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Pathophysiological and Diagnostic Implications of Cardiac Biomarkers Pathophysiological and diagnostic implications of cardiac biomarkers and antidiuretic hormone release in distinguishing immersion pulmonary edema from decompression sickness Article Published Version Creative Commons: Attribution-Noncommercial-No Derivative Works 4.0 Open access Louge, P., Coulange, M., Beneton, F., Gempp, E., Le Pennetier, O., Algoud, M., Dubourg, L., Naibo, P., Marlinge, M., Michelet, P., Vairo, D., Kipson, N., Kerbaul, F., Jammes, Y., Jones, I. M., Steinberg, J.-G., Ruf, J., Guieu, R., Boussuges, A. and Fenouillet, E. (2016) Pathophysiological and diagnostic implications of cardiac biomarkers and antidiuretic hormone release in distinguishing immersion pulmonary edema from decompression sickness. Medicine, 95 (26). e4060. ISSN 0025-7974 doi: https://doi.org/10.1097/MD.0000000000004060 Available at http://centaur.reading.ac.uk/66136/ It is advisable to refer to the publisher’s version if you intend to cite from the work. See Guidance on citing . To link to this article DOI: http://dx.doi.org/10.1097/MD.0000000000004060 Publisher: Lippincott, Williams & Wilkins All outputs in CentAUR are protected by Intellectual Property Rights law, including copyright law. Copyright and IPR is retained by the creators or other copyright holders. Terms and conditions for use of this material are defined in the End User Agreement . www.reading.ac.uk/centaur CentAUR Central Archive at the University of Reading Reading’s research outputs online ® Observational Study Medicine OPEN Pathophysiological and diagnostic implications of cardiac biomarkers and antidiuretic hormone release in distinguishing immersion pulmonary edema from decompression sickness Pierre Louge (MD)a, Mathieu Coulange (MD)b,c, Frederic Beneton (MD)b, Emmanuel Gempp (MD)a, Olivier Le Pennetier (MSc)c, Maxime Algoud (MSc)d, Lorene Dubourg (MSc)d, Pierre Naibo (MSc)d, Marion Marlinge (MSc)d, Pierre Michelet (MD)c, Donato Vairo (MSc)c, Nathalie Kipson (MSc)c, François Kerbaul (MD)c, Yves Jammes (MD)c, Ian M. Jones (PhD)e, Jean-Guillaume Steinberg (PhD)c, ∗ Jean Ruf (DSc)c, Régis Guieu (MD)c,d, , Alain Boussuges (MD)c, Emmanuel Fenouillet (DSc)c,f Abstract Immersion pulmonary edema (IPE) is a misdiagnosed environmental illness caused by water immersion, cold, and exertion. IPE occurs typically during SCUBA diving, snorkeling, and swimming. IPE is sometimes associated with myocardial injury and/or loss of consciousness in water, which may be fatal. IPE is thought to involve hemodynamic and cardiovascular disturbances, but its pathophysiology remains largely unclear, which makes IPE prevention difficult. This observational study aimed to document IPE pathogenesis and improve diagnostic reliability, including distinguishing in some conditions IPE from decompression sickness (DCS), another diving-related disorder. Thirty-one patients (19 IPE, 12 DCS) treated at the Hyperbaric Medicine Department (Ste-Anne hospital, Toulon, France; July 2013–June 2014) were recruited into the study. Ten healthy divers were recruited as controls. We tested: (i) copeptin, a surrogate marker for antidiuretic hormone and a stress marker; (ii) ischemia-modified albumin, an ischemia/hypoxia marker; (iii) brain-natriuretic peptide (BNP), a marker of heart failure, and (iv) ultrasensitive-cardiac troponin-I (cTnI), a marker of myocardial ischemia. We found that copeptin and cardiac biomarkers were higher in IPE versus DCS and controls: (i) copeptin: 68% of IPE patients had a high level versus 25% of DCS patients (P<0.05) (mean±standard-deviation: IPE: 53±61pmol/L; DCS: 15±17; controls: 6±3; IPE versus DCS or controls: P<0.05); (ii) ischemia-modified albumin: 68% of IPE patients had a high level versus 16% of DCS patients (P<0.05) (IPE: 123±25 arbitrary-units; DCS: 84±25; controls: 94±7; IPE versus DCS or controls: P<0.05); (iii) BNP: 53% of IPE patients had a high level, DCS patients having normal values (P<0.05) (IPE: 383±394ng/L; DCS: 37±28; controls: 19±15; IPE versus DCS or controls: P<0.01); (iv) cTnI: 63% of IPE patients had a high level, DCS patients having normal values (P<0.05) (IPE: 0.66±1.50mg/L; DCS: 0.0061±0.0040; controls: 0.0090±0.01; IPE versus DCS or controls: P<0.01). The combined “BNP-cTnI” levels provided most discrimination: all IPE patients, but none of the DCS patients, had elevated levels of either/both of these markers. We propose that antidiuretic hormone acts together with a myocardial ischemic process to promote IPE. Thus, monitoring of antidiuretic hormone and cardiac biomarkers can help to make a quick and reliable diagnosis of IPE. Abbreviations: ADH = antidiuretic hormone, AU = arbitrary units, BNP = brain natriuretic peptide, CRP = C-reactive protein, DCS = decompression sickness, H+6 = 6 hours after admission to the hospital, H0 = time of emergency admission to the hospital, IMA = ischemia-modified albumin, IPE = immersion pulmonary edema, us cTnI = ultrasensitive cardiac troponin I. Keywords: antidiuretic hormone, cardiac biomarkers, decompression sickness, diving, immersion pulmonary edema Editor: Anastasios Lymperopoulos. Funding: Aix-Marseille University and Assistance Publique-Hôpitaux de Marseille. These sources were not involved in study design, results, and writing. The authors have no conflicts of interest to disclose. Ethical Approval: informed consents were obtained before inclusion. The Ethics Committee at the university hospital gave its agreement. The protocol followed the guidelines of the 1975 Declaration of Helsinki. Alain Boussuges and Emmanuel Fenouillet contributed equally to this work. a Department of Hyperbaric Medicine, Sainte-Anne Hospital, Toulon, b Department of Hyperbaric Medicine, Sainte-Marguerite Hospital, Marseille, c UMR MD2, Aix- Marseille University and Institute of Biological Research of the Army, d Laboratory of Biochemistry, Timone University Hospital, Marseille, e School of Biological Sciences, University of Reading, United Kingdom, f Institut des Sciences Biologiques, CNRS, France. ∗ Correspondence: Régis Guieu, Faculty of Medicine, Bd Dramard, (e-mail: [email protected]). Copyright © 2016 the Author(s). Published by Wolters Kluwer Health, Inc. All rights reserved. This is an open access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially. Medicine (2016) 95:26(e4060) Received: 10 March 2016 / Received in final form: 28 May 2016 / Accepted: 2 June 2016 http://dx.doi.org/10.1097/MD.0000000000004060 1 Louge et al. Medicine (2016) 95:26 Medicine 1. Introduction distinguish IPE from DCS in some challenging conditions by Immersion pulmonary edema (IPE) is a serious environmental characterizing the biomarkers outlined above in each disorder. illness caused by water immersion, cold, and exertion, and occurs In summary, the present observational study was aimed at during popular water sports such as SCUBA diving, snorkeling, understanding the pathophysiology of IPE by evaluating cardiac and swimming. Cases are also reported among professional function, kidney function, and hypoxia biomarkers, and to – divers, military swimmers, and triathletes.[1 4] IPE pathophysiol- review the resulting data to improve the reliability of IPE ogy is unclear and its incidence is difficult to determine accurately diagnosis, particularly to distinguish IPE from DCS. because many cases are thought to be misdiagnosed. IPE is characterized by dyspnea, cough, haemoptysis, hypoxemia, and 2. Methods [1–4] extreme fatigue. Most patients recover from IPE with rest and 2.1. SCUBA divers’ inclusion oxygen and/or betamimetic therapy, but IPE is sometimes associated with myocardial injury and/or loss of consciousness, In this prospective approach, all the 31 patients (19 IPE, 12 DCS) – which may have a fatal outcome in a water environment.[4 9] The treated at the Emergency Unit of the Department of Hyperbaric fragmented knowledge of IPE pathophysiology is a hurdle to Medicine (Sainte-Anne Hospital, Toulon, France) between July deducing new approaches to prevent the disorder and identifying 2013 and June 2014 were consecutively included. None of the patients with IPE as soon as possible in a context where patients refused to participate, and none were excluded. Ten established biochemical markers are not available. healthy divers were recruited as controls for biochemical analysis, First, the pathogenesis of IPE is thought to imply hemodynamic and blood samples were collected after SCUBA diving. The Ethics and cardiorespiratory disorders that induce leakage of fluid out of Committee at the university hospital gave its agreement, the lumen of the capillary into the interstitial space, and informed consents were obtained before inclusion, and the – eventually into the alveolar airspace.[1 4] Various events are protocol followed the guidelines of the 1975 Declaration of involved in fluid leakage including (i) increased capillary pressure Helsinki. Blood pressure measurement and venous blood resulting from increased cardiac preload following blood sampling (5mL of whole blood on sodium heparinate, or on redistribution from peripheral to thoracic vessels induced by sodium EDTA for the BNP assay) were performed on hospital exertion in immersion conditions, and afterload following admission for all groups. Blood gas analysis was performed on vasoconstriction induced by cold and/or emotional stress,[2,10,11] admission for IPE patients only (2 mL of
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