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[Perinatal influences on blood coagulation in healthy newborn infants with special reference to vitamin K
Insights
Late feeding impacts blood clotting factors in newborns. Higher factor II levels in infants with abnormal heart rate monitoring suggest stress-induced liver maturation.
Area of Science:
- Neonatal physiology
- Hematology
Context:
- Investigating early life factors affecting newborn health.
- Understanding the development of coagulation factors in infants.
Purpose:
- To examine the relationship between early feeding patterns, birth weight, and coagulation factors (II, V, VII) in newborns.
- To assess the influence of delivery and postnatal factors on these coagulation factors.
Summary:
- Daily milk intake and weight gain were monitored in 169 newborns during their first week.
- Coagulation factors II, V, and VII were measured on day four.
- Late feeding significantly affected factor II and VII levels. Factor II correlated with birth weight in full-term infants.
- Abnormal cardiotocographic findings were associated with higher factor II levels, potentially due to stress-induced liver maturation.
Impact:
- Highlights the critical role of timely feeding in neonatal hemostasis.
- Provides insights into physiological responses to stress in newborns.
- Informs clinical practices regarding neonatal monitoring and feeding protocols.
Abstract:
In a prospective study the daily milk intake and weight gain were recorded in 169 healthy newborn infants during the first week of life. Factor II, V and VII activities were determined on the fourth day using a capillary blood method with hematocrit correction factor. Late onset of feeding showed a major influence on factor II and VII activities. In full-term newborns factor II was correlated to the birth weight. Mode of delivery, color of amniotic fluid, umbilical cord round the neck, Apgar score and postnatal vitamin K prophylaxis showed no significant influence. In infants with abnormal cardiotocographic findings higher levels of factor II were determined. This can be explained by stress-induced liver maturation.