Pediatric sepsis remains a major cause of morbidity and mortality worldwide, particularly in low- and middle-income countries where delayed recognition, limited intensive care resources, and late referral may worsen outcomes [1]. Sepsis is a leading cause of morbidity and mortality in children globally, especially in low and middle-income countries where delayed recognition, inadequate intensive care facilities and late referral may contribute to poor outcomes [1]. Sepsis in children is now recognized as a life-threatening organ dysfunction resulting from a dysregulated host response to infection, and recent consensus criteria for children focus on organ dysfunction in the respiratory, cardiovascular, coagulation, and neurological systems, in addition to systemic inflammatory response [2]. Early recognition of children at risk of deterioration is therefore critical for timely escalation of care, appropriate antimicrobial therapy, hemodynamic support and improved survival [3]. Thrombocytopenia is a common haematological abnormality in paediatric sepsis and can be caused by platelet consumption, endothelial activation, disseminated intravascular coagulation, immune-mediated destruction, bone marrow suppression and sequestration. In addition to hemostasis, platelets are also involved in inflammation, microvascular integrity, host defense, and immunothrombosis. Thus, a decrease in platelet count in sepsis may not only indicate bleeding risk but also disease severity, organ dysfunction and adverse outcome. Several pediatric studies have shown that thrombocytopenia is associated with worse clinical outcomes. Agrawal et al. found that children with thrombocytopenia who were admitted to the pediatric intensive care unit were at a higher risk of bleeding, had a longer stay in the intensive care unit, and had a higher mortality rate [4]. But platelet count alone may not be a complete indicator of platelet activation and turnover. Other platelet indices, including mean platelet volume, platelet distribution width, plateletcrit, and platelet-large cell ratio, are available with automated hematology analyzers. These parameters are readily available, inexpensive, and are routinely produced with complete blood count testing, which makes them potentially useful markers in resource-limited clinical settings. MPV is a measure of the average platelet size and is thought to be a marker of platelet activation and increased thrombopoietic activity. Platelet distribution width is a measure of platelet size variability and can be elevated in platelet activation and in heterogeneous platelet production. Plateletcrit is a measure of total circulating platelet mass and is dependent on platelet count and platelet size. Golwala et al. showed that platelet count, plateletcrit, MPV/platelet count ratio, MPV/plateletcrit ratio, and PDW/platelet count ratio were associated with in-hospital pediatric mortality [5]. Evidence specifically in pediatric sepsis also supports the prognostic value of platelet indices. Sayed et al., in children with severe sepsis, found that non-survivors had significantly lower platelet count and plateletcrit, higher mean platelet volume, and higher platelet-index ratios than survivors; plateletcrit showed high sensitivity for prediction of death [6]. Choi et al. found that thrombocytopenia was a good predictor of mortality in pediatric septic shock, and that platelet count had good discriminatory power for survival, especially in children without underlying hemato-oncological disease [7]. Recent studies have also indicated that platelet-index ratios can give further prognostic information. MPV/platelet count and PDW/platelet count ratios were significantly higher in non-survivors and were independently associated with 28-day mortality in pediatric septic shock, as found by Celegen et al. [8]. Meliani et al. also showed that platelet count and platelet indices, especially platelet distribution width, may be useful in predicting mortality in children with sepsis [9]. These results suggest that baseline platelet indices and their serial changes can be used for risk stratification. However, data from Indian paediatric population is still scarce, particularly on the association of sepsis associated thrombocytopenia with severity and outcome. Platelet indices are simple, low cost and routinely available, and assessing their prognostic value could be useful for early identification of high-risk children. The present study was thus designed to assess the platelet indices as a predictor of severity and outcome in children with sepsis associated thrombocytopenia. OBJECTIVES 1. To assess platelet indices, including platelet count, mean platelet volume, platelet distribution width, plateletcrit, and platelet-large cell ratio, in children with sepsis-associated thrombocytopenia. 2. To correlate platelet indices with severity of sepsis, organ dysfunction, and need for intensive care support. 3. To evaluate the association of platelet indices with clinical outcomes such as duration of hospital stay, need for mechanical ventilation, vasoactive support, and mortality.

Study design and setting This prospective observational study was conducted in the Department of Pediatrics at JIET Medical College, Jodhpur, Rajasthan, over a period of one year, from March 2025 to March 2026. The study evaluated the role of platelet indices in predicting severity and clinical outcomes in children with sepsis-associated thrombocytopenia. Study population A total of 120 children with sepsis-associated thrombocytopenia were included. Children aged 1 month to 18 years admitted with clinically suspected or microbiologically confirmed sepsis and platelet count <150,000/µL were enrolled after obtaining written informed consent from parents or guardians. Patients were categorized according to clinical severity into three groups: sepsis, sepsis with organ dysfunction, and septic shock. Organ dysfunction was assessed using clinical, laboratory, and hemodynamic parameters, including the pediatric Sequential Organ Failure Assessment score. Inclusion criteria Children aged 1 month to 18 years with suspected or confirmed sepsis and thrombocytopenia, defined as platelet count <150,000/µL at admission or during hospital stay, were included. Only patients with available complete blood count-derived platelet indices and adequate clinical outcome data were enrolled. Exclusion criteria Neonates below 1 month of age were excluded. Children with pre-existing hematological disorders, leukemia, aplastic anemia, immune thrombocytopenia, congenital platelet disorders, malignancy, chronic liver disease, chronic kidney disease, autoimmune disease, or non-septic causes of thrombocytopenia such as dengue, malaria, megaloblastic anemia, drug-induced thrombocytopenia, or hypersplenism were excluded. Patients who had received platelet transfusion before the initial platelet-index assessment and those with incomplete records were also excluded. Data collection Baseline demographic and clinical details were recorded, including age, sex, infection focus, culture positivity, organ dysfunction count, pediatric Sequential Organ Failure Assessment score, serum lactate, and procalcitonin. The primary focus of infection was classified as pneumonia or lower respiratory tract infection, bloodstream infection, gastrointestinal or intra-abdominal infection, meningitis or central nervous system infection, skin and soft tissue infection, urinary tract infection, or undifferentiated/unknown focus. Platelet indices assessment Complete blood count was performed using an automated hematology analyzer. Platelet parameters recorded included initial platelet count, platelet nadir, 72-hour platelet count, mean platelet volume, platelet distribution width, plateletcrit, and platelet-large cell ratio. Platelet nadir was defined as the lowest platelet count recorded during hospitalization. Thrombocytopenia severity was categorized according to platelet count as mild thrombocytopenia: 100,000–149,999/µL, moderate thrombocytopenia: 50,000–99,999/µL, and severe thrombocytopenia: <50,000/µL. Outcome measures The primary outcome was the association of platelet indices with sepsis severity. Secondary outcomes included association of platelet indices and thrombocytopenia severity with pediatric Sequential Organ Failure Assessment score, organ dysfunction count, PICU admission, need for mechanical ventilation, vasoactive support, platelet transfusion after assessment, duration of PICU stay, duration of hospital stay, and mortality. Statistical analysis Data were analyzed using appropriate statistical software. Continuous variables were expressed as median with interquartile range, and categorical variables as frequency and percentage. Comparisons across sepsis severity categories and thrombocytopenia severity groups were performed using the Kruskal–Wallis H test for continuous variables and the chi-square test for categorical variables. Correlations between platelet indices and severity or hospital-course variables were assessed using Spearman correlation coefficient. A p-value <0.05 was considered statistically significant. Ethical considerations The study was conducted after approval from the Institutional Ethics Committee of JIET Medical College, Jodhpur. Written informed consent was obtained from parents or legal guardians before enrolment. Patient confidentiality was maintained throughout the study.

Study cohort and baseline clinical profile A total of 120 children with sepsis-associated thrombocytopenia were included. The cohort comprised 38 (31.7%) children with sepsis, 55 (45.8%) with sepsis with organ dysfunction, and 27 (22.5%) with septic shock. Baseline characteristics are summarized in Table 1. Clinical severity markers showed the expected stepwise increase across severity categories, whereas age, sex distribution, and culture-confirmed sepsis were broadly comparable across groups. Table 1. Baseline clinical characteristics according to sepsis severity Characteristic Overall N=120 Sepsis n=38 Sepsis with organ dysfunction n=55 Septic shock n=27 Test statistic p-value Age, years, median (IQR) 3.8 (0.9-8.4) 4.0 (0.8-8.9) 3.9 (1.1-7.6) 2.8 (0.9-7.0) H=0.32 0.852 Male sex, n (%) 63 (52.5%) 21 (55.3%) 28 (50.9%) 14 (51.9%) χ²=0.18 0.915 Culture-confirmed sepsis, n (%) 66 (55.0%) 23 (60.5%) 32 (58.2%) 11 (40.7%) χ²=2.91 0.233 Primary infection focus, n (%) χ²=20.81 0.053 Pneumonia/Lower respiratory infection 42 (35.0%) 8 (21.1%) 22 (40.0%) 12 (44.4%) — — Bloodstream infection 18 (15.0%) 2 (5.3%) 12 (21.8%) 4 (14.8%) — — Gastrointestinal/intra-abdominal infection 25 (20.8%) 12 (31.6%) 10 (18.2%) 3 (11.1%) — — Meningitis/CNS infection 12 (10.0%) 3 (7.9%) 5 (9.1%) 4 (14.8%) — — Skin/soft tissue infection 9 (7.5%) 5 (13.2%) 3 (5.5%) 1 (3.7%) — — Urinary tract infection 6 (5.0%) 4 (10.5%) 0 (0.0%) 2 (7.4%) — — Undifferentiated/unknown focus 8 (6.7%) 4 (10.5%) 3 (5.5%) 1 (3.7%) — — Organ dysfunction count, median (IQR) 2 (1-3) 1 (1-1) 2 (2-3) 3 (3-4) H=79.63 <0.001 pSOFA score, median (IQR) 7 (5-10) 4 (3-5) 8 (6-9) 13 (11-14) H=85.18 <0.001 Lactate, mmol/L, median (IQR) 3.3 (2.2-4.3) 1.7 (1.3-2.4) 3.4 (2.8-4.1) 5.4 (4.6-6.2) H=75.92 <0.001 Procalcitonin, ng/mL, median (IQR) 4.8 (2.7-7.4) 2.5 (1.3-3.6) 5.3 (3.4-7.3) 7.6 (5.2-17.2) H=36.35 <0.001 Values are presented as median (IQR) or n (%). Kruskal-Wallis H test was used for continuous variables and chi-square test for categorical variables. Platelet indices and sepsis severity Platelet indices demonstrated a clear severity gradient (Table 2). Initial platelet count, platelet nadir, 72-hour platelet count, and plateletcrit decreased with increasing sepsis severity, while MPV, PDW, and P-LCR increased. The distribution of initial platelet count across sepsis severity categories is shown in Figure 1. Table 2. Platelet indices according to sepsis severity Characteristic Overall N=120 Sepsis n=38 Sepsis with organ dysfunction n=55 Septic shock n=27 Test statistic p-value Initial platelet count, /µL, median (IQR) 79000 (57000-117250) 105500 (73250-122750) 87000 (62500-119500) 50000 (38000-77000) H=22.23 <0.001 Platelet nadir, /µL, median (IQR) 64000 (41000-105250) 88000 (59250-110250) 66000 (45000-106000) 26000 (16000-45500) H=31.07 <0.001 72-hour platelet count, /µL, median (IQR) 98500 (64500-132250) 115500 (87500-143250) 108000 (73500-131500) 52000 (27500-71500) H=31.85 <0.001 MPV, fL, median (IQR) 10.0 (9.4-10.7) 9.5 (9.0-10.1) 10.0 (9.4-10.4) 10.7 (10.5-11.1) H=33.09 <0.001 PDW, %, median (IQR) 15.4 (14.5-16.4) 14.7 (14.0-15.9) 15.2 (14.5-16.2) 16.5 (15.8-17.4) H=20.78 <0.001 Plateletcrit, %, median (IQR) 0.081 (0.058-0.111) 0.096 (0.075-0.117) 0.088 (0.059-0.111) 0.052 (0.039-0.080) H=19.11 <0.001 P-LCR, %, median (IQR) 30.0 (24.5-34.2) 26.1 (22.8-29.8) 30.4 (24.6-33.6) 34.8 (31.6-38.0) H=27.18 <0.001 Thrombocytopenia severity, n (%) χ²=25.61 <0.001 Mild 46 (38.3%) 20 (52.6%) 24 (43.6%) 2 (7.4%) — — Moderate 53 (44.2%) 17 (44.7%) 23 (41.8%) 13 (48.1%) — — Severe 21 (17.5%) 1 (2.6%) 8 (14.5%) 12 (44.4%) — — Values are presented as median (IQR) or n (%). P-LCR, platelet-large cell ratio; MPV, mean platelet volume; PDW, platelet distribution width. Figure 1. Initial platelet count according to sepsis severity. Box-and-point plot showing lower initial platelet counts with increasing sepsis severity. Correlation of platelet indices with organ dysfunction and hospital course Correlation analyses are presented in Table 3. Lower platelet count, lower plateletcrit, and lower platelet nadir were associated with higher pSOFA scores, greater organ dysfunction, and longer PICU and hospital stay. Conversely, higher MPV, PDW, and P-LCR were positively correlated with clinical severity, with the strongest associations observed for pSOFA score and PICU stay. Table 3. Correlation of platelet indices with severity and hospital-course variables Platelet index pSOFA score Organ dysfunction count PICU stay Hospital stay Initial platelet count ρ=-0.359; t=-4.18; p=<0.001 ρ=-0.286; t=-3.24; p=0.002 ρ=-0.254; t=-2.86; p=0.005 ρ=-0.248; t=-2.78; p=0.006 MPV ρ=0.476; t=5.88; p=<0.001 ρ=0.432; t=5.20; p=<0.001 ρ=0.340; t=3.93; p=<0.001 ρ=0.195; t=2.16; p=0.033 PDW ρ=0.363; t=4.23; p=<0.001 ρ=0.293; t=3.33; p=0.001 ρ=0.292; t=3.31; p=0.001 ρ=0.173; t=1.91; p=0.059 Plateletcrit ρ=-0.345; t=-3.99; p=<0.001 ρ=-0.258; t=-2.90; p=0.005 ρ=-0.236; t=-2.64; p=0.009 ρ=-0.242; t=-2.71; p=0.008 P-LCR ρ=0.525; t=6.71; p=<0.001 ρ=0.444; t=5.39; p=<0.001 ρ=0.395; t=4.67; p=<0.001 ρ=0.128; t=1.40; p=0.165 Platelet nadir ρ=-0.436; t=-5.26; p=<0.001 ρ=-0.364; t=-4.25; p=<0.001 ρ=-0.280; t=-3.16; p=0.002 ρ=-0.262; t=-2.94; p=0.004 Each cell shows Spearman correlation coefficient, approximate t statistic, and p-value. Clinical outcomes according to thrombocytopenia severity Clinical outcomes according to thrombocytopenia severity are summarized in Table 4 and illustrated in Figure 2. Increasing thrombocytopenia severity was associated with greater need for PICU admission, vasoactive support, platelet transfusion, and mortality. Severe thrombocytopenia was also associated with longer PICU and hospital stay. Table 4. Clinical outcomes according to thrombocytopenia severity Outcome Overall N=120 Mild n=46 Moderate n=53 Severe n=21 Test statistic p-value PICU admission, n (%) 86 (71.7%) 25 (54.3%) 43 (81.1%) 18 (85.7%) χ²=11.17 0.004 Mechanical ventilation, n (%) 31 (25.8%) 6 (13.0%) 18 (34.0%) 7 (33.3%) χ²=6.37 0.041 Vasoactive support, n (%) 38 (31.7%) 6 (13.0%) 20 (37.7%) 12 (57.1%) χ²=14.57 <0.001 Platelet transfusion after assessment, n (%) 35 (29.2%) 8 (17.4%) 13 (24.5%) 14 (66.7%) χ²=17.93 <0.001 Mortality, n (%) 27 (22.5%) 6 (13.0%) 12 (22.6%) 9 (42.9%) χ²=7.35 0.025 PICU stay, days, median (IQR) 3 (0-6) 1 (0-4) 3 (1-6) 5 (3-7) H=10.34 0.006 Hospital stay, days, median (IQR) 11 (8-15) 11 (7-13) 11 (8-16) 13 (10-17) H=8.36 0.015 pSOFA score, median (IQR) 7 (5-10) 6 (4-7) 8 (5-11) 10 (8-13) H=19.40 <0.001 Values are presented as median (IQR) or n (%). Kruskal-Wallis H test was used for continuous variables and chi-square test for categorical variables. Figure 2. Clinical outcomes according to thrombocytopenia severity. Grouped bar chart showing the proportion of children requiring mechanical ventilation, vasoactive support, and mortality across thrombocytopenia severity categories.

In the current study, platelet indices were found to be well correlated with severity and outcome in paediatric sepsis associated thrombocytopenia. Septic shock was present in 22.5% of 120 children and was correlated with higher pSOFA score, higher organ dysfunction count, higher lactate and higher procalcitonin. Platelet parameters varied gradually according to the severity of the disease: initial platelet count, platelet nadir, platelet count at 72 hours, plateletcrit decreased, while MPV, PDW, and P-LCR increased from sepsis to septic shock. Severe thrombocytopenia was clinically associated with increased PICU admission, vasoactive support, platelet transfusion, PICU and hospital length of stay, increased pSOFA score and mortality. The severity gradient seen in our cohort is similar to that seen in the pediatric sepsis literature, where markers of organ dysfunction and laboratory abnormalities are strongly associated with poor outcomes. In a systematic review and meta-analysis, the Pediatric Sepsis Definition Taskforce analyzed 106 studies, 81 of which were included in the meta-analysis, and found that platelet count, lactate, procalcitonin, organ dysfunction, PELOD score, PIM-3, and PRISM score were significantly and consistently associated with mortality in children with sepsis, severe sepsis, or septic shock [10]. This is in line with the current finding that platelet indices were not isolated hematological abnormalities but paralleled pSOFA score, organ dysfunction count, lactate and procalcitonin. The correlation between decreasing platelet count and poor outcome in our study is similar to that of Sriram et al., who prospectively studied 151 children with sepsis in South India. They found that 67.5% of children had thrombocytopenia, 27.8% died, there was a significant difference in platelet count between survivors and nonsurvivors, there was a significant difference in plateletcrit between survivors and nonsurvivors, and there was a significant association between the severity of the thrombocytopenia before discharge and outcome [11]. In our study, platelet count similarly decreased with increasing severity, with septic shock patients having the lowest initial platelet count, platelet nadir, and 72-hour platelet count. Mortality also increased with increasing severity of thrombocytopenia, from 13.0% in mild thrombocytopenia to 42.9% in severe thrombocytopenia, further supporting the prognostic significance of platelet depletion. Lu et al. further support the importance of severe thrombocytopenia and platelet recovery by analyzing 4,848 critically ill children in a pediatric intensive care database. Early severe thrombocytopenia was an independent risk factor for in-hospital mortality, and short-term platelet recovery to ≥150 ×10⁹/L was protective, with OR 0.301, 95% CI 0.139–0.648, p=0.002 [12]. We also included dynamic platelet behaviour in our study, as platelet nadir and 72-hour platelet count. The septic shock group had a significantly lower nadir platelet count and poor recovery at 72 hours compared with less severe categories, indicating that persistent thrombocytopenia may be a marker of continued platelet consumption, endothelial damage, and unresolved organ dysfunction. Our results are also consistent with those of Zhang et al., who investigated septic shock in children and found that thrombocytopenia within 24 hours of septic shock onset was linked to higher 28-day mortality, fewer ventilation-free days, fewer PICU-free days, more bleeding events, more blood product transfusion, and more organ dysfunction [13]. This is similar to our findings, which showed that severe thrombocytopenia was linked to increased requirement for mechanical ventilation, vasoactive support, platelet transfusion, PICU length of stay and pSOFA score. In our study, MPV levels were found to be increasing gradually from sepsis to septic shock and were positively correlated with pSOFA score, organ dysfunction count, PICU stay, and hospital stay among platelet activation markers, whereas MPV was negatively correlated with platelet count. İşgüder et al. investigated 186 septic children and found that nonsurvivors had significantly higher admission MPV, 72-hour MPV, and change in MPV, and lower platelet counts. Logistic regression showed that admission MPV, 72-hour MPV, ΔMPV, platelet count and mechanical ventilation were significant factors associated with 28-day mortality, with ROC cutoffs of 9 fL for admission MPV and 9.86 fL for 72-hour MPV [14]. The median MPV in the present cohort was 9.5 fL in sepsis and 10.7 fL in septic shock, which is consistent with MPV as a marker of platelet activation and severe inflammatory stress. PDW and P-LCR also increased with disease severity in our study. Yanni and Saragih assessed platelet profile in 83 critically ill children, of which 51.8% were diagnosed with sepsis, and found that platelet count on day 1 and PDW on day 3 were significant factors associated with mortality. They also found that the change in MPV from day 1 to day 3 was correlated with the change in PELOD-2 score, but the individual platelet indices did not consistently correlate with PELOD-2 at each time point [15]. Our findings confirm this association in a septic thrombocytopenic population, with PDW and P-LCR being positively associated with pSOFA score and organ dysfunction count, respectively, and P-LCR being the most strongly associated platelet index with pSOFA. The biological pattern seen in our pediatric cohort is also supported by the adult septic shock literature. Gao et al. studied 124 patients with septic shock and found that nonsurvivors had higher MPV, increasing trends in PDW and P-LCR, and decreasing trends in platelet count and plateletcrit. MPV was the most powerful platelet index with AUC 0.81 and a cutoff of 10.5 fL for mortality prediction [16]. While data for adults cannot be directly extrapolated to children, the direction of change is very similar to the present study, which showed that septic shock was associated with decreased platelet count and plateletcrit and increased MPV, PDW, and P-LCR. Serial MPV behaviour has also been demonstrated to have prognostic significance. Kim et al. prospectively studied 345 patients with severe sepsis or septic shock and found 28-day mortality of 10.1%. MPV increased over the first 72 hours in both survivors and nonsurvivors, but the rate of increase was significantly higher in non survivors. ΔMPV from admission to 72 hours independently predicted 28-day mortality with hazard ratio 1.44, 95% CI 1.01–2.06, p=0.044 [17]. In our study, platelet count at 72 hours and platelet nadir were highly correlated with severity, and MPV was positively correlated with pSOFA and PICU stay. These results indicate that serial platelet evaluation may be more useful than a single platelet count. Vélez-Páez et al. also highlighted the role of platelet indices and platelet-index ratios in the severity of sepsis. MPV and MPV-to-platelet ratio on the first 3 days of septic ICU predicted clinical severity and 28-day mortality in a prospective cohort of 163 septic ICU patients. MPV cutoffs on days 1, 2, and 3 were >9.45 fL, >8.95 fL, and >8.85 fL, respectively, and MPV/P independently predicted mortality with hazard ratios up to 4.43 [18]. Our study did not calculate MPV/platelet count ratios or ROC cutoffs, but our correlation results suggest the same idea: higher platelet size indices and lower platelet mass are associated with more severe sepsis physiology in children. The clinical outcome trends in our study are also similar to the Indian paediatric sepsis data. Kaur et al. conducted a study on 50 children with sepsis, severe sepsis and septic shock in Rohtak, Haryana and found high mortality rate of 58% in tertiary PICU. Their cohort had a median age of 18 months and looked at mortality in relation to age, PICU stay, transfer delay, PRISM score, and organ dysfunction, but none of these factors alone predicted mortality [19]. By contrast, our mortality rate was 22.5%, but adverse outcomes were clearly related to the severity of the thrombocytopenia. This discrepancy could be due to variations in case mix, definitions, treatment era, and the fact that only thrombocytopenic septic children were included in the current study. The current results have implications for practice. Platelet indices are inexpensive, readily available, and routinely ordered as part of a complete blood count. In environments where more sophisticated biomarkers are not readily available, a trend of decreasing platelet count and plateletcrit, and increasing MPV, PDW, and P-LCR may be useful for identifying children at risk for organ dysfunction, PICU admission, vasoactive support, transfusion, prolonged hospitalization, and death. Importantly, there was no significant difference in culture positivity between severity groups in our cohort, indicating that platelet indices may reflect the severity of the host response even in the absence of microbiological confirmation. There are some limitations to this study. This was an observational study with 120 children in a single centre. Platelet indices can be different depending on the type of analyzer, anticoagulant used, and time from sampling to processing. The study was based on associations and not causality, and ROC-derived cutoffs for individual platelet indices were not calculated. Furthermore, platelet transfusion following assessment may have affected subsequent platelet trajectories. The study has important clinical implications, as platelet indices are associated with the severity of sepsis and with important outcomes in pediatric sepsis-associated thrombocytopenia despite these limitations.

Platelet indices showed a significant association with sepsis severity and clinical outcomes in children with sepsis-associated thrombocytopenia. Lower platelet count, platelet nadir, 72-hour platelet count, and plateletcrit, along with higher MPV, PDW, and P-LCR, were associated with greater organ dysfunction, higher pSOFA score, longer PICU stay, and adverse outcomes. Severe thrombocytopenia was linked to increased need for PICU admission, mechanical ventilation, vasoactive support, platelet transfusion, and mortality. These routinely available platelet parameters may serve as simple and useful adjunctive markers for early risk stratification in pediatric sepsis.

1. Fleischmann-Struzek C, Goldfarb DM, Schlattmann P, Schlapbach LJ, Reinhart K, Kissoon N. The global burden of paediatric and neonatal sepsis: a systematic review. Lancet Respir Med. 2018;6(3):223–230. doi: 10.1016/S2213-2600(18)30063-8 2. Schlapbach LJ, Watson RS, Sorce LR, Argent AC, Menon K, Hall MW, et al. International consensus criteria for pediatric sepsis and septic shock. JAMA. 2024;331(8):665–674. doi: 10.1001/jama.2024.0179 3. Weiss SL, Peters MJ, Alhazzani W, Agus MSD, Flori HR, Inwald DP, et al. Surviving Sepsis Campaign international guidelines for the management of septic shock and sepsis-associated organ dysfunction in children. Pediatr Crit Care Med. 2020;21(2):e52–e106. doi: 10.1097/PCC.0000000000002198 4. Agrawal S, Sachdev A, Gupta D, Chugh K. Platelet counts and outcome in the pediatric intensive care unit. Indian J Crit Care Med. 2008;12(3):102–108. doi: 10.4103/0972-5229.43678 5. Golwala ZM, Shah H, Gupta N, Sreenivas V, Puliyel JM. Mean platelet volume, platelet distribution width, platelet count and plateletcrit as predictors of in-hospital paediatric mortality: a case-control study. Afr Health Sci. 2016;16(2):356–362. doi: 10.4314/ahs.v16i2.3 6. Sayed SZ, Mahmoud MM, Moness HM, Mousa SO. Admission platelet count and indices as predictors of outcome in children with severe sepsis: a prospective hospital-based study. BMC Pediatr. 2020;20:387. doi: 10.1186/s12887-020-02278-4 7. Choi SJ, Ha EJ, Jhang WK, Park SJ. Platelet indices as predictive markers of prognosis in pediatric septic shock patients. Iran J Pediatr. 2017;27(3):e7212. doi: 10.5812/ijp.7212 8. Celegen M, Kesici S, Yavuz S, Celegen K, Bayrakci B. Are platelet indices promising ratios for predicting pediatric septic shock prognosis? Bratisl Lek Listy. 2022;123(6):444-448. doi: 10.4149/BLL_2022_069. 9. Meliani M, Siregar J, Lubis IND. The use of platelet count and indices as prognostic factors for mortality in children with sepsis. Iran J Med Sci. 2024;49(8):494–500. doi: 10.30476/IJMS.2023.99084.3113 10. Menon K, Schlapbach LJ, Akech S, Argent A, Biban P, Carrol ED, et al. Criteria for pediatric sepsis—a systematic review and meta-analysis by the Pediatric Sepsis Definition Taskforce. Crit Care Med. 2022;50(1):21–36. doi: 10.1097/CCM.0000000000005294 11. Sriram SM, Aroor S, Kini PG, Kanaparthi S, Konda KC. Platelet indices in children with sepsis and their relation to the outcome. Sri Lanka J Child Health. 2018;47(4):301–305. doi: 10.4038/sljch.v47i4.8589 12. Lu Y, Ren C, Guo H, Chen Y, Chen R, Wang Y, et al. Association of early severe thrombocytopenia and platelet course with in-hospital mortality in critically ill children. Front Pediatr. 2022;10:922674. doi: 10.3389/fped.2022.922674 13. Zhang R, Huang H, Lu S, Chen J, Pi D, Dang H, et al. Relationship between thrombocytopenia and prognosis in children with septic shock: a retrospective cohort study. Platelets. 2024;35:2363242. doi: 10.1080/09537104.2024.2363242 14. İşgüder R, Ceylan G, Ağın H, Nacaroğlu HT, Korkmaz HA, Devrim İ, et al. Increased mean platelet volume in children with sepsis as a predictor of mortality. Turk J Pediatr. 2016;58(5):503–511. doi: 10.24953/turkjped.2016.05.007 15. Yanni GN, Saragih RAC. Platelet profile as prognostic factor in critically ill children. Open Access Maced J Med Sci. 2020;8(B):966–968. doi: 10.3889/oamjms.2020.4448 16. Gao Y, Li Y, Yu X, Guo S, Ji X, Sun T, et al. The impact of various platelet indices as prognostic markers of septic shock. PLoS One. 2014;9(8):e103761. doi: 10.1371/journal.pone.0103761 17. Kim CH, Kim SJ, Lee MJ, Kwon YE, Kim YL, Park KS, et al. An increase in mean platelet volume from baseline is associated with mortality in patients with severe sepsis or septic shock. PLoS One. 2015;10(3):e0119437. doi: 10.1371/journal.pone.0119437 18. Vélez-Páez JL, Legua P, Vélez-Páez P, Irigoyen E, Andrade H, Jara A, et al. Mean platelet volume and mean platelet volume to platelet count ratio as predictors of severity and mortality in sepsis. PLoS One. 2022;17(1):e0262356. doi: 10.1371/journal.pone.0262356 19. Kaur G, Vinayak N, Mittal K, Kaushik JS, Aamir M. Clinical outcome and predictors of mortality in children with sepsis, severe sepsis, and septic shock from Rohtak, Haryana: a prospective observational study. Indian J Crit Care Med. 2014;18(7):437–441. doi: 10.4103/0972-5229.136072]