Objective: Characteristics of preterm infants who develop pulmonary hypertension (PHT) and their response to inhaled nitric oxide (iNO) are not well described. Our objective was to identify risk factors for PHT in infants <37 weeks gestational age (GA) and to evaluate their response to iNO.Study design: A retrospective chart review was conducted in infants <37 weeks GA born from July/2000 to October/2005 who had an echocardiographic diagnosis of PHT in the first 4 weeks of life. A comparison non-PHT group was generated matched for GA and birth date. Data on prenatal and postnatal characteristics, response to iNO and mortality were collected.Results: Low Apgar scores, preterm premature rupture of membranes, oligohydramnios, pulmonary hypoplasia and sepsis were independently predictive of PHT. Mortality was significantly higher in the PHT group (26.2% versus 4.1%; P<0.0001) compared to the control group. Low birth weight, severe intraventricular hemorrhage and male sex were significantly associated with death in infants with PHT. Thirty-seven percent (23/61) of infants with PHT were treated with inhaled NO. Infants <29-week GA had poor response to iNO and the response to iNO increased with GA (P<0.02).Conclusions: Low Apgar scores, oligohydramnios and pulmonary hypoplasia are associated with the development of PHT in premature infants. The percentage of infants responding to iNO increases with advancing GA.
A B S T R A C T The effects of Escherichia coli endotoxin on lung mechanics, hemodynamics, gas exchange, and lung fluid and solute exchange were studied in 12 chronically instrumented unanesthetized sheep. A possible role for cyclooxygenase products of arachidonate metabolism as mediators of the endotoxin-induced alterations in lung mechanics was investigated by studying sheep before and after cyclooxygenase inhibition with sodium meclofenamate and ibuprofen. Sheep were studied three times in random order: (a) sodium meclofenamate (or ibuprofen) infusion alone; (b) E. coli endotoxin alone; and (c) meclofenamate (or ibuprofen) and endotoxin. Meclofenamate alone had no effect on any of the variables measured. Endotoxin alone caused early marked changes in lung mechanics: resistance to airflow across the lungs (RL) increased 10-fold, dynamic lung compliance (Cdyn) decreased 80% and functional residual capacity (FRC) decreased by >30%. The alveolar-to-arterial oxygen difference (AAaPO2) increased markedly following endotoxemia. In the presence of sufficient meclofenamate to inhibit accumulation of thromboxane-B2 and 6-keto-prostaglandin Fl. in lung lymph, endotoxin caused no increase in RL, Cdyn decreased by <40%, and FRC decreased by only 6%. Meclofenamate significantly attenuated the hypoxemia and early pulmonary hypertension caused by endotoxemia but had no effect on the late increases in lung fluid and solute
The nature and control of early neonatal respiratory patterns were determined in 10 premature, asphyxiated lambs. Severe retardation of early expiratory airflow (braking) characterized an initial pattern (A), but was absent in a final one (B). During a transition pattern (pattern T), pattern A and B airflow types occurred. Close temporal relationships between the airflow patterns and posterior cricoarytenoid (PCA), thyroarytenoid (TA), and diaphragm (D) integrated muscle activities were demonstrated quantitatively. Specifically, in pattern A, the duration of braked expiratory airflow was related to the durations of TA burst activity and the absence of PCA burst activity (r2 = 0.99). In pattern A, pH, but not arterial PCO2 or arterial PO2, differed from that in patterns T and B [7.01 +/- 0.14 (A), 7.11 +/- 0.12 (T), 7.19 +/- 0.08 (B) (P < 0.03)]. Within-breath airflow and respiratory muscle activity relationships and differences in neural and mechanical respiratory timing intervals between patterns suggested that neural feedback was important in the control of central pattern generation. Thus activities of PCA, TA, and D shape the early neonatal airflow patterns and are influenced mainly by neuromechanical, and not chemical, feedback.
Prognostic factors for survival of 62 fetuses and neonates with nonimmune hydrops fetalis (NIHF) were studied retrospectively. Twenty-eight infants survived ≥28 days which is 45% for all fetuses and newborns diagnosed with NIHF and 61% for liveborns with unresolved NIHF. Univariate analysis identified that mortality was associated with the presence of ≥2 serous cavity effusions and a need for chest compressions at birth. Multivariate logistic regression analysis confirmed that the presence of ≥2 serous cavity effusions was significantly associated with mortality from NIHF <28 days after birth [OR = 48.2 (CI 3.6, 662.9) (p < 0.004)]. We conclude that, compared to published cases from the 1970s and early 1980s, survival of liveborns with NIHF seems improved. The decrease in stillbirths is more notable. The severity of hydrops at birth is the key determinant for survival.
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