Pathophysiological and diagnostic implications of cardiac biomarkers and antidiuretic hormone release in distinguishing immersion pulmonary edema from decompression sickness

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 ± 61 pmol/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 ± 394 ng/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 ± 1.50 μg/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.

Galectin-3 and Cardiovascular Biomarkers Reflect Adaptation Response to Scuba Diving

“…Several studies have ob-served a significant increase in the plasma level of N-terminal prohormone of brain natriuretic peptide (NT-proBNP), a myocardial stress/stretching biomarker, after diving at low depths (10 or 15 meters) during 30-60 min [6][7][8]. However, cardiac troponin-I (TnI), a myocardial injury biomarker, level has only been measured in patients with decompression sickness [9] or immersion pulmonary edema [9,10]. A study on the effects of technical diving, which differs from rSCUBA diving because it allows dives deeper than 40 m with an obligatory decompression stop [11,12], on the vascular antioxidant system detected the decrease in endothelin-1 (ET-1) and increase in vascular endothelial growth factor (VEGF) immediately after diving [13].…”

Troponins in scuba divers with immersion pulmonary edema

“…Finally, high BNP level has been previously reported in IPE [ 6 ], sometimes associated with hypertension [ 8 ]. Here, we observed a high level in BNP that is consistent with an increased filling pressure.…”

“…IPE occurs typically during scuba diving, snorkeling, and swimming. IPE is sometimes associated with myocardial injury or dysfunction [ 6 ], mostly in the context of a Takotsubo syndrome triggered by cold immersion, stress, and effort [ 11 ]. In these cases, troponin dosage is welcome.…”

“…Symptomatology includes dyspnea, cough, hemoptysis, blood-tinged sputum, cyanosis, and sometimes fainting. Most patients recover from IPE with appropriate treatment including oxygen, β-mimetic, diuretics, and/or aerosols [ 6 ]. The pathophysiology of this syndrome remains elusive but implies hemodynamic and cardiorespiratory disorders leading to the leakage of water into the pulmonary alveolar interstitial spaces [ 3 , 7 ].…”

“…Because myocardial injury impacts the therapeutic management, cardiac biomarkers could help in screening of patients with IPE. As an example, it was shown that cardiac biomarker profile may help to distinguish IPE from decompression sickness [ 6 ]. Thus, the aim of the present study was to evaluate the profile of cardiac biological markers of divers in a context of IPE, and specially the behavior of brain natriuretic peptide (BNP), creatine phosphokinase (CPK), and troponins.…”