Nitric oxide in acute hypoxic respiratory failure: From the bench to the bedside and back again  

Oleh:

Bohn, Desmond

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: The Journal of Pediatrics vol. 135 no. 01 (Jul. 1999), page 387-389.
Topik: AHRF ; Acute hypoxic respiratory failure; ARDS ; Acute respiratory distress syndrome; iNO ; Inhaled nitric oxide; NO ; Nitric oxide; OI ; Oxygenation index; RCT ; Randomized controlled clinical trial

Ketersediaan

Perpustakaan FK Nomor Panggil: J45.K.1999.02 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

Lihat Detail Induk

Isi artikel

Few therapies introduced into critical care medicine in the past 10 years have stimulated the degree of excitement and enthusiasm as that generated by the discovery of the pulmonary vasodilating properties of inhaled nitric oxide. It has made the journey from bench to bedside in rapid order. In the neonatal unit nitric oxide would seem to be a real advance in the management of hypoxic respiratory failure associated with primary pulmonary hypertension. This heightened the expectation that NO would also prove to be a life-saving therapy in older children and adults with the acute respiratory distress syndrome, based on uncontrolled studies with physiologic end points. The study by Dobyns et al1 in this issue of The Journal puts iNO to the more rigorous test of a randomized controlled clinical trial with, in this instance, a physiologic end point of an improvement in oxygenation. The study involves 108 patients with acute hypoxic respiratory failure from 8 different centers. The principal investigators were masked as to patient assignment. The underlying causes of AHRF were pneumonia with and without chronic lung disease, sepsis, and diseases associated with immunocompromise. Eligibility criteria were an oxygenation index =15, although the mean OI was =30 at enrollment in study patients, with exit from the study at an OI =15 or treatment failure within 72 hours (OI >40 × 3 hours or OI >25 × 6 hours). The primary end point was a difference in treatment failure. Patients received iNO at a concentration of 10 ppm. The markers of oxygenation (OI and PaO2 /fraction of inspired oxygen) showed a more significant improvement in the iNO group compared with the control group at 4 and 12 hours, but this difference was not sustained for the 72 hours of the study. There was no difference in the percentage of treatment failures (non-responders) between the 2 groups (iNO, 46%; control, 54%). This result is similar to that recently reported in adult patients with ARDS in the study by Michel et al2 in which the initial improvement in oxygenation in the NO group was matched by the control subjects after 24 hours. Perhaps in an attempt to salvage a positive result from an essentially negative study, the authors have used a post hoc analysis to support their claim that iNO may be a more effective therapy for patients with more severe hypoxemia (OI >25) and immunocompromise because of the fewer treatment failures in these groups. Because the study did not stratify for this factor and there were twice as many immunocompromised patients enrolled in the control arm as in the iNO arm (18 vs 9), it is difficult to support this contention.

Opini Anda

Klik untuk menuliskan opini Anda tentang koleksi ini!

Kembali