PNEUMOPERITONEUM IN SARS-COV-2: A RARE AND OMINOUS CLINICAL SIGN

Abstract

TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: Over a year into the pandemic, SARS-CoV-2 continues to perplex healthcare workers with several atypical clinical manifestations. There is growing literature on SARS-CoV-2-induced pneumothorax, pneumomediastinum, and pneumopericardium. Scarce are cases illustrating this novel pathogen presenting with pneumoperitoneum. It remains unclear whether this relatively rare finding is benign or ominous of impending cardiorespiratory failure. CASE PRESENTATION: A 56yoM presents to the ER with dyspnea and hypoxia. He is PCR-positive for COVID-19. An ABG drawn after he is placed on BIPAP shows 7.072/99.5/66.9/29 with 80% SpO2. Due to PaO2:FiO2 ratio of 66, indicating severe ARDS, the patient was intubated. Follow-up CXR shows multifocal opacities. Within 1 hour, he becomes hypotensive and repeat CXR (Fig1.1a) shows a right pneumothorax. Physical exam findings include apical crepitus and diffuse rales. Labs show elevated inflammatory markers (Fig2.1). He is given high-dose dexamethasone, remdesevir, and tocilizumab. CXR 1 day later reveals free air under the diaphragm. A follow-up CT chest/abdomen (Fig3.1) shows bilateral pneumothoraces, pneumomediastinum, and pneumoperitoneum. Bilateral chest tubes are placed within 48 hours (Fig1.1b), infraclavicular incisions (Gills' procedures) are made to release trapped subcutaneous air, and ventilator adjustments are made. His prognosis remains guarded and he continues to require ventilatory support. DISCUSSION: COVID-19 induced ARDS occurs via the angiotensin-converting enzyme 2 (ACE2) receptor. The diaphragm surface is lined with ACE2 receptors and surface myofibers bind viral RNA. Highlighted via RNA in-situ hybridization, a post-mortem analysis has shown diaphragm fibrosis is >2x higher in COVID-ICU patients compared with other ICU patients. In our case, one possible mechanism of pneumoperitoneum is from mediastinal air seeding through one of many fibrosed diaphragmatic weak points to the peritoneal cavity. Other explanations for COVID-19 related pneumoperitoneum include the Macklin effect or direct intestinal penetration via ACE2 receptors expressed on intestinal mucosa. Our patient developed a small pneumothorax upon being placed on mechanical ventilation. This correlates to PRMV (Pneumothorax/pneumomediastinum related to mechanical ventilation) inducing further barotrauma. Nonetheless, direct diaphragmatic myopathy from SARS-CoV-2 is also contributory. CONCLUSIONS: Patients with severe ARDS from COVID-19 are at significantly higher risk of barotrauma, as up to 40% of patients will have some form due to reduced lung compliance. A higher incidence of diaphragmatic fibrosis predisposes patients to an increased risk of pneumoperitoneum, especially in the setting of severe ARDS with PRMV-related barotrauma. We recommend clinicians to be vigilant about this complication as it poses a therapeutic challenge in patients continuing to require mechanical ventilation. REFERENCE #1: Shi Z, de Vries HJ, Vlaar APJ, et al. Diaphragm Pathology in Critically Ill Patients With COVID-19 and Postmortem Findings From 3 Medical Centers. JAMA Intern Med. 2021;181(1):122–124. doi:10.1001/jamainternmed.2020.6278 REFERENCE #2: Li S, Chau E, Ghasem W, Sohn J, Yaghmour B. Air Should Not be There: A Case of Pneumomediastinum and Pneumopericardium in COVID-19. Cureus. 2020;12(11):e11696. Published 2020 Nov 25. doi:10.7759/cureus.11696 REFERENCE #3: Duarte R, Duarte E, Gutierrez J, et al. (February 07, 2021) Pneumoperitoneum in a COVID-19 Patient Due to the Macklin Effect. Cureus 13(2): e13200. doi:10.7759/cureus.13200 DISCLOSURES: No relevant relationships by David Lindner, source=Web Response No relevant relationships by Sankalp Patel, source=Web Response No relevant relationships by Vishal Patel, source=Web Response No relevant relationships by Anshika Singh, source=Web Response No relevant relationships by Carla Williams, source=Web Response