Endovascular thrombectomy is the optimal treatment option in patients with large vessel occlusion acute ischemic stroke (1). Although 90% of patients achieved successful recanalization and the procedure is generally relatively safe, some of the patients still suffer from unfavorable outcomes at 90 days (2–4). Reperfusion injury and hemorrhagic transformation, which are mainly attributed to impaired cerebral blood flow autoregulation and disrupted blood–brain barrier (BBB), have been identified as important complications in the acute phase of recanalization (5–7).

Early identification of potential candidates who may suffer from neurological deterioration should be performed for a timely experimental treatment to improve the outcome of patients with reperfusion therapies. While timely neurological assessment is unavailable in patients who received general anesthesia or mild sedation during endovascular reperfusion therapies. Transcranial duplex (TCD) sonography or transcranial color-coded sonography (TCCS) may be one of the early hemodynamic predictors of outcome, while there are numerous confounding factors affecting middle cerebral artery (MCA) flow velocity. It may be difficult to reverse the prognosis when the intracranial lesion is detected on cerebral computed tomography (CT) or MRI 24 h routinely after the endovascular procedure or in the event of clinical deterioration.

In clinical practice, we often find that patients with poor prognoses have decreased bicarbonate (HCO3-) levels in arterial blood gas (ABG) testing or even have metabolic acidosis or elevated lactate in the early phase of recanalization. Patients with cerebral infarction are less likely to suffer from hemodynamic disorders in the early stages, so changes in the acid–base balance in peripheral blood may be related to cerebral metabolism. There have been few studies exploring the relationship between ABG testing results and poor prognosis in patients with reperfusion therapies. We, therefore, explored the ABG testing results in the early phase of recanalization and analyzed their association with poor prognosis in patients with successful revascularization.

Despite revascularization after thrombectomy, a relevant proportion of patients with large vessel occlusion acute ischemic stroke do not achieve a favorable prognosis. Early identification of patients with possible neurological deterioration may be critical to improving prognosis. Our study demonstrated that ABG testing results were closely related to clinical outcomes after EVT. Our main finding was that acidosis in arterial blood gas testing was strongly associated with poor prognosis. Decreased HCO3- levels at 8 h after EVT were independently related to higher odds of sICH, hemicraniectomy, and mortality. Decreased HCO3- levels, decreased pH at 8 h after EVT, and elevated lactate levels at 8 h after EVT were also presented in patients with poor clinical outcomes. To the best of our knowledge, this was the first study to investigate the relationship between ABG testing results and clinical outcomes after successful recanalization. Our findings may be useful for screening patients with possible neurological deterioration in the acute early phase of recanalization. ABG could detect exacerbations earlier than routine TCD, CT, or MRI.

After successful recanalization, a series of complex pathophysiological changes occur in the cerebral tissue, which may involve the intricate interplay of mitochondrial dysfunction, overload of calcium, excitotoxicity, free radical-mediated toxicity, endothelial pathology, and edema formation (9–13). In another view, recanalization after EVT does not always lead to downstream reperfusion, a state that has been known as the no-reflow phenomenon, which may be due to capillary compression and luminal narrowing in cerebral circulation (14–16). These pathophysiologic derangements may result in cerebral microcirculation disorders. The larger the infarct size, the more severe the microcirculation disorders may be. Impaired microcirculation could lead to excessive acid production, increased toxic substances, and elevated lactic acid. Due to exacerbation of BBB disruption after reperfusion, these acid productions are released into peripheral blood (17). Dysfunctional cerebral blood flow autoregulation after thrombectomy aggravates these processes (18).

The existence of a buffer system in the body will maintain pH in the normal range during the initial phase. However, HCO3- as the main component of the biological buffer may change at the onset. Under normal conditions, lactate is continually being produced and metabolized, maintaining dynamic balance. When lactate production predominates, lactate levels rise. Impaired microcirculation can lead not only to elevated lactate levels but also to excessive production of other acids. For example, in the area of cerebral infarction, the Na⁺/H⁺ exchange isoform 1 (NHE1) function is augmented (19). As a result, Na⁺ enters the cells in return for H⁺ extrusion, which may aggravate acidosis (20). Thus, bicarbonate, as the main component of biological buffer, is a more comprehensive and earlier indicator of cerebral metabolism, whereas lactate is only a major part of metabolic acidosis. Acidosis (drop in pH) may present when the buffering system fails to compensate. Excluding causes such as systemic hypoperfusion and other causes of secondary metabolic abnormalities, pH, lactate levels, and HCO3- levels may be optimal candidates for embodying a cerebral metabolic state, which may indicate the severity of cerebral postischemic reperfusion injury.

Previous studies have explored cerebral metabolism in cerebral ischemia under experimental and clinical conditions by using microdialysis catheters. In animal experiments, the biochemical pattern of cerebral tissue during ischemia is characterized by a marked increase in cerebral lactate (21, 22). Elevated intracerebral lactate and glutamate were also demonstrated in patients with MCA infarcts and malignant brain swelling (23, 24). In addition, the Na⁺/H⁺ exchange is augmented and tissue pCO₂ rises during ischemia, which may also contribute to cerebral tissue acidosis (19, 25). Acidic amino acids, lactate, and other acidic metabolites were released into the peripheral blood through the damaged BBB, and these products resulted in altering biological buffers, even metabolic acidosis.

The previous study has shown that bedside TCD indicated a significantly higher MBF velocity in the recanalized MCA in patients who experienced ICH following recanalization (26). Although there was a tendency for MBF velocity to increase in patients with sICH in our study, the MBF velocity was not a statistically significant difference between the two groups. The difference between our results and the previous study could be related to the fact that TCD in the present study was performed within 0–30 min and 8 h after EVT, Markus et al. performed a TCD examination within 24 h after EVT. However, the two studies were similar in that MBF velocity was not an independent predictor of sICH following recanalization. Therefore, MBF velocity may not be an optimal biomarker to identify patients with possible neurological deterioration in the acute early phase of recanalization.

Cerebral metabolism is accompanied by complex pathophysiological changes in patients with large vessel occlusion acute ischemic stroke. After successful recanalization, cerebral metabolism may suffer from aggravation due to postischemic reperfusion injury. There are more published articles using bedside TCD to explore cerebral blood flow in patients with cerebral infarction (27, 28). However, it is surprising that so scant attention has been given to bedside cerebral metabolic markers. Cerebral metabolic indicators may contribute appropriate information on cerebral impairment much earlier. In this context, ABG testing as an efficient bedside screening method is certainly more readily available than other examinations and provides more information about prognosis.

In this study, we observed that decreased HCO3- levels at 8 h after EVT were a reliable predictor of clinical outcome in patients with successful revascularization. In the case of conventional treatment after recanalization, decreased HCO3- levels at 8 h after EVT indicated that acid production from cerebral metabolism is still increasing, implying deteriorating cerebral function. This study demonstrated that increased lactate at 8 h after EVT was closely associated with hemicraniectomy, which was regarded as a surrogate for malignant edema. Increased lactate levels may result from microcirculatory disorders provoking secondary brain impairment. Due to severe deterioration of cerebral function and excessive acid production release, patients who died may be accompanied by a decrease in pH levels after endovascular therapy.

Some limitations need to be considered in this study. First, all newly admitted patients had their ABG testing routinely collected within 30 min and reviewed 8 h later in our intensive care unit. BBB permeability was increased in the ischemic hemisphere 1 h after reperfusion (29), and whether an earlier review of the ABG testing could provide useful information about the prognosis needs to be further explored. Second, although we included only patients with ASPECTS ≥ 6, we could not obtain the final infarct volume. The correlation of final infarct volume with ABG testing results may provide more useful information. Third, the sample sizes were relatively small, this was a single-center study, and more patients need to be included to confirm these findings. Fourth, a lot of patients with malignant cerebral edema may not choose to undergo hemicraniectomy due to age, hemispheric laterality, and other reasons. But the prognosis of these patients may be worsened and eventually be classified in the death group.

In the present study, we have indicated that post-EVT ABG testing might be an effective bedside method for assessing prognosis in patients with large vessel occlusion acute ischemic stroke. Acidosis in arterial blood gas testing is associated with clinical outcomes after endovascular therapy and may help to select patients with poor prognosis in the acute early phase of recanalization.

The original contributions presented in the study are included in the article/supplementary material, further inquiries can be directed to the corresponding authors.

The studies involving human participants were reviewed and approved by the study was approved by the Ethics Committee of the Shengli Oilfield Central Hospital (Approval No. Q/ZXYY-ZY-YWB—LL202251). The patients/participants provided their written informed consent to participate in this study.

ZT and MX conceived and designed the study. RS, LL, JX, PL, GW, HS, RL, YZ, SH, YL, and PZ acquired the data. RS and LL analyzed the data, which was discussed with ZT and MX. RS and ZT drafted and critically revised the manuscript. All authors gave final approval for manuscript publication and agree to be accountable for all aspects of this work. All authors contributed to the article and approved the submitted version.