PULMONARY EDEMA AND HEMOPTYSIS AFTER AN ORTHOPEDIC SURGERY

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: Negative pressure pulmonary edema(NPPE) is an acute respiratory failure usually caused after a strong inspiratory effort generated against an obstructed upper airway[1]. CASE PRESENTATION: A 29-year-old man was admitted to the hospital for an elective open reduction with internal fixation of left bimalleolar ankle fracture. The surgery was uneventful. After extubation, he became hypoxic and started coughing up bloody phlegm without evidence of vomiting. He was afebrile, HR 96, RR 22 and BP 146/96. Chest x-ray showed bilateral alveolar consolidations in the upper and mid zones(Fig1). He was given Lasix 40 mg IV once and was transferred to the ICU. He was hemodynamically stable on high-flow oxygen. Arterial blood gas was showing pH of 7.41, PO2 98, pCO2 46 and HCO3 28.4. There was no evidence of swelling in the posterior pharynx. Lung exam showed good air entry on both sides, bilateral crepitations without wheezes. Laboratory work was unremarkable. Echocardiogram revealed normal ejection fraction, no significant valvular heart disease. He made a strong inspiratory effort after extubation due to upper airway laryngospasm and developed NPPE with alveolar hemorrhage. He was started on steroids. CT chest with contrast showed bilateral ground-glass opacities with alveolar infiltration in parenchymal hemorrhagic pattern(Fig2). He was continued on supportive treatment. Hemoptysis resolved in a day. He was transitioned to nasal cannula. Follow up chest x-ray showed significant improvement in alveolar infiltrates(Fig3). He was discharged home after a 48-h stay in the hospital. DISCUSSION: In adults, the most reported causes of airway obstruction leading to NPPE are in the context of laryngospasm following surgery[2]. The incidence of NPPE is as low as 0.1% of laryngospasm cases [3]. The first case of NPPE was reported and published in 1973 by Capitano and Kirkpatrick. There was a question whether NPPE was a result of high vessel permeability or hydrostatic pressure edema formation[1]. The high negative intrathoracic pressure generated to overcome the upper airway obstruction can reach -140 cm H2O[1]. The hydrostatic pressure in the pulmonary capillaries increases, the rate of interstitial fluid accumulation outgrows the capacity of the lymphatic drainage and fluid floods into the alveoli. Stress fracture can develop in the pulmonary capillaries leading to high permeability edema and blood-tinged secretions. Most cases of NPPE resolve in 24-48h. Diuretics have been used to hasten the resolution of the pulmonary edema. Beta agonist improves the clearance of the fluid by increasing active cation transport. In case of severe obstruction, cricothyroidotomy or tracheostomy can been used. Sedating and paralyzing the patient prevent more laryngospasm or biting of the endotracheal tube. CONCLUSIONS: NPPE is an entity not frequent encountered, but life threatening if not recognized or managed appropriately. Reference #1: M. Bhattacharya, R. H. Kallet, L. B. Ware, and M. A. Matthay, “Negative-Pressure Pulmonary Edema,” Chest, vol. 150, no. 4, pp. 927–933, Oct. 2016. Reference #2: A. Udeshi, S. M. Cantie, and E. Pierre, “Postobstructive pulmonary edema,” J. Crit. Care, vol. 25, no. 3, p. 538.e1-538.e5, 2010. Reference #3: B. Bhaskar and J. F. Fraser, “Negative pressure pulmonary edema revisited: Pathophysiology and review of management,” Saudi J. Anaesth., vol. 5, no. 3, pp. 308–313, 2011. DISCLOSURES: No relevant relationships by Arul Chandran, source=Web Response No relevant relationships by Michele Obeid, source=Web Response