Case report

We present the case of a neonate born at 32 + 4 weeks by planned caesarean section because of intra-uterine growth restriction. Neonatal stabilisation with inflations and ventilations was required to achieve adequate breathing at minute 10 (Apgar-score 3/5/7 at 1–5–10 minutes, respectively). Nasal continuous positive airway pressure was started because of neonatal respiratory distress syndrome, and the patient was stably admitted to the neonatal ICU. Clinical examination revealed an asymmetric intra-uterine growth restriction with a birthweight of 900 g (−2.51 standard deviations) and a head circumference of 28 centimetres (−1.28 standard deviations), a single umbilical artery, and a hypospadias. Single nucleotide polymorphism array and trio-based whole-exome sequencing were normal. An umbilical venous and arterial catheter were inserted according to the Dunn method. Blood could easily be aspirated. After chest and abdominal X-ray suggested correct positioning of both catheter tips (Supplementary Figure S1A-B), total parenteral nutrition was started. At 39 hours of life, the infant developed increasing respiratory distress with bilateral reduced air entry on clinical examination and FiO₂ up to 1.0. A chest X-ray showed bilateral opacities (Supplementary Figure S1C). The patient was intubated and mechanically ventilated. Surfactant was administered intratracheally, resulting in temporary stabilisation of the respiratory condition. Within four hours, respiratory distress recurred, with increasing oxygen requirement and haemodynamic compromise. Chest ultrasound revealed bilateral pleural and pericardial effusion, while the umbilical venous catheter tip could not be visualised and blood could no longer be aspirated via the catheter. Because of suspicion of extravasation of total parenteral nutrition through the umbilical venous line, total parenteral nutrition administration was stopped and the catheter removed immediately. Due to impending hypovolemic shock, peripheral venous access was obtained, and a normal saline bolus was administered followed by an emergency pericardiocentesis by subxiphoid approach under ultrasound guidance. During this procedure, 2 mL of a serous bloody fluid was aspirated. Biochemical analysis of the aspirated fluid showed high glucose (1017 mg/dL) and triglycerides (597 mg/dL), confirming the presence of total parenteral nutrition in the pericardial space. The patient’s clinical condition improved after pericardiocentesis with a decrease in tachycardia and normalisation of arterial blood pressure. Echocardiography showed minor residual pericardial effusion but a new intrapericardial thrombus (15 × 8 mm) adjacent to the right ventricle, without haemodynamic compromise (Fig. 1a-b; Supplementary Video S1). The patient was transferred to a paediatric cardiac surgery centre to allow pericardiotomy and thrombus removal, if necessary. Chest ultrasound upon arrival demonstrated stable sizes of the pericardial thrombus and effusion, as well as the pleural effusion. Because of the absence of signs of impending cardiac tamponade and surgical risk associated with a birthweight of 900 g, a conservative approach with close monitoring of vital signs (e.g. continuous arterial blood pressure measurement via arterial umbilical catheter, heart rate, and oxygen saturation) and serial imaging was adopted. Cardiac ultrasound after six hours showed a spontaneous decrease of the pleural effusion and stable size of the pericardial thrombus and effusion. Hence, close monitoring was continued without further interventions. One day after transfer, the pleural and pericardial effusion, as well as the pericardial thrombus, had completely resolved. Four days after initial transfer, the patient was retransferred to our centre. Echocardiography could no longer visualise any residual pericardial thrombus (Fig. 1c). Our patient was successfully weaned from mechanical ventilation and switched back to nasal continuous positive airway pressure and remained haemodynamically stable throughout the rest of his stay in the neonatal ICU.

Figure 1. (a ). Echocardiography performed after pericardiocentesis demonstrates the intrapericardial thrombus (asterisk) with a maximal diameter of approximately 8 × 15 mm and a minor residual pericardial effusion. ( b ). Parasternal short-axis view shows the intrapericardial thrombus (asterisk) adjacent to the right ventricle. ( c ). Repeat echocardiography after retransfer shows complete resolution of the intrapericardial thrombus and pericardial effusion. RA = right atrium, RV = right ventricle, LV = left ventricle.