LAUSR

© BMJ Publishing Group Limited 2021. No commercial reuse. See rights and permissions. Published by BMJ. DESCRIPTION The case is of a twin A male infant born preterm vaginally at 31 weeks as a product of dichorionic diamniotic twins gestation. The mother was 23 years old, gravida 3 para 0, with gestational diabetes on a diet regimen. She did not have any risk factors for infection. She was seen in the antenatal clinic 5 weeks before the onset of labour with no maternal or fetal concerns. Her twins were growing normally with no congenital anomalies seen in the antenatal ultrasound scans. On the delivery day, she arrived at the emergency room fully dilated with premature rupture of membranes (PROM) at the onset of labour. She did not receive any antenatal steroids before the delivery. The infant was born in a good condition with an Apgar score of 9 and 10 at 1 and 5 min, respectively. He was admitted to the neonatal intensive care unit (NICU) together with his twin due to prematurity and respiratory distress syndrome. Regarding his respiratory support, he was supported by nasal continuous positive airway pressure (NCPAP) since birth for 11 hours and by nasal cannula for another 2 days. The treating team started empiric initial antibiotic therapy at birth by ampicillin and amikacin based on the preterm labour and the PROM. The antibiotic therapy was continued for 5 days despite the sterile blood culture at 48 hours of age and repeatedly negative Creactive protein (CRP). The other twin B received ampicillin and amikacin at birth and it was stopped after 2 days due to negative cultures. He was supported by NCPAP for 12 hours and by nasal cannula for 13 days. He had a smooth NICU course with no complications. On the fifth day of life, this infant (twin A) was noted to have poor activity, lethargy with frequent attacks of bradycardia and desaturation. Based on the clinical presentation, the neonatal team considered lateonset sepsis and necrotising enterocolitis (NEC) as possible initial differential diagnoses. Complete blood count (CBC) and peripheral smear were of normal values and blood culture was negative at that time. CRP was elevated to 49 mg/L. Capillary blood gases showed partially compensated metabolic acidosis while the coagulation profile and serum electrolytes were normal. Anteroposterior (figure 1) and cross table (figure 2) abdominal Xray was done and showed pneumatosis intestinalis, portal venous gas and gastric pneumatosis with no free air. Ultrasound of the abdomen showed scanty free ascites with tiny bright foci within hepatic parenchyma, indicating portal tract air foci (figure 3). The infant was supported by NCPAP for few hours which was escalated to conventional mechanical ventilation for 2 days before extubation to a nasal cannula for another 2 days. The paediatric surgery team was consulted and the infant was kept nil per mouth for 14 days. A peripherally inserted central catheter was placed and the infant received intravenous teicoplanin, intravenous amikacin and intravenous metronidazole for 14 days. Lateonset sepsis was excluded based on the negative blood culture and normal CBC parameters. As a final diagnostic aetiology, the neonatal Figure 1 Anteroposterior Xray of the abdomen shows gastric pneumatosis (blue arrow), pneumatosis intestinalis (red arrow) and air in the portal tract (black arrow).