Post-extubation Glossoptosis Complicated by Negative Pressure Pulmonary Edema: A Case Report of a 12-year-old Child Following Laparoscopic Appendectomy Under General Anesthesia

Negative pressure pulmonary edema (NPPE) is a known non-cardiogenic complication of upper-airway obstruction, yet it remains underrecognized in children. Although laryngospasm is well reported, the role of post-extubation tongue fallback as a trigger for NPPE has not been described in the literature. Delayed emergence from anesthesia, due to synergistic effects of anesthetic agents, can reduce airway tone and predispose to transient backward and downward displacement of the tongue (glossptosis) which may trigger NPPE. While post-extubation tongue fallback is usually benign and easily corrected, even a brief obstruction in a struggling child can generate sufficient negative intrathoracic pressure to cause NPPE. A brief tongue fallback can rapidly evolve into life-threatening NPPE within minutes. We report a child who developed acute NPPE after extubation from transient tongue fallback despite standard extubation practices, with full recovery after rapid recognition and supportive care. The child was tachypneic and started having recurrent cough and on auscultation there were de-novo coarse crackles heard on both lung fields more extensively on the left side of the chest. Immediate chin lift and jaw thrust maneuvers were performed, mouth opening for laryngoscopy showed a posteriorly displaced flaccid tongue obstructing the supraglottic area causing airway occlusion with no laryngospasm. Chest X-ray revealed bilateral diffuse pulmonary infiltrates suggestive of pulmonary edema. The child responded to furosemide and hydrocortisone. The child recovered uneventfully. NPPE diagnosis was based on high index of clinical suspicion and close monitoring in our reported child. Clinicians and medical staff should maintain high index of suspicion for NPPE in any child with post-extubation airway obstruction, as early identification and prompt management are critical to preventing NPPE.