Chicken-fat clots and pulmonary intravascular neutrophil density: a retrospective autopsy study

The purpose of this study was to explore the association between chicken-fat clots (CFCs) and neutrophil-related parameters in postmortem samples. Based on previous studies suggesting a potential role of neutrophils in CFC formation, the study aimed to assess whether CFCs are associated with increased neutrophil levels or intravascular neutrophil accumulation, rather than being explained solely by the traditional concept of "slow death".

A retrospective observational study was conducted using autopsy data from November 2020 to November 2024. A total of 152 autopsies were screened, of which 122 met the inclusion criteria and were included in the final cohort. Autopsy reports were reviewed together with available clinical documentation, including information on anticoagulants, vasoactive amines, corticosteroids, ongoing infections, and laboratory tests (leukocyte count, neutrophil percentage, and absolute neutrophil count). Because premortem laboratory data were frequently unavailable, particularly in traumatic deaths, lung tissue samples from all 122 decedents were analyzed. Digital pathology techniques, including scanning and analysis using QuPath software, were employed to quantify pulmonary intravascular neutrophil density. The association between intravascular neutrophil density and CFC presence was statistically analyzed using ROC curves, χ² tests, and odds ratios.

CFCs were present in 34 of 122 cases (27.9%), with septic shock representing the largest cause-of-death group among CFC-positive cases (29.4%). Increased pulmonary intravascular neutrophil density was significantly associated with CFC presence (OR 21.0, p < 0.001). A threshold of 2286 neutrophils/mm² showed good discrimination for CFC presence, with an AUC of 0.840. No significant associations were identified between CFCs and anticoagulants, antiplatelet agents, or the other evaluated blood parameters.

Chicken-fat clots were associated with increased pulmonary intravascular neutrophil density in this retrospective autopsy cohort, suggesting a possible relationship with systemic inflammatory or neutrophil-mediated processes. These findings do not establish pulmonary intravascular neutrophil density as a validated marker of antemortem neutrophilia and do not exclude the contribution of agonal duration or postmortem processes to CFC formation. Further studies incorporating well-defined agonal timing and closely timed premortem laboratory data are needed to clarify the biological and temporal determinants of CFC formation.