Objective To explore the mediating effects of potential mediating factors on occurrence of stroke-associated pneumonia (SAP) in patients with varying degrees of neurological deficit based on real-world case data.

Methods A total of 902 hospitalized patients in the acute phase of stroke were selected as study subjects. Clinical characteristics were compared among patients with different degrees of neurological deficit and those with SAP. R studio was employed to generate a correlation heatmap of potential mediating factors, enabling the identification of primary potential mediating factors. Multivariate logistic regression analysis was conducted to assess the impact of the degree of neurological deficit, potential mediating factors, and stroke-associated pneumonia. R studio was also used to analyze the interaction between the degree of neurological deficit and potential mediating factors, as well as the mediating role of potential mediating factors in the association between neurological deficit and SAP.

Results Based on the results of the correlation heatmap, this study screened out five major potential mediating factors, namely consciousness level, neutrophil-to-lymphocyte ratio (NLR), chlorine (Cl), fasting blood glucose (FBG) and albumin (ALB). Multivariate logistic regression analysis revealed that the degree of neurological deficit was significantly associated with the level of consciousness, NLR, Cl, FBG levels and the occurrence of SAP. Interaction analysis demonstrated an interaction between the degree of neurological deficit and FBG levels. Mediation analysis indicated that the total effect of the association between neurological deficit and SAP was 0.302. Both the level of consciousness and NLR exhibited partial mediating effects in the association between neurological deficit and SAP, with mediating effect proportions of 25.92% and 15.15%, respectively.

Conclusion Consciousness level and NLR have partial mediating effects in the occurrence of SAP in patients with different neurological deficits. There is an interaction between the degree of neurological deficit and the level of FBG.