aaHigh-frequency ventilation (HFV) is widely used for rescue treatment of hypoxaemic neonates and premature infants [1]. Although its role as a first-line mode of ventilation has not been established, it is often applied in newborns with respiratory failure, who cannot be successfully managed with conventional mechanical ventilation (CMV). The results of recent studies investigating the theoretically diminished baro-and volutrauma remain equivocal. Nonetheless there is evidence for a decreased secretion of inflammatory mediators [2] and a reduced amount of lung oedema [3] using high-frequency oscillatory ventilation (HFOV) with or without additional application of exogenous surfactant.Inhaled nitric oxide (iNO) as a treatment for neonatal pulmonary hypertension has been in use for the past few years, both in premature infants and in term neonates [4][5][6][7][8][9]. It is worth noting that the first published application of iNO in a premature infant, and the subsequent improvement of oxygenation, occurred during HFOV [10]. Although still an experimental treatment, NO inhalation plays an important therapeutic role in severe hypoxaemia of the newborn due mainly to extrapulmonary shunting [11,12].Recently, a randomized, multicentre trial showed that the combination of iNO and HFOV was superior in term neonates, as compared to either treatment alone [13]. We report a similar experience in a full-term neonate, but also in a premature infant of 29 weeks of gestation.
Case 1The term infant was delivered by caesarean section because of maternal hypertension. There was no maternal history of infection. The infant was male and had a birth weight of 3,810 g and Apgar 9,10,10 (1',5',10'); he became symptomatic at the age of 15 min with intercostal retractions and grunting. At that stage, capillary blood gases were: pH 7.23, capillary carbon dioxide tension (Pc,CO 2 ) 8.0 kPa (60 mmHg), capillary oxygen tension (Pc,O 2 ) 4.0 kPa (30 mmHg) in combination with an increasing inspiratory oxygen fraction (FI,O 2 ). At the age of 2 h the neonatal transport team was called, which arrived about 1 h later. The infant was intubated and ventilated because of persistent cyanosis, antibiotic treatment was started and he was transferred to our neonatal intensive care unit. Upon arrival, bovine surfactant (100 mg·kg -1 ) was applied; in order to achieve adequate oxygenation, peak inspiratory pressures (PIPs) up to 4.6 kPa were required (positive endexpiratory pressure (PEEP) 0.5 kPa, rate 70 breaths·min -1 , inspiratory time 0.35 s, mean airway pressure (MAP) 1.8 kPa, FI,O 2 1.0). After approximately 6 h a sudden deterioration of oxygenation and arterial blood pressure occurred, caused by a pneumopericard, which was relieved by drainage. During this event, profound hypoxia occurred for about 15 min, the continuously recorded arterial oxygen saturation (Sa,O 2 ) (measured by pulsoximetry) was approximately 20%. Following drainage of the pneumopericard We report two cases of newborn infants with profound hypoxaemia, who did not respond with ...