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Abnormal proteolysis in sick newborns.

P Henriksson, H Ekelund

Acta Paediatrica Scandinavica

|March 1, 1975

Summary

This summary is machine-generated.

Newborn infants often show coagulation and fibrinolytic system defects, particularly those with severe illness. "Multiple defects" were linked to illness severity and outcomes, not specific neonatal disorders.

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Area of Science:

Neonatal Medicine
Hematology
Pediatrics

Background:

Neonatal hemostasis is complex and differs significantly from adult hemostasis.
Infants are prone to bleeding and thrombotic disorders due to immature coagulation and fibrinolytic systems.

Purpose of the Study:

To investigate defects in the coagulation and fibrinolytic systems in newborn infants on their first day of life.
To determine if specific patterns of hemostatic abnormalities are associated with Idiopathic Respiratory Distress Syndrome (IRDS) or mixed neonatal disorders.
To explore the relationship between illness severity, clinical course, and the presence of multiple hemostatic defects.

Main Methods:

Studied 87 newborn infants within the first 24 hours of life.
Assessed coagulation and fibrinolytic system parameters, including Factor V, fibrinogen, and fibrin/fibrinogen degradation products (FDP).

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Categorized infants into groups based on diagnosis (IRDS vs. mixed neonatal disorders) and clinical outcomes (survival vs. death).

Main Results:

Factor V, fibrinogen, and FDP abnormalities were most frequent among the studied parameters.
The presence of "multiple defects" in hemostasis was significantly associated with illness severity and mortality (85% of deceased infants had multiple defects vs. 28% of survivors).
No significant difference in the pattern of hemostatic abnormalities was observed between infants with IRDS and those with mixed neonatal disorders.

Conclusions:

Neonatal hemostatic defects are common and can be severe, particularly in critically ill infants.
Multiple hemostatic defects are linked to poor prognosis in newborns.
Potential mechanisms for these defects include impaired synthesis (e.g., vitamin K deficiency, liver damage) and abnormal proteolytic activity leading to dysregulated coagulation and/or fibrinolysis.