Immersion pulmonary edema in scuba divers is a rare disorder that tends to recur and can be potentially fatal, even in the absence of underlying cardiac disease. Anecdotal cases of reversible myocardial dysfunction have been described in this setting, but little is known of its pathogenesis. The purpose of the present study was to determine the clinical outcomes and the determinants associated with this condition. The data from 54 consecutive divers admitted for acute immersion pulmonary edema during a 5.5-year period were retrospectively studied. A diagnosis of myocardial dysfunction was established by the presence of elevated cardiac troponin T levels, coupled with electrocardiographic changes and/or wall motion abnormalities on the echocardiogram. The demographic, clinical, biologic, and diving characteristics were tested as potential predictors of this disorder. All the patients had complete resolution of symptoms within 72 hours, but 3 required intensive ventilation or hemodynamic support at admission. Reversible myocardial dysfunction was observed in 28% and was associated more with age >50 years (odds ratio [OR] 5.5, 95% confidence interval [CI] 1.5 to 21, p = 0.013), hypertension (OR 8.2, 95% CI 2.1 to 32, p = 0.002), diabetes (OR 22.1, 95% CI 1.1 to 458; p = 0.002), and release of natriuretic peptides (OR 9.1, 95% CI 2.4 to 35, p = 0.001). Follow-up investigations at 1 month were obtained for 49 patients and revealed a significant number of patients with occult hypertension. In conclusion, reversible myocardial dysfunction is not uncommon in divers with immersion pulmonary edema. The short-term overall prognosis is not adversely altered, but severe heart failure with a fatal outcome is unpredictable. Close monitoring of older divers with latent cardiovascular risk factors is warranted.
Recent published reports have outlined that immersion pulmonary edema (IPE) during diving can have a potentially fatal outcome, particularly in older divers without evidence of underlying cardiac disease. Sporadic cases of IPE were found to be associated with myocardial injury that was clinically inconsequential ; however, the pathophysiology linking these 2 conditions in the specific clinical arena of the medicine of diving has received little attention. To date, reversible myocardial dysfunction (RMD), described as myocardial stunning with left ventricular contractile abnormalities, has largely been observed after a variety of neurologic events, emotional sources of stress, or acute medical illness. It is the prevailing view that the cardiac decompensation in these situations could be neurogenic, with sympathetic stimulation of the myocardium, leading to direct myocyte injury or reduction of the coronary flow with the development of microvascular spasm resulting in ischemia. It is not known whether the RMD that occurs in the setting of IPE is the cause or the effect. However, it has been assumed that the detection of cardiac abnormalities evocative of myocardial injury at admission indicates that such patients are at greater risk of acute heart failure and arrhythmias, which might explain some of the fatalities associated with IPE while diving. Therefore, the purpose of the present study was to analyze the diving data and clinical characteristics of divers admitted for IPE with the aim of identifying the potential determinants of cardiac impairment sometimes detected with this presentation. We also assessed the cardiovascular functional status and clinical course of the outpatients 1 month after discharge.
Methods
We retrospectively reviewed the medical records and diving parameters of scuba divers treated in 2 French hyperbaric facilities (Toulon near the Mediterranean Sea and Brest near the Atlantic Ocean) from January 2007 to June 2012, who met the clinical criteria for IPE (i.e., onset of dyspnea during diving, cough, frothy sputum, bilateral rales) documented by chest computed tomography in the 6 hours after their admission. We excluded the patients with historical and clinical evidence of water aspiration and pulmonary barotrauma or when IPE occurred during breath-hold diving. A total of 61 consecutive patients were initially identified during the 5.5-year study period for this injury. Of the 61 patients, 7 were not included in the present study because laboratory investigations had not been obtained or the patients had presented 12 hours after surfacing with resolving symptoms, leaving 54 divers for analysis.
Pre-existing pulmonary, cardiac, and coronary diseases with cardiovascular (CV) risk factors, including cigarette smoking, hypertension, diabetes mellitus, and dyslipidemia, were determined for each patient at presentation. For the purposes of the present study, the number of patients with hypertension or dyslipidemia was the sum of those who had been treated with appropriate medication before the acute event and those with hypertension or dyslipidemia detected during the hospitalization or the follow-up study period and medicated thereafter.
Cardiac troponin T (cTnT) was measured at the initial presentation to the emergency department, and repeated measurements were done within the first 12 hours of admission to obtain a concentration curve. The absence of myocardial injury was established by a minimum of 2 negative serum biomarkers measured ≥4 to 6 hours apart with cut-off values of 0.05 μg/L before 2012 and 15 μg/L thereafter (high-sensitivity cTnT assay). Twelve-lead electrocardiograms with potential ST-segment and T-wave changes recorded were taken within the first hour of clinical presentation. If necessary, serial electrocardiograms were recorded at 6, 12, and 24 hours after admission. Transthoracic echocardiography was performed early for all the patients in whom cardiac impairment was suspected from the biologic and electrocardiographic findings to identify wall motion abnormalities and to assess the left ventricular ejection fraction. The diagnosis of myocardial dysfunction (MD) was established by the coexistence of elevated cTnT levels with electrocardiographic and/or echocardiographic abnormalities.
Some patients underwent emergency coronary angiography or exercise testing within 48 hours of admission, when acute ischemic heart disease was suspected. Natriuretic peptide biomarker levels were also available for all patients at admission and were used for statistical analysis with a normal limit of <100 pg/ml for brain natriuretic peptide and <350 pg/ml for N-terminal pro-brain natriuretic peptide.
The patients were followed up at 1 month with a physical examination by a cardiologist, echocardiography, exercise testing, and the determination of the blood lipid levels (triglycerides, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol). In some cases, cardiac magnetic resonance imaging and ambulatory blood pressure monitoring were performed, as indicated by the physician in charge of the patient.
Continuous variables are presented as the mean ± SD after passing the normality test, and categorical variables are presented as absolute values and percentages. A comparison of the variables between the groups was performed using the unpaired t test and the Fisher exact test, as appropriate. Odds ratios (ORs) with 95% confident intervals (CIs) were calculated, when needed, with the p values, for which the level of significance was set as <0.05. Statistical analysis was done with Graphpad Prism, version 5.00 (GraphPad Software, San Diego, California). Informed consent of the patients was waived because of the retrospective nature of our study.
Results
The mean age of the study population was 46 ± 13 years; 18 (33%) were women. Of the 54 patients, 43 (80%) originated from Toulon and 11 (20%) from the area of Brest. The divers with IPE treated in Toulon during the study period represented 12% of all patients referred for a diving injury to this facility, if we included those with incomplete data.
All the patients were admitted to the emergency unit or the intensive care unit for a minimum of 12 hours with usual treatment consisting of normobaric oxygen. All but 2 patients had complete resolution of symptoms within 6 to 24 hours. Three patients required initial continuous positive airway pressure ventilation because of respiratory distress at hospital admission. Of these, 2 received inotropes (dobutamine, neosynephrin) for hemodynamic support. No patient died during the hospital stay.
The demographic, medical history, and biologic data and details of the incident dives as a function of myocardial impairment are listed in Table 1 .
| Variable | MD | p Value | OR (95% CI) | |
|---|---|---|---|---|
| Yes (n = 15) | No (n = 39) | |||
| Gender | 0.53 | — | ||
| Male | 9 | 27 | ||
| Female | 6 | 12 | ||
| Age (yrs) | 0.013 | 5.5 (1.5–21) | ||
| >50 | 11 | 13 | ||
| ≤50 | 4 | 26 | ||
| Mean BMI (kg/m 2 ) | 27.5 ± 2 | 24.7 ± 3 | 0.06 | — |
| Previous IPE | 3 (20) | 6 (15) | 0.7 | — |
| Pre-existing pulmonary disease ∗ | 0 | 2 (5) | 1 | — |
| Pre-existing heart disease † | 0 | 1 (3) | 1 | — |
| Cigarette smoker | 3 (20) | 3 (8) | 0.3 | — |
| Hypertension | 9 (60) | 6 (15) | 0.002 | 8.2 (2.1–32) |
| Diabetes mellitus | 3 (20) | 0 | 0.002 | 22.1 (1.1–458) |
| Hyperlipidemia ‡ | 6 (40) | 6 (15) | 0.07 | — |
| Elevated natriuretic peptides | 10 (67) | 7 (18) | 0.001 | 9.1 (2.4–35) |
| Mean depth (msw) | 32 ± 12 | 30 ± 12 | 0.5 | — |
| Mean total dive time (min) | 21 ± 8 | 29 ± 15 | 0.08 | — |
| Violation of decompression guidelines | 3 (20) | 8 (21) | 1 | — |
| Breathing gas | 0.25 | — | ||
| Air | 14 | 39 | ||
| Nitrox | 1 | 9 | ||
| Mean water temperature (°C) | 16.5 ± 4 | 15 ± 3 | 0.2 | — |
| Loss of consciousness | 4 (26) | 5 (13) | 0.24 | — |
| Exertion in diving/after surfacing | 5 (33) | 10 (26) | 0.73 | — |
| Emotional stress | 3 (20) | 16 (41) | 0.2 | — |
† Coronary artery disease previously treated by revascularization.
‡ Determined by serum low-density lipoprotein cholesterol levels >3.5 mmol/L or triglycerides >1.8 mmol/L.
The findings from the laboratory and clinical investigations ruled out a cardiac disorder in 39 patients (72%), who were considered the MD-negative group. The remaining 15 patients (28%) had elevated cTnT levels within the 6 to 12 hours after admission with electrocardiographic and/or echocardiographic disturbances and were included in the MD-positive group ( Table 2 ).
| Pt. No./Gender | Age (yrs) | BMI (kg/m 2 ) | CV Risk Factors | ECG Findings | cTnT (μg/L) | NP (pg/ml) | Initial Echo, LVEF | CAD Testing During Hospitalization | Follow-Up Investigations |
|---|---|---|---|---|---|---|---|---|---|
| 1/M | 60 | 28 | HTN, Chol, DM | ST-segment depression D 1 –aVL–V 1 –V 2 | 0.2 | 61 † | Mild cLVH, 60% | — | ECG: N; ET: N; Echo: cLVH, 62%, |
| 2/M | 64 | 28.7 | None | ST-segment depression D 1 –aVL | 1.6 | 272 † | LBH, 40% | CA: N | ECG: N; ET: N; Echo: N, 61% |
| 3/M | 62 | 24.1 | None | ST-segment depression D 1 –aVL–V 5 –V 6 | 0.5 | 170 † | LBH, 45% | CA: N | ECG: N; Chol; ET: N; Echo: N, 55% |
| 4/M | 56 | 26.6 | None | LBBB | 0.1 | 1,200 | SBH, 50% | CA: N | ECG: N; ET: N; Echo: N, 55% |
| 5/M | 63 | 28.8 | HTN, Chol, DM | ST-segment inversion D 2 –D 3 –aVF | 0.6 | 7,000 | IBH, 55%; mild cLVH; MR | CA: mild irregularities LADA | ECG: N; ET: N; Echo: mild cLVH, 61% |
| 6/F | 51 | 26.1 | Smoking | LBBB | 0.08 | 1,180 | SH, 60% | — | ECG: N; ET: N; BPm: HTN; Echo: N |
| 7/M | 45 | 31.1 | None | ST-segment inversion D 2 –D 3 –aVF | 0.15 | 35 | N, 61% | — | ECG: N; ET: N; BPm: HTN |
| 8/F | 55 | 30.5 | Chol | N | 0.9 | 635 | Discrete SH, 50% | ET: N | ECG: N; Echo: N, 55%; BPm: HTN |
| 9/F | 66 | 30 | HTN, TG | N | 102 ∗ | 425 | GH, 45% | CA: N | ECG: N; Echo: N, 55%; cMRI: N |
| 10/M | 61 | 27.4 | HTN | ST-segment depression D 1 –aVL | 75 ∗ | 2,000 | LBH, 62%; cLVH | — | ECG: N; ET: HTN; Echo: cLVH, 70% |
| 11/M | 64 | 24.6 | Smoking | N | 0.3 | 715 | GH, 55% | — | ET: HTN; Echo: N, 65%; BPm: HTN |
| 12/F | 45 | 27.5 | HTN, smoking | ST-segment depression V 1 –V 2 –V 3 | 0.4 | 320 | ASH, 48% | CA: N | ECG: N; Echo: N, 58% |
| 13/M | 47 | 26 | None | ST-segment depression D 1 –aVL | 0.12 | 300 | GH, 55% | ET: N | ECG: N; Echo: N, 72% |
| 14/F | 57 | 25 | Chol, DM | T-wave inversion V 5 –V 6 | 0.6 | 250 † | SBH, 45% | — | ECG: N; ET: N; Echo: N |
| 15/F | 43 | 26.7 | None | ST-segment depression D 1 –aVL | 4 | 88 † | LBH, 50% | ET: N | ECG: N; Echo: N, 62%; cMRI: N |
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