IntroductionPleural effusion is defined as fluid accumulation in the pleural space. This potential space exists between the parietal pleura lining the chest wall and the visceral pleura around the lung. (1) The incidence ranging from 1/10,000 to 1/15,000. (2,3) There is a wide spectrum of aetiology ranging from idiopathic, chromosomal anomalies, inflammatory association, or structural malformations. (4) It is usually chylous. (5,6) Currently, there is no sufficient data regarding the incidence of isolated pleural effusion associated with inflammation or genetic syndromes. The aetiology can be classified in primary and secodary aetiologies. The primary causes could be hydrothorax or chylothorax. Secondary causes usually associated with hydrops fetalis either immune or non-immune. Non-immune causes usually associated with infection, bronchopulmonary sequestration, congenital heart disease, congenital lung lesion, chromosomal -genetic syndromes or congenital diaphragmatic hernia. (7)
Case reportA term baby girl 40+1 weeks of gestational age, weighing 3 kg, appropriate for gestation, was born by Kiwi assisted vaginal delivery done for foetal distress to a 25-year-old booked mother G2P1 with "O" positive blood group. The antenatal scan at 12 weeks of gestational age showed the nuchal translucency thickness at the upper normal limit (2.5 mm). The Foetal anomaly scan at 20 weeks of gestational age was reported normal. The repeated antenatal ultrasound at 31 weeks was normal but the antenatal scan at 39+5 weeks showed pleural effusion. Baby required resuscitation and intubation at birth and the Apgar scores were 5 and 7 at 1 and 5 minutes, respectively. She was in severe respiratory distress after resuscitation in the form of tachypnoea, with subcostal and intercostal recessions and breath sounds were diminished over the left hemithorax with right sided apex heartbeats auscultated for which she was admitted to the neonatal intensive care unit. She was observed with dysmorphic features in the form of upward slanting eyes, short neck, sandal gap deformity sign [Figure 1], but there was no signs of hydrops fetalis. Rest of the systemic examination was normal. The blood gas analysis revealed severe mixed acidosis with pH 6.8, PaO2 90 mmHg, and PaCO2 113 mmHg, HCO3 and BE were unrecordable. The baby was connected to conventional mechanical ventilation; IV fluids and antibiotics were charted but there was progressive worsening with increasing Fio2 requirements up to 100%. An urgent bedside chest X-ray was done revealed left side pleural effusion with mediastinal shift of the airway and heart to the right side [Figure 2]. Echocardiography was done and showed large sized patent ductus arteriosus with severe persistent pulmonary hypertension. Chest tube was inserted which drained straw-coloured fluid around 100 ml.