Case April 2025 - Warm Distributive Shock

Case by Dr Gabriel Altit and Dr Pasinee Kanaprach - April 2025

This is a case of a preterm infant born at 24 weeks’ gestation, now 27 weeks postmenstrual age, on day of life 20. The patient was diagnosed with perforated necrotizing enterocolitis (NEC) and presented with hypotension and anuria for the past 12 hours. The infant weighs approximately 1 kilogram and had already received volume resuscitation totaling 75 mL/kg, in addition to a total fluid intake of 120 mL/kg/day.

At the time of assessment, the patient was receiving vasoactive support including dopamine at 5 mcg/kg/min, norepinephrine at 0.2 mcg/kg/min, and hydrocortisone. Despite these measures, blood pressure remained low at 27/15 mmHg (mean arterial pressure of 20), with significant tachycardia at 186 beats per minute. The patient was on volume-guaranteed ventilation with a tidal volume of 5.5 mL/kg, PEEP of 7, and an FiO2 between 55 and 60 percent. Arterial blood gas analysis revealed a pH of 7.15, a pCO2 of 57, a Bicarbonate of 19, and a base deficit of -8. Serum sodium was 125 mmol/L, and potassium was elevated at 8 mmol/L (re-evaluated arterial at 4.5). The baby was anuric.

Given the ongoing hemodynamic instability, several management adjustments were recommended following the clinical and echocardiographic evaluation. A bolus of 3% normal saline at 1 mL/kg was advised to address the hyponatremia and help with volume optimization. Potassium was discontinued from all intravenous infusions..

After the TnECHO presented below outlining adequate cardiac function and a hyperdynamic heart with appropriate filling, due to the persistent tachycardia and limited effect of dopamine, it was recommended to stop dopamine and to not initiate epinephrine. Vasopressin was introduced to provide more targeted vasoconstrictive support, and norepinephrine was to be gradually tapered as vasopressin was titrated up. The idea was to limit the chronotropic effect of norepinephrine to favour filling time and use vasopressin for its effect on increasing systemic vascular resistance. Hydrocortisone was continued to support adrenal function in the context of vasopressor-resistant shock.

Further recommendations included optimizing intravascular volume and perfusion by ensuring a hemoglobin level above 100 g/L, platelet count above 25 x10⁹/L, and an INR less than 2. The overall approach aimed to stabilize the infant’s hemodynamic status through tailored fluid, hormonal, and vasoactive management, recognizing the complexity of caring for extremely preterm infants with advanced NEC and evolving multi-organ dysfunction. The patient progressively improved over the period of the next 24 hours and all vasopressors were weaned off at around 24 hours following the consultation, with recovery of the blood pressures and the improvement in urine output, as well as metabolic indicators of organ perfusion.

Blood pressure is determined by the product of cardiac output and systemic vascular resistance. When systemic resistance falls significantly, the body attempts to maintain perfusion pressure by increasing cardiac output, which is the product of heart rate and stroke volume. In this case, the patient was already markedly tachycardic, and preload had been optimized in an effort to enhance stroke volume. However, there comes a point where these compensatory mechanisms are no longer sufficient, and blood pressure declines because the drop in resistance outweighs the body's ability to augment flow.

In such scenarios, increasing systemic vascular resistance with agents like vasopressin, norepinephrine, dopamine or phenylephrine becomes necessary to restore perfusion pressure. Norepinephrine and dopamine were already in use at an appropriate dose but were likely contributing to further tachycardia through their chronotropic effects, potentially compromising diastolic filling. Phenylephrine, while not affecting heart rate, has limited evidence supporting its use in neonates outside of specific indications like tet spells. Given these considerations, vasopressin was selected due to its ability to increase vascular tone without exacerbating tachycardia. The idea was also to drop the norepinephrine and dopamine to remove their significant effects on heart rate, avoid polypharmacy and their side-effects, while optimizing the effect on SVR of using one single agent (i.e.: Vasopressin). Following its initiation, the patient’s hemodynamic profile improved. Importantly, the patient was also managed with appropriate broad-spectrum antibiotics to address the underlying infection. This case highlights the value of TnECHO and comprehensive hemodynamic assessment in cases of neonatal sepsis that are not responding as expected. A physiology-driven approach can help guide targeted interventions to restore perfusion, reduce the risk of tissue ischemia, and improve clinical outcomes.

Targeted Neonatal Echocardiography

RV and septal TDI outlining Tachycardia, appropriate systolic velocities.

A5C with Colour. There is flow originating below the LVOT and going through the LVOT. No LVOT obstruction. Intra-cavitary acceleration by colour. 

LVO estimation based on HR, LVOT diameter and VTI was 350-400 mL/kg/min (increased). There is mid-systolic notching in the LVOT VTI. In septic shock, high sympathetic tone and circulating catecholamines drive tachycardia. This leads to: Shortened diastolic filling time; Reduced preload; Impaired ventricular filling, especially in a non-compliant or immature myocardium (as in neonates). This can lead to early peaking of flow in systole followed by a relative drop mid-systole, creating the appearance of a notch. Septic shock disrupts normal ventriculo-arterial coupling. The heart pumps into a vasoplegic, low-resistance system, and the forward flow is not well sustained throughout systole, there's a mismatch between ventricular ejection and peripheral vascular tone, resulting in flow deceleration mid-systole. Finally, reflected pressure waves from the periphery can cause mid-systolic flow deceleration.

Here the E wave velocity is much higher than the A wave velocity for both the RV and LV. There is significant tachycardia during these PW-Dopplers. In neonatal septic warm shock, when the E wave velocity is significantly lower than the A wave velocity on mitral inflow Doppler (or tricuspid, similarly), it typically reflects a high cardiac output, low systemic vascular resistance (SVR) state, with associated short diastolic filling time and myocardial stiffness due to tachycardia and immature myocardium. If preload is low (e.g., hypovolemia, third spacing, or high PEEP), early filling may be blunted due to reduced venous return. The atrial contraction compensates by pushing more forcefully to fill the underfilled ventricle, increasing the A wave velocity. If E and A waves are not fused and clearly separated and A > E, it indicates the ventricle is relying on atrial kick for filling — a red flag in neonates who have limited atrial reserve.

Bidirectional PFO (mostly left to right), often seen when the baby is tachycardic and the RA pressure and LA pressure are similar. Indeed, because SVR are very low, the LV  empties fully in systole, dropping the LV end-diastolic pressure and having the LA pressure similar to RA pressure.

Aortic arch outlines accelerated flow. There is no PDA on the PDA sweep that could be contributive to low total peripheral resistance in the systemic compartment. 

Flow in the Descending Aorta. One may appreciate the short systolic time. There is Tachycardia. 

IVC is nicely opened in the subcostal view. This is an indirect indicator that preload systemically was adequate after volume repeltion. There is forward flow in the Doppler of the subhepatic veins outlining that the RA pressure is unlikely high. 

Review of the physiology of this particular case.

Once Vasopressin was started, blood pressure progressively increased. Urine output restarted at 2.1 mL/kg/hour.