Case - Premature baby with severe LV dysfunction

Dr Nina Nouraeyan - NeoPremLab - Neonatologist at the Jewish General Hospital; McGill University

Case - October 2023

A baby was delivered at 25+0 weeks with a birthweight of 810 grams. The mother, a G5P2A3, had been taking Synthroid, citalopram, vitamins, and iron during her pregnancy. This was a spontaneous pregnancy with no identified abnormalities, as the 21-week ultrasound had yielded normal results. The mother initially presented at a community hospital with painful contractions and was administered dexamethasone (due to shortage of betamethasone availability). She was subsequently transferred to our institution, the Jewish General Hospital, where she received an additional dose of dexamethasone, along with magnesium sulfate, nifedipine, and indomethacin (300mg).

Due to the progression of contractions, cervical dilatation, and a breech presentation, the decision was made to perform a C-section. The baby's APGAR scores were 2, 6, and 8, and the cord pH was recorded at 7.11/-2.4. The newborn initially had a stable postnatal course but later required intubation and surfactant administration within 16 hours of birth. The infant's condition deteriorated rapidly, necessitating high-frequency oscillation (yielding a pCO2 level of 45), oxygen supplementation up to 100%, and initiation of inhaled nitric oxide (iNO) at 20ppm. Additionally, the baby experienced persistent hypotension, despite receiving normal saline boluses and packed red blood cells, leading to the initiation of dopamine and norepinephrine support.

On the first day of life, there was ongoing low blood pressure (22/10 mmHg) observed via invasive blood pressure monitoring, even with maximum dopamine and norepinephrine infusions. The infant's hemoglobin was found to be elevated at 202 g/L, with a hematocrit of 0.667. A bedside point-of-care ultrasound (POCUS), specifically a 4-chamber view of the heart, revealed severe left ventricular dysfunction and right ventricular hypertrophy. Notably, the patent ductus arteriosus (PDA) was not identified. A decision was made to initiate prostaglandin E1 (PGE) infusion at 0.005 mcg/kg/min to promote systemic flow in the context of LV dysfunction. Moreover, there was a prompt wean in the ongoing inotropic support (dopamine and norepinephrine), both of which exert vasoconstrictive effects that may have contributed to increased left ventricular afterload. Simultaneously, epinephrine was introduced at a rate of 0.1 mcg/kg/min to support left ventricular function. The baby demonstrated swift improvement, with blood pressure normalization, a reduction in FiO2 requirements to 50%, and enhanced clinical perfusion (improved color, capillary refill time, and peripheral pulses).

A repeat cardiac POCUS (4-chamber view) performed two hours after these interventions revealed improved flow within the left ventricular structures and enhanced contractility, albeit with some residual dysfunction. The epinephrine infusion was increased to 0.15 mcg/kg/min. After 8 hours, PGE was discontinued once blood pressure had stabilized. A follow-up cardiac POCUS, performed 12 hours after the initiation of epinephrine at 0.15 mcg/kg/min, showed significant improvement in left ventricular function. A subsequent bedside POCUS conducted three days later confirmed complete normalization of left ventricular function. At this time, the epinephrine infusion was maintained at 0.1 mcg/kg/min and weaned. The exact etiology of the cardiogenic shock remains unclear, as there was no evidence of significant perinatal asphyxia (normal cord pH, absence of high lactate on arterial blood gas). It is uncertain whether this condition resulted from a combination of cardiogenic shock induced by antenatal administration of dexamethasone and indomethacin, superimposed on rising afterload due to exposure to systemic vasoconstrictors.


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