Rescue Treatment with Terlipressin for Persistent Pulmonary Hypertension and Refractory Shock in a Preterm Infant
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Rescue Treatment with Terlipressin for Persistent Pulmonary Hypertension and Refractory Shock in a Preterm Infant
in oxygenation (OI from 38 to 15). In the next 24 hours, he developed left to right ductal shunt and he was progressively weaned from pulmonary vasodilators. Terlipressin was maintained for 48 hours and then tapered gradually (1 µg/kg/h) allowing the infant to be weaned from catecholamines (7th day of life) and finally extubated at 12th day of life. The child was discharged home without any clinically significant sequelae. At 2 years follow up, the child has age-appropriate developmental status. With terlipressin we observed a rapid raise in MAP with a marked improvement in pulmonary hypertension and oxygenation, allowing tapering of catecholamines. Terlipressin has been used to treat catecholamine-resistant vasodilatory shock in adults, showing restoration of arterial blood pressure. Terlipressin has also been used in pediatric and neonatal refractory shock with unclear clinical benefits [2,3]. Unlike adults, pure vasodilatory shock is uncommon in the pediatric and neonatal population and in consequence excessive vasoconstriction can induce tissue ischemia and worsen heart function and is not generally recommended.
Persistent pulmonary hypertension of the newborn (PPHN) affects about 2/1000 newborn. The mainstay of therapy is supportive high frequency oscillatory ventilation (HFOV) and inhaled nitric oxide (NO), which have decreased the need for Extracorporeal membrane oxygenation (ECMO) in these patients [1].However, still there is significant mortality and affected infants are at risk of long-term neurological impairment. We present the case of a preterm infant with severe PPHN and shock that failed all available therapies and was successfully rescued with the administration of terlipressin.
Terlipressin is a vasopressin analogue with long half-life that exerts effects via V1 and V2 receptors.The main clinical effect is mediated by V1-receptor that causes smooth muscle contraction and induces a potent increase in systemic vascular resistance (SVR) and blood pressure.Terlipressin is reported to increase SVR without a concomitant increase in pulmonary vascular resistance (PVR) [4]. In fact terlipressin may induce direct pulmonary vasodilatation via NO-release and lower pulmonary arterial pressure. Terlipressin-induced increase in SVR also improves coronary perfusion and right heart function contributing to increased pulmonary blood flow and oxygenation; which is newborn infants may be further facilitated by reversal of right to left intra-cardiac shunts as a consequence of increased MAP/PAP ratio [5].
A 33-week male preterm baby (birthweight 2010 g) was admitted to our neonatal intensive care unit. Soon after birth he developed respiratory distress and hypoxemia. He was intubated and a surfactant dose was administered but without significant improvement. An echocardiogram showed a structurally normal heart and a near-systemic pulmonary artery systolic pressure (PASP) of 55-60 mmHg. HFOV and inhaled
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