{'fraction_non_alphanumeric': 0.02544529262086514, 'fraction_numerical': 0.016398077466779758, 'mean_word_length': 5.363309352517986, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 3, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Is an increased hematocrit at birth a trigger for UVC‐related thrombosis in preterm very low birth weight neonates?

I n the pediatric population, neonates are at greatest risk for thromboembolism with an incidence of about 5.1 per 100,000 live births or 2.4 per 1,000 neonatal care unit admissions [1,2]. Up to 90% of pediatric thromboses are related to central venous catheters with a morbidity of up to 12% and a related mortality of 2% [3]. Significant morbidity has been reported after renal vein thrombosis and vena cava occlusion. Approaches to prevention have included optimal positioning of the catheter, restriction of catheter duration, and continuous heparin infusion. However, up to 30% of neonates with a central venous catheter still develop a related thrombosis [4]. Multiple acquired risk factors for neonatal thrombosis have been described including polycythemia with a hematocrit >65%, while the influence of inherited thrombophilia is controversial [1,5]. In this issue of Pediatric Blood & Cancer Narang et al. retrospectively evaluated acquired risk factors for thrombosis in a cohort of preterm, very low birth weight (VLBW) infants who had had a systematic echocardiography assessment for umbilical vein catheter (UVC)-related thrombosis during a prospective randomized study [6]. The study included 210 preterm, VLBW newborns with an in situ duration of the UVC for 7–28 days. Using a predetermined imaging schedule, UVC-related thrombus in the right atrium or inferior vena cava was detected by echocardiography in 10.4% of patients between day 5 and 30. While several factors including a lower platelet count, small for gestational age, maternal pre-eclampsia, and increased gestational age were significant in univariate analysis, multivariate logistic regression analysis identified only a hematocrit >55% within the first week of life to be independently associated with thrombosis (OR 3.6, P1⁄4 0.03). Polycythemia has generally been defined as a hematocrit above 65%; the finding that even a hematocrit of >55% may be a risk factor for clot formation will require a shift in the assessment of neonatal hematocrit with attention paid to these lower levels, or rather to age and developmentally appropriate hematocrit levels. Polycythemia is a known risk factor for thrombosis in other clinical settings; a positive correlation between hematocrit and vascular occlusion has been well described in polycythemia vera and idiopathic erythrocytosis [7]. Polycythemia leads to increased viscosity and decreased blood flow which causes red cell axial migration and dispersion of the platelets to the peripheral zones next to the vessel wall where shear forces are highest and activation of platelets and local procoagulants can easily be achieved [7–9]. The strength of this study includes having assessed the outcome measure of thrombosis prospectively and in a systematic and controlled manner. Narang et al. make an important point in assessing the hematocrit and its impact on clot formation during the first week of life arguing that clot formation most likely starts during early interactions between catheter surface, blood, and endothelium. However compelling these results appear to be, they still need to be treated with caution and confirmed in a controlled prospective study. Being aware that thrombosis is multifactorial, including thrombogenic predispositions plus recent or acute thrombogenic triggers, multiple issues and questions remain and should be considered when planning future evaluations: