Background
Bacteraemia in neonates is a major cause of morbidity and mortality.1
Despite advancements in medicine, the rapid and precise identification of neonatal sepsis through clinical evaluation and laboratory investigations still poses a significant challenge. It is imperative to detect bacteraemia and sepsis as early as possible, as delayed diagnosis and/or late commencement of antibiotic therapy can cause severe complications, including multisystem failure and death. The clinical manifestations of neonatal infections are often indistinct and could mimic various newborn conditions. Clinical signs such as apathy, compromised perfusion, respiratory distress and haemodynamic instability increase the suspicion of sepsis. The recent advances in technological utilities that facilitate the identification of sepsis-related genes, mRNA, proteins and metabolites in biological samples (such as integration of AI software and OMIC technology), are being considered tools for early sepsis detection, however, these utilities are still under investigation.2
Systemic inflammatory responses can be triggered by blood infections leading to multiorgan failure affecting, among others, the brain, lungs, kidneys and haematopoietic system. Haematological abnormalities such as leucocytosis, leucopenia and thrombocytopaenia are common during infections and serve as indicators of disease severity. Another established marker is the elevation of C reactive protein (CRP) levels, usually observed from around the second day of infection.3
Neonatal sepsis is broadly categorised into early sepsis, caused by organisms acquired perinatally, and late-onset sepsis (LOS), which appears after three calendar days from birth in hospitalised neonates (defined by ‘Identifying Healthcare Associated Infection, January 2024), usually, due to postnatal hospital-acquired organisms.4 While early sepsis incidence has declined due to antibiotic administration during childbirth, late sepsis episodes have risen. Preterm neonates or those with low birth weight are 3–10 times more susceptible to sepsis than full-term, normal-weight infants.5 6
Thrombocytopaenia in neonates, defined as platelet counts below 150 x10ˆ9/L, is frequently perceived as an indicator of severity during sepsis.7 This finding is often concurrent with early infection signs and might worsen rapidly, with the platelet count nadir typically noted between 24 and 48 hours.8
The half-life of platelets in the blood circulation is 7–10 days. Newly released platelets are comparatively large relative to ‘older’ platelets. The average size and maturity of circulating platelets are expressed as mean platelet volume (MPV), which is calculated as the plateletcrit divided by the total platelet count (TPC) and is part of a complete blood count (CBC).9–12 The average volume of the platelets in the blood circulation is between 7 and 9 fL.13 A high MPV value indicates an increased production of platelets by the bone marrow to compensate for destroyed platelets. Platelet volume in the blood offers a more comprehensive picture of platelet functionality when compared with platelet count.
There are several studies that have demonstrated the use of a high MPV as a predictor of mortality in early sepsis.14–18 There is one case–control study that suggests a relationship between MPV and LOS in preterm infants.19
Our study aims to evaluate the association between MPV and LOS in preterm infants.