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Published on: August 25, 2022
Hyperviscosity of the blood and haemostasis in the newborn infant
Insights
Newborn infants with polycythaemia (high red blood cell count) and hyperviscosity syndrome showed no significant coagulation or fibrinolysis abnormalities. Low antithrombin III levels may increase thrombotic risk, suggesting haemodilution therapy.
Area of Science:
- Neonatal Medicine
- Hematology
- Pediatric Coagulation
Background:
- Neonatal polycythaemia can lead to hyperviscosity syndrome, increasing the risk of thromboembolic events.
- The coagulation and fibrinolytic status in infants with hyperviscosity syndrome requires further elucidation.
Purpose of the Study:
- To investigate the coagulation and fibrinolytic systems in newborn infants diagnosed with hyperviscosity syndrome.
- To identify potential hemostatic abnormalities contributing to thrombotic complications in this population.
Main Methods:
- Analysis of coagulation parameters and fibrinolytic activity in 15 newborn infants with central haematocrit ≥65% and elevated blood viscosity.
- Assessment included platelet counts, ethanol gelation tests for fibrin/fibrinogen degradation products (FDP), and plasma fibrinolytic activity assays.
- Evaluation of antithrombin III (heparin cofactor activity) levels.
Main Results:
- No significant defects were found in the coagulation system of the infants.
- Most patients exhibited no demonstrable abnormal proteolysis in circulation; FDP were detected in only two infants.
- Low antithrombin III levels were noted, potentially exacerbated by impaired microcirculation.
Conclusions:
- Newborns with hyperviscosity syndrome due to polycythaemia do not typically present with overt coagulation or fibrinolysis activation.
- Reduced antithrombin III levels, coupled with microcirculatory impairment, may elevate the risk of thrombotic complications.
- Haemodilution, preferably with plasma, is recommended for symptomatic infants to mitigate thrombotic risks.
Abstract:
15 newborn infants with the hyperviscosity syndrome due to polycythaemia i.e. a central haematocrit of at least 65% and a raised whole blood viscosity, were examined for changes in their coagulation and fibrinolytic systems. 5 were thrombocytopenic but showed no other signs of activated coagulation. Neither did the only patient with positive ethanol gelation test measuring circulating fibrin/fibrinogen degradation products (FDP) appeared in only two and, with only one exception, an assay for fibrinolytic activity in plasma was negative. No defects were found in the coagulation system. Thus, in most of the patients there was no demonstrable abnormal proteolysis in the circulation. However, in such infants the normally low levels of antithrombin III (heparin cofactor activity) in combination with the impairment of the microcirculation might increase the risk of thrombotic complications. Haemodilution, preferably with plasma, is therefore advocated in the symptomatic patients.
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