Persistent Pulmonary Hypertension Of The Neonate Research Articles

Adverse effects of drugs on the immature kidney.

The immature kidney may be adversely affected by a variety of vasoactive or diuretic drugs, either administered to the mother during pregnancy, or to the neonate. Inhibitors of the angiotensin-converting enzyme administered to the hypertensive pregnant woman can severely and sometimes definitely impair renal function in the fetus, leading to postnatal anuria. Pathogenesis involves interference with the renin-angiotensin system and the prostaglandins. Beta-adrenergic agents administered during labor depress glomerular filtration rate transiently. Tolazoline, an alpha-adrenergic blocking agent useful in the treatment of persistent pulmonary hypertension of the neonate induces intense renal vasoconstriction with consequent hypoperfusion. Indomethacin, a prostaglandin synthetase inhibitor used for the pharmacological closure of a patent ductus arteriosus, also increases renal vascular resistance, and decreases urine output. Furosemide, the drug most often used in oliguric neonates, may also adversely affect the newborn infant. Its use has been associated with an increase in the incidence of patent ductus arteriosus, hypercalciuria, nephrocalcinosis and secondary hyperparathyroidism. These observations demonstrate that the proper use of drugs requires that the therapeutic endpoint be clearly defined and the predictable side effects be anticipated.

Transition phase during hyperventilation therapy for persistent pulmonary hypertension of the neonate.

It is important for the clinician who is hyperventilating infants with persistent pulmonary hypertension (PPHN) to recognize a transition phase during therapy when pulmonary hypertension is no longer the primary cause of hypoxemia, because infants who are hyperventilated develop parenchymal lung disease after 2 to 3 days. This study reports ten infants who showed PaO2 lability early in the course of PPHN, with an inverse relationship between PaO2 and PaCO2. At a mean age of 79 +/- 14 (SEM) there was a transition phase, after which PaO2 lability decreased and the infants did not require hyperventilation. The mean change in PaO2 per change in PaCO2 was significantly (p less than .05) higher pretransition (22.4 +/- 5.2) compared to during transition (5.1 +/- 1.4) or post-transition (1.9 +/- 1.2). Mean alveolar-arterial oxygen gradient was higher (p less than .05) pretransition (495 +/- 36) vs. post-transition (405 +/- 52) and was more labile relative to PaCO2 change pretransition (20.3 +/- 5.9) compared to post-transition (.3 +/- 2.4). When ventilator settings were reduced after the transition phase, PaCO2 rose by 12.2 torr.

Pulmonary thromboemboli after neonatal asphyxia

Two surviving neonates with pulmonary thromboembolism, diagnosed by ventilation-perfusion lung scan, are described. Both infants had respiratory distress, and one had features consistent with persistent pulmonary hypertension of the neonate. These reports demonstrate that substantive pulmonary emboli can occur in neonates and may not be recognized without an appropriate level of clinical suspicion.

TRACHEAL SECRETION INPACTION DURING HYPERVENTILATION FOR PERSISTENT PULMONARY HYPERTENSION OF THE NEONATE

We have recently observed at two institutions the occurrence of tracheal secretion casts or extensive mucous plugging in five neonates hyperventilated for Persistent Pulmonary Hypertension of the Neonate. This finding represents a significant clinical problem that can be recognized by pneumothoraces or CO2 retention often in the face of adequate oxygenation. Tracheal suctioning or bronchoscopy may be necessary to remove the thick secretions. Five neonates were reviewed with mean BWt 3.51 kg, mean GA 39.6 wks. All infants were on the Bournes Bear Cub infant ventilator and all required max. insp. O2 concentration of 100%. Ventilation was initiated at a mean of 11 hrs and these infants had been ventilated a mean of 191.4 hrs when the secretions were removed. At the time of recognition of tracheal plugs, mean ventilator settings were: inspired O2 concentration 92%, rate 80 breaths/min, peak inspiratory pressure 55 cmH2O, PEEP 4.4 cmH2O, and mean arterial blood gas values were: PO2 68, PCO2 133, pH 7.25. All patients were on pancuronium and all had pneumothoraces associated with tracheal plugging. Large tracheal plugs were removed by suctioning in 2 infants, bronchoscopy in 2 infants and following jet ventilation in 1 infant. An increase in PCO2 during hyperventilation with high rate and pressures and adequate PO2 may signal tracheal plugs. Aggressive suctioning or bronchoscopy may be necessary to remove these plugs. Effective airway humidification systems are necessary for hyperventilation.