Intracranial hemorrhage is a severe complication affecting preterm neonates. Schmid and colleagues (1) in their article say that the rate of intracranial hemorrhage can be notably reduced by prospective risk factor monitoring. This is a useful prophylactic measure. An investigation into neonates in Baden-Württemberg in 2009 showed that sepsis owing to bacterial pathogens is the most common cause of intraventricular hemorrhage; no hemostaseological causes were mentioned (2).
Germinal matrix hemorrhage often occurs as a consequence of a venous infarction. The ischemia causes hemorrhage and is accompanied by periventricular leukomalacia. The protective use of magnesium sulfate is currently under discussion (3).
If, however, it really is venous thrombosis that triggers the hemorrhage then the use of heparin should be considered—for example, 5–10 IU per hour per kg given intravenously—since monitoring cerebral perfusion is too elaborate for routine clinical practice to be used as a prophylactic measure for hemorrhage. Beforehand, the clotting status needs to be determined in citrate blood (1.6 mL syringe), in order to rule out a coagulation disorder, often seen in neonates (4). If a plasma related bleeding tendency is confirmed, then heparin must not be administered; rather, clotting factors should be given, for example, clotting factors I, VII, IX, and X (PPSB) at a dosage of 20–50 IU per kg body weight.
A thrombocyte count should be obligatory in order to rule out thrombocytopenia—for example, neonatal alloimmune thrombocythemia (NAIT).
References
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