Persistent Bradycardia and Hypoperfusion in an Infant Despite Neonatal Resuscitation

A monochorionic, diamniotic twin male infant is born at 30 weeks and 5 days gestational age via extramural precipitous vaginal delivery. He is initially intubated due to respiratory distress syndrome, receives endotracheal surfactant, and is subsequently extubated to continuous positive airway pressure (CPAP) on day of life 1, which is well tolerated. An umbilical venous catheter (UVC) is placed in preparation to initiate parenteral nutrition (PN). Appropriate UVC positioning is confirmed with imaging, per standard protocol using 2 views. In our institution, anterior-posterior and lateral radiographs are used to confirm placement. Sometimes point-of-care ultrasonography (POCUS) can be used for insertion or to confirm location, but not in this case (Figure 1). The radiograph in this case was interpreted as having a UVC projecting over the right atrium with no suggestions for adjustment.On day of life 4, he is noted to be dusky in color and found to be hypoxic on pulse oximetry. Positive pressure ventilation is initiated. He initially demonstrates grimace, tone, and cry with heart rate (HR) in the low 150s. Two minutes later, his HR drops precipitously and is sustained in the 50s, during which cardiopulmonary resuscitation (CPR) is initiated. Code-dose epinephrine is given once through the UVC. Four minutes after CPR initiation, he is successfully intubated with a 3.0 uncuffed endotracheal tube, confirmed with appropriate color change using an end-tidal CO2 detector and later with a chest radiograph. He continues to demonstrate poor perfusion with HR sustained in the low 90s despite following standard neonatal resuscitation protocol.There are several possible etiologies for hypoperfusion and persistent bradycardia, despite neonatal resuscitation measures. Differential diagnosis includes, but is not limited to, etiologies of distributive shock (septic shock or adrenal crisis), hypovolemic shock (internal bleeding or severe third spacing), and obstructive shock (tension pneumothorax, mediastinal or thoracic mass, cardiac tamponade, or traumatic injury to the lungs or major cardiac vessels).Prior to decompensation, the patient did not exhibit signs suggestive of sepsis or hypovolemia, as there was no tachycardia, temperature instability, abnormal neurologic examination, or hemodynamic instability. Additionally, previous chest imaging did not demonstrate anomalous structures of the thorax or abdomen or the presence of free fluid.Given that he required high pressures on bag-mask ventilation with subsequent emergent intubation, trauma to the thoracic structures resulting in tension physiology is possible. A central UVC was recently placed, infusing PN prior to decompensation. Thus, cardiac tamponade from accumulating PN in pericardium from malpositioned UVC cannot be excluded.POCUS was readily available and was used during acute resuscitation measures to discern etiology of shock. Pleural effusion and pneumothorax were ruled out with lung POCUS. Four-chamber and parasternal long axis cardiac views were significant for a large, circumferential pericardial effusion, severely diminished biventricular systolic function, and severe diastolic dysfunction with absence of ventricular diastolic filling (Figure 2 and Video 1). These findings were diagnostic for cardiac tamponade physiology. POCUS also illustrated the position of the UVC being within the pericardial space (Figure 3).Pericardial effusions (PCEs) are rare in neonates and entail the accumulation of more than 5 mL of fluid between cardiac visceral and parietal layers. Clinical presentation depends on the speed of fluid accumulation, size, onset, distribution, and hemodynamic impact.1 Small or moderate PCEs are hemodynamically insignificant and tend to resolve overtime, with close monitoring. PCEs are most commonly iatrogenic in critically ill infants, due to malpositioned central venous catheters (CVCs).2–5 In these cases, CVCs are used for administration of large volume fluids, which can inadvertently accumulate in the pericardium, resulting in a slowly increasing PCE, subsequently resulting in cardiac tamponade. PCEs can also be due to infection, fetal hydrops, thyroid dysfunction, autoimmune diseases, and diaphragmatic hernias. The major complication of PCEs is cardiac tamponade, classified by severely restricted diastolic filling, stunted cardiac output, and akinesia or hypokinesia of many cardiac structures, contributing to obstructive shock.PCEs causing cardiac tamponade must be evacuated as soon as possible to facilitate return of cardiac function and end organ perfusion. Pericardiocentesis is essential for removal of the PCE and thus the global compressive forces on the myocardium.6 This procedure involves attaching a 10-cm3 syringe to a 3-way stopcock and 21- or 22-gauge needle or angiocath, inserting the needle 0.5 to 1 cm inferior to the xyphoid, and advancing the needle until air or fluid enters the syringe.7 Additionally, as CVCs are commonly implicated in neonatal PCEs, they must also be removed promptly, if in place, especially in the setting of clinical instability such as cardiac tamponade. The ideal location for placement of a CVC is at the junction of the right atrium and inferior vena cava, which is the level of thoracic vertebral bodies 7 to 9. As this position cannot be seen on radiography, the diaphragm is often used as a landmark.8 Postevacuation transthoracic echocardiogram is used to confirm return of cardiac function and to evaluate for remaining effusion. Routine postarrest evaluation and monitoring is conducted per standing critical care practices.Bedside pericardiocentesis is performed using a 23-gauge butterfly needle, advanced with a subxiphoid approach under ultrasonography guidance, yielding 11 mL of milky fluid (Figure 4), which is promptly evacuated. There is real-time resolution of gross cardiac function on POCUS, and the patient’s HR increases back to the 150s. A pericardial fluid sample is sent for laboratory analysis and the UVC is removed. A postpericardiocentesis transthoracic echocardiogram shows normal right and left ventricular systolic function and small inferior and anterior PCE without evidence of hemodynamic compromise (Figure 5). Analysis of the PCE fluid showed glucose more than 3000 mg/dL and triglycerides of 755 mg/dL, confirming that the fluid was infusate.Obstructive shock physiology, although rare, is on the differential for neonates that do not respond to initial neonatal resuscitation measures.1,9Cardiac POCUS is an immensely helpful tool for rapid evaluation and intervention for structural etiologies of shock.6Umbilical CVC malpositioning is one of the most common causes of neonatal pericardial effusions and may result in cardiac tamponade if large fluid volumes are administered via these catheters.2–5 To more accurately position CVCs prior to use, protocols are still being optimized to use methods such as POCUS and cross table films.Emergent pericardiocentesis is curative above any and all other measures, once the diagnosis is made.American Board of Pediatrics Neonatal-Perinatal Content SpecificationUnderstand cardiac tamponade.Know procedures regarding resuscitation of a newborn infant.Recognize indications, management, and complications of medical technology (eg, central lines, gastronomy, tracheostomy, ostomy, ventriculoperitoneal shunt, extracorporeal membrane oxygenation).