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Extracorporeal Membrane Oxygenation for Infant of a Diabetic Mother with Congenital Heart Defect
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A5248 - Extracorporeal Membrane Oxygenation for Infant of a Diabetic Mother with Congenital Heart Defect
Author Block: A. Y. Wen1, T. Chadha2, H. M. Dapul1, J. C. Fisher3, A. Chopra1; 1Pediatric Critical Care Medicine, NYU Langone Medical Center, New York, NY, United States, 2Pediatric Critical Care Medicine, Wolfson Children's Hospital, Jacksonville, FL, United States, 3Surgery, NYU Langone Medical Center, New York, NY, United States.
Infants of diabetic mothers (IDMs) are at increased risk for developing congenital heart defects. We present the case of a newborn male delivered at 38 weeks gestational to a mother with untreated pregestational diabetes with hemoglobin a1c of 11.2%. The patient was large for gestational age with birth weight of 4250 grams, and was born hypotonic with respiratory failure necessitating endotracheal intubation. Apgar scores were 1, 6, 6, and 7 at 1, 5, 10, and 15 minutes, respectively. Transthoracic echocardiogram (TTE) showed a patent ductus arteriosus, hypertrophic ventricles, elevated pulmonary pressures, and dynamic left ventricular outflow tract obstruction consistent with hypertrophic obstructive cardiomyopathy associated with infants of diabetic mothers (HOCM-IDM) further complicated by persistent pulmonary hypertension of the newborn (PPHN). The infant’s condition deteriorated, and he became hypotensive to 44/34 and hypoxemic with PaO2 30.8 mmHg, despite therapy with esmolol, fluid administration to maintain preload, inhaled nitric oxide, and high frequency oscillator ventilation. On day of life 3, the patient was placed on veno-venous extracorporeal membrane oxygenation (ECMO). Repeat TTEs showed improved filling of the left ventricle and decreased pulmonary pressures, so the patient was successfully decannulated on day of life 7 while on esmolol for rate control, and a combination of inhaled nitric oxide, sildenafil, and iloprost for pulmonary vasodilation. HOCM-IDM is a well-recognized cardiomyopathy distinguished from other forms of HOCM by its transient nature. Pathophysiology is attributed to fetal hyperinsulinemia with subsequent synthesis and deposition of fat and glycogen in cardiac myocytes as a result of poorly controlled maternal gestational diabetes. The natural history of HOCM-IDM is spontaneous regression once removed from the maternal environment making supportive therapy with ECMO a viable treatment option to allow for resolution of ventricular hypertrophy over time. Concurrent PPHN worsens pulmonary vascular resistance and further complicates medical management. Due to the reversibility of course, ECMO should be considered for patients with HOCM-IDM and longer ECMO duration may be considered for patients with concurrent PPHN.
Author Block: A. Y. Wen1, T. Chadha2, H. M. Dapul1, J. C. Fisher3, A. Chopra1; 1Pediatric Critical Care Medicine, NYU Langone Medical Center, New York, NY, United States, 2Pediatric Critical Care Medicine, Wolfson Children's Hospital, Jacksonville, FL, United States, 3Surgery, NYU Langone Medical Center, New York, NY, United States.
Infants of diabetic mothers (IDMs) are at increased risk for developing congenital heart defects. We present the case of a newborn male delivered at 38 weeks gestational to a mother with untreated pregestational diabetes with hemoglobin a1c of 11.2%. The patient was large for gestational age with birth weight of 4250 grams, and was born hypotonic with respiratory failure necessitating endotracheal intubation. Apgar scores were 1, 6, 6, and 7 at 1, 5, 10, and 15 minutes, respectively. Transthoracic echocardiogram (TTE) showed a patent ductus arteriosus, hypertrophic ventricles, elevated pulmonary pressures, and dynamic left ventricular outflow tract obstruction consistent with hypertrophic obstructive cardiomyopathy associated with infants of diabetic mothers (HOCM-IDM) further complicated by persistent pulmonary hypertension of the newborn (PPHN). The infant’s condition deteriorated, and he became hypotensive to 44/34 and hypoxemic with PaO2 30.8 mmHg, despite therapy with esmolol, fluid administration to maintain preload, inhaled nitric oxide, and high frequency oscillator ventilation. On day of life 3, the patient was placed on veno-venous extracorporeal membrane oxygenation (ECMO). Repeat TTEs showed improved filling of the left ventricle and decreased pulmonary pressures, so the patient was successfully decannulated on day of life 7 while on esmolol for rate control, and a combination of inhaled nitric oxide, sildenafil, and iloprost for pulmonary vasodilation. HOCM-IDM is a well-recognized cardiomyopathy distinguished from other forms of HOCM by its transient nature. Pathophysiology is attributed to fetal hyperinsulinemia with subsequent synthesis and deposition of fat and glycogen in cardiac myocytes as a result of poorly controlled maternal gestational diabetes. The natural history of HOCM-IDM is spontaneous regression once removed from the maternal environment making supportive therapy with ECMO a viable treatment option to allow for resolution of ventricular hypertrophy over time. Concurrent PPHN worsens pulmonary vascular resistance and further complicates medical management. Due to the reversibility of course, ECMO should be considered for patients with HOCM-IDM and longer ECMO duration may be considered for patients with concurrent PPHN.
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