Late morbidity among survivors of respiratory failure treated with tolazoline.

Late morbidity among survivors of respiratory failure treated with tolazoline.
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用妥拉唑啉治疗的呼吸衰竭幸存者的晚期发病率。

DOI:
10.1016/s0022-3476(80)80032-1
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发表时间:
1980
期刊:
The Journal of pediatrics
影响因子:
--
通讯作者:
Sunshine,P
Sunshine,P
中科院分区:
--
文献类型:
--
作者:
Cohen,RS;Stevenson,DK;Malachowski,N;Ariagno,RL;Johnson,JD;Sunshine,P

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6 4 4简短的临床和实验室观察1980年10月儿科杂志证实,被一个器官强迫进入一个小的腹腔,可能减少了肾脏的灌注量,激活了肾素-血管紧张素-醛固酮系统。与主动脉血流量显著减少时可能预期的那样,下肢血压并未降低。然而,有三名婴儿腹壁紧绷并伴有下肢水肿,这可能是由于静脉或淋巴闭塞所致。他们的正常外周血浆肾素值不排除肾脏肾素生成增加的可能贡献。8控制内脏床的交感神经供应可能导致内脏血管收缩、肾动脉痉挛或增加儿茶酚胺而导致全身血压升高。2两名婴儿尿儿茶酚胺排泄正常。最后,压迫或牵拉腹壁、臀部或骨盆区域的神经可能会导致高血压。要矫正这些相当大的缺陷,需要对腹壁施加严重的牵引。此外,婴儿通常在腹部重量增加的情况下以仰卧姿势固定,这可能导致供应骨盆或臀部的神经受到不寻常的压力。总而言之,4名婴儿在失去腹壁缺陷后发展为轻度至中度系统性高血压。高血压似乎与缺陷的大小、腹膜发育不良的程度以及关闭缺陷所需的牵引力程度有关。两名婴儿接受了3至6个月的降压治疗。这种疾病的发病机制尚不清楚。我们感谢M.PIBBS的秘书协助,以及加州大学戴维斯分校、医学中心和萨克拉门托凯撒基金会医院的医疗和护理人员的合作。我们特别感谢儿科外科医生Dennis Vitale在这些婴儿的管理方面给予的关怀和建议。
6 4 4 Brief clinical and laboratory observations The Journal of Pediatrics October 1980 sure by an organ forced into a small abdominal cavity, may have decreased renal perfusion and activated the renin-angiotensin-aldosterone system. Lower extremity blood pressures were not reduced, as might be expected with a marked decrease in aortic blood flow. However, three infants had a taut abdominal wall associated with edema of the lower extremities, which may have been due to venous or lymphatic occlusion. Their normal peripheral plasma renin values do not exclude the possible contribution of increased renal production of renin. 8 Manipulation of the sympathetic supply to the splanchnic bed may caUse elevated systemic blood pressure due to splanchnic vasoconstriction, renal artery spasm, or increased catecholamine production2 Urinary catecholamine excretion was normal in the two infants in whom it was measured. Finally, compression or traction involving nerves within the abdominal wall, gluteal or pelvic areas, may have contributed to the hypertension. TM Correction of these rather large defects required severe traction upon the abdominal wall. In addition, infants were usually immobilized in a supine position under an increased abdominal weight, which may have led to unusual pressure upon nerves supplying the pelvic or gluteal areas. in summary, four infants developed mild to moderate systemic hypertension following-~ losure of a defect of the abdominal wall. The hypertension appeared related to the size of the defect, the extent of hypoplasia of the abdominal cavity, and the degree of traction required for closure of the defect. Antihypertensive therapy was required for three to six months in two infants. The pathogenesis of this disorder remains unknown.We gratefully acknowledge the secretarial assistance of M. Pibbs and the cooperation of the medical and nursing staffs at the University of California, Davis, Medical Center and Kaiser Foundation Hospital, Sacramento. We are especially grateful to Dennis Vitale, MD, pediatric surgeon, for his care and advice in the management of these infants.