Vasopressin improves hemodynamic status in infants with congenital diaphragmatic hernia

Abstract

Objective: To assess the ability of vasopressin to stabilize hemodynamics in infants with systemic hypotension secondary to congenital diaphragmatic hernia (CDH).

Study design: A retrospective chart review was performed to identify 13 patients with CDH treated with vasopressin for refractory hypotension to assess the effect of vasopressin on pulmonary and systemic hemodynamics and gas exchange in this setting. Data collected included demographics, respiratory support, inotropic agents, pulmonary and systemic hemodynamics, urine output, and serum and urine sodium levels during vasopressin therapy.

Results: Vasopressin therapy increased mean arterial pressure and decreased pulmonary/systemic pressure ratio, heart rate, and fraction of inspired oxygen. In 6 of 13 patients, extracorporeal membrane oxygenation therapy was no longer indicated after treatment with vasopressin. Improvement in left ventricular function and oxygenation index after vasopressin initiation was associated with a decreased need for extracorporeal membrane oxygenation therapy. Prolonged vasopressin treatment was associated with hyponatremia, increased urine output, and increased urine sodium.

Conclusions: Vasopressin stabilized systemic hemodynamics without adverse effects on pulmonary hemodynamics in a subset of infants with CDH. Our results suggest a potential role for vasopressin therapy in patients with CDH with catecholamine-resistant refractory hypotension.

Figure 1

A, Among all patients (n=13), heart rate (HR) decreased and mean arterial pressure (MAP) increased after initiation of vasopressin therapy (P=0.0021). B, Same trends in HR and MAP in those patients not treated with ECMO (n=6). C, Among all patients (n=13), FiO2 decreased significantly and SaO2 increased with vasopressin therapy. D, Same trends in SaO2 and FiO2 in those patients not treated with ECMO (n=6).

Figure 2

A, Among those patients treated with ECMO, heart rate decreased and MAP increased slightly immediately following vasopressin initiation (n=7). B, SaO2 increased slightly and FiO2 was quickly weaned to room air following initiation of ECMO therapy.

Figure 3

A, Pulmonary to systemic pressure ratio pre and post vasopressin treatment (available data for 8 patients). B, Oxygenation index decreased following vasopressin administration in patients treated with ECMO (n=7) and those not treated with ECMO (n=6).

Figure 4

A, Urine output increased significantly following initiation of vasopressin therapy in the six patients with prolonged vasopressin exposure. (P=0.0022). B, Serum sodium decreased following vasopressin initiation (average nadir 117.8mmol/L; range 111-121) due to excessive urinary excretion. C, Urine sodium was elevated during days 2, 3, and 4 of vasopressin therapy but decreased by day 5 and following vasopressin withdrawal. D, Serum creatinine decreased significantly by day 3 and 4 of vasopressin infusion.