Introduction: Clinically significant feto–maternal haemorrhage (FMH), defined as fetal blood loss exceeding 30 mL, occurs in approximately 1 in 300–1,000 deliveries, while massive FMH is considerably rarer. Severe cases may present with abnormal cardiotocography (CTG), profound neonatal anaemia and multiorgan dysfunction. Secondary persistent pulmonary hypertension of the newborn (PPHN) due to chronic intrauterine hypoxia may closely mimic structural congenital heart disease. Case presentation: A baby girl was delivered at 36+6 weeks’ gestation by emergency lower segment caesarean section for abnormal CTG. Birth weight was 3 kg and Apgar scores were 3, 4 and 8. She required immediate intubation due to significant pre and post ductal saturation difference and hypotension. Initial blood gas revealed severe metabolic acidosis (pH 7 .07 , lactate 11.5 mmol/L, base excess −19). Profound anaemia was detected (haemoglobin 5 g/dL) with elevated reticulocyte count. Echocardiography demonstrated PDA, ASD, VSD and moderate PPHN. Modified Kleihauer–Betke test showed 0.7% fetal red cells, consistent with >35 mL FMH. Following 20 mL/kg packed red cell transfusion, oxygen requirement reduceddramatically with haemodynamic stabilisation. The infant developed acute kidney injury (serum creatinine 2.9 mg/dL) and transaminitis (AST 330 U/L), both resolving with supportive management. Sepsis evaluation was negative. Conclusions: Massive FMH should be suspected in neonates with severe unexplained anaemiaand abnormal CTG. Prompt recognition and correction of anaemia can reverse secondary PPHN and prevent further organ injury .