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[Prostacyclin in the treatment of persistent fetal circulation syndrome].

Persistent pulmonary hypertension of the neonate (PPHN), described initially by Gersony in 1969 as persistent foetal circulation (PFC syndrome), results from a flawed transition from foetal to extrauterine pulmonary circulation. It is primarily characterised by persistence of, or return to, the suprasystemic pulmonary vascular resistance and pressure normally found in the foetus. The increased pulmonary pressure causes right to left shunting through the ductus arteriosus or the foramen ovale, or both. The resulting hypoxaemia and acidosis may produce further pulmonary vasoconstriction and lead to a vicious cycle of shunting, hypoxia and acidosis. Infants with a wide variety of underlying clinical conditions develop PPHN. This condition is reversible, but can cause very severe and unrelenting respiratory failure and ultimate death when uncontrolled. Although vasodilating agents, such as tolazoline, have been used with variable success in the treatment of PPHN, a generally acceptable therapy is still lacking. We report here the use of prostacyclin (epoprostenol, PGI2) in two infants with severe and refractory hypoxaemia secondary to pulmonary vasoconstriction.

Epoprostenol↗
PubMed1983

[Tolazoline and dopamine in the treatment of the persistent fetal circulation syndrome].

The combined application of Tolazoline and Dopamine for the treatment of the persistent fetal circulation syndrome showed that Dopamine prevented the most common side effects of Tolazoline i.e. systemic hypotension and oliguria. The authors emphasize the importance of continuous monitoring of the systemic blood pressure in infants during this treatment.

Dopamine↗
PubMed1983

[Persistent fetal circulation syndrome: long-term clinical and treatment results].

The definition, pathophysiology, signs and symptoms, diagnostic and therapeutic procedures of the persistent fetal circulation syndrome are presented. A description of the clinical characteristics of 38 patients, admitted during a 3 years period, is included. The results of a follow-up investigation amongst the 20 surviving children are discouraging, because a maximum of only 5 children appears to be totally normal. At least half of the children is more or less handicapped, the majority of which severely!

Child Development↗
PubMed1982

[PFC syndrome (persistent fetal circulation). Central cyanosis in a full-term newborn infant without congenital heart defect].

In a case report the main features of the PFC-syndrome (persistent fetal circulation) are demonstrated: 1. general central cyanosis, 2. pulmonary hypertension, 3. right-to-left shunting via foramen ovale and (or) ductus arteriosus. At postmortem analysis in some of these patients the muscular thickness of the pulmonary vessels was found to be increased: primary PFC-syndrome. Hypoxia, shock, and many pulmonary disturbances of the newborn can produce the clinical picture of "persistent fetal circulation": secondary PFC-syndrome. Under adequate therapy with O2-insufflation, vasodilatory drugs, and if necessary mechanical ventilation the prognosis in the majority of cases is good.

Cyanosis↗
PubMed1987

Treatment of persistent fetal circulation syndrome of the newborn. Comparison of different doses of tolazoline.

The effects of two doses of tolazoline have been compared in 2 groups of newborns suffering from the persistent fetal circulation syndrome. The effects on PaO2 and AaDO2 were similar in the 2 groups who received either a bolus of 1 or 0.5 mg X kg-1 tolazoline, followed by a continuous infusion of 1 or 0.5 mg X kg-1 X h-1. The observed changes did not differ significantly from those previously observed in babies treated with 2 mg X kg-1. A rise in PaO2 and a reduction in AaDO2 were usually observed shortly after the bolus injection and at plasma levels between 1.5 and 4 micrograms X ml X -1. A progressive rise in plasma level over time occurred after 1 mg X kg-1 (and in the previous study of 2 mg) but not with 0.5 g/kg tolazoline. The elimination half-life of tolazoline in 6 patients was 5 to 13 h. The data suggest that continuous infusion of tolazoline is not necessarily required and that the dose of 0.5 mg/kg is more appropriate and safer than the higher doses usually proposed.

Blood Pressure↗
PubMed1983

Persistent pulmonary hypertension of the neonate (persistent fetal circulation syndrome).

This 15-year-old disease has been clearly described anatomically. Some understanding of possible in utero predisposing conditions has emerged from clinical and animal studies. However, we have very little understanding of the cellular processes that trigger and/or prolong the abnormal medial smooth muscle hypertrophy underlying the condition. Empiric observation has resulted in the development of hyperventilation as a fairly successful treatment modality, although the underlying mechanism of this salubrious effect is unknown. Drugs, a major focus of clinical and laboratory investigations, sometimes are marginally successful (and sometimes are utter failures). Translated into the neonatal intensive care unit, the disease is more frequently accurately diagnosed than in the past, but it remains frustratingly difficult to manage, and thus far is impossible to prevent. The research foundations laid in the past decade provide impetus for accelerated search into the fundamental cellular and biochemical derangements that cause persistent pulmonary hypertension. It is to be hoped that the next decade will yield major advances in both mechanistic understanding and in treatment.

Acetylcholine↗
PubMed1977

Persistence of fetal circulation syndrome: an echocardiographic study.

Serial echocardiograms were performed on 17 infants with persistence of fetal circulation syndrome to measure right ventricular systolic time intervals from pulmonic valve echograms and left ventricular systolic time intervals from aortic valve echograms. Right ventricular pre-ejection period/right ventricular ejection time ratio was prolonged in PFCS when compared to that in normal newborn infants, and diminished with clinical improvement. Left ventricular pre-ejection period/left ventricular ejection time ratio was prolonged in infants with PFCS. Echographic RPEP/RVET was consistent with the elevated pulmonary artery pressure and pulmonary vascular resistance of PFCS; elevated LPEP/LVET suggested left ventricular dysfunction.

Blood Circulation↗
PubMed1999

Cytokines, pulmonary surfactant and consequences of intrauterine infection.

Excess of inflammatory cytokines is implicated in the sequence of inflammatory diseases during the perinatal period. Specific cytokines induce spontaneous premature labor and accelerate fetal lung maturity in case of chorioamnionitis. In addition, they are involved in the pathogenesis of chronic lung disease, periventricular white matter damage, shock and multiorgan damage. Deficient cytokine response of the immature lung is associated with severe respiratory distress syndrome and persistent fetal circulation syndrome. Surfactant supplementation remains the cornerstone among therapies in the premature infant. Brief courses of glucocorticoids, antioxidants or inhaled nitric oxides remain to be fully evaluated as possible adjunct therapies shortly after birth in small premature infants with severe cardiorespiratory failure.

Animals↗