The Nonlinear Relationship Between Temperature and Prognosis in Sepsis-induced Coagulopathy Patients: A Retrospective Cohort Study from MIMIC-IV Database

TL;DR

This study found that a body temperature of 37.0–38.0°C is linked to lower mortality in sepsis-induced coagulopathy patients compared to normal temperature.

Contribution

The study reveals a nonlinear relationship between body temperature and mortality in sepsis-induced coagulopathy patients.

Findings

A body temperature of 37.0–38.0°C was associated with significantly lower 28-day mortality.

Hypothermia (≤36.0°C) correlated with higher mortality compared to the normal temperature group.

The temperature-mortality relationship was nonlinear, with no significant increase in mortality risk above 38.0°C.

Abstract

The prognostic value of body temperature in sepsis-induced coagulopathy (SIC) remains unclear. In this study we aimed to investigate the association between temperature and mortality among SIC patients.

We analyzed data for 9,860 SIC patients from an intensive care database. Patients were categorized by maximum temperature in the first 24 hours into the following: ≤36.0°C; 36.0–37.0°C; 37.0–38.0°C; 38.0–39.0°C; and ≥39.0°C. The primary outcome was 28-day mortality. We used multivariate regression to analyze the temperature-mortality association.

The 37.0–38.0°C, 38.0–39.0°C and ≥39.0°C groups correlated with lower 28-day mortality (adjusted HR 0.70, 0.76 and 0.72, respectively), while the <36.0°C group correlated with higher mortality compared to the 36.0–37.0°C group (adjusted HR 2.60). A nonlinear relationship was observed between temperature and mortality. Subgroup analysis found no effect modification except in cerebrovascular disease.

A body temperature in the range of 37.0–38.0°C was associated with a significantly lower mortality compared to the normal temperature (36.0–37.0°C) group. Additionally, a gradual but statistically insignificant increase in mortality risk was observed when body temperature exceeded 38.0°C. Further research should validate these findings and elucidate involved mechanisms, especially in cerebrovascular disease subgroups.

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