Severe bronchospasm in a premature infant during induction of anesthesia caused ventilation failure

provided the original work is properly cited. CC A 3-month-old (39 weeks postconceptual age) male infant weighing 2.9 kg was scheduled for laser photocoagulation with a diagnosis of retinopathy of prematurity. He was born at 27 weeks gestation with a birth weight of 970 g. He had been mechanically ventilated from birth for 20 days for respiratory insufficiency due to respiratory distress syndrome (RDS) and bronchopulmonary dysplasia (BPD). A chest X-ray performed before the subsequent ligation of the patent ductus arteriosus showed bilateral haziness in the entire lung field due to the RDS and BPD during tracheal intubation. The infant required ventilation with a high concentration of oxygen and received surfactant therapy. Twenty days after birth, patent ductus arteriosus (PDA) ligation was done under general anesthesia in which induction was achieved with inhalation of sevoflurane and 1 mg of rocuronium. The operation proceeded uneventfully and the extubation was performed five days after the surgery. After extubation, the infant was able to breathe spontaneously with an incubator oxygen supply, and the oxygen saturation was maintained above 90%. After PDA ligation, the infant was diagnosed with retinopathy of prematurity, and he was then scheduled for laser photocoagulation. On the chest X-ray, improvement of haziness was observed from five days before the operation. After consultation with pediatrics, the decision was made to operate. Upon arrival in the operating room, electrocardiography, pulse oximetry, and noninvasive blood pressure were monitored, and the patient’s vital signs were stable. Induction of anesthesia was achieved with thiopental (15 mg), rocuronium (2 mg), and sevoflurane. The tracheal intubation was performed with an uncuffed 3.5 mm internal diameter endotracheal tube, but there was no capnogram trace after three breaths. At this time, the oxygen saturation rapidly dropped to below 80%. The endotracheal tube was removed because the anesthesiologist suspected esophageal intubation and the patient was ventilated with 100% oxygen via face mask. Mask ventilation was not performed well, and peak inspiratory pressure was revealed to be above 25 mmHg. The anesthesiologist suspected stiff lungs, which suggested bronchospasm. Hydrocortisone sodium succinate (SoluCortef, Pfizer Inc., New York, NY, USA) 20 mg was intravenously injected. Five minutes later, oxygen saturation slowly increased up to 99% and reintubation was attempted. Although it was confirmed by direct laryngoscopy that the tube had passed between the vocal cords, proper ventilation of the lungs was not achieved. No expired carbon dioxide was noted on the capnograph, and chest auscultation was equivocal. The oxygen saturation was then in the low sixties. After sevoflurane was administered by inhalation, a slight chest movement was noted, and oxygen saturation increased up to 80%. During that time, a portable chest radiograph was taken which revealed severe consolidation with air bronchograms (Fig. 1A). Despite ventilatory support for 10 minutes, the oxygen saturation failed to increase beyond 80%. Hydrocortisone sodium succinate 20 mg was then intravenously injected once more. Afterwards, SaO2 was maintained at 88-93%. The surgery was cancelled, and glycopyrrolate