Funato M, Tamai H, Noma K, Kurita T, Kajimoto Y, Yoshioka Y, Shimada S
Department of Pediatrics, Yodogawa Christian Hospital, Osaka, Japan.
J Pediatr. 1992 Oct;121(4):614-9. doi: 10.1016/s0022-3476(05)81157-6.
To ascertain whether any routine practices or clinical manipulations in a neonatal intensive care unit could induce intraventricular hemorrhage (IVH) in preterm infants, we performed ultrasonic monitoring of the germinal layer continuously for 48 hours in 33 extremely premature infants with respiratory distress. Intraventricular hemorrhage developed in 16 of these infants. In four infants the timing of the germinal layer hemorrhage was confirmed with ultrasonic monitoring. Three of the four cases were apparently associated with clinical events occurring at the moment of IVH: manual ventilation for improvement of hypercapnia associated with primary pulmonary hypertension of the newborn; correction of hyperkalemia, which was causing an arrhythmia, with administration of calcium gluconate and sodium bicarbonate; and administration of surfactant-TA to improve respiratory failure caused by pulmonary hemorrhage. In these three infants it appeared that one of the basic factors inducing IVH might be an increase in blood pressure with or without hypercapnia, causing cerebral reperfusion after ischemic damage of the germinal layer.
为确定新生儿重症监护病房中的任何常规操作或临床处置是否会诱发早产儿脑室内出血(IVH),我们对33例患有呼吸窘迫的极早产儿的生发层进行了连续48小时的超声监测。这些婴儿中有16例发生了脑室内出血。通过超声监测确定了4例婴儿生发层出血的时间。4例中的3例显然与脑室内出血发生时的临床事件有关:为改善与新生儿原发性肺动脉高压相关的高碳酸血症而进行的人工通气;通过静脉注射葡萄糖酸钙和碳酸氢钠纠正引起心律失常的高钾血症;以及给予表面活性物质TA以改善由肺出血引起的呼吸衰竭。在这3例婴儿中,似乎诱发脑室内出血的基本因素之一可能是无论有无高碳酸血症的血压升高,导致生发层缺血损伤后的脑再灌注。