Nitric Oxide-Associated Pulmonary Edema in Children With Pulmonary Venous Hypertension.

Oct 2012

Baird JS, Havalad V, Aponte-Patel L, Ravindranath TM, October TW, Starc TJ, Smerling AJ.

Source

College of Physicians and Surgeons, Children's Hospital of New York-Presbyterian, Columbia University, 3959 Broadway, CHN 10-24, New York, NY, 10032, USA, jsb106@columbia.edu.

Abstract

Nitric oxide (NO)-associated pulmonary edema is rarely reported in children; in adults, it is often associated with left-sided heart failure. We report a case series of children with NO-associated pulmonary edema, which was defined as new multilobar alveolar infiltrates and worsening hypoxemia within 24 h of initiation or escalation of NO and radiologic or clinical improvement after NO discontinuation. We identified six patients (0.4-4 years old) with ten episodes of NO-associated pulmonary edema. Diagnoses included atrioventricular canal defect with mitral valve disease (n = 2), pulmonary atresia and major aorta-pulmonary collateral arteries (n = 2), total anomalous pulmonary venous return (n = 1), and pulmonary veno-occlusive disease (n = 1). All patients had evidence of pulmonary venous hypertension, and two had mitral valve disease resulting in clinical evidence of left-sided heart failure. Pulmonary edema improved or resolved within 24 h of discontinuing NO. At cardiac catheterization, mean left atrial pressure was <15 artery="artery" disease="disease" in="in" mitral="mitral" mmhg="mmhg" nbsp="nbsp" none="none" occlusion="occlusion" of="of" patients="patients" pressure="pressure" pulmonary="pulmonary" three="three" valve="valve" was="was" whereas="whereas" with="with">15 mmHg in two of five patients. In conclusion, we describe six young children with NO-associated pulmonary edema and pulmonary venous hypertension. Only two of these children had left-sided heart failure: Left atrial pressure as well as pulmonary artery occlusion pressure may not be helpful in identifying children at risk for NO-associated pulmonary edema.

Springerlink

Inhaled nitric oxide does not prevent postpneumonectomy pulmonary edema in pigs

Inhaled nitric oxide does not prevent postpneumonectomy pulmonary edema in pigs
2007 The American Association for Thoracic Surgery

Marc Filaire, MDa, Elie Fadel, MDb, Benoît Decanteb, Frédéric Seccatoreb, Guy-Michel Mazmanian, MDb, Philippe Hervé, MDb,*
a CHU Clermont-Ferrand, Service de Chirurgie Générale et Thoracique, Hôpital Gabriel Montpied, and Université d’Auvergne, Laboratoire d’Anatomie, Clermont-Ferrand, Franceb Experimental Surgery Laboratory and Department of Thoracic and Vascular Surgery and Heart-Lung transplantation, Centre Chirurgical Marie Lannelongue, Paris-Sud University, Le Plessis-Robinson, France.

Received for publication May 11, 2006; revisions received July 22, 2006; accepted for publication September 5, 2006.

* Address for reprints: Philippe Hervé, MD, Centre Chirurgical Marie Lannelongue, Paris-Sud University, Le Plessis-Robinson, France. (Email: pherve@ccml.com)

Objective: Increase in lung permeability is an inevitable consequence of pneumonectomy in relation to inflammatory injury and increased perfusion flow. We tested whether inhaled nitric oxide, a potent vasodilatator and anti-inflammatory agent, prevents postpneumonectomy edema in the first 24 hours after pneumonectomy in pigs.

Methods: We assessed hemodynamics, gas exchange, extravascular lung water estimated with the double-indicator dilution method, and lung neutrophil sequestration measured on the basis of lung myeloperoxidase activity at 1 and 24 hours after left pneumonectomy in 14 pigs randomly assigned to inhaled nitric oxide (10 ppm) or control groups.

Results: Extravascular lung water content markedly increased at 1 and 24 hours after pneumonectomy, with no difference between the 2 groups. Hemodynamics did not differ between the 2 groups. Myeloperoxidase activity was higher and PaO 2 values were lower in the nitric oxide group compared with in the control group.

Conclusions: Over the 24 hours after pneumonectomy, intraoperative inhaled nitric oxide levels neither improved gas exchange nor attenuated accumulation of lung water. On the contrary, they were associated with an increase in lung neutrophil sequestration and deterioration of arterial oxygenation, suggesting the occurrence of an early and toxic effect of nitric oxide.

Abbreviations and Acronyms: CI = cardiac index; EVLW = extravascular lung water; FIO 2 = inspired oxygen fraction; MPAP = mean pulmonary artery pressure; MPO = myeloperoxidase; MSAP = mean systemic artery resistance; NO = nitric oxide; PBV = pulmonary blood volume; SVRI = indexed value of systemic vascular resistance