1. Introduction In acute ischemic stroke (AIS), one of the leading causes of mortality and long-term morbidity worldwide, early diagnosis and rapid intervention directly impact patient prognosis. In the emergency department (ED)—the primary point of care for most of these patients—diagnosis is based on neurological examination and imaging, while the severity of the disease is estimated using neurological scoring systems; however, there is a critical need for practical biomarkers that can provide early prognostic insights. Various studies have shown that immune and inflammatory responses increase following an AIS [ 1, 2]. Although the primary pathology in AIS is ischemia due to vascular occlusion, neuroinflammation is being investigated as a secondary mechanism of damage. Existing evidence suggests that inflammatory factors are associated with both stroke severity and prognosis [ 3]. Damaged cells activate the immune system when brain tissue remains hypoxic following an AIS [ 4]. The subsequent inflammatory cytokine storm leads to the release of factors that damage the blood–brain barrier and recruit peripheral immune cells to the lesion site [ 4]. This triggers the early onset of nerve damage and delays cell repair. Prior studies demonstrate that heightened inflammation subsequent to a stroke can aggravate cerebral damage and deteriorate the prognosis [ 3]. Therefore, appropriate inflammatory biomarkers may be effective in predicting prognosis in AIS. The extent of ischemic brain injury can directly influence the magnitude of the systemic inflammatory response, depending on the infarct volume. Larger infarct volumes lead to greater neuronal loss. The release of damage-associated molecular patterns activates peripheral immune cells and strengthens the systemic inflammatory cascade [ 3]. As a consequence of this mechanism, infarct volume is expected to correlate with composite inflammatory indexes such as SII and SIRI. The aim of this study is to investigate the relationship between SII and SIRI scores with infarct volume, as well as short-term and long-term mortality, in patients diagnosed with AIS. 2. Materials and Methods 2.1. Study Design and Population This research was designed as a retrospective cohort study with a level of evidence of 2+ according to the Scottish Intercollegiate Guidelines Network (SIGN 100) criteria [ 12]. Patients diagnosed with AIS at the ED of Bilecik Training and Research Hospital between 1 March 2022, and 30 September 2023, were retrospectively evaluated. Inclusion criteria were patients aged ≥ 18 years presenting to the ED within 24 h of symptom onset, diagnosed with AIS via diffusion-weighted magnetic resonance imaging (DWI), and with a CBC drawn at presentation. Patients were excluded if their records contained missing information regarding medical history, physical examination, laboratory results, or radiological findings. Additionally, the following exclusion criteria were applied: (i) documented infection before stroke onset or within 72 h of admission; (ii) known hematological disorders; (iii) acute metabolic disease or poisoning; (iv) cancer or current use of steroids or immunosuppressive agents; (v) patients who were transferred to a comprehensive stroke center for potential thrombolytic therapy or mechanical thrombectomy, as these interventions were not available at our facility during the study period; and (vi) patients with intracranial hemorrhage or mass lesions identified on brain computed tomography. The patient recruitment and exclusion process is summarized in the study flow chart ( Figure 1). A sample size of 240 was determined to be sufficient based on the aim of detecting a minimum biomarker difference level of 20% between patients who were alive and those who died, with a two-to-one expected ratio (such as 160 alive and 80 deceased patients). Type I errors (α-level, two-sided) were set to 0.05, and Type II errors (β-level) were set to 0.2 for 80% statistical power. 2.2. Data Collection and Indexes Data were extracted from the hospital information management system, including age, sex, medical history, and blood parameters (white blood cell, platelet, neutrophil, lymphocyte, and monocyte counts), as well as hospital length of stay and mortality dates. Additionally, infarct volumes were calculated based on patients’ DWI images, and SII and SIRI scores were calculated based on laboratory values. SII and SIRI values were calculated using the CBC performed at hospital admission as follows [ 5, 13]: SII = N e u t r o p h i l ୍ଠ P l a t e l e t L y m p h o c y t e SIRI = N e u t r o p h i l ୍ଠ M o n o c y t e L y m p h o c y t e 2.3. Imaging and Volumetric Analysis DWI was performed on a 1.5T scanner (Magnetom Essenza, Siemens, Erlangen, Germany). DWI was acquired using single-shot echo-planar imaging with the following parameters: TE 105 ms, TR 3800 ms, matrix 160 × 160, b-value-1 = 0 and b-value-2 = 1000 s/mm 2, 5.5 mm slice thickness, 1.65 mm interslice gap, and approximately 20 slices. Two experienced radiologists independently analyzed all DWI data, each blinded to the other’s assessments as well as to clinical and laboratory results, for the presence, location, and number of hyperintensities on DWI. In cases of discordance, consensus was reached through discussion. Lesion volumes were calculated offline using an image post-processing software package (syngo.via, Siemens Healthcare, Erlangen, Germany). The radiologists manually contoured the areas of diffusion hyperintensity on each slice; the total infarct volume was then determined by multiplying the sum of these areas by the slice spacing (slice thickness + interslice gap). Infarcts were categorized as lacunar ( 1364) 2.5 (1.0–7.0) 0.05 2.3 (1.3–4.2) 0.008 2.2 (1.3–3.9) 0.004 SIRI Group 1 (≤2.87) Ref Ref Ref Ref Ref Ref Group 2 (>2.87) 3.1 (1.2–9.1) 0.02 3.3 (1.8–6.3) 0.0002 2.9 (1.7–5.1) 0.0002 Disclaimer/Publisher’s Note: The statements, opinions and data contained in all publications are solely those of the individual author(s) and contributor(s) and not of MDPI and/or the editor(s). MDPI and/or the editor(s) disclaim responsibility for any injury to people or property resulting from any ideas, methods, instructions or products referred to in the content. © 2026 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license.
