Ekkehard Schleusner in his article explains the problem clearly. In spite of this fact, however, we wish to add several comments on the topic of cerebral intraventricular hemorrhage. Unfortunately, cerebral hemorrhage occurs in more than 70% of neonates weighing 500–750g and 15% in those weighing 1500–2000g. Some 10–15% of surviving, very small preterm babies will have lifelong disabilities (1). In order to investigate the incidence of cerebral hemorrhage, 11 887 neonates were sonographically examined on the 3rdto 10th day of life in the years 1985–94. 303 babies (2.5%) had intraventricular or periventricular bleeds (2). The study found that the most important risk factor was prematurity, but the duration of gestation, birth weight, and body length correlated inversely. Furthermore, a correlation exists between pediatric infections passed by the mother and twin pregnancies (2). A possible coagulation disorder was not investigated. Schleusner mentions the problem of cerebral hemorrhage after administration of magnesium sulfate and glucocorticoids (reduction of cerebral intraventricular hemorrhage), magnesium sulfate combined with fenoterol (the highest rate of cerebral intraventricular hemorrhage altogether), and when using calcium antagonists (reduction of cerebral intraventricular hemorrhage). The causes of cerebral hemorrhage are the subject of controversy, whereas coagulation disorders hardly find any mention. In preterm babies, plasmatic coagulation becomes subject to a tendency to hemorrhage, and neonatal alloimmune thrombocytopenia (NAIT) may be present (3). Both should be considered on obstetric medicine, in order to prevent, or at least ameliorate, cerebral hemorrhage. In preterm babies, the recommendation is to determine as rapidly as possible the thrombocyte count and coagulation status, in order to alleviate postnatal hemorrhage by early administration of thrombocytes or clotting factors. This should be followed by a diagnostic evaluation of the causes by measuring thrombocyte antibodies.
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