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Objective-To determine the efficacy of fibrinolytic therapy with tissue

Inhaled nitric oxide may play an important role in the management of transient critical pulmonary perfusion caused by reactive elevated pulmonary vascular resistance in the early postoperative period after Fontan-type operations and bidirectional Glenn anastomosis.

This study was a prospective, randomized design to compare oxygenation and pulmonary hemodynamics between inhaled nitric oxide (NO) and inhaled prostacylcin (PGI,), and between inhaled and i.v. PGI, in acute respiratory failure with pulmonary hypertension. Acute respiratory failure with pulmonary hypertension was induced in 12 piglets weighing 9-12 kg by repeated lung lavages and a continuous infusion of the stable endoperoxane analogue of thromboxane. Thereafter the animals were randomly assigned either for NO or PGI, application. All animals were treated with different concentrations of NO or different doses of PGI, applied i.v. and inhaled in random order. Continuous monitoring included ECG, central venous pressure (CVP), mean pulmonary artery pressure (MPAP), mean arterial pressure (MAP), artertial oxygen saturation (SaO,), and mixed venous oxygen saturation (SvO,) measurements. NO inhalation of 10 ppm resulted in a significant increase in Pao,/fraction of inspired oxygen (FiO,) from 7.5 2 1.34 kPa to 46.1 2 9.7 kPa. MPAP decreased significantly from 5.1 -t 0.26 kPa to 3.7 i 0.26 kPa during inhaled NO of 40 ppm; i.v. infusion of PGI, slightly increased oxygenation parameters. A significant increase in Pao,/ FiO, up to 32.4 2 3.lkPa was observed during PGI, aerosol delivery (11 < 0.01); i.v. PGI, decreased MAP from 11.5 -+ 0.39 kPa to 9.8 2 0.66 kPa ( p < 0.05) and MPAP from 5.8 -+ 0.53 kPa to 4.5 2 0.66 kPa, respectively ( p < 0.05). PGI, aerosol delivery significantly decreased the MPAP to 3.7 2 0.53 kPa ( p < 0.05) without influencing the MAP. It was concluded that inhaled NO and inhaled PGI, act as selective pulmonary vasodilators in acute respiratory Cdilure with pulmonary hypertension In 1987 N O was reported to be an important endotheliumderived relaxing factor (1, 2). NO is synthesized in the vascular endothelial cell from L-arginine by NO synthase. It rapidly diffuses into the vascular smooth muscle cell and acts by stimulation of guanylate cyclase producing cGMP which me-

Continuous arterio-venous haemofiltration (CAVH) and continuous veno-venous haemofiltration (CVVH) were used as renal support in 52 critically ill infants and children with acute renal failure. The majority of the patients were on mechanical ventilation (90%) and needed vasopressor support (85%). Uraemia was satisfactorily controlled with both treatment modes. Post-treatment serum urea levels were not different between survivors (94 +/- 8.8 mg/dl) and non-survivors (99.5 +/- 8.8 mg/dl). There were significant differences between survivors and non-survivors in the mean arterial pressure (64.7 +/- 3.8 vs 48.0 +/- 2.2 mmHg, p less than 0.001), the number of organ system failures (2.9 +/- 0.16 vs 3.8 +/- 0.21, p less than 0.025), and the severity of illness assessed by the acute physiologic score for children (APSC 19.4 +/- 1.9 vs 26.3 +/- 1.9, p less than 0.01). The overall mortality was 48%. The mortality in the CVVH group (65%) was higher than in the CAVH group (40%). Death was significantly related to sepsis (p less than 0.005) and multiple system organ failure (p less than 0.005). A major complication during CAVH was one femoral artery thrombosis after 12 days of treatment. Technical problems were only observed during CVVH. CAVH and CVVH are safe and effective methods of continuous renal support for critically ill paediatric patients with multiple system organ failure. CAVH is simpler, needs no specially trained staff and seems to the ideal renal replacement system for critically ill infants.