Late morbidity among survivors of respiratory failure treated with tolazoline.
Late morbidity among survivors of respiratory failure treated with tolazoline.
复制标题
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
复制
发表时间:
1980
期刊:
影响因子:
--
通讯作者:
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
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.