Tang S F, Miller O I
Department of Intensive Care, Royal Alexandra Hospital for Children, Westmead, New South Wales, Australia.
J Paediatr Child Health. 1996 Oct;32(5):419-23. doi: 10.1111/j.1440-1754.1996.tb00942.x.
Inhaled nitric oxide (iNO) has been shown to cause selective pulmonary vasodilatation and improve ventilation-perfusion matching and may be an important therapeutic option for the treatment of persistent pulmonary hypertension of the newborn (PPHN). We report our experience on the use of iNO in neonates with severe PPHN.
Inhaled NO was administered to 10 infants with PPHN and persistent hypoxaemia (meconium aspiration syndrome, n = 9; pneumonia, n = 1) after failure of conventional therapy to improve oxygenation. With the exception of one infant, iNO was commenced at 10 ppm.
After 30 min exposure to iNO, the arterial oxygen tension (PaO2) rose from a median of 49 mmHg (6.5 kPa) [range 12-82 mmHg (1.6-10.9 kPa)] to 75 mmHg (10 kPa) [range 17-450 mmHg (2.3-60 kPa)] (P = 0.005), while the median oxygenation index fell (pre-iNO of 37 vs post-iNO 20) (P = 0.005) and median systemic arterial pressure rose (pre-iNO 46.5 mmHg (6.2 kPa) [range 32-63 mmHg (4.3 to 8.4 kPa vs post-iNO 54.5 mmHg (7.3 kPa) [range 36-74 kPa]) P = 0.005). All infants subsequently continued to receive iNO with the duration of exposure to iNO ranging from 12 to 168 h (median duration 100 h). Three infants died despite showing an initial beneficial response to iNO. The mean duration of intubation for survivors was 11.9 +/- 2.6 days. Methaemoglobinaemia and toxic levels of nitrogen dioxide were not seen during iNO administration. Of the seven survivors, 12 month follow up in two infants and 4 month follow up in four infants showed age-appropriate neurodevelopmental skills, with one infant having very mild hearing loss.
Inhaled NO reduces the oxygenation index by improving the PaO2 and decreasing ventilation pressures, and appears to be clinically useful in severely hypoxaemic infants with PPHN refractory to conventional treatment.
吸入一氧化氮（iNO）已被证明可引起选择性肺血管扩张，改善通气-灌注匹配，可能是治疗新生儿持续性肺动脉高压（PPHN）的重要治疗选择。我们报告了我们在严重PPHN新生儿中使用iNO的经验。
在10例PPHN且持续性低氧血症（胎粪吸入综合征，n = 9；肺炎，n = 1）的婴儿中，在常规治疗未能改善氧合后给予吸入NO。除1例婴儿外，iNO均从10 ppm开始使用。
暴露于iNO 30分钟后，动脉血氧分压（PaO2）从中位数49 mmHg（6.5 kPa）[范围12 - 82 mmHg（1.6 - 10.9 kPa）]升至75 mmHg（10 kPa）[范围17 - 450 mmHg（2.3 - 60 kPa）]（P = 0.005），而氧合指数中位数下降（iNO前为37，iNO后为20）（P = 0.005），全身动脉压中位数升高（iNO前46.5 mmHg（6.2 kPa）[范围32 - 63 mmHg（4.3至8.4 kPa）]，iNO后54.5 mmHg（7.3 kPa）[范围36 - 74 kPa]）P = 0.005）。所有婴儿随后继续接受iNO治疗，iNO暴露时间为12至168小时（中位数持续时间100小时）。尽管3例婴儿最初对iNO有有益反应，但仍死亡。幸存者的平均插管持续时间为11.9±2.6天。在iNO给药期间未观察到高铁血红蛋白血症和二氧化氮中毒水平。7名幸存者中，2名婴儿进行了12个月随访，4名婴儿进行了4个月随访，结果显示其神经发育技能与年龄相符，1名婴儿有非常轻微的听力损失。
吸入NO通过提高PaO2和降低通气压力降低氧合指数，对于常规治疗难治的严重低氧血症PPHN婴儿似乎具有临床应用价值。
