Radiographic lung disease and response of persistent pulmonary hypertension to mean airway pressure and alkalosis.

Persistent pulmonary hypertension of the newborn (PPHN) is associated with multiple cardiopulmonary diseases. Therapy often includes hyperventilation/alkalosis despite little evidence as to its efficacy in diverse conditions. To determine (1) if part of the improvement of arterial oxygen tension (PaO2) attributed to alkalosis is actually related to increased mean airway pressure (P(aw)) and (2) if the presence of radiographic pulmonary disease predicts the response to alkalosis or mean airway pressure, we reviewed records of 19 newborns with well-documented PPHN. Arterial blood gases and corresponding ventilator settings were recorded during the first day of life. To adjust for lower FiO2, corrected PaO2 (cPaO2) was calculated when the FiO2 < 1.0, such that cPaO2 = calculated arterial/alveolar oxygen ratio x (713 - PaCO2/0.8). Regression equations were obtained and mean slopes of these were compared for P(aw) vs. cPaO2, and pH vs. cPaO2 by one group t-tests (with assumed population slope of zero). There was no correlation between P(aw) and cPaO2 (mean slope +/- SD = -8.4 +/- 30.8, P = 0.25), but there was a moderate correlation between pH and cPaO2 (mean slope = 333.1 +/- 480.5, P = 0.007). Patients were then classified by chest radiographs as having severe or minimal/no lung disease. Relationships of P(aw) and pH to cPaO2 were then re-examined. No correlation was present between P(aw) and cPaO2 in 11 patients with PPHN and severe radiographic disease (mean slope = -7.4 +/- 26.9, P = 0.38) or in eight patients with PPHN and minimal/no lung disease (mean slope = -9.8 +/- 37.5, P = 0.48).(ABSTRACT TRUNCATED AT 250 WORDS)

Fetal exposure to lisinopril: neonatal manifestations and management.

The use of angiotensin-converting enzyme (ACE) inhibitors in pregnancy has been associated with neonatal morbidity and mortality. The mechanism of renal dysfunction likely is related to fetal hypotension and prolonged decreased glomerular filtration. Six of 14 previously published cases of neonatal renal failure after maternal ACE inhibitor therapy resulted in death. Eight infants survived after peritoneal dialysis, some with residual renal impairment. Serum lisinopril levels and ACE activity in our patient indicate that during the anuric state the drug has an extremely prolonged half-life, and that it is removed by peritoneal dialysis. In view of this prolonged half-life and the drug's continued suppression of ACE activity and renal function, we recommend institution of early dialysis in infants with renal failure after maternal therapy with lisinopril.

Effect of indomethacin on edema following single and repetitive cerebral ischemia in the gerbil.

BACKGROUND AND PURPOSE: Repetitive periods of cerebral ischemia result in more severe injury than a single period of ischemia of similar total duration. We investigated the possibility of prostaglandin mediation of this increased injury by attempting to modify brain edema formation with indomethacin pretreatment. METHODS: Under halothane/N2O anesthesia, groups of gerbils underwent bilateral carotid occlusion to induce forebrain ischemia. Group I underwent a single 15-minute period of carotid occlusion. Group II underwent three 5-minute periods of occlusion at hourly intervals. Groups III and IV were similar to groups I and II, respectively, but received 0.2 mg/kg indomethacin before carotid occlusion. Cortical and cerebellar water and sodium contents were determined in control animals (n = 6) at time zero and in experimental animals 24, 48, and 72 hours after ischemia (n = 6-10 gerbils/group at each time point). RESULTS: Cortical water and sodium contents in group II peaked 48 hours after insult (82.15 +/- 0.31% and 420 +/- 14 meq/kg dry wt, respectively) and were significantly higher than control and group I values at both 24 and 48 hours. Cortical water did not change from control in group I animals. Indomethacin pretreatment significantly attenuated increases in water and sodium content seen at 48 hours in gerbils undergoing repetitive ischemia (peak 80.02 +/- 0.45% and 300 +/- 39 meq/kg dry wt), but did not affect mortality. CONCLUSIONS: Indomethacin lessens edema after repetitive cerebral ischemia, suggesting that elevations of cyclooxygenase products are responsible, at least in part, for severe brain edema following repetitive ischemia.

Spontaneous focal gastrointestinal perforation in very low birth weight infants.

Spontaneous, focal gastrointestinal perforation occurred in six very low birth weight infants. The first recognized clinical sign of perforation in five of the six infants was striking blue-black discoloration of the abdominal wall. In all cases the clinical and radiographic presentations, as well as the histologic findings, were distinct from those associated with necrotizing enterocolitis. All 4 infants who underwent exploratory laparotomy and repair had excellent surgical outcomes.

Double-blind, randomized trial of a calf lung surfactant extract administered at birth to very premature infants for prevention of respiratory distress syndrome.

Organic solvent extraction of surfactant obtained by lavage of calf lungs yields a highly surface-active material. A double blind, randomized clinical trial to determine the effect of this material on respiratory distress syndrome in premature infants was initiated in the Neonatal Intensive Care Unit at the University of Rochester in December 1983. Infants 25 to 29 weeks gestational age were eligible for entry into the trial. At the time of this interim analysis 32 patients had been randomly selected and entered into the trial, 16 surfactant-treated patients and 16 in a control group who received only saline. At birth, intrapulmonary instillation of the calf lung surfactant extract dispersed in saline or saline alone occurred in the delivery room immediately after intubation and prior to ventilation; infants were then ventilated and treated as usual. At 6, 12, 24, 48, and 72 hours after birth, the severity of respiratory distress was categorized as either minimal, intermediate, or severe based on oxygen and mean airway pressure requirements. Differences observed at six hours after birth were of marginal significance, but at 12 and 24 hours the surfactant-treated group had significantly (P less than .01) less severe respiratory distress compared with the control group. Differences between treated and control infants were not statistically significant at 48 and 72 hours after birth. In four surfactant-treated infants the severity of respiratory distress worsened between 24 and 48 hours after birth, suggesting that one dose of surfactant at birth may not be sufficient for some infants.