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在一名哮喘持续状态的婴儿中使用异氟烷治疗危及生命的高碳酸血症。

Treatment of life-threatening hypercapnia with isoflurane in an infant with status asthmaticus.

作者信息

Masuda Yoshiki, Tatsumi Hiroomi, Goto Kyoko, Imaizumi Hitoshi, Yoshida Shin-ichiro, Kimijima Tomohiko, Yamakage Michiaki

机构信息

Department of Intensive Care Medicine, Sapporo Medical University, School of Medicine, West 16 South 1, chuo-ku, Sapporo, Hokkaido, 060-8543, Japan,

出版信息

J Anesth. 2014 Aug;28(4):610-2. doi: 10.1007/s00540-013-1751-0. Epub 2013 Dec 6.

Abstract

We encountered a 2-year-old child with life-threatening hypercapnia, with a PaCO(2) of 238 mm Hg and severe respiratory and metabolic acidosis, due to status asthmaticus that was refractory to steroid and bronchodilator therapy. Suspecting ventilatory failure and excessive ventilation-induced obstructive shock, we started respiratory physiotherapy in synchrony with her respiration, to facilitate exhalation from her over-inflated lungs. Isoflurane inhalation was commenced in preparation for extracorporeal circulation, to reduce the hypercapnia. The combination of respiratory physiotherapy and isoflurane inhalation resulted in a rapid decrease in ventilatory resistance and PaCO(2) levels within a few minutes, with recovery of consciousness within 60 min. Isoflurane inhalation was gradually discontinued and steroid and aminophylline therapy were commenced. The patient recovered completely without any recurrence of her bronchospasm and without any residual neurological deficits. In our patient with a severe asthmatic attack, decreased exhalation secondary to asthma and overventilation during artificial ventilation resulted in overinflation of the lungs, which in turn led to cerebral edema and obstructive cardiac failure. The favorable outcome in this case was due to the short duration of hypercapnia. Hence, we conclude that the duration of hypercapnia is an important determinant of the morbidity and mortality of status asthmaticus-induced severe hypercapnia.

摘要

我们遇到一名2岁儿童,因哮喘持续状态对类固醇和支气管扩张剂治疗无效,出现危及生命的高碳酸血症,动脉血二氧化碳分压(PaCO₂)为238 mmHg,并伴有严重的呼吸性和代谢性酸中毒。怀疑存在通气衰竭和过度通气诱发的梗阻性休克,我们开始与她的呼吸同步进行呼吸物理治疗,以促进过度膨胀的肺部呼气。开始吸入异氟烷以准备体外循环,降低高碳酸血症。呼吸物理治疗和异氟烷吸入相结合,在几分钟内使通气阻力和PaCO₂水平迅速下降,60分钟内意识恢复。逐渐停用异氟烷吸入,并开始类固醇和氨茶碱治疗。患者完全康复,未再出现支气管痉挛,也没有任何残留神经功能缺损。在我们这位患有严重哮喘发作的患者中,哮喘继发的呼气减少以及人工通气期间的过度通气导致肺部过度膨胀,进而导致脑水肿和梗阻性心力衰竭。该病例的良好结局归因于高碳酸血症持续时间较短。因此,我们得出结论,高碳酸血症的持续时间是哮喘持续状态诱发的严重高碳酸血症发病率和死亡率的重要决定因素。

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