Mathieu Coulange

Post-mortem computed tomography in a case of suicide by air embolism

a Laboratoire d’imagerie interventionnelle expérimentale, faculté de médecine, Aix-Marseille université, boulevard Jean-Moulin, 13385 Marseille cedex 5, France b Pôle imagerie médicale, service de radiologie, hôpital de la Timone, Assistance publique des Hôpitaux de Marseille, 264, rue Saint-Pierre, 13385 Marseille cedex 5, France c Pôle RUSH, service de médecine hyperbare, hôpital Sainte-Marguerite, 270, boulevard Sainte-Marguerite, 13274 Marseille cedex 9, France d UMR MD2, dysoxie tissulaire, Aix-Marseille université, boulevard Pierre-Dramard, 13916 Marseille cedex 20, France e Service de médecine légale et droit à la santé, hôpital de la Timone, Assistance publique des Hôpitaux de Marseille, 264, rue Saint-Pierre, Marseille cedex 05, France

Retrograde cerebral venous air embolism: a rare cause of intracranial gas.

The emergency department requested a head computed tomography (CT) without contrast media for a brain trauma (fall from height) in a 92-year-old female patient followed for Alzheimer’s disease. The patient presented an acute confusional status but neurological examination was considered to be normal. Head CT detected several intracranial bubbles of air density. They were mainly right-sided, at the contact of orbital fissure and jugular foramen (Fig. 1). A careful bone window examination was not able to identify any fracture of the vault or base of the skull. Analysis of the topography of the gas bubbles found them all within venous structures: right cavernous sinus and right inferior ophthalmic vein, left cavernous sinus and right sigmoid sinus. Moreover, the CT technologist reported that the patient ripped out her peripheral venous catheter, inserted at the crook of her right elbow, immediately before the examination. The final diagnosis was therefore retrograde venous air embolism. i s v i

Plasma adenosine release is associated with bradycardia and transient loss of consciousness during experimental breath-hold diving

Plasma adenosine release is associated with bradycardia and transient loss of consciousness during experimental breath-hold diving Fabrice Joulia , Mathieu Coulange , Frederic Lemaitre , Guillaume Costalat , Frederic Franceschi , Vlad Gariboldi , Laetitia Nee , Julien Fromonot , Laurie Bruzzese , Gilles Gravier , Nathalie Kipson , Yves Jammes , Alain Boussuges , Michele Brignole , Jean Claude Deharo , Regis Guieu a,g,⁎

Scuba diving and portal vein thrombosis: a case report.

INTRODUCTION SCUBA (self-contained underwater breathing apparatus) diving is a well-recognized recreational activity. Most of the medical health problems in SCUBA diving result from decompression during the ascent of the diver. As the diver descends, the surrounding hydrostatic pressure is increased. Because body tissues absorb nitrogen from the inhaled gas in proportion to the ambient hydrostatic pressure, increased depth leads to increased dissolved nitrogen accumulating in the tissues. When the pressure is reduced during ascent, the nitrogen comes out of solution and forms bubbles in the tissues. These bubbles may gain access to the capillary or lymphatic bed by migration and thus can enter the venous circulatory system. Small bubbles are filtered by the lung and exhaled. In mild decompression sickness (Type I), periarticular soft tissue gas bubbles form and patients complain of symptoms like musculoskeletal pains or ‘‘skin bends’’ with rash and pruritus. In severe decompression sickness (Type II), bubbles cause venous stasis in the spinal cord or paradoxical cerebral arterial embolization, which are characterized by neurological symptoms. Other important diving injuries include barotrauma because of overexpansion of air-filled spaces during ascent (mainly the lung, ear, and sinuses, but rarely the stomach). Gas embolism is a rare event that complicates pulmonary or gastric barotraumas. Some authors report an activation of hemostasis by SCUBA diving. In particular, increased levels of Factor VIIa, increased levels of circulating microparticles, and platelet activation have been reported. Many other factors that potentially favor a prothrombotic state, like activation of platelets, complement activation, and increased leukocyte chemotaxis, have been associated with SCUBA diving. However, symptomatic portal vein thrombosis has never been reported in conjunction with SCUBA diving. Here, we report the case of a young recreational diver who experienced a portal vein thrombosis after a diving accident. Despite extensive investigations, no other etiology to this thrombosis could be found.

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

AbstractImmersion 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 &mgr;g/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.

Acute coronary syndrome and cerebral arterial gas embolism in a scuba diver

Background Pulmonary barotrauma is a rare but feared complication of scuba diving, with around 30% mortality. Objective We report an uncommon case of pulmonary barotrauma complicated by arterial gas embolism with both coronary and neurological ischemic injuries after scuba diving. Case report A 46-year-old-man was admitted to our hospital for acute coronary syndrome and stroke following a scuba dive. After hyperbaric oxygen therapy, the patient recovered fully with a subsequent normal coronary angiogram. Conclusion Myocardial ischemia can be a complication of scuba diving, but does not always reveal significant obstructive coronary artery disease.

Ischaemia-modified albumin during experimental apnoea

Ischaemia-modified albumin (IMA) is a marker of the release of reactive oxygen species (ROS) during hypoxaemia. In elite divers, breath-hold induces ROS production. Our aim was to evaluate the kinetics of IMA serum levels during apnea. Twenty breath-hold divers were instructed to perform a submaximal static breath-hold. Twenty non-diver subjects served as controls. Blood samples were collected at rest, every minute, at the end of breath-hold, and 10 min after recovery. The IMA level increased after 1 min of breath-hold (p < 0.003) and remained high until recovery. Divers were separated into 2 groups: subjects who held their breath for less than 4 min (G-4) and those who held it for more than 4 min (G+4). After 3 min of apnoea, the increase of IMA was higher in the G-4 group than in the G+4 group (p < 0.008). However, at the end of apnoea, the IMA level did not differ between groups. If IMA level was globally correlated with the apnoea duration, it is interesting to note that the higher IMA level was not found in the best divers. Similarly, if arterial blood oxygen saturation (SpO2) was globally inversely correlated with apnoea duration, the lowest SpO2 at the end of breath-hold was not found in the divers that performed the best apnoea. We concluded that these divers save their oxygen. The IMA level provides a useful measure of resistance to hypoxaemia.

Glossopharyngeal Insufflation and Breath-Hold Diving: The More, the Worse?

OBJECTIVE The glossopharyngeal insufflation maneuver (lung packing) is largely performed by competitive breath-hold divers to improve their performance, despite observational evidence of fainting and loss of consciousness in the first seconds of apnea. METHODS We describe here the time course of hemodynamic changes, induced by breath-holding with and without lung packing, in 2 world-class apnea competitors. RESULTS When compared with apnea performed after a deep breath (100% vital capacity), lung packing leads to a decrease in cardiac output, blood pressure, and cerebral blood flow during the first seconds after the beginning of apnea. The major hemodynamic disorders were observed in diver 1, who exhibited the greater increase in pulmonary volume after lung packing (+22% for diver 1 vs +10% for diver 2). After the initial drop in both cardiac output and blood pressure, the time course of hemodynamic alterations became quite similar between the two apneas. CONCLUSIONS Some recommendations, such as limiting the number of maneuvers and performing lung packing in the supine position, should be expressed to avoid injuries secondary to the use of glossopharyngeal insufflation.

Evaluation of Transport Ventilators at Mild Simulated Altitude: A Bench Study in a Hypobaric Chamber

BACKGROUND: Previous studies on ventilators used for air transport showed significant effects of altitude, in particular with regard to accuracy of the tidal volume (VT) and breathing frequency. The aim of the study was to evaluate transport ventilators under hypobaric conditions. METHODS: We conducted a bench study of 6 transport ventilators in a Comex hypobaric chamber to simulate mild altitude (1,500 m [4,920 feet] and 2,500 m [8,200 feet]). The ventilators were connected to a test lung to evaluate their accuracy: (1) to deliver a set VT under normal resistance and compliance conditions at FIO2 = 0.6 and 1, (2) to establish a set PEEP (0, 5, 10, and 15 cm H2O), and (3) to establish a set inspiratory pressure in pressure controlled mode, (4) at a FIO2 setting, and (5) and at a frequency setting. RESULTS: Four ventilators kept an average relative error in VT of < 10% without effect of altitude. The Medumat ventilator was affected by the altitude only at FIO2 = 1. The Osiris 3 ventilator had > 40% error even at 1,500 m. We found no change in frequency as a function of altitude for any ventilators studied. No clinically important differences were found between all altitudes with the PEEP or inspiratory pressure setting. Although FIO2 was affected by altitude, the average error did not exceed 11%, and it is unclear whether this fact is an experimental artifact. CONCLUSIONS: We have shown that most of the new transport ventilators tested require no setting adjustment at moderate altitude and are as safe at altitude as at sea level under normal respiratory conditions. Older technologies still deliver more volume with altitude in volumetric mode.

Pelvic Radiation Disease Management by Hyperbaric Oxygen Therapy: Prospective Study of 44 Patients

Pelvic radiation disease (PRD) occurs in 2–11% of patients undergoing pelvic radiation for urologic and gynecologic malignancies. Hyperbaric oxygen therapy (HBOT) has previously been described as a noninvasive therapeutic option for the treatment of PRD. the purpose of study was to analyze prospectively the results of HBOT in 44 consecutive patients with PRD who were resistant to conventional oral or topical treatments. Material and Methods. The median age of the cohort was 65.7 years (39–85). Twenty-seven percent of patients required blood transfusion (n = 12). The median of delay between radiotherapy and HBOT was 26 months (3–175). We evaluated the results of HBOT, using SOMA-LENT Scale. Results. SOMA-LENT score was decreased in 59% of patient. The median of SOMA-LENT score before HBOT was significantly higher, being equal to 14 (0–36), than after HBOT with the SOMA-LENT score of 12 (0–38) (P = 0.003). Tenesmus (P = 0.02), bleeding (P = 0.0001), and ulceration (P = 0.001) significantly decreased after HBOT. Regarding patients with colostomy, 33% (n = 4) benefited from colostomies closure. HBOT was generally well tolerated. Only one patient stopped precociously due to transient myopia. Conclusion. This study is in favor of the interest of HBOT in pelvic radiation disease treatment (PRD).