A life-threatening complication of umbilical vein catheter in an extremely low birthweight infant.

A second twin, preterm female, was born at 27 weeks of gestational age, with appropriate weight, through caesarean due to maternal pre-eclampsia. Corticosteroid therapy was administered before delivery. Antenatal history was otherwise irrelevant. The Apgar scores were 8/9/9 and the initial physical examination was normal. Despite prompt initiation of nasal continuous positive airway pressure (nCPAP) after delivery, the patient developed signs of respiratory distress within the first hours of life, needing surfactant replacement therapy by minimal invasive technique and progression to invasive ventilation. A 2.5 Fr double lumen umbilical venous catheter (UVC) (Vygon®), was easily inserted, under sterile conditions, on the second day of life and total parenteral nutrition (TPN) was initiated. In chest x-ray, the UVC tip was in infradiaphragmatic position, but continued to be in use as there was no immediate alternate central vein access available and the UVC was functional. Two days later, the patient's condition suddenly deteriorated, showing a marked increase in respiratory support, a hypotensive trend as well as pronounced abdominal distension and tenderness. The chest x-ray showed an image consistent with fluid in the abdominal cavity, a paucity of bowel gas and the UVC tip in infradiaphragmatic position. It also revealed poorly ventilated lungs, and pulmonary ultrasound (US) confirmed an alveolar-interstitial pattern (Figure 1). The echocardiography performed at that time showed good biventricular function and apparently adequate filling. The abdominal US confirmed the presence of abdominal fluid, consistent with ascites/TPN extravasation (Figure 1), so a diagnostic and therapeutic paracentesis was promptly performed and 23 mL of a milky fluid was drained. Abdominal fluid analyses revealed high glucose and triglyceride levels consistent with TPN. A diagnosis of intraperitoneal extravasation from UVC was made. UVC was removed immediately, and TPN was resumed through an alternative central venous access. The patient recovered well after ventilatory optimization, inotropic support, diuretics, and antibiotics, quickly suspended. An abdominal US performed 2 days after paracentesis exhibited an irregular hyperechoic image in the left lobe of the liver, within the IV segment, measuring approximately 0.6 cm × 0.4 cm, probably reflecting liver parenchymal injury (Figure 2). No associated liver dysfunction was documented. The patient was electively extubated on the 19th day to nCPAP. She was kept under non-invasive ventilation until the 74th day, due to bronchopulmonary dysplasia. She was discharged on the 80th day, in spontaneous ventilation and tolerating enteral nutrition per os. At 6 weeks follow-up, the liver collection was completely reabsorbed (Figure 2). The authors present a case of TPN extravasation secondary to UVC malposition, complicated by parenchymal liver collection and ascites in a preterm newborn, without liver dysfunction. UVC is widely used in neonatal intensive care units because it is one of the fastest and easiest methods to access a deep vein allowing higher osmolality fluids and safe administration of drugs when compared to peripheral venous cannulas.1 Nevertheless, it is also associated with short-term and long-term complications such as infection, embolism, thrombosis, migration of the catheter, pericardial or pleural effusion, arrhythmia, endocarditis, cardiac tamponade, intestinal perforation or necrotizing enterocolitis, portal hypertension, liver hematoma and hepatic necrosis.1, 2 TPN extravasation in liver parenchyma is rare3 and malposition is the most important risk for hepatic extravasation.3, 4 Like other authors reported, concerning the injury dynamics, the catheter tip has the capacity to inflict direct harm on the vessel wall, resulting in the direct escape of TPN fluid into the peritoneum. Beyond the mechanical aspect, the hyperosmolar nature of TPN fluid can instigate portal phlebothrombosis and liver necrosis, leading to TPN fluid seepage into necrotic foci, compromised sinusoids, and small subcapsular veins. It's plausible that fluid accumulates beneath the liver capsule, subsequently seeping into the peritoneum and potentially causing ascites.4 The authors believe the phlebothrombosis was the main mechanism in this case. The diagnosis should always be considered when a patient under UVC-administered TPN presents with abdominal distension.1 A high level of suspicion and a quick actuation were essential to the resolution. Recovery of TPN extravasation is usually good with spontaneous resorption.1 However, acute abdominal distension is life-threatening and in some cases may require paracentesis.1 The use of US constitutes a more accurate method for the confirmation of UVC proper placement when compared to radiography.2 Even when the UVC position is suitable, complications can occur; therefore if this is suspected, catheter removal should not be delayed.2 D.E.R. and I.P.F. collected the data, analyzed scientific reports to review the literature and wrote the draft of the manuscript. A.C., S.D. and E.P. gave technical support, conceptual advice and critical review of the manuscript. All authors read and approved the submission. No undisclosed authors contributed to the manuscript. The authors have nothing to report. Informed consent was obtained from the patient's parents for the publication of this case report. The authors declare no conflict of interest.