Strategies of Cardiovascular and Ventilatory Management in Preterm Infants With Prolonged Rupture of Fetal Membranes and Oligohydramnios

Abstract

We read with interest the case presentations describing the use of nitric oxide for preterm infants with apparent pulmonary hypoplasia related to oligohydramnios.1 Geary and Whitsett describe two infants, each having experienced midtrimester ruptured membranes and prolonged oligohydramnios before delivery, who developed refractory hypoxia that was apparently responsive to inhaled nitric oxide. We have recently reported similar experience with infants having sublethal pulmonary hypoplasia following preterm premature rupture of membranes (PPROM) and oligohydramnios occurring as early as 14 weeks' gestation.2 Six of eight cases were treated with nitric oxide and four survived, each with an immediate response similar to that described in the cases of Geary and Whitsett. Although, these infants had been exposed to severe oligohydramnios, in at least two of the four cases, there was ongoing vaginal fluid leaking, suggesting continued fetal fluid production. Our experience has suggested even small amounts of fluid may modulate the degree of pulmonary hypoplasia 2,3 With current technology, some infants may survive now who would not have in the past decade. 2The clinical presentation of pulmonary hypertension with secondary hypoxemia in these cases is consistent with postmortem histopathologic findings of markedly increased alveolar ductal artery muscularization. 4 Another lung structural change that may be an important determinant of clinical outcome relates to elastic tissue, which is severely diminished in infants with PPROM.5 These hypoplastic lungs, particularly with surfactant deficiency, are uniquely susceptible to volutrauma.6 For this reason, we have recommended early installation of surfactant (possibly lower volume, consistent with size of lung, rather than total body weight). If high peak-inflating pressures are needed with conventional ventilation, early use of high-frequency oscillation may be better tolerated.2,7 As we noted previously, 2 following resolution of the pulmonary hypertension, a patent ductus arteriosis with the left-to-right shunt may occur and prolong clinical recovery, another factor related to risk of chronic lung disease.In summary, infants born after midtrimester PPROM are at high risk for significant pulmonary complications. These complications should be anticipated and clinical management should be based on the unique pathophysiologic changes. We agree with Geary and Whitsett that nitric oxide should be used cautiously in preterm infants until more data are available regarding long-term implications. However, its use in early midtrimester PPROM patients with severe oligohydramnios is reasonable based on the high mortality rate and underlying pathophysiology.

Combination therapy for life-threatening pulmonary hypertension in a premature infant: first report on bosentan use

“…Perinatal infection is a further established independent risk factor for PPHN in such circumstances [12]. Several reports point out that these infants may benefit from iNO [1,7,10,16,23], although premature infants<29 week gestation may have poor response to this drug [12]. Alternative therapeutic options like PDE5 inhibitors were studied in a small number of preterm infants [6,13], while no report exists on ET-1 receptor antagonists use at this age.…”