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SummaryAutomated microanalytic chromogenic coagulation assays allow serial monitoring of critically ill newborn infants. In this study 84 premature infants 126 healthy prematures and 58 neonates with idiopathic respiratory distress syndrome (IRDS)] were studied daily during the first week of life, to investigate the possible significance of hemostatic abnormalities in IRDS.In neonates with IRDS, coagulation factors I1 and X, antithrombin I11 (AT-111), plasminogen, and a2-antiplasmin were significantly lower than control values. Recovery of the initially low AT-111 levels was delayed relative to the other coagulation parameters measured. An AT-I11 r 0.15 U/ml was present within the first 6 h of life in eight patients who developed IRDS, seven of whom died within 48 h. Autopsy of these neonates showed widespread fibrin deposition and hemorrhage in vital organs consistent with intravascular coagulation. These findings indicate that very low levels of AT-I11 are associated with disseminated intravascular coagulation in neonates with IRDS and suggest that a deficiency of AT-I11 is predictive of a poor outcome. AbbreviationsAT-111, antithrombin 111 DIC, disseminated intravascular coagulation IRDS, idiopathic respiratory distress syndrome IVH, intraventricular hemorrhage DIC is frequently encountered in premature newborn infants suffering from IRDS. Deficiencies in clotting factors and fibrinogen, increased levels of fibrinogenlfibrin degradation products and thrombocytopenia (2,4,19,22,23) have been reported to be caused by DIC. These coagulation abnormalities are associated with clinical symptoms of bleeding (7,8,16,25,29) particularly IVH and fibrin thrombi at autopsy (3,7, 16,3 1) suggesting that DIC contributes to the fatal outcome of this disease. Decreased levels of AT-I11 have been described in early stages of DIC in adult patients (6,26). In cord blood samples of premature infants who developed IRDS, reduced AT-I11 levels have been reported (1 8, 2 1, 34); however, the relationship between AT-I11 activity and the clinical course of IRDS has not yet been thoroughly investigated. The availability of automated chromogenic coagulation assays enables the serial study of several coagulation parameters, and of AT-I11 in particular, in premature neonates with IRDS. These results are correlated with clinical signs and autopsy findings.

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Despite numerous well-described causes of stroke in infancy and childhood, a significant proportion remains unexplained. Venous thromboembolism is a common complication in adult patients undergoing surgery, and after severe trauma, but not in otherwise healthy children less than 10 years old. However, it may also occur spontaneously without recognizable cause. It has been known for a long time that some patients are particularly prone to venous thrombosis and in recent years great efforts have been made to identify the risk factors. The attention of haematologists has been focused on the possibility that certain abnormalities of coagulation may be associated with a tendency to thrombosis, but only in a few instances a clear causal relationship has been established. One such example is a deficiency of antithrombine III, but such a deficiency has hitherto been recognized as a cause for thrombosis in children only in very particular circumstances. We present two young children with stroke of which one was purely ischemic and the other ischemic with secondary hemorrhage. Both our patients showed an AT III deficiency. Patient one also had a cyanotic congenital heart disease with right to left shunting which made cerebral embolism originating from a thrombus in the iliac vein possible to occur. We consider her hematocrit values too low to be a predisposing factor for this thrombosis. AT III deficiency may be caused by several different mechanisms. Either it exists as a congenital (hereditary) or as an acquired disorder. In patient two the family history was positive for hereditary AT III deficiency.(ABSTRACT TRUNCATED AT 250 WORDS)