Effects of terlipressin on pulmonary artery pressure in a septic cooled infant: an echocardiographic assessment

Abstract

Experience with terlipressin (TP) in the neonatal field is scarce. We describe the effects of TP on pulmonary circulation, studied with echocardiography, in an asphyxiated septic cooled infant with pulmonary hypertension (PH) who developed catecholamine-resistant hypotension and exacerbation of PH shortly after the beginning of the rewarming. TP was added to norephinephine and adrenaline infusions at the dose of 0.02 mg kg À1 every 6 h, because of refractory hypotension and oliguria. After 10 min, blood pressure dramatically and definitely increased, and urinary output was re-established after 60 min. Echocardiographic evaluation 30 min after the second bolus of TP showed unchanged velocity of the tricuspidal valve regurgitation and improved biventricular functional indexes respect to the pre-treatment assessment. TP was continued for 12 h (three doses) without significant adverse effect except for a transient increase in troponin levels. Addition of TP boluses to catecholamine infusion in our newborn was effective in increasing systemic vascular resistance without increasing pulmonary vascular resistance, successfully reversing the hemodynamics of severe PH, and suggesting a potential primary vasodilator effect on pulmonary circulation. Transient increase of troponin levels during TP treatment confirms the risk of excessive coronary vasoconstriction when TP boluses are added to high dose catecholamines.

Vasopressin Improves Hemodynamic Status in Infants with Congenital Diaphragmatic Hernia

“…Failure of LV function and OI to improve after initiation of vasopressin predicted the need for ECMO in our patient population. This effect has been demonstrated previously in neonates with similar hemodynamic status and pulmonary hypertension (10,12,13). .…”

“…Vasopressin is used in the setting of cardiac arrest, sepsis, vasodilatory shock, and cardiac surgery with reported effects including improved systemic blood pressure, a decline in catecholamine requirements, and increased urine output (17,18). In studies of patients with pulmonary hypertension, vasopressin improves systemic hemodynamics without adverse effects on the pulmonary vasculature, making it an ideal agent for treatment of infants with CDH who have pulmonary hypertension and systemic hypotension (12,19). …”

Rescue Treatment with Terlipressin for Persistent Pulmonary Hypertension and Refractory Shock in a Preterm Infant

“…Various genes are associated with Bartter syndrome [4]; MAGED2 mutation described recently is associated with transient Bartter syndrome which starts antenatally with severe phenotype and usually resolves by six weeks of age. Our case presented at around six weeks with acute kidney injury without hypomagnesemia [5].…”

“…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.…”

Vasopressin in Pediatric Critical Care

“…Because of its potential for pulmonary vasodilation, terlipressin has been used as rescue therapy in the management of severe pulmonary hypertension in neonates with congenital diaphragmatic hernia, perinatal asphyxia, and therapeutic hypothermia. 50,51 These studies are limited to case reports, and this indication has not been further evaluated in prospective trials to date.…”