MiscellaneousReversible Myocardial Dysfunction and Clinical Outcome in Scuba Divers With Immersion Pulmonary Edema
Section snippets
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
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
Discussion
The present series is the largest series of IPE in scuba divers in the published data. Our results have tended to demonstrate that RMD accompanying IPE is common, with 28% of patients having cardiac injury, documented by cTnT release and echocardiographic and/or electrocardiographic abnormalities. This phenomenon has rarely been depicted, making a direct comparison with other studies difficult. In a series of 19 scuba divers with documented IPE, Henckes et al5 identified only 2 patients who
Acknowledgment
We gratefully acknowledge the medical team of the cardiology department of Sainte Anne's military hospital (Toulon, France) for conducting the laboratory investigations and performing the echocardiography. We thank P. Constantin, MD, for his participation in our study.
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Swimming-Induced Pulmonary Edema: Evaluation of Prehospital Treatment With CPAP or Positive Expiratory Pressure Device
2022, ChestCitation Excerpt :The rationale for β2-agonist inhalation can be increased alveolar fluid absorption of pulmonary edema or comorbidity of SIPE and acute asthma.2,18,30,33 Simultaneously, reports have been published of patients with SIPE and immersion pulmonary edema with reversible myocardial dysfunction or Takotsubo cardiomyopathy.12,34,35 In such cases, safety using β2-agonist inhalation may be uncertain, and more knowledge about adrenergic activation as a trigger of SIPE is required.36
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