Early Platelet Counts Distinguish Viral and Bacterial Pulmonary Sepsis

Abstract

Rationale: Respiratory viruses are commonly detected pathogens in pulmonary sepsis. Prior studies have demonstrated that patients with respiratory viral infections may have transient lymphocytopenia and thrombocytopenia. Leukocyte parameters including lymphocyte to monocyte ratio (LMR) and neutrophil to lymphocyte ratio (NLR) have been reported as screening tools for viral infections. Platelet counts and dynamics have been described as quantitative traits for ARDS risk and mortality. Therefore, we hypothesized that early hematologic parameters including lymphocyte count, monocyte count, platelet count, NLR, and LMR may distinguish viral from bacterial pulmonary sepsis. Methods: We enrolled 1,158 critically ill patients with pulmonary sepsis from 2009 to 2020 and measured lymphocyte count, monocyte count, platelet count, NLR, and LMR on ICU admission and at 24-hrs. Respiratory viruses were detected via PCR panel on nasopharyngeal swabs. Pulmonary sepsis was adjudicated by a physician panel. APACHE III scores were collected during the first 24-hrs. Shock was assessed by vasopressor use or mean arterial pressure <65mmHg despite 30cc/kg fluid resuscitation. ARDS was defined per Berlin criteria. We assessed mortality at 30 days. We used multivariable linear regression to test the association between each of the laboratory studies and a positive respiratory pathogen panel (RVP) adjusting for APACHE III score, age, sex, malignancy, and race. We used multivariable logistic regression to assess for associations between a positive RVP and outcomes. Results: The incidence of respiratory virus detection was 33.9%. The incidence of ARDS and mortality were 52.7% and 49.0%, respectively. The most commonly detected pathogens were SARS-CoV-2 and rhinovirus (Table 1). Lower platelet counts at 24-hrs were significantly associated with respiratory virus detection (β-41.59 × 109/L [95%CI-79.03,-4.15], p=0.03), whereas admission platelet counts were not significantly associated (β-22.38 × 109/L [95%CI-63.26, 20.49], p=0.32). The significant association at 24-hrs was also present on sensitivity analyses excluding patients with SARS-CoV-2. There were no statistically significant differences between the populations with respect to lymphocyte count, monocyte count, NLR, LMR, ARDS, shock, and mortality. Conclusion: Lower early platelet counts were identified in patients with viral pulmonary sepsis. Although LMR and NLR have been reported as screening tools for viral infections in non-critically ill populations, we did not detect significant associations between lymphocyte count, monocyte count, NLR or LMR and viral detection in pulmonary sepsis. Our findings suggest that platelet counts in combination with other validated parameters may warrant further investigation for the early discrimination of viral versus bacterial pulmonary sepsis.