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Unlabelled: Inhaled nitric oxide is a potent vasodilator in acute severe pulmonary hypertension and is increasingly used as rescue treatment in intensive care algorithms aiming at reducing severe hypoxaemia in neonates and children. Although the immediate effects may seem impressive, long-term outcome regarding residual pulmonary hypertension and other sequelae has been studied in only a very few patients. The aim of the present study was to evaluate residual pulmonary hypertension, cardiopulmonary or neurological symptoms in children after treatment with inhaled nitric oxide in severely hypoxaemic and/or pulmonary hypertensive mechanically ventilated children. The study was performed in four paediatric intensive care units in university hospitals in Sweden, Norway and Australia. Patients who had received inhaled nitric oxide as part of their intensive care treatment for severe hypoxaemia and/or pulmonary hypertension, and in whom 6 mo had elapsed since treatment, were included for evaluation. Thus 36 paediatric or neonatal patients were examined for circulatory, respiratory or neurological disorders with clinical examination, echocardiography, chest X-ray and a capillary blood sample. Four patients with congenital heart disease had residual pulmonary hypertension. Nine patients were receiving bronchodilators. Sixteen patients had minor (n = 15) or moderate (n = 1) changes on a chest X-ray. One patient had a possible delay in psychomotor development.Conclusions: In spite of the severity of their primary illness, we found that the overwhelming majority of the surviving children were asymptomatic and doing well. The few residual circulatory and respiratory symptoms could be related to the initial condition. [ABSTRACT FROM AUTHOR]

Twelve patients (median age 3.8 months) with pulmonary hypertension in the postoperative period after congenital heart surgery on cardiopulmonary bypass were given inhaled nitric oxide. Effects on cardiovascular and respiratory systems were measured. Mean pulmonary artery pressure decreased from 33+/-2 to 28+/-2 mmHg (p < 0.001) and arterial oxygen tension increased from 13.3+/-2.3 to 16.7+/-2.7 kPa (p < 0.05). The mean change in arterial oxygen tension in percent was 29.8+/-6.3% (p < 0.05). The response was significant only in the first step from 0 to 3 or 5 ppm with no further significant changes in mean pulmonary artery pressure or oxygenation at higher doses. The decrease in mean pulmonary artery pressure was concomitant with a significant increase in arterial oxygen tension. No dose-response relationship was found with increasing doses to 80 ppm. [ABSTRACT FROM AUTHOR]

Methods: Fourteen children aged 4-15 months were studied after corrective cardiac surgery. Heart rate was increased by 20% with an external pacemaker. Cardiac output (CO) was measured with thermodilution. Oxygen saturation was measured in systemic artery (SaO2), central vein (ScvcO2) and pulmonary artery (SvO2). Inspiratory to endtidal oxygen difference (FI-ETO2) was measured using a paramagnetic technique. SvO2 was measured continuously using a spectrophotometric technique., Results: CO increased in three patients and decreased in 11 patients during pacing. Regression between DeltaCO and Delta(1/Sa-vO2), Delta(FI-ETO2/Sa-vO2), Delta(FI-ETO2/Sa-cvcO2) showed r=0.70, r=0.76 and r=0.75, respectively. DeltaCO exceeded 10% in 17 of 26 interventions. Changes in FI-ETO2 of equal direction as changes in CO occurred in 12 of these 17 interventions., Conclusion: Estimations of CO changes, based on SvO2, can be enhanced if changes in FI-ETO2 are also measured. ScvcO2 instead of SvO2 gives equivalent results. Sudden changes in FI-ETO2 after pacemaker initiation or termination can predict the direction of CO changes.

Extracorporeal membrane oxygenation was used as a bridge for three infants with complicated long segment congenital tracheal stenosis to tracheal homograft transplantation with cadaveric tracheal homograft and for one child, with an extensive traumatic tracheal laceration caused by aspiration of a sharp foreign body, to definitive tracheal repair. In all four cases mechanical ventilation was impossible and death almost certain without extracorporeal membrane oxygenation.

Early-onset neonatal group B beta-hemolytic streptococcus (GBS) infection exhibits pathophysiologic characteristics of a toxic shock syndrome, in which a cascade of inflammatory mediators are involved. Thromboxane A2 (TXA2) is thought to play an important role as a mediator of the pulmonary response to GBS toxin, because high lung lymph concentrations of a TXA2 metabolite have been observed after GBS toxin injections in sheep. The aim of this study was to evaluate the effects of a selective antagonist of the TXA2-prostaglandin endoperoxide receptor (SQ 29,548). Six unanesthetized young lambs, each serving as its own control, were given SQ 29,548 or vehicle control followed by GBS toxin challenge. Hemodynamic and lung function (lung mechanics, lung volume, ventilation) responses were followed for 5 h. When compared with the control studies, treatment with SQ 29,548 significantly altered the response to GBS toxin. SQ 29,548 reduced the increase in pulmonary and systemic vascular resistance, improved cardiac output and stroke volume, improved dynamic lung compliance but not airway resistance, and improved oxygenation. The attenuating effect of SQ 29,548 was most pronounced during the first phase of toxin response (15-90 min after toxin infusion), but significant treatment effects were also seen during the second phase (120-300 min after toxin infusion). This study demonstrates that TXA2 is an important mediator of the response to GBS toxin and is responsible for hemodynamic and lung function changes. Thromboxane receptor blockade may offer a potential therapeutic approach to infants with severe early-onset GBS sepsis.

Prophylactic treatment with ovine surfactant was evaluated in preterm lambs at risk for development of hyaline membrane disease. Eight mechanically ventilated newborn lambs were treated before delivery and 10 served as controls (gestational age 129-131 d). Lung mechanics, functional residual capacity, alveolar ventilation, efficiency of ventilation, and distribution of ventilation were tested using pressure, flow, and nitrogen elimination (nitrogen washout during 100% oxygen breathing) measurements in the endotracheal tube. The surfactant-treated animals showed significantly improved gas mixing efficiency in the lung with improved alveolar ventilation. Single exponential washout pattern dominated in both groups. Adequate functional residual capacity was established earlier after birth in the treated lambs than in the control animals. Lung mechanics in the treated group showed significant improvement in dynamic lung compliance. Surfactant treatment also improved gas exchange and reduced respirator pressure requirement. We speculate that the main functional effect of surfactant treatment in preterm lambs at risk to develop hyaline membrane disease is to maintain the patency of the peripheral airways in the lung, which improves diffusive gas mixing, alveolar ventilation, and gas exchange. The techniques used in this study should also be useful to evaluate lung function in preterm human infants after specific adaptation of the equipment size.