Abstract

SESSION TITLE: Wednesday Medical Student/Resident Case Report Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/23/2019 09:45 AM - 10:45 AM INTRODUCTION: Obstructive sleep apnea (OSA) is associated with fragmented sleep caused by intermittent narrowing or occlusion of the upper airways leading to hypoxia. Uvulopalatopharyngoplasty (UPPP) is a common surgical treatment for adult patients with OSA. Complications are infrequent post-UPPP and include respiratory failure, hemorrhage, and hypertension. We report a serious complication of negative pressure pulmonary edema (NPPE) leading to respiratory failure after a UPPP procedure. CASE PRESENTATION: A 33 year-old-male with a past medical history of morbid obesity and OSA underwent UPPP without intraoperative complications. Immediately following extubation, he developed hypoxia refractory to increasing oxygen supplementation requiring intubation. The post intubation chest X-ray (CXR) showed diffuse pulmonary edema with a deep sulcus sign on the right. Extensive pink frothy secretions were suctioned repeatedly and required an endotracheal tube exchange. The repeat CXR showed worsening pulmonary edema and a right-sided pneumothorax which failed to improve despite right-sided chest tube placement. He subsequently required a second right-sided chest tube which expanded the right lung, decreased the peak pressures, and improved oxygenation. Echocardiogram was consistent with longstanding OSA and revealed a moderate to severely dilated right ventricle with reduced function. Patient’s condition improved rapidly with diuretics and aggressive mechanical ventilation; he was weaned off the ventilator and the chest tubes were quickly removed. After a short hospital course, he was discharged home in stable condition. DISCUSSION: The temporal cause of events following the relief of upper airway obstruction after UPPP suggests that NPPE was the cause of the respiratory failure. Clinicians need to be aware of this serious complication as rapid recognition can improve outcomes. NPPE can be classified as either Type I or Type II. Type I develops in patients who generate a negative intrathoracic pressure against acute airway obstruction. This can occur in patients with upper airway infections and laryngospasms leading to increased venous return and pulmonary edema. Type II develops after relief of chronic upper airway obstruction with loss of positive end-expiratory pressure (PEEP). The rapid removal of PEEP leads to interstitial fluid transudation and pulmonary edema. Regardless of type, patients usually present with hypoxia, pulmonary edema, and pink frothy sputum. Manifestations of acute airway obstruction may be present and include stridor with use of accessory muscles. Management is supportive with or without the use of diuretics. The use of positive airway pressure ventilation has been suggested for both acute management and prevention of pulmonary edema. CONCLUSIONS: Although a benign surgical procedure, UPPP has complications that need to be rapidly identified in the immediate post-operative period. Reference #1: Bhaskar B, Fraser JF. Negative pressure pulmonary edema revisited: Pathophysiology and review of management. Saudi J Anaesth. 2011;5(3):308-13. Reference #2: Miro AM, Shivaram U, Finch PJ. Noncardiogenic pulmonary edema following laser therapy of a tracheal neoplasm. Chest. 1989;96:1430–1. Reference #3: Guffin TN, Harel G, Sanders A, Lucente FE, Nash M. Acute postobstructive pulmonary edema. Otolaryngol Head Neck Surg. 1995;112:235–7. DISCLOSURES: No relevant relationships by Abdullah Al Twal, source=Web Response No relevant relationships by Kristin Fless, source=Web Response No relevant relationships by Sasa Ivanovic, source=Web Response No relevant relationships by Nirav Mistry, source=Web Response No relevant relationships by Vagram Ovnanian, source=Web Response No relevant relationships by Anish Patel, source=Web Response No relevant relationships by Fariborz Rezai, source=Web Response No relevant relationships by Paul Yodice, source=Web Response

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