SECONDARY SPREAD OF IATROGENIC SINGLE LUNG INJURY: AN UNUSUAL AND FATAL CAUSE OF ARDS

Abstract

SESSION TITLE: Medical Student/Resident Critical Care Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Acute lung injury may occur following thoracotomy. We describe a fatal case of acute respiratory distress syndrome (ARDS) resulting from the combination of one-lung ventilation (OLV), ventilator induced lung injury (VILI) and patient self-induced lung injury (P-SILI) following routine lobectomy. CASE PRESENTATION: A 69-year-old man with lung adenocarcinoma and OSA was admitted after open thoracotomy for right upper lobectomy which required several hours of OLV. Postoperatively, he developed dyspnea for which diuresis, bronchodilators and frequent CPAP use were tried. On post-op day 3, CT chest revealed interstitial ground glass opacifications, greater on the left. This pattern was worrisome for hypersensitivity pneumonitis, and steroids were initiated. He was transitioned to BIPAP and transferred to the ICU. Repeat CT revealed worsening interstitial disease bilaterally and left pneumothorax for which pleural drainage catheter was placed. Due to respiratory compromise, he was transferred to a tertiary center. He continued to receive noninvasive ventilation with tidal volumes exceeding 1L. He was intubated prior to bronchoscopy with bronchial alveolar lavage which was unrevealing. He continued to have increased oxygen needs with PaO2/FiO2 and imaging consistent with ARDS and multifocal high density alveolar infiltrates. Despite adjustment to low tidal volume ventilation, prone positioning and paralysis, his hypoxemia did not improve. He was placed on VV-ECMO. Ultimately, he did not recover and died after withdrawal of ECMO. DISCUSSION: During a thoracotomy, functional residual capacity decreases about 40% with complete loss upon surgical pneumothorax. The intact lung relies on positive pressure to maintain volumes and therefore is dependent on tidal volume and positive end expiratory pressure. Overdistention in OLV with large tidal volumes causes excess strain. This strain produces an inflammatory response at the alveolar-capillary membrane with release of cytokines resulting in greater injury in the ventilated lung during OLV. While lung overdistention contributes to VILI during OLV, ventilation at low absolute lung volumes causes frequent opening and closing of lung units, regional hypoxia and surfactant dysfunction i.e. atelectrauma. Our patient was exposed to OLV in surgery causing left lung injury with a unique unilateral ARDS picture. We speculate that increased respiratory drive and impaired gas exchange due to this injury caused him to develop P-SILI in his right lung. These initial injuries were likely compounded by VILI through gratuitous use of noninvasive ventilation and unchecked tidal volumes generated by the patient’s effort. Failure to identify these factors ultimately resulted in continuous insults and irreparable damage. CONCLUSIONS: Proper identification of lung injury pattern after OLV is crucial in reducing effects of VILI and P-SILI in the development of ARDS. Reference #1: Henderson, W.R., Chen, L., Amato, M.B.P, & Brochard, L.J. (2017). Respiratory mechanics in acute respiratory distress syndrome. American Journal of Respiratory and Critical Care Medicine 2017 Oct 1; 196 (7): 822-833. doi:10.1164/rccm.201612-2495CI. Reference #2: Lohser, J. and Slinger, P. (2015). Lung injury after one-lung ventilation: a review of the pathophysiologic mechanisms affected the ventilation and the collapsed lung. Anesthesia & Analgesia 122 (2):302-18. doi: 10.1213/ANE.0000000000000808. Reference #3: Slutsky, A.S. & Marco Ranieri, V. (2013). Ventilatory-induced lung injury. New ENgland Journal of Medicine 2013; 369:2126-2136 doi:10.1056/NEJMra1208707. DISCLOSURES: No relevant relationships by Paul Bergl, source=Web Response No relevant relationships by Marium Khan, source=Web Response