Study of Platelet Indices for Assessment of Severe Sepsis: A Hospital-Based Prospective Observational Study.

Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection and remains a leading cause of morbidity among critically ill patients worldwide. Despite advances in antimicrobial therapy and organ support, severe sepsis and septic shock. ¹⁻³ Rudd et al. estimated approximately 48.9 million sepsis cases and 11 million sepsis-related deaths globally in 2017, with a disproportionately greater burden in low- and middle-income countries.⁴

 

Sepsis is characterised by immune dysregulation, endothelial injury, coagulation activation, microvascular dysfunction, and multi-organ impairment. Cytokine-driven inflammation activates the coagulation cascade, producing platelet consumption, microthrombi, and tissue ischaemia.5,6 Consequently, haematological derangements—particularly thrombocytopenia—are common and correlate with disease severity and outcome.⁷ However, platelet count alone may not adequately reflect platelet function or the bone marrow’s thrombopoietic response.

Platelet indices generated routinely by automated haematology analysers—mean platelet volume (MPV), platelet distribution width (PDW), plateletcrit (PCT), and immature platelet fraction (IPF)—offer additional insight into platelet biology at no incremental cost. Larger, younger platelets released in response to peripheral consumption produce a rise in MPV and IPF, while heterogeneity in platelet size manifests as elevated PDW. Multiple studies have linked these parameters to sepsis severity.⁸⁻¹² Compared with composite scores such as SOFA or APACHE II, platelet indices are objective, rapidly available, and accessible even in resource-limited settings.¹³

 

Against this background, the present study was designed to evaluate platelet indices (MPV, PDW, and IPF) as markers of sepsis severity in patients admitted to a tertiary care ICU in Jaipur, India.

Study design and setting

This was a hospital-based, prospective observational study conducted in the Department of General Medicine, Mahatma Gandhi Medical College & Hospital, Jaipur, Rajasthan, from April 2024 to September 2025 (1.5 years).

 

Ethics and consent

The study was approved by the Institutional Ethics Committee. Written informed consent was obtained from each participant; in patients unable to consent due to their clinical condition, consent was obtained from a legally authorised attendant or relative.

 

Study population

Adults aged 18–65 years of either sex admitted to the ICU with sepsis fulfilling the inclusion criteria were enrolled consecutively. Exclusion criteria were trauma, pulmonary embolism, myocardial infarction, known immune thrombocytopenic purpura, platelet dysfunction disorders, coagulopathy, and non-infectious causes of a systemic inflammatory response.

 

Definitions

Sepsis was defined as Systemic Inflammatory Response Syndrome (SIRS) with a proven or suspected source of infection. SIRS required ≥2 of: temperature >38°C or <36°C; heart rate >90/min; respiratory rate >20/min or PaCO₂ <32 mmHg; total leukocyte count >12,000/mm³ or <4,000/mm³ or >10% immature forms. Severe sepsis was defined as sepsis with organ dysfunction and/or hypoperfusion abnormality.

 

Sample size

Sample size was estimated using MedCalc software (comparison of means) with α = 0.01, β = 0.10, mean difference = 2.6, standard deviation = 3 in each group, and 1:1 allocation, yielding 84 patients.

 

Investigations and data collection

All patients underwent a complete blood count with platelet indices (MPV, PDW, IPF), arterial blood gas analysis, urine routine, renal and liver function tests with total protein, prothrombin time/INR, activated partial thromboplastin time, CRP, random blood sugar, serum electrolytes, chest radiography, erythrocyte sedimentation rate, and ultrasonography of the abdomen. Treatment followed standard hospital protocol; no intervention was performed for the study. Clinical, laboratory, and outcome data were captured on a pre-designed proforma.

 

Statistical analysis

Data were analysed using SPSS version 29.0. Continuous variables are expressed as mean ± standard deviation and compared using Student’s t-test; categorical variables are expressed as frequencies (percentages) and compared using the chi-square test or Fisher’s exact test, as appropriate. A two-sided p-value <0.05 was considered statistically significant.

Eighty-four patients fulfilling the inclusion criteria were analysed. The majority (n = 51; 60.71%) had severe sepsis/septic shock and 33 (39.29%) had sepsis (Table 1). Pneumonia was the most frequent source of infection (33.3%), followed by urinary tract infection (21.4%) and intra-abdominal infection (14.2%) (Table 4).

 

Table 1. Distribution of patients according to severity of sepsis (n = 84)

 

Table 2. Age distribution among patients with sepsis and severe sepsis

 

The mean age was 62.33 ± 2.40 years in severe sepsis versus 59.52 ± 8.12 years in sepsis (p = 0.057). Most patients in both groups were aged 55–64 years (Table 2). Males predominated in both groups (63.64% in sepsis; 56.86% in severe sepsis), but gender distribution did not differ significantly (p = 0.48) (Table 3).

Table 3. Gender distribution among patients with sepsis and severe sepsis

 

Table 4. Distribution of causes of sepsis in the study population

 

Inflammatory and haematological parameters by severity

Mean CRP was significantly higher in severe sepsis than in sepsis (202.08 ± 41.32 vs 153.07 ± 41.41 mg/L; p < 0.001), while mean platelet count was significantly lower (185 ± 86 vs 263 ± 68 × 10³/µL; p < 0.001). Leukocyte and neutrophil counts did not differ significantly between groups (Table 5).

Table 5. Inflammatory and haematological parameters in sepsis vs severe sepsis

 

Platelet indices by severity

All three platelet indices were significantly higher in severe sepsis compared with sepsis: MPV (8.08 ± 0.87 vs 7.61 ± 0.85 fL; p = 0.03), PDW (18.02 ± 0.87 vs 17.61 ± 0.69%; p = 0.018), and IPF (6.17 ± 5.64 vs 4.08 ± 3.69%; p = 0.04) (Tables 6).

Table.6 Comparison of Platelet Indices According to Severity of Sepsis

 

In this prospective observational study of 84 ICU patients, platelet indices—MPV, PDW, and IPF—were significantly elevated in severe sepsis compared with sepsis. The findings support the role of these inexpensive, routinely reported parameters as adjuncts to clinical assessment in early risk stratification.

 

Prevalence and aetiology

Severe sepsis/septic shock predominated in our cohort (60.71%), likely reflecting the tertiary referral nature of the study centre, delayed presentation, and prior treatment at peripheral facilities. Comparable variability has been reported across settings: the multicentric INDICAP study from India documented severe sepsis in 28.3% of ICU admissions, whereas European studies have reported figures around 27%. 14-17 Differences likely reflect heterogeneity in setting, study design, sepsis definitions (SIRS-based vs Sepsis-3), and population characteristics.

 

Pneumonia was the leading source of infection (33.3%), followed by urinary tract and intra-abdominal infections (21.4% and 14.2%, respectively). This distribution is consistent with the INDICAP and ANZICS cohorts and with Western series, in which respiratory infection consistently ranks first.3,14 Contributing factors include the rapid systemic dissemination from extensive alveolar involvement, frequent catheterisation predisposing to urinary infection, and the prevalence of post-procedural and skin/soft-tissue infections in older comorbid patients.

 

Demographic features

The mean age was higher in severe sepsis than in sepsis (62.33 ± 2.40 vs 59.52 ± 8.12 years; p = 0.057) and most patients in both groups were 55–64 years old, but age was not a significant determinant of severity or outcome in this cohort. A male predominance was observed without statistical significance for severity (p = 0.48) or outcome (p = 0.37).

 

Mean Platelet Volume

MPV reflects platelet size, activation status, and bone marrow response. Larger platelets are metabolically and enzymatically more active and have greater prothrombotic potential. Accelerated peripheral platelet destruction in sepsis prompts release of younger, larger platelets, raising MPV. In our cohort, MPV was significantly higher in severe sepsis (8.08 ± 0.87 vs 7.61 ± 0.85 fL; p = 0.03), in keeping with Becchi et al. and Vardon-Bounes et al., who reported higher MPV values in critically ill septic patients and association with adverse outcomes.8,9

 

Platelet Distribution Width

Platelet Distribution Width (PDW) reflects the variability in platelet size and tends to increase in conditions associated with accelerated platelet turnover, where both newly released larger platelets and older senescent platelets coexist. In the present study, PDW was significantly higher among patients with severe sepsis compared to those with sepsis (18.02 ± 0.87% vs 17.61 ± 0.69%; p = 0.018). These findings are consistent with the observations of Yadav et al., who reported significantly elevated PDW values in patients with sepsis compared to healthy controls. Similarly, studies conducted by Zhang et al. and Gao et al. demonstrated that increased PDW was associated with greater severity of sepsis and could serve as a predictor of severe sepsis.15–17

 

Immature Platelet Fraction

IPF measures circulating platelets that still contain residual RNA, providing a direct estimate of bone marrow thrombopoietic activity. It is particularly useful for distinguishing decreased production from increased peripheral destruction. Inflammatory mediators including interleukin-1 can promote megakaryocyte rupture, releasing larger, immature platelets and raising IPF in sepsis.¹²

In our cohort, IPF was significantly higher in severe sepsis than in sepsis (6.17 ± 5.64 vs 4.08 ± 3.69%; p = 0.04), consistent with reports by Di Mario et al., Enz Hubert et al., De Blasi et al., and Buoro et al., who described elevated IPF in confirmed sepsis—often rising approximately 2 days before clinical onset.16-19

 

Inflammatory and standard haematological parameters

CRP was significantly higher in severe sepsis (202.08 ± 41.32 vs 153.07 ± 41.41 mg/L; p < 0.001), and platelet count significantly lower (185 ± 86 vs 263 ± 68 × 10³/µL; p < 0.001), reinforcing their role as severity markers. Leukocyte and neutrophil counts did not discriminate severity (p = 0.06 and 0.68, respectively), consistent with the known limited specificity of total leukocyte indices in critically ill patients. Lobo et al. and Póvoa et al. have shown that absolute CRP values, and particularly their trends, correlate with severity and treatment response.20,21

 

Strengths and limitations

Strengths include the prospective design, exclusion of confounders that affect platelet indices, and use of routinely available analyser-derived parameters that are translatable to most clinical laboratories. Limitations include the single-centre setting, a relatively small sample size particularly for outcome analysis , measurement at a single time point rather than serially, the use of SIRS-based definitions of sepsis severity (predating Sepsis-3 in concept), and the absence of receiver-operating-characteristic analysis to define optimal cut-offs. Multivariable adjustment for comorbidities, organ dysfunction scores, and source of infection was not performed.

Platelet indices derived from routine complete blood count analysis—MPV, PDW, and IPF—were significantly higher in patients with severe sepsis than in those with sepsis, reflecting heightened platelet activation, consumption, and bone marrow turnover with increasing systemic infection.

 

DECLARATIONS

Ethics approval and consent to participate: Approved by the Institutional Ethics Committee. Written informed consent was obtained from all participants or their legally authorised representatives.

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