Dube B, Das B K, Kolindewala J K, Dube R K, Bhargava V
Indian Pediatr. 1989 Jan;26(1):26-31.
Hemostatic profile (prothrombin time (PT), thrombin time (TT), kaolin cephalin clotting time (KCCT), plasma fibrinogen, serum fibrin/fibrinogen degradation products (FDP) and platelet counts) was examined in 153 neonates with birth anoxia and 86 with sepsis. Remarkable hemostatic alterations occurred in neonates with severe anoxia and sepsis, while those with moderate anoxia exhibited minimal or no change. Vitamin K administration to anoxic babies showed no improvement in the hemostatic profile after 48-72 hours. The hemostatic alterations were presumably due to incipient disseminated intravascular coagulation (DIC). In spite of the marked coagulation changes, only 3 neonates with sepsis and none of the anoxic newborns presented with clinical bleeding indicating a well balanced hemostatic mechanism.
对153例出生时缺氧的新生儿和86例患败血症的新生儿进行了止血指标检查(凝血酶原时间(PT)、凝血酶时间(TT)、白陶土部分凝血活酶时间(KCCT)、血浆纤维蛋白原、血清纤维蛋白/纤维蛋白原降解产物(FDP)和血小板计数)。患有严重缺氧和败血症的新生儿出现了显著的止血改变,而中度缺氧的新生儿则表现出极小的变化或无变化。对缺氧婴儿给予维生素K,48 - 72小时后止血指标未见改善。止血改变可能是由于早期弥散性血管内凝血(DIC)所致。尽管有明显的凝血变化,但只有3例患败血症的新生儿出现临床出血,而缺氧新生儿均未出现临床出血,这表明止血机制保持良好平衡。