Acute Coronary Syndrome and Cerebral Arterial Gas Embolism in a Scuba Diver

Journal of Cardiology Cases (2011) 3, e22—e25

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

Pierre-Julien Moro (MD) a,∗, Mathieu Coulange (MD, PhD) b, Olivier Brissy (MD) a, Thomas Cuisset (MD, PhD) a, Jacques Quilici (MD) a, Jean-Philippe Mouret (MD) a, Jean-Louis Bonnet (MD) a, Alain Barthélémy (MD) b

a Département de Cardiologie A, CHU Timone, 264, rue saint Pierre, 13005 Marseille, France b Centre de Médecine Hyperbare, Pôle RUSH, CHU Sainte Marguerite, Marseille, France

Received 4 August 2010; received in revised form 19 October 2010; accepted 21 October 2010

KEYWORDS Summary Pulmonary Background: Pulmonary barotrauma is a rare but feared complication of scuba diving, with barotrauma; around 30% mortality. Cerebral gas Objective: We report an uncommon case of pulmonary barotrauma complicated by arterial gas embolism; embolism with both coronary and neurological ischemic injuries after scuba diving. Acute coronary Case report: A 46-year-old-man was admitted to our hospital for acute coronary syndrome and syndrome; stroke following a scuba dive. After hyperbaric oxygen therapy, the patient recovered fully with Scuba diving 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. © 2010 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.

Introduction Case report

Pulmonary barotrauma is a rare but feared complication of A 46-year-old-man was admitted to our hospital after scuba diving, with approximately 30% mortality. Moreover, a scuba dive. His past medical history included current arterial gas embolism is the second cause of death after smoking (3 cigarettes/day), viral hepatitis, and gout. His drowning [1,2]. sole medication was daily allopurinol. After a dive to a depth of 12 m (39 ft), during approximately 1 h, he sur- faced quickly, panic-stricken, probably with closed glottis. Clinical symptoms consisted of malaise and chest pain. ∗ Corresponding author. Tel.: +33 4 91 38 95 74; Physical examination revealed confusion, agitation, altered fax: +33 4 91 38 47 26. mental state, left hemiplegia, and total bilateral blind- E-mail address: [email protected] (P.-J. Moro). ness. Glasgow Coma Scale score was 12. Heart rate was

1878-5409/$ — see front matter © 2010 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved. doi:10.1016/j.jccase.2010.10.002 Acute coronary syndrome and cerebral arterial gas embolism in a scuba diver e23

Figure 1 Initial electrocardiogram showing inverted T-waves in anterior and inferior leads.

53 beats per minute. Blood pressure was 120/60 mmHg. A 12-lead electrocardiogram (ECG) revealed inverted T-waves in anterior and inferior leads (Fig. 1). Cardiac troponin Ic was 12 ng/mL (normal range 0—0.04 ng/mL), creatinine phosphokinase: 529 IU/L (normal range 33—145 IU/L), and myoglobin: 894 ␮g/L (normal range 10—92 ␮g/L). Determi- nation of arterial blood gases at room air revealed: pH: 7.42; PaO2: 85.4 mmHg; PaCO2: 38.3 mmHg; HCO3: 24.3 mmol/L; and SaO2: 97%. Thoracic scanner ruled out a pneumothorax or a pneumomediastinum but revealed a right perihilar bullous dystrophy (Fig. 2). Brain magnetic resonance imaging showed a right fronto-parietal ischemic process (Fig. 3). Initial echocardiogram and electroencephalogram

Figure 2 Thoracic scanner revealing a right perihilar bullous Figure 3 Diffusion-weighted brain magnetic resonance imag- dystrophy. ing revealing right fronto-parietal ischemic process. e24 P.-J. Moro et al.

Figure 4 Electrocardiogram after hyperbaric therapy showing normalization of T-waves. were normal. The patient received aspirin and preven- diver surfacing, which allows the differential diagnosis with tive anti-epileptic treatment by phenobarbital. During the decompression sickness. Furthermore, the small depth and subsequent course, the patient presented full recovery of the short duration of the dive ruled out decompression the initial symptoms after four hyperbaric oxygen sessions. sickness in our case. Myocardial and cerebral ischemia is ECG significantly changed after hyperbaric therapy, with probably due to coronary and cerebral gas embolism. Micro- normalization of T-waves (Fig. 4). A subsequent coronary bubbles obstructed and decreased myocardial blood flow in angiogram revealed normal coronary arteries, without sig- the capillary system, leading to ischemic injury [3]. nificant obstructive lesion or evidence of coronary plaque This clinical observation raised the question of the tim- rupture (Figs. 5 and 6). Left ventricular ejection fraction ing of the coronary angiogram. If the myocardial ischemia is was 65%, and did not show any wall motion abnormali- ties. Transesophageal echocardiography did not detect any patent foramen ovale.

Discussion

While diving, divers present relatively stable pulmonary volumes, but during ascent, the compressed gas in their lungs expands and the pulmonary volumes increase as the ambi- ent pressure falls. If intrapulmonary gas is prevented from escaping through the airways by gas trapping, excessive transpulmonary pressures will result and rupture can occur in the pulmonary capillaries. Escaping gas can enter pulmonary veins (which transit the left heart leading to arterial gas embolism). Air bubbles are then released in the sys- temic circulating blood ﬂow and can produce acute cerebral and coronary arterial embolic manifestations. Pulmonary diseases predisposing to gas trapping (bullous lung disease, asthma) may favor the occurrence of pulmonary barotrau- mas [2]. In this case, the perihilar bullous dystrophy and rapid ascent may have precipitated the accident. Symptoms of arterial gas embolism complicating pulmonary barotrauma classically occur within a few minutes after the Figure 5 Coronary angiogram: normal left coronary arteries. Acute coronary syndrome and cerebral arterial gas embolism in a scuba diver e25

Our observation also shows the value of transesophageal echocardiography, which did not detect any patent foramen ovale. In the absence of a patent foramen ovale, another likely mechanism to explain arterial gas embolism is the opening of pulmonary arteriovenous shunts by accumulation of nitrogen bubbles in the capillary bed site, causing tran- sient pulmonary arterial hypertension, leading to arterial bubbles. However, in this case, paradoxical gas embolism caused by decompression illness remains unlikely. In summary, myocardial ischemia can be a complication of scuba diving, but does not always reveal a signiﬁcant obstructive coronary artery disease. A coronary angiogram must be performed in this situation, but must not delay hyperbaric therapy.

Acknowledgments

Jean-Vincent Zink and Sébastien Rodriguez, Radiology Department, CHU Sainte Marguerite, Marseille.

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