Case by Dr Nina Nouraeyan (Neonatologist at the Jewish General Hospital)
Monthly Case – August 2026 - Dr. Nina Nouraeyan - Posted: August, 2026
A 28-week gestation infant weighing 1210 grams was delivered by emergency cesarean section following a pregnancy complicated by threatened preterm labour from 21 weeks and prolonged rupture of membranes. The mother had completed antenatal corticosteroids and magnesium sulfate. Daily fetal non-stress tests had remained reassuring, and weekly ultrasound examinations demonstrated normal fetal Doppler studies. Shortly before delivery, the mother reported a sudden reduction in fetal movements. An urgent non-stress test demonstrated recurrent deep decelerations, prompting an immediate cesarean section.
The infant was born depressed, with Apgar scores of 1, 5, and 8 and a cord pH below 7.00, consistent with profound perinatal compromise. Following delivery, the infant was intubated, received surfactant, and was transferred to the NICU. Despite optimal ventilation, the infant remained critically ill. Oxygen saturation was 80% despite an FiO₂ of 100%. Clinical examination demonstrated profound shock with weak peripheral pulses, capillary refill greater than four seconds, and blood pressure of 50/30 mmHg; mean arterial pressure 28 mmHg. Over the following hours, perfusion failed to improve and the oxygen requirement remained between 80% and 100%.
An augmented cardiac POCUS was performed to identify the underlying hemodynamic abnormality and guide management.
Subjectively, ventricular filling appears adequate. Left ventricular systolic function is depressed. Although the LV free wall appears to contract relatively well, the interventricular septum contributes minimally to overall contraction. Right ventricular systolic function is also depressed, although tricuspid annular motion is preserved. Fractional area change could be used to quantify global RV systolic function, while TAPSE could quantify longitudinal tricuspid annular excursion. Overall, RV function appears subjectively better preserved than LV function. This biventricular dysfunction is likely related to the preceding perinatal distress and associated acidosis.
Opening and closure of the aortic and mitral valves. The interventricular septum demonstrates a rocking motion rather than contributing effectively to ventricular contraction.
This represents a more advanced cardiac POCUS (with components of a TNE assessment), focusing on ductal flow. In this view, the ductus arteriosus demonstrates predominantly right-to-left shunting. The pulmonary valve opens normally, confirming forward right ventricular ejection into the pulmonary artery. The right-to-left ductal flow indicates that pulmonary artery filling pressure (and likely PVR) exceeds aortic pressure during part of the cardiac cycle (however, because the PDA is unrestrictive, it will equalize the pressure on both end quite quickly). This may reflect elevated pulmonary vascular resistance and pulmonary artery pressure, reduced systemic arterial pressure, or a combination of both. In this case, depressed left ventricular output may also be contributing to the lower aortic filling pressure (although the systemic BP were within acceptable range - prompting concern for significantly high PVR and low pulmonary blood flow).
This represents a more advanced application of cardiac POCUS. Pulsed-wave Doppler interrogation of the left ventricular outflow tract provides the velocity–time integral, or stroke distance, reflecting the distance travelled by the blood column during each cardiac cycle. In this case, the low Doppler velocities produce a reduced stroke distance and, at a heart rate of 136 beats per minute, a reduced minute distance. In more advanced applications, the minute distance can be combined with measurement of the LVOT diameter in the parasternal long-axis view, following the NH-TNE approach, to estimate left ventricular output. This patient had dramatically decreased estimated LV output.
The infant was transitioned to high-frequency oscillatory ventilation (MAP 12 cmH₂O, frequency 15 Hz, tidal volume goal 1.5 mL/kg) and inhaled nitric oxide (20 ppm) was initiated. Dobutamine was started at 5 mcg/kg/min and progressively increased to 15 mcg/kg/min. Blood pressure gradually improved, but peripheral perfusion remained poor, with persistently weak pulses and prolonged capillary refill.
LV function has improved but the RV function is still depressed.
LV function improved.
PDA is now mostly left to right, indicating that the PVR is likely below SVR.
Here, the LVOT VTI has increased to 7.18 cm, indicating a greater stroke distance (prior 1.7 cm). The Doppler envelope is also more robust and densely filled, supporting improved left ventricular output at a stable heart rate of 136 beats per minute. The envelope remains consistent across successive cardiac cycles, suggesting reproducible flow measurements.
Serial cardiac POCUS examinations were performed to reassess function, filling and monitor the ductus arteriosus. As pulmonary vascular resistance improved, inhaled nitric oxide was gradually weaned. However, despite improving blood pressure, the infant remained clinically underperfused. Epinephrine was therefore initiated and titrated from 0.03 to 0.1 mcg/kg/min while maintaining dobutamine at 15 mcg/kg/min.
Significantly improved LV function with forward flow through the LVOT.
PDA fully left to right.
Normalizing LV and RV function subjectively with improvement of the septal motion.
Here the VTI has increased to 9.63 cm. Of note, the scale of the Y-Axis has been compressed to 200 cm/s compared to 150 cm/s prior.
Following optimization of left ventricular performance, the infant's pulses became stronger, capillary refill improved, blood pressure normalized, and oxygen requirements steadily decreased to approximately 50%. Inhaled nitric oxide was successfully discontinued, followed by gradual weaning of both dobutamine and epinephrine. Over the next 48 hours, serial POCUS examinations demonstrated normalization of cardiac function. The infant was subsequently extubated and continued to make an excellent recovery.
This case illustrates that not all neonatal shock is the same. Although the infant initially presented with profound hypoxemia, and poor perfusion, the primary hemodynamic problem was impaired left ventricular function. Identifying this physiology allowed therapy to be directed toward improving cardiac output rather than simply escalating vasopressor support.
Equally important was the use of serial cardiac POCUS examinations throughout the infant's course. Continuous assessment of ventricular performance and ductal physiology allowed inhaled nitric oxide to be discontinued at the appropriate time, avoiding prolonged pulmonary vasodilation in the setting of evolving ductal shunting—a situation that can precipitate significant complications, including pulmonary hemorrhage. This case demonstrates how repeated bedside cardiac assessment enables individualized, physiology-based management rather than a one-size-fits-all approach to neonatal shock.