Hemostasis is a dynamic age-related process, which gradually evolves from fetal life throughout childhood until adulthood. Although at birth there is a hemostatic deficit of most coagulation factors, studies have shown that this “hemostatic immaturity” is functionally counterbalanced in healthy term or preterm newborns. This delicate hemostatic balance is, however, deranged in sick neonates, resulting in an enhanced risk of hemorrhage and/or thrombosis. In critically ill neonates, conventional coagulation tests do not seem to provide reliable information or indications regarding the functional status of platelets or fibrinolysis. In contrast, viscoelastic tests, namely thromboelastography/thromboelastometry (TEG/TEM) hold promise for rapid assessment of the whole hemostatic potential, allowing immediate intervention should this be required. However, neonatal data are limited due to lack of reference values, especially in premature neonates. In this narrative review, we provide some insights around current knowledge regarding TEG/TEM applications in healthy and sick newborns. Overall, the use of viscoelastic tests in diagnosis and management of coagulation disorders in neonates is definitely worth further exploration. Consideration should be made to include these tests in the routine laboratory investigation of neonates and specific transfusion algorithms should also be developed in order to avoid treatment pitfalls.

Perinatal hypoxia is associated with an increased risk of coagulation disorders by enhancing the consumption of platelets and some clotting factors due to the associated severe hypoxemia, acidemia, and compromised oxygen and blood supply to the neonatal liver and bone marrow. Thromboelastometry (TEM), which estimates the dynamics of blood coagulation, may represent an attractive tool for studying the coagulation status of these neonates. We aimed at assessing the hemostatic profile of neonates with perinatal hypoxia using the standard extrinsically activated TEM (ex-TEM) assay. In total, 164 hospitalized neonates with perinatal asphyxia and/or fetal distress comprised the study subjects, and 273 healthy neonates served as controls. Ex-TEM assay was performed, SNAPPE (Score for Neonatal Acute Physiology Perinatal Extension) was calculated, and clinical findings and laboratory results were recorded in all study subjects. Hypoxic neonates expressed a prolonged clotting time (CT) and clot formation time (CFT) and reduced amplitude at 10 minutes (A10), α-angle, and maximum clot firmness compared with healthy neonates. Furthermore, asphyxiated neonates had a significantly prolonged CT and CFT and reduced A10 and α-angle compared with neonates with fetal distress. Hypoxic neonates demonstrate a hypocoagulable ex-TEM profile relative to healthy neonates, indicating a potential role of TEM in the early detection of coagulation derangement in perinatal hypoxia.

Background and Purpose: The aim of this study was to prospectively validate our prior findings of smaller hematoma volume and lesser neurologic deficit in Non Vitamin K oral anticoagulant (NOAC)- compared to Vitamin K antagonist (VKA)- related intracerebral hemorrhage (ICH). Methods: Prospective 12-month observational study in 15 tertiary stroke centers in the USA, Europe and Asia. Consecutive patients with premorbid modified Rankin Scale (mRS) score <2 with acute non-traumatic anticoagulant-related ICH divided in two groups according to the type of anticoagulant; NOAC vs VKA. We recorded baseline ICH volume, significant hematoma expansion [absolute (>12.5ml) or relative (>33%) increase], neurologic severity measured by National Institutes of Health Stroke Scale (NIHSS) score, 90-day mortality and functional status (mRS score). Results: Our cohort comprised 196 patients; 62 NOAC-related (mean age 75.0±11.4 years, 54.8% men) and 134 VKA-related (mean age 72.3±10.5, 73.1% men). There were no differences in vascular comorbidities, antiplatelet and statin use; NOAC-related ICH patients had lower median baseline hematoma volume [13.8 (2.5–37.6) vs. 19.5 (6.6–52.0) ml, p=0.026] and were less likely to have severe neurologic deficits (NIHSS>10 points) on admission (37% vs. 55.3%, p=0.025). VKA-ICH were more likely to have significant hematoma expansion (37.4% vs. 17%, p=0.008). NOAC pretreatment was independently associated with smaller baseline hematoma volume [standardized linear regression coefficient:−0.415 (95%CI:−0.780, −0.051] resulting in lower likelihood of severe neurological deficit (OR: 0.44; 95%CI: 0.22, 0.85) in multivariable adjusted models. Conclusion: Patients with NOAC-related ICH have smaller baseline hematoma volumes and lower odds of severe neurological deficit compared to VKA-related ICH. These findings are important for practicing clinicians making anticoagulation choices.

There is a complex and not fully elucidated association between pulmonary arterial hypertension (PAH) and coagulation disorders. The goal of this study was to evaluate platelet function, coagulation and fibrinolysis in PAH patients at diagnosis, before PAH-specific treatment initiation. We enrolled 20 healthy controls and 30 PAH patients (20 with connective tissue disease (CTD-PAH) and 10 idiopathic (iPAH)). None of the participants was on any antiplatelet or anticoagulation therapy. Blood samples from PAH patients were collected during the initial right heart catheterization. All subjects were assessed with platelet function analyzer-100 (PFA-100), epinephrine (Epi) and ADP-induced light transmission aggregometry (LTA), thromboelastometry (ROTEM) and endogenous thrombin potential (ETP). Our results showed that Epi and ADP-LTA values were significantly lower in newly diagnosed PAH patients compared to controls. Disaggregation was present in 73% of patients, a characteristic not seen in healthy individuals. In ROTEM assay, CT and CFT measurements were significantly higher and a angle lower compared to controls. ETP testing revealed significantly reduced outcomes in AUC, Cmax and Tmax. When CTD-PAH and iPAH patient groups were compared, iPAH ADP-LTA values were significantly decreased compared to CTD-PAH. In conclusion, newly diagnosed PAH patients presented with decreased platelet aggregation, clot propagation and thrombin generation, along with delayed initiation of the coagulation process. These hemostatic deficits could indicate an "exhaustion" of the coagulation process that could be caused by endothelial dysfunction and chronic activation of the procoagulant pathways. Further studies are warranted to confirm these laboratory findings and assess their potential clinical significance.