Thrombocytopenia is a frequent hematological abnormality during the neonatal period, particularly in neonates hospitalized in neonatal intensive care units (NICUs) and premature infants. It occurs in 30% of neonates hospitalized in intensive care units [1], in 0.8% to 4% of healthy full-term neonates [2], in 22% of premature or sick infants [3], and in around 0.2% to 4.5% of fetuses [4]. It is defined by a drop in the number of blood platelets below 150,000/mm3. Its prevalence is still poorly known worldwide, due to its polymorphism in etiology. The causes of thrombocytopenia in the intensive care unit are often multifactorial, both central due to a production defect, and peripheral due to destruction and/or increased sequestration of platelets in the circulating blood. Peripheral etiology appears to be involved in over 50% of cases, while 10% of isolated cases are at least of central origin. It may be secondary to infection, inflammation, or consumption coagulopathy [5].  A study reports that 20% - 50% of severely ill neonates develop thrombocytopenia, with 5% - 10% having a platelet count of less than 50,000/mm3.

In children with more than 20% body surface burns, 82% of them undergo thrombocytopenia during the first week, and 18% was experience it afterward, the main etiology being sepsis [6]. According to the World Health Organization (WHO), infections are the leading cause of infant mortality worldwide.

Thrombocytopenia, defined as a platelet count below 150_109/L, is a frequent problem in neonatal intensive care units, complicating the clinical course in 22±35% of intensive care admissions[7]. Recently, there has been wide interest in thrombocytopenia and especially the correlation between platelet count and clinically significant bleeding. This correlation appears to be less clear than initially assumed, while platelet counts are still universally used in transfusion guidelines. Factors other than platelet count seem to be more important determinants of the bleeding risk in neonates, warranting more research in the field of thrombocytopenia[8].

One of the major cause of thrombocytopenia in neonates is sepsis and thrombocytopenia may rapidly become very severe with the lowest platelet count reached within 24±48 hours after onset of infection.

The study was be conducted in Neonatal Intensive Care Unit of Paediatric Department and Obstetrics and Gynaecology Department of Amaltas Institute of Medical sciences. All neonates admitted in NICU of AIMS, Dewas with features of probable sepsis or with sepsis screen positive.

All babies who fulfil the criteria and admit in NICU of AIMS, DEWAS was be enrolled into the study. An informed consent was be obtained from the mother or any other caretaker (if mother unable to give consent for any reason). Parents were informed that blood sample was taken for complete blood count and culture. Mother’s details regarding illness before and during pregnancy were obtained from OG records. Risk factors for sepsis were also noted from mother's case sheet. It is recommended to take two different samples, preferably from two different regions. Minimum amount of blood required for blood culture should be 0.5-1 ml(1 mL is ideal; there is a 10% to 40% decrease in detection rated by taking only 0.5 mL). It is recommended to take two different samples, preferably from two different regions.

Inclusion Criteria:

All neonates aged 0 to 28 days admitted in NICU (Paediatric department) with risk factors of sepsis or clinical features of sepsis as described in introduction was be included in the study and with screening positive sepsis.

Exclusion Criteria:

Mother with history suggestive of (s/o) ITP, SLE other autoimmune disorders, on medication during pregnancy (Sulfonamides, Quinine/ Quinidine) (Thiazides, Tolbutamide, Vancomycin, Hydralazine and Heparin) Neonate with history s/o bleeding disorder in family, trisomies, Turner /Noonan’s syndromes. Severe Hemolytic disease of newborn (marked erythropoiesis is in bone marrow → Neutropenia and thrombocytopenia) massive bleed from causes like birth trauma, transfusion (dilutional NNT). Sick neonate with RVT, CHD, Congenital leukemia. Neonate who had received IV antibiotics for ≥ 48 h prior to our study.

Table No. 1: Age Group

The chi-square statistic is 9.9792. The p-value is .001583. The result is significant at p < .05.

Table No. 2: Thrombocytopenia

In this study, 150 had thrombocytopenia, of which (20%) had mild (platelets: 101-150 cells/L), (26%) had moderate (platelets: 50-100 cells/L), and (21%) had severe thrombocytopenia (platelets: >50 cells/L). The chi-square statistic is 0.4718. The p-value is .049163. The result is significant at p < .05.

Table No. 3: Neonatal thrombocytopenia according to onset (hours)

The table categorizes thrombocytopenia onset into three groups. The vast majority of individuals (82%) have normal platelet counts. A small proportion (7%) experiences early onset thrombocytopenia, while 11% have a delayed onset after 72 hours. This suggests that thrombocytopenia is relatively uncommon in this group, with the majority having normal platelet counts, but it also indicates some cases of delayed onset, which may warrant further investigation into underlying causes. The chi-square statistic is 22.1822. The p-value is < .00001. The result is significant at p < .05.

Table No. 4: Mean Haematological and infective markers of the neonates admitted to the NICU

This data shows a variety of hematological parameters with some exhibiting more variability (e.g., WBC count, CRP) and others being more consistent (e.g., platelet count). The mean values reflect typical blood profile characteristics, but the standard deviations highlight the range and variation in these measures within the sample group. The chi-square statistic is 12.6456. The p-value is .001795. The result is significant at p < .05.

Thrombocytopenia is a common complication of neonatal sepsis and is one of the most prognostic independent causes of sepsis-related death. Every year, over 1.6 million newborn deaths occur worldwide, with 40% of them occurring in poorer nations, primarily Asia and Africa. This condition is a prevalent concern in neonates with confirmed sepsis, with thrombocytopenia happening in 66% of the total cases in our cross-sectional study. The results of our study are in good correlation with a cohort study, where 20% had severe onset of the disease, and the results revealed an almost fourfold increase in mortality in neonatal sepsis with thrombocytopenia [9]. Earlier, Charoo et al. investigated 200 VLBW infants with sepsis, and thrombocytopenia was detected in 61.5% of them. The increased incidence of thrombocytopenia in VLBW newborns may be due to a partial response to thrombocytopenia in terms of platelet and thrombopoietin production, mostly during sepsis with diminished energy reserves in the host [10].

The use of vascular catheters is strongly linked to intravascular thrombosis. Catheters can enhance platelet consumption [16]. They ultimately lead to vascular wall damage mechanically by altering the flow of blood, but they can also contain possibly thrombogenic agents or be used to inject toxic chemicals into the vascular walls. In our study, males were more affected. This is in accordance with the study of Fanaroff et al., who found that the incidence of sepsis is considerably higher in male newborns than in female ones [11].

The severity of thrombocytopenia differs depending on the causative bacteria. In this study, gram-negative sepsis had a considerably higher rate of early thrombocytopenia than gram-positive sepsis. In 30.43% of gram-negative sepsis episodes, there was severe early thrombocytopenia, while in gram-positive sepsis, only 4.34% were investigated for severe thrombocytopenia. This finding supports a prior study that found that thrombocytopenia was more common in gram-negative sepsis [12]. The likely mechanisms of thrombocytopenia associated with gram-negative sepsis are augmented destruction of platelets by absorption, antibody-mediated binding, and activation. In animal models, cell-free extracts comprising lipopolysaccharide and a constituent of gram-negative bacteria’s cell wall have been demonstrated to cause thrombocytopenia.

Bhat et al. [13] investigated an association between the organism responsible for the infection and thrombocytopenia in 415 very-low-birth-weight infants. The frequency and duration of thrombocytopenia were significantly greater in children with Gram-negative bacterial or yeast infections. Thrombocytopenic patients had significantly more persistent bacteremia, greater multivisceral failure, and higher mortality.

Guida et al. [14] reported in their cohort of 943 very-low-birth-weight infants that sepsis due to Gram-negative bacteria was associated with lower platelet counts and prolonged duration, compared with those due to Gram-positive bacteria.

In our study, we found that in neonatal sepsis, more than half of the neonates developed thrombocytopenia and 20% developed severe thrombocytopenia. It was independently associated with high CRP. To conclude, it is critical to screen for and treat thrombocytopenia in all babies brought to the NICU, including those who appear to be at low risk, because the incidence and mortality linked with this illness are significant. Because sepsis is still a common cause of newborn thrombocytopenia and the severity of thrombocytopenia in sepsis varies from mild to moderate to severe, the fact that thrombocytopenia is present in more than half of sepsis cases with positive blood cultures indicates the severity of the condition.

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