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Case by Dr Sarah Spenard (NH-TNE Specialist at the Montreal Children's Hospital). Written by Dr Gabriel Altit (NH-TNE Specialist at the Montreal Children's Hospital)
August 10, 2025
This was a 24 week preterm infant, born via emergency cesarean section for footling breech presentation. The baby was initially intubated at birth, received surfactant, and was empirically started on ampicillin and gentamicin. The initial blood culture was negative, and antibiotics were discontinued after 48 hours. At 72 hours old, the infant experienced acute clinical deterioration, marked by refractory hypotension and severe hypoxemia. The patient was transitioned to HFJV for worsening respiratory failure and started on dopamine for hemodynamic support by the clinical team due to hypotension. FiO₂ requirements escalated to 100%, prompting the initiation of inhaled nitric oxide (iNO) at 20 ppm for suspected suprasystemic pulmonary hypertension. Despite these interventions, the infant remained poorly perfused. She developed new-onset anemia, received a pRBC transfusion, and was found to severe IVH on head ultrasound. A repeat blood culture was positive for E. coli bacteremia, and the patient had reduced urine output. A Targeted Neonatal Echocardiography (TNE) was requested to assess the hemodynamic profile and guide further cardiovascular management.
Based on the TnECHO, the patient was maintained on inhaled nitric oxide (iNO) for management of acute pulmonary hypertension. Dopamine was discontinued due to its potential to increase pulmonary vascular resistance. Dobutamine was initiated to support left ventricular inotropy, given an acceptable heart rate of 140 bpm, and was titrated up to 12.5 mcg/kg/min. Norepinephrine was trialed without significant hemodynamic response, prompting a switch to vasopressin, which was increased to 0.8 mU/kg/min and resulted in improved blood pressure and stabilization of perfusion. Hydrocortisone dosing was increased to 1 mg/kg every 8 hours. Ventricular filling was deemed adequate following volume resuscitation with packed red blood cells and normal saline in the context of sepsis.
Here is below the interpretation of the TnECHO
The Parasternal Long Axis view outlines that there is hyperdynamic left ventricule. The mitral valve opens and closes. The LV function is vigorous (likely facing some degree of low SVR). The Aortic valve opens and closes.
The LVOT is measured at 0.358 cm
The RVOT is here visualized in the PLAX. The pulmonary valve opens and closes.
The RVOT is measured at 0.361 cm.
Flow is seen going through the pulmonary valve from the PLAX view.
RV inflow view in the PLAX. There is some trivial tricuspid regurgitant jet.
PLAX. We can observe the RVOT and the pulmonary valve, as well as the aortic and tricuspid valves. The LA is about the size of the aorta (no LA dilatation). LA dilatation would be seen in the context of a left to right PDA due to increased Qp:Qs.
Some flattening of the septum at peak of systole. The LV contraction is vigorous. There is near kissing ventricles, possibly secondary to the low state of SVR.
PAAT/RVET is 30/164 = 0.18 (concerning for high PVR)
RVOT - VTI by PW-Doppler is 0.095 m. With a heart rate of 141, the RVO is estimated at 221.13 mL/kg/min. However, a large part of this output is diverged via the right to left ductus arteriosus as seen later.
The PDA is large / unrestrictive. It is larger than the LPA and RPA.
The PDA flow is right to left completely. This may be secondary to high PVR. There is possibly a component of low SVR from the sepsis. As such, the net flow is from the PA to the Aorta. This unloads the right ventricle.
The PDA flow is unrestrictive and right to left. The peak systolic gradient is 0.68 m/s. Knowing that the PDA is wide open, the pressure transmission occurs fully without restriction, and the PA pressure, by definition, becomes near-systemic by pressure equalization. As such, it is the PVR/SVR ratio that drives the directonality of flow.
There is good RV and LV function from this view (apical 4 chamber view). The LA and RA are of good caliber. Atrio-ventricular valves open and closes. The filling from an atrial point of view seems appropriate. The LV walls are not kissing, although there is some subjective signs of hyperdynamic contraction.
TAPSE is 0.45 cm (within normal limit).
Pulmonary venous flow is observed by PW-Doppler with limited velocities. As such, this goes in line with decreased pulmonary blood flow. Just based on the PDA, it is clear that the Qp is much less than Qs.
Mild to moderate Tricuspid Regurgitation seen here.
Apical 5 chamber view. We can appreciate some trivial aortic insufficiency (red flow). There is good filling of the LVOT with flow initating before the aortic valve and going through the valve (no LVOT obstruction).
The VTI is 0.077 m. At this assessment, the heart rate was 165. Cardiac Output: 206.27 mL/kg/min - which is within normal limit. The descending aorta flow is higher than this since there is contribution of the RVO to the descending aortic flow via the PDA.
Subcostal view demonstrates a right-to-left shunt across the foramen ovale, directing hypoxic blood from the right atrium (RA) to the left atrium (LA). This contributes to desaturation in the pre-ductal limb. The right-to-left flow through the patent foramen ovale (PFO) is secondary to altered compliance between the right and left ventricles (RV vs LV). Additionally, underfilling of the LA—due to reduced pulmonary venous return and diminished pulmonary blood flow—further promotes this interatrial shunt. Elevated RA pressure is partly attributable to mild-to-moderate tricuspid regurgitation (TR). Importantly, RV function may appear deceptively normal, as a portion of its stroke volume is regurgitated into the RA, which offers less resistance than the pulmonary circulation.
PW-Doppler of the PFO confirming the right to left shunt (negative velocities).
This patient presents with acute pulmonary hypertension (PH) secondary to E. coli sepsis. Right-to-left shunting is evident, driven by elevated pulmonary vascular resistance (PVR) and, paradoxically, also by low PVR in certain vascular beds. The elevated PVR reduces pulmonary blood flow, contributing to underfilling of the left atrium (LA) and promoting interatrial shunting via a patent foramen ovale (PFO). At the time of evaluation, the patient’s mean arterial pressure was 29 mmHg, considered adequate. Due to a large patent ductus arteriosus (PDA), pulmonary artery (PA) pressure is systemic, rendering the right ventricle (RV) systemic as well. This pressure equalization explains the flattening of the interventricular septum. Notably, PVR exceeds systemic vascular resistance (SVR), further impairing pulmonary perfusion. Reduced pulmonary venous return leads to LA underfilling, reinforcing the right-to-left atrial shunt. This shunt is also driven by elevated RV end-diastolic pressure (reflecting decreased RV compliance) and mild-to-moderate tricuspid regurgitation (TR). The increased right atrial (RA) pressure—into which the coronary sinus drains—combined with low SVR, may compromise coronary perfusion. Thus, maintaining adequate diastolic pressure is critical. Management focused on acute PH with concurrent concern for low SVR. The patient was supported with inhaled nitric oxide (iNO), optimized ventilation, and titrated oxygen therapy. While oxygen can aid pulmonary vasodilation, it does not improve extra-pulmonary shunting (e.g., via PFO or PDA). Vasopressin was used to support SVR, and dobutamine was administered to enhance RV inotropy, given signs of RV strain and TR.
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