Case May 2025 - Severe biventricular dysfunction

Case written by Dr. Gabriel Altit 

This is a case of a late preterm infant, born at 34 weeks gestation with a birth weight of 2 kg, transferred to our center following an initially uneventful pregnancy. The mother presented with spontaneous rupture of membranes and significant vaginal bleeding. Delivery was by emergency cesarean section due to breech presentation and ongoing fetal decelerations. The estimated maternal blood loss was approximately 800 mL. At birth, the neonate was anemic (hemoglobin 90 g/L) but transitioned relatively well, requiring only CPAP. The infant was admitted to the nursery and weaned to room air without difficulty. However, around 12 hours of life, the baby developed recurrent desaturations and apneic events. A repeat hemoglobin revealed a further drop to 75 g/L. A Kleihauer-Betke (KB) test from the mother returned positive, confirming a significant fetomaternal hemorrhage as a contributing factor to the anemia. Initial blood gases were unremarkable. At that point, the infant was restarted on CPAP and transfused with packed red blood cells (pRBCs). Despite this, the clinical condition deteriorated—manifesting as ongoing desaturation events, poor perfusion, and progressive hypotension. Notably, the maternal history included greenish vaginal discharge for two weeks prior to delivery, raising concerns for chorioamnionitis. A full septic workup was initiated, including a lumbar puncture which was reassuring. 

Given signs of escalating shock and hypotension, the referring team initiated transport. A peripheral umbilical venous line (UVL) was inserted, and norepinephrine was started under the working diagnosis of sepsis superimposed on a significant anemia event. A second transfusion was given, bringing the total to 25 mL/kg, which normalized hemoglobin levels. Norepinephrine was titrated up to 0.2 mcg/kg/min. 

Upon arrival to our center, the infant was in profound shock: encephalopathic, anuric, with a capillary refill time >4 seconds, heart rate of 190 bpm, and severe metabolic acidosis (pH 7.10, CO₂ 19 mmHg, HCO₃ 8 mmol/L, base excess -18, lactate 17 mmol/L on arterial sample). Central access was obtained via a femoral double-lumen catheter, with an initial central venous pressure of 11 cm H₂O. An umbilical arterial line was placed showing a blood pressure of 32/15 mmHg (mean 28 mmHg). 

Targeted neonatal echocardiography (TnECHO) revealed a picture of severe cardiogenic shock. Norepinephrine was discontinued, and dobutamine was initiated at 5 mcg/kg/min and gradually increased to 12.5 mcg/kg/min over 12 hours. Due to ongoing hypotension, epinephrine was added 30 minutes after dobutamine initiation, and titrated progressively up with ongoing monitoring of the LV contractility. The infant responded to epinephrine with some improvement in blood pressure and lactate clearance. Ventilator settings were minimal (FiO₂ 21%, tidal volume 5 mL/kg, rate 20 breaths per minute, PEEP 5 cm H₂O). The infant, however, remained profoundly encephalopathic. Due to gestational age and size, the infant was not considered a candidate for ECMO. Despite escalation of inotropic support, both left and right ventricular function remained severely depressed over the following 24 hours, with minimal signs of recovery. Hydrocortisone had been added for adrenal support. After extensive discussions with the family, a decision was made to redirect care toward comfort. This case highlights a rare and severe presentation of neonatal cardiogenic shock.

Parasternal long axis view

Parasternal short axis view

PSAX. One may appreciate that we can visualize nicely the coronary arteries. This is often seen in situation where the RA pressure rises (such as in this case where the central venous pressure is around 10-11 mmHg). This is because the coronary sinus drains into the right atrium, which may lead to upstream coronary dilatation. This view outlines nicesly the left atrial appendage, which ressembles a small finger. 

Mid-papillary view in PSAX, we can appreciate that the septum is relatively immobile. The contraction is very poor. The RV and LV are dilated. 

The PDA is moderate in size and bidirectional by colour. There is pulmonary insufficiency. The aortic valve is tri-leaflet. The pulmonary valve opens and closes. 

Apical views

Despite the poor LV function, there is LV output generated. This view was obtained post-initiation of Dobutamine and Epinephrine. The LVO increased from 80 mL/kg/min to 140 mL/kg/min.

When diastole starts, the already high LA pressure drops upon mitral valve opening, temporarily reducing LA pressure and making it easier for pulmonary venous blood to "rush" into the LA, resulting in a higher D-wave. This is seen in the left lower pulmonary vein and right upper pulmonary vein. 

Subcostal view

The PFO is mostly left to right. We can appreciate that the subhepatic veins are dilated upon this sweep. 

In these 2 views we can appreciate that the IVC is diilated. This patient was intubated but on minimal settings on the ventilator (the IVC caliber is unlikely to be the reflection of the positive intra-thoracic pressure). The dilated IVC indicates that the RA pressure is relatively high. It is unlikley that this patient would benefit from further volume at this point. 

Suprasternal view

No obvious coarctation on the arch view. There is also some trivial retrograde (one red flash seen during the loop) flow in the pre-ductal descending aorta. This may be secondary to poor LV output, with some retrograde flow by the duct feeding the pre-ductal aorta (systemic RV in systole). It may also be secondary to cerebral vasodilatation in some infants with perinatal depression.