The firstborn male of a healthy G1, P0, 21-year old mom, was born at 41+1 weeks gestation, birth weight 3,700 g, by vaginal delivery after spontaneous rupture of membrane (SROM) of 15 h; two vacuum tractions were performed because of a prolonged active second stage of labor. Cardiotocographic monitoring was normal for the expulsive period. After the extraction of the fetal head, a maneuver of digital hooking (Bourgeois maneuver) was performed for the disengagement of the shoulders. The delay between the extraction of the fetal head and the disengagement of the shoulders was 2 min. There was a presence of thick meconium-stained amniotic fluid after the fetal extraction. At birth, the umbilical cord was immediately clamped. The baby was in cardiac asystole at auscultation, without spontaneous respiratory efforts, pale, and hypotonic. Cardiopulmonary resuscitation was started and continued according to the neonatal resuscitation program (NRP). A pulse oximeter was immediately positioned, followed by probe-ECG monitoring. Resuscitation included positive-pressure ventilation, chest compressions, intubation, and epinephrine. At 7 min of life, the heart rate was >100 beats per minute (bpm). The baby showed severe hypotonia and passive hypothermia was started at about 10 min of life. He was transferred to the neonatal intensive care unit (NICU), mechanically ventilated with a fraction of inspired oxygen (FiO2) 0.3. His Apgar scores were 0, 0, 5 at 1, 5, and 10 min, respectively. The cord blood gas analysis revealed an arterial pH 7.16, pCO2 58 mmHg (kPa 7.7), base excess (BE) -8.4 mmol/l, lactate 10.2 mmol/l; the pH from the venous sample was 7.26, pCO2 42 mmHg (kPa 5.6), BE -7.5 mmol/l, lactate 8.8 mmol/l.
Upon arrival in the NICU, his umbilical vein was catheterized, and blood work was done. Capillary gas performed on the neonate at about 30 min of life showed a pH 6.8, pCO2 83 mmHg (kPa 11.0), BE -21 mmol/l, lactate 14 mmol/l, and glucose 4.7 mmol/l. A neurologic exam showed moderate hypoxic-ischemic encephalopathy. Amplitude-integrated electroencephalography (aEEG) monitoring showed a burst suppression type trace. The arterial gas at 1 h of life showed pH 7.01, pCO2 58 (kPa 7.7), BE -21 mmol/l, and lactate 18 mmol/l. Hemoglobin at 14 h of life was 12.1 g/dl. Active hypothermic treatment was started and maintained for 72 h. Because of clinical suspicion of seizures, the baby was loaded with Phenobarbital but not maintained due to a lack of electroencephalographic abnormalities and normalization of the clinical picture. At about 4 h after birth, as spontaneous respiration improved, the newborn was extubated and gradually weaned off any ventilatory support. At 13 days of life (DOL), the overall neurologic exam showed a favorable evolution. The otoacoustic emission test results were normal, bilaterally. He was discharged on 14 DOL. His first head magnetic resonance imaging (MRI), done at 1 month of life, was normal. Follow-up at 30 months of age showed only a mild developmental delay in language and he required follow-up sessions with a speech therapist.