembolic sources can arise from direct cardiac arterial manipulation, from venous thromboembolism passing through a cardiac shunt, or via procedurally associated occurrence of atrial fibrillation. Atrial fibrillation may be previously known, newly discovered, or only recently detected in the intra- or post-operative period. The latter circumstance may be independently associated with increased risk of short- and long-term stroke [11]. However, there remains more to be learned about the frequency and duration of atrial fibrillation after certain procedures. In a recent publication, it was shown, for example, that, although the incidence of atrial fibrillation detected by insertable cardiac monitors was high after coronary artery bypass grafting in the first year (48%), the burden at 30 days was low (0.04%) [12]. Other embolic sources may include fat, gas, and other particulate material introduced during orthopedic and other types of surgery such as endovascular embolization procedures [13].
Role of Blood Pressure. Blood pressure may play an important role in mediating perioperative strokes. It has been reported that up to a third of intraoperative strokes may be due to brain injury in watershed (also called border zone) vascular territories in the brain due to hypoperfusion [5]. These areas are susceptible as they are in end-artery territories with poor collateral flow (e.g., between middle and posterior cerebral artery territories). Cerebral hypoperfusion may be associated with anesthesia-induced hypotension; however, the patient circumstances may be more complicated in that there may be known or previously unknown significant atherosclerotic disease serving as a confounding mechanism and making it difficult to determine the precise mechanism of brain injury in these cases. Surgical positioning may also affect cerebral perfusion pressure and may, for example, be compromised in seated positions [4]. Conversely, elevated postoperative blood pressure is a major risk factor for developing cerebral hyper-perfusion syndrome after carotid revascularization. This is thought to be due to impaired cerebral autoregulation in a chronically hypoperfused brain vascular territory that is suddenly flooded with blood after the downstream highly stenotic artery (e.g., carotid artery in the neck) is opened after carotid endarterectomy or angioplasty and stenting [14].
Neurosurgical Procedures and Stroke. Stroke may occur as a complication of neurosurgical procedures via additional mechanisms. Vascular manipulation as a consequence of brain surgery may cause embolic or thrombotic events [15]. Tumor resection may result in iatrogenic vascular injury. For example, a glioma located in an insular location of the brain may be a risk for intraoperative ischemia during glioma resection surgery due to compromise of nearby arterial perforators in the region. Such compromise may be associated with poor collateral flow patterns and greater likelihood of ischemic complications [16]. Another example is delayed cerebral ischemia which may occur as a well-known consequence of subarachnoid hemorrhage or as a complication of endovascular treatment of aneurysms which may introduce thromboembolism via device-related thrombosis and other thrombo-embolic mechanisms [17]. Venous infarction occurs as a consequence of meningioma resection due to the propensity of meningiomas to invade veins and venous sinuses and as a consequence of the necessity of sacrificing certain veins to achieve adequate surgical resection of the neoplasm [18].
Other Mechanisms. Mechanisms of covert infarcts are less well-studied but may occur by mechanisms like those described for general infarcts (see above paragraphs of this section). The perioperative period is also associated with systemic inflammation and a prothrombotic state that may also play a role in the genesis of stroke [4].

2.2. Epidemiology and Risk Factors for Stroke

Overall Incidence. Because the total volume of surgeries performed is high, a low incidence rate of perioperative stroke translates to a high absolute burden of events. An analysis of over 3 million surgical encounters in California found an overall stroke rate of 0.32%, with highest incidence in neurological, followed by vascular, and cardiac surgeries [19]. Swedish and Chinese registry studies have found similar incidences of 0.22% and 0.23%, respectively [20,21]. An analysis of over 10 million hospitalizations in the United States found the incidence of perioperative stroke to increase from 2004 to 2014 despite reductions in the rate of death and acute myocardial infarction [22]. Most overt strokes occur early, with nearly half detected within the first 24 h after surgery [4]. The vast majority of perioperative strokes are ischemic, while a small proportion are hemorrhagic [4]. One should interpret the data with caution as studies that do not include estimates of stroke based not only on clinically manifest strokes but also on neuroimaging detected covert strokes may underestimate the true magnitude of the problem [3].
Though covert strokes have been studied in the cardiac and carotid intervention literature, two major recent studies have established the broader incidence of covert infarcts and their association with cognitive outcomes (Table 1). The NeuroVISION study was a seminal, international, prospective cohort study of 1114 patients over the age of 65 undergoing non-cardiac surgery, and found 7% suffered a perioperative covert stroke, and 13% had multiple brain infarcts, suggesting an embolic etiology [7]. The PRECISION study was a prospective cohort study of 934 patients undergoing elective non-cardiac surgery and found 11.9% of patients had covert strokes. Notably, two-thirds of the participants underwent craniotomies [23].
Risk Factors in Neurosurgical, Neuro-endovascular, and Cardiac Interventions. The risk of perioperative stroke varies substantially by surgical procedure. Across all neurosurgical procedures, estimates of overt stroke range from 0.73% [24] to 1.5% [25]. Higher stroke rates can be found in neurovascular procedures, reaching as high as 8% in patients undergoing aneurysm clipping [26]. Five to six percent of patients undergoing meningioma resection may have a clinical ischemic stroke [27,28], whereas rates in spinal neurosurgical procedures are similar to non-cardiac, non-neurologic surgeries and less than 1% [29,30,31]
Covert strokes may be observed in a high proportion of neurosurgical procedures. Post-operative diffusion weighted imaging has shown as many as 23% of patients may have ischemic strokes after low-grade glioma resection [16], and up to 35% of patients undergoing meningioma resection have postoperative peritumoral infarctions, the majority of which are not associated with an immediate neurological deficit [27]. In the PRECISION study, 16.3% of patients aged ≥ 60 undergoing elective neurosurgery had a new postoperative covert infarct, most commonly multiple, small, watershed-pattern lesions (i.e., ischemic strokes in the border-zone regions between major arterial territories due to hypoperfusion) [23].
As previously mentioned, the risk of covert infarction is high in neuro-endovascular interventions. In the diffusion-weighted imaging (DWI) MRI sub-study of the International Carotid Stenting Trial, new ischemic lesions occurred in 50% of patients undergoing carotid artery stenting (CAS) and 17% undergoing carotid endarterectomy (CEA), and the majority were covert infarcts [32]. In endovascular brain aneurysm treatment, a systematic review found an incidence of DWI lesions of 47% but no statistical difference by aneurysm treatment technique [33]. Longer procedure time has been shown to be a risk factor for developing DWI lesions during endovascular aneurysm repair [34].
Cardiac Interventions. The highest rates of overt stroke in cardiology procedures are seen in coronary artery bypass grafting (CABG) (2%) [35], surgical aortic valve replacement (SAVR) (5.1%), and transcatheter aortic valve implantation (TAVR) (5.3%) [36,37]. Pooled prevalence rates of covert infarcts are reported as high as 74% with TAVR and 58% with SAVR, likely related to atherosclerotic plaque disruption in the ascending aorta [36]. In other cardiac procedures, the prevalence decreases, reaching 15% in percutaneous coronary intervention [36].
Patient-Specific Risk Factors. Patient-level characteristics exert a strong influence on perioperative stroke risk. Advanced age is a consistent predictor. For example, the NeuroVISION trial demonstrated 7% of the patients aged 65 and older had a covert stroke after surgery, and other studies consistently demonstrate advanced age as a risk factor [7,19,20,21]. Frailty also independently increases the risk of perioperative stroke across surgical populations, with reported odds ratios ranging from 1.5 to 4.2 depending on procedure type [38,39]. History of prior stroke or TIA is another risk factor and recent stroke even more so. Elective non-cardiac surgery performed within 30 days of an ischemic stroke carries an up to 8-fold-higher risk of major cardiovascular events, including recurrent stroke, and the risk that remains elevated for at least 3 months, before it plateaus [40].
Atrial fibrillation (AF), either pre-existing or newly detected postoperatively, increases perioperative stroke risk approximately two-fold in non-cardiac surgery [41]. Post-operative atrial fibrillation is also common in cardiac procedures, and may be independently associated with stroke risk [42]. Amongst the traditional vascular risk factors, carotid stenosis, heart failure, and diabetes mellitus may be risks for perioperative stroke in patients undergoing cardiac procedures [43,44].
Anesthesia-Related Factors. The role of anesthesia in perioperative stroke risk is complex. In surgeries where a choice of regional or general anesthesia exists, Cochrane reviews have not reported a significant difference between either approach [45,46]. Similarly, general versus local anesthesia for carotid surgery shows nonsignificant differences in stroke and death rates between the two approaches [47]. Stroke rates across TAVR are also comparable across anesthesia techniques [48].
Anesthesia is responsible for various physiological parameters that may influence risk of stroke. The PRECISION study specifically analyzed the relationship between intraoperative hypotension and stroke risk. There was no statistically significant association between the duration or extent of hypotension (using a MAP threshold of 75 mmHg) and the occurrence of postoperative stroke [23]. Conversely, early postoperative hypertension (especially systolic BP > 180 mmHg) after carotid endarterectomy or stenting is a well-documented risk for cerebral hyper-perfusion syndrome and can precipitate malignant cerebral edema in the context of impaired cerebrovascular autoregulation [49,50]. Both hypocarbia or hypercarbia may increase stroke risk via cerebral vasoconstriction or steal phenomenon, respectively [51].

2.3. Risk Stratification and Mitigation

Introduction. Before launching into a discussion of risk stratification and mitigation and treatment strategies for perioperative stroke, one should be reminded that the field of perioperative brain health is a relatively new one, and there is much work to be done to close knowledge gaps in this field [3]. Hassani and Gorelick provide a roadmap of the work that lies ahead of periprocedural brain health, and it includes such domains as improving our understanding of mechanisms of periprocedural strokes, development of validated models of periprocedural stroke risk, better understanding of long-term cognitive outcomes, optimization of patient education on brain health risks, and wider scale testing of prevention strategies [3].
Stratification Methods and Prevention. Several risk-prediction calculators exist for assessing perioperative stroke risk, including the Perioperative Stroke Risk Index, the Stroke Risk Analysis Score (SRAS), the American College of Surgeons National Surgical Quality Improvement Program (ACS-NSQIP) Stroke Risk Model, the 301 Perioperative Stroke Risk Calculator (301PSRC), and the Cong et al. model (Table 2) [5,21,40,52,53,54,55,56]. These all show predictive ability for perioperative stroke risk, but are not without limitations, including a lack of prospective validation, different statistical methods, an absence of certain key risks, and concerns about their generalizability to all populations [5,21,52,53,54,55,56].
Additionally, these models are not applicable to patients undergoing cardiac surgery, with the only validated risk calculator applying to this population being the Society of Thoracic Surgeons Adult Cardiac Surgery Database (STS ACSD) Risk Calculator [56].
Notably, however, the predictive ability of this model is not as robust as the aforementioned models [56]. These tools also vary considerably with respect to the variables included, the patient populations studied, and their intended time frames. The American Heart Association recommends the ACS-NSQIP as it demonstrates high predictive accuracy despite not being developed to predict stroke risk and because it is an accessible, web-based calculator [4,57]. The STRAS predicts 1-year postoperative stroke risk instead of 30-day risk, which limits its use as a perioperative risk stratification tool [53]. The 301 PRSC is a new stratification tool developed in 2025 showing a high discriminative ability; however, it has been developed and validated in Chinese populations and therefore has limited potential applicability to non-Chinese populations [21]. The Cong et al. model is also a newer tool developed in 2025, but its use is also limited due to lack of external validation and a development cohort derived retrospectively from a single center [55].
Approach to Prevention. We discuss the approach to prevention of perioperative stroke according to general and specific underlying medical conditions.
  • General Guidance: In the absence of substantially validated prediction models for perioperative stroke and absence of a plethora of clinical trials to guide prevention, periprocedural stroke prevention may begin with customary and usual guideline optimization for risks and medication management.
  • Major Underlying Medical Conditions: The main conditions that may elevate risk of stroke that may be acted on in the preoperative period include history of recent stroke or TIA, extracranial carotid disease, patent foramen ovale (PFO), and anemia [4,52].
    • Elective Surgery: Non-urgent, elective surgery should be postponed a minimum of 3 months after ischemic stroke or TIA, if possible, though further delay to 6 months may be optimal [4,52].
    • Carotid Stenosis: Patients with recent symptomatic high-grade carotid stenosis should undergo revascularization prior to other major elective surgery, though prophylactic revascularization of asymptomatic high-grade carotid stenosis prior to elective surgery is not recommended [52].
    • PFO: The data regarding the relationship between PFO and perioperative stroke risk is limited. Therefore, prophylactic PFO closure is generally not recommended [4]. In patients who have already been determined to be candidates for PFO closure, it is reasonable to delay elective surgery until after PFO closure [4].
    • Anemia: Management of perioperative anemia is complex, as both the presence of anemia as well as the transfusion of blood have been shown to increase the risk of perioperative stroke [58,59]. Utilizing a restrictive transfusion threshold (7–8 g/dL) or administration of tranexamic acid to reduce intraoperative blood loss may decrease perioperative stroke risk [40,58].
    • β-blocker and Antithrombotic Medications: Medications that play a key role in perioperative stroke mitigation include β-blockers, antiplatelet agents, and anticoagulant medications. β-blockers should not be newly initiated directly preceding surgery, as this may confer an increased risk of periprocedural stroke [60]. However, continuation of chronic stable β-blocker use does not seem to increase the risk of stroke [40].
Aspirin for secondary stroke prevention should be continued in the periprocedural period, unless the surgery carries a high risk of bleeding, in which case it may be held for 7 days pre-procedure [61,62]. There are currently no randomized control trials addressing periprocedural P2Y12 inhibitor (e.g., clopidogrel, ticagrelor, and prasugrel) use; however, in patients undergoing carotid artery stenting for symptomatic carotid stenosis, preoperative initiation of dual antiplatelet therapy (DAPT) with aspirin and a P2Y12 inhibitor therapies decreases the risk of periprocedural stroke, and is therefore recommended [63,64]. For patients undergoing carotid endarterectomy (CEA) for symptomatic carotid stenosis, it is recommended to initiate DAPT prior to CEA, though there is no consensus on whether DAPT should be stopped prior to CEA or continued, as studies have found conflicting information regarding its effect on perioperative stroke risk [64,65].
Periprocedural management of oral anticoagulation (OAC) medication is a complex issue, though it is generally recommended to continue OAC in patients undergoing procedures with minimal bleeding risk [40]. Routine periprocedural parental bridging anticoagulation is not recommended, instead being reserved for patients with high thrombotic risk such as those with mechanical heart valves, CHA2DS2VASc scores of ≥7, or history of severe thrombophilia, based on increased risk of periprocedural thromboembolic stroke [40,62]. Additionally, bridging therapy should be avoided in patients on direct oral anticoagulants, as this may result in an increased bleeding risk without a reduction in stroke risk [40,62]. In the setting of urgent/emergent surgery, pharmacologic reversal of OAC may be necessary, but can lead to increased risk of perioperative stroke. Decisions regarding whether to reverse OAC can be guided by measurement of INR for warfarin, or DOAC levels if available, to minimize perioperative stroke risk [62,66]. Resumption of OAC therapy and antiplatelet agent administration after a procedure is discussed at the end of this section.
Intraoperative Detection and Mitigation of Stroke. Detection of clinically manifest intraoperative stroke is complicated by multiple factors including administration of anesthesia and analgesia use. Intraoperative neuromonitoring using EEG, evoked potentials, near-infrared spectroscopy, and transcranial doppler can allow for early identification of ischemia, though the sensitivity and specificity of these techniques is limited [42]. The most sensitive brain imaging technique to detect ischemic stroke is MRI. More recently, portable MRI units have become available for use in inpatient hospital units such as the intensive care unit and in the operating theater. Nevertheless, there has not been widespread adaptation of the portable units as they continue to undergo study.
Data regarding specific intraoperative blood pressure goals to mitigate intraoperative risk of stroke is limited. Based on the available evidence, maintaining a mean arterial pressure of 60 to 65 mmHg and a systolic blood pressure ≥ 90 mmHg is recommended as a general hemodynamic safety rule per guidelines [4,42]. One must keep in mind that the cerebral autoregulatory curve parameters may vary by individual patient, making it difficult to precisely predict blood pressure targets and ranges in an individual case.
Thromboembolic risk can be mitigated through the use of “no-touch” techniques during cardiac and thoracic aortic procedures, and the use of embolic protection devices and flow reversal techniques in cardiac and carotid artery surgeries [42,52]. Currently, evidence does not support the use of a specific anesthesia technique or agent to reduce the risk of perioperative stroke. Observational level III evidence from a retrospective cohort study has suggested that the use of volatile anesthetics decreases the risk of early perioperative stroke, but further prospective validation of this finding is needed [4,67].
Postoperative Detection and Mitigation. Like intraoperative detection of strokes, postoperative detection can be difficult due to multiple factors including prolonged intubation and residual effects from anesthesia, which can obscure the identification of new focal neurologic deficits. Additionally, a large proportion of patients with early perioperative stroke may present with non-focal findings [4]. Given these issues, routine neurologic evaluation in post-anesthesia care units utilizing standard scales, such as the NIH Stroke Scale (NIHSS), should be considered, though these scales lack validation in the perioperative setting [4]. The NIHSS is a well-studied tool to document neurological impairment in practice and in research.
Atrial Fibrillation. The risk of postoperative atrial fibrillation can be assessed using one of several validated risk scores, which can assist in determining which patients might benefit from continuous or prolonged cardiac monitoring [52]. Discussion of these scores is beyond the scope of this review, and the reader is referred to another authoritative source for additional details [52]. Initiation of anticoagulation for new onset atrial fibrillation should be individualized and should, in general, be considered for a CHA2DS2-VASc score of greater than 2 for men or greater than 3 for women and who do not have a contraindication related to bleeding risk [52,68].
Resumption of Antithrombotic Therapies. A key factor in the mitigation of postoperative stroke is the resumption of anticoagulant and antiplatelet medications. Generally, anticoagulation should be resumed 24 h postoperatively after low-bleeding-risk surgeries and 48–72 h after surgeries with an elevated bleeding risk, assuming post-operative conditions allow for administration of such therapy [4,40,52]. Resumption of warfarin should generally be done within 24 h of a procedure, as it typically takes at least 4 days to reach a full anticoagulant effect [40,62]. In those who received preoperative bridging or are in need of such therapy based on clinical risk assessment, this should be resumed 24–72 h after the procedure based on postprocedural bleeding risk, and continued until the INR is ≥2.0 [62,69]. Antiplatelet medications should generally be resumed within 24 h after surgery, for both secondary stroke prevention and for maintenance of stent patency (i.e., extracranial carotid or intracranial stents), except in cases with a high bleeding risk [52,62].

3. Treatment and Outcomes of Clinically Manifest and Covert Infarcts

Perioperative stroke may be associated with significantly worse outcomes than non-operative strokes [9]. However, there is a lack of high-quality data on long-term patient outcomes, and the current data may be biased towards the selection of patients with more severe strokes [9]. Patients with perioperative stroke may have a higher mortality and more severe disability than other stroke patients. The delayed recognition of stroke, surgical contraindications to intravenous thrombolysis, and lower rates of admission to stroke units may be some of the factors associated with worse outcomes [4,58]. Mortality rates in patients undergoing mechanical thrombectomy are higher in perioperative stroke patients, despite similar rates of reperfusion, which may also be due to the risks associated with the non-candidacy of these patients for intravenous thrombolysis or other surgical factors [70]. Periprocedural stroke also predicts longer hospital length of stays, and increases the likelihood of in-hospital mortality [42,71].
Covert Infarcts. Covert infarcts in the perioperative setting are understudied due in part to the inherent challenge in diagnosis. They may be recognized acutely on brain imaging but otherwise may have subtle or no clinical findings. Thus, covert infarcts pose an inherent challenge in treatment due to a high likelihood of being undetected. In the NeuroVISION study of elective non-cardiac, non-neurologic surgery patients, 7% had a periprocedural covert stroke detected by brain MRI [7]. Cognitive decline occurred in 42% of patients with a covert stroke and 29% of patients without a covert stroke [7]. In addition, the primary analysis showed that a covert stroke was associated with an increased risk of perioperative delirium, and overt stroke or TIA at 1-year of follow-up [7]. Similar findings were observed in the PRECISION study where one in nine patients suffered a covert stroke which was associated with a more-than-doubled risk of post-operative delirium and long-term neurocognitive decline [23]. Of interest, the occurrence of post-operative atrial fibrillation was associated with incident dementia [72].
There are several authoritative sources that address the management of persons with covert stroke [73,74]. Overall, the assessment and management of lifestyle and cardiovascular risks are recommended. However, the administration of statin therapy without a clear-cut customary indication is not recommended, and the use of antiplatelet agents to reduce the ischemic stroke risk is of uncertain value [74].
Acute Treatment of Stroke. The acute treatment of periprocedural stroke should follow typical guideline-based principles for the treatment of acute hemorrhagic or ischemic stroke with respect to blood pressure management, thrombolysis and mechanical thrombectomy administration, and other guideline-based recommendations [75]. Similar guideline recommendations should be followed for secondary prevention [76]. Acute infarcts are apparent on diffusion-weighted magnetic resonance imaging, whereas chronic covert infarcts may present as lacunes or other subcortical small strokes or irregularly shaped T2 hyperintensities of a chronic nature [77]. For acute symptomatic perioperative stroke, management should be similar to that of clinically manifest acute stroke in other settings including additional investigations based on the determination of stroke mechanism [73]. Embolic sources comprise a large proportion of covert infarcts, particularly in association with cardiac and vascular procedures. A proper investigation for an embolic source should be considered when clinically indicated [7]. A vascular neurologist, stroke team, or a general neurologist should be consulted in the absence of an available vascular neurologist to help guide acute stroke management and subsequent prevention recommendations. Expert input from these sources or other experts in the management of acute stroke, its prevention, and recurrent stroke prevention can add value to the overall patient management.
There is a lack of high-quality evidence to support specific interventions to prevent perioperative stroke. There is also a lack of high-quality evidence regarding interventions to reduce the risk of cognitive impairment when covert infarcts occur. Following the American Heart Association’s Life’s Essential 8 and other established guidance on the maintenance of brain health may be a prudent strategy when covert infarcts are discovered [74,78,79].

4. Limitations

This review has several limitations. As an expert opinion/narrative piece, it may be subject to selection bias in relation to the included studies. It is also limited by a paucity of randomized controlled data and study heterogeneity with respect to patient populations, procedure types, the definition of stroke, and data analytic methods. Conclusions should be interpreted in the context of these limitations.

5. Future Directions

Periprocedural covert brain infarcts are understudied, and there is a major need for high-quality research to further characterize them and their long-term consequences. A call for multidisciplinary action to better understand periprocedural infarcts and brain health has been proposed by Hassani and Gorelick [3]. Prevention is a cornerstone of modern stroke management, and high-quality randomized studies are needed to determine efficacious prevention strategies. From an intraoperative perspective, additional information is needed to better understand clinical phenotypes and risk markers. With the ever-expanding breadth of endovascular neurological procedures, the continued refinement of technology and techniques to minimize perioperative stroke is anticipated; however, many specific clinical questions, such as what the optimal intraoperative blood pressure targets are with known large-artery atherosclerosis, remain unanswered.
Data from the non-operative and perioperative settings repeatedly suggest an association between covert infarcts and later adverse cognitive outcomes. Additional high-quality longitudinal data is needed to further characterize this association, and the adoption of standardized post-operative cognitive measurements would assist in the systematic collection of such data [80]. Furthermore, there is a paucity of information from which to address the role of specific brain health interventions to reduce adverse cognitive outcomes when a covert perioperative stroke occurs. With rates of covert infarcts ranging from 7% in low-risk procedures (non-cardiac, non-neurologic procedures) to as high as 74% in high-risk cardiac procedures, the failure to detect them may be a missed opportunity to initiate general guideline-based treatments and preventives, particularly when cognition is at stake.

6. Conclusions

Periprocedural stroke is a major cause of morbidity and mortality related to surgeries and endovascular procedures. Perioperative death is estimated to be as high as the third leading cause of mortality worldwide. Such procedural complications as stroke are not only associated with a high mortality, but, in addition, are associated with the prolongation of hospitalization and adverse cognitive outcomes. The mechanisms by which they occur are multiple and range from traditional stroke mechanisms to neuro-inflammation and others [81]. We have just begun to understand the mechanisms and clinical manifestations of this group of adverse events. A multidisciplinary call to action has been recommended to bridge important knowledge gaps and reduce these preventable complications of brain injury. Anesthesiologists and other healthcare professionals working in the surgical and procedural field are well-positioned to make important contributions to this growing discipline of the prevention of brain injury in the perioperative period.

Author Contributions

Conceptualization, K.Q. and P.B.G.; methodology, K.Q. and P.B.G.; formal analysis, K.Q., P.B.G., J.S., M.U.F. and A.H.; investigation, K.Q., P.B.G., J.S., M.U.F. and A.H.; resources, K.Q., P.B.G., J.S., M.U.F. and A.H.; data curation, K.Q., P.B.G., J.S., M.U.F. and A.H.; writing—original draft preparation, K.Q., P.B.G., J.S., M.U.F. and A.H.; writing—review and editing, K.Q., P.B.G., J.S., M.U.F. and A.H.; visualization, K.Q., P.B.G., J.S., M.U.F. and A.H.; supervision, K.Q. and P.B.G.; project administration, K.Q. and P.B.G. All authors have read and agreed to the published version of the manuscript.

Funding

This research received no external funding.

Institutional Review Board Statement

Not applicable.

Informed Consent Statement

Not applicable.

Data Availability Statement

No new data were created or analyzed in this study. Data sharing is not applicable to this article.

Conflicts of Interest

The authors declare no conflicts of interest.

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Table 1. Comparison of study design, patient population, outcome measures, results, and key takeaways between the NeuroVISION and PRECISION studies [7,23].
Table 1. Comparison of study design, patient population, outcome measures, results, and key takeaways between the NeuroVISION and PRECISION studies [7,23].
Name NeuroVISION PRECISION
Study Design Prospective cohort study across 12 international sites. Prospective cohort study across 2 Chinese academic sites.
Patient Population 1114 patients aged ≥ 65 years undergoing elective non-cardiac surgeries (excluded carotid artery or intracranial surgeries). 934 patients ≥ 60 years undergoing elective non-cardiac inpatient surgery (2/3 had craniotomies).
Key Outcome Measures Primary: Cognitive decline at 1-year (decrease in Montreal Objective Cognitive Assessment of 2 or more points from baseline).
Secondary: Incidence of perioperative stroke, delirium within 3 days, other clinical outcomes. 		Primary: Incidence of postoperative stroke (evaluated by MRI within 7 days of surgery).
Secondary: Post-operative delirium within 5 days, post-operative cognitive decline at 3 months, and 1 year, and other clinical outcomes.
Covert Stroke Incidence 78 patients (7%; 95% CI 6–9%). 111 patients (11.9%; 95% CI 9.8–14.0%).
Postoperative Delirium Incidence 10% in covert stroke group, 5% in no covert stroke group. Covert stroke associated with increased risk of delirium. 23% in covert stroke group, 11% in no covert stroke group. Covert stroke associated with increased risk of delirium.
One-Year Cognitive Decline 42% in covert stroke group and 29% in no covert stroke group (adjusted OR 1.98 95% CI 1.22–3.20). 147 patients across both groups (18.8%; 95% CI, 16.0 to 21.5%). Association seen between covert stroke and 1-year cognitive decline (adjusted OR 2.33; 95% CI, 1.31 to 4.13).
Key Takeaways One in 14 patients had a covert stroke which increased the risk of delirium and neurocognitive decline at one year. One in nine patients had a covert stroke which increased the risk of delirium and neurocognitive decline at one year.
Table 2. Perioperative stroke risk models. Area under the curve (AUC) quantifies discriminative ability of perioperative risk stratification models, i.e., how well they distinguish patients who will experience stroke from those who will not. An AUC of 1.0 represents perfect discrimination, while 0.5 indicates no better than chance. Abbreviations: ACE, angiotensin-converting enzyme; AUC, area under the curve; ASA, American Society of Anesthesiologists; CABG, coronary artery bypass grafting; COPD, chronic obstructive pulmonary disease; CV, cardiovascular; MAP, mean arterial pressure; MI, myocardial infarction; NSAID, non-steroidal anti-inflammatory drug; PFO, patent foramen ovale; TIA, transient ischemic attack; WBC, white blood cell.
Table 2. Perioperative stroke risk models. Area under the curve (AUC) quantifies discriminative ability of perioperative risk stratification models, i.e., how well they distinguish patients who will experience stroke from those who will not. An AUC of 1.0 represents perfect discrimination, while 0.5 indicates no better than chance. Abbreviations: ACE, angiotensin-converting enzyme; AUC, area under the curve; ASA, American Society of Anesthesiologists; CABG, coronary artery bypass grafting; COPD, chronic obstructive pulmonary disease; CV, cardiovascular; MAP, mean arterial pressure; MI, myocardial infarction; NSAID, non-steroidal anti-inflammatory drug; PFO, patent foramen ovale; TIA, transient ischemic attack; WBC, white blood cell.
Model NameSize of Derivation CohortType of SurgeryKey Risk Factors AssessedOutcome(s)Performance (AUC)ValidationLimitations
Perioperative Stroke Risk Index [5]350,031Non-cardiac, non-neurological surgeriesAge ≥ 62 year, MI within 6 months, acute renal failure, history of stroke, history of TIA, preoperative dialysis, hypertension, severe COPD, current smoker, body mass indexPostoperative stroke and mortality within 30 days0.78 (95% confidence interval (CI) 0.76–0.80)Internally validatedOldest model/data, suboptimal performance for vascular surgery
Stroke Risk Analysis Score (STRAS) [53]107,756Non-cardiac surgeriesAge, sex, race/ethnicity, ASA classification, history of ischemic stroke or TIA, carotid artery stenosis, PFO, migraine, hypertension, atrial fibrillation, emergency surgery, surgery type (vascular surgery or high-risk neurosurgery)Ischemic stroke within 1 year0.88 (95% CI 0.86–0.89)Internally validatedRisk prediction extends well beyond the typical perioperative period
American College of Surgeons National Surgical Quality Improvement Program (ACS-NSQIP) Stroke Risk Model [54]1,165,750Non-cardiac, non-neurological surgeriesAge, history of coronary artery disease, history of stroke, ASA classification, hematocrit, serum sodium, creatinine, emergency surgery, surgery typePostoperative stroke, major cardiovascular event, and mortality within 30 days0.876 (95% CI not reported)Internally validatedExclusion of critical risk factors such as atrial fibrillation and carotid stenosis
301 Perioperative Stroke Risk Calculator (301PSRC) [21]223,415Non-cardiac surgeriesAge, ASA classification, hypertension, previous stroke, valvular heart disease, preoperative steroid hormones, preoperative ß-blockers, preoperative MAP, preoperative fibrinogen to albumin ratio, preoperative fasting plasma glucose, emergency surgery, surgery type, surgery lengthPostoperative stroke within 30 days0.897 (95% CI 0.872, 0.922).Externally validatedMay lack generalizability outside Chinese populations
Cong et al. Model [55]106,328Non-cardiac, nonvascular, non-neurological surgeriesAge, drinking history, angina pectoris, cerebrovascular disease history, intraoperative MAP, serum sodium, preoperative ACE inhibitor use, preoperative NSAID usePostoperative stroke within 30 days0.869 (95% CI, 0.827–0.910)Internally ValidatedMay lack generalizability outside Chinese populations
Society of Thoracic Surgeons 2018 Cardiac Surgery Stroke Risk Model [56]CABG: 439,092
Valve: 150,150
CABG + Valve: 81,588		Adult cardiac surgeriesSurgery type, surgery priority, prior CV surgery, patient demographics, comorbidities, preoperative medications, creatinine, hematocrit, WBC count, platelet countPostoperative stroke during hospitalizationCABG: 0.697 Valve: 0.656 CABG + valve: 0.632 (95% CI not reported)Internally validatedModest discriminative ability for stroke risk, difficult to implement due to complexity
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Qureshi, K.; Schick, J.; Hasan, A.; Farooq, M.U.; Gorelick, P.B. Periprocedural Stroke: Stroke Mechanisms, Risks, Outcomes, Prevention, and Treatment. Anesth. Res. 2026, 3, 7. https://doi.org/10.3390/anesthres3010007

AMA Style

Qureshi K, Schick J, Hasan A, Farooq MU, Gorelick PB. Periprocedural Stroke: Stroke Mechanisms, Risks, Outcomes, Prevention, and Treatment. Anesthesia Research. 2026; 3(1):7. https://doi.org/10.3390/anesthres3010007

Chicago/Turabian Style

Qureshi, Kasim, Jason Schick, Ahmedyar Hasan, Muhammad U. Farooq, and Philip B. Gorelick. 2026. "Periprocedural Stroke: Stroke Mechanisms, Risks, Outcomes, Prevention, and Treatment" Anesthesia Research 3, no. 1: 7. https://doi.org/10.3390/anesthres3010007

APA Style

Qureshi, K., Schick, J., Hasan, A., Farooq, M. U., & Gorelick, P. B. (2026). Periprocedural Stroke: Stroke Mechanisms, Risks, Outcomes, Prevention, and Treatment. Anesthesia Research, 3(1), 7. https://doi.org/10.3390/anesthres3010007

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