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Cerebral arterial gas embolism (CAGE) from breath-holding or inadequate exhalation during ascent is a well-recognised complication of scuba diving. It does not usually occur with breath-hold (BH) diving in those with normal lungs, as the volume of gas in the lungs on surfacing cannot exceed what it was on leaving the surface. However, a BH diver who breathes from a compressed gas supply at depth essentially becomes a scuba diver and is at risk of pulmonary barotrauma (PBt) and CAGE on ascent. In this case, a 26-year-old male experienced BH diver breathed from a scuba set at approximately 10 metres' sea water depth and ascended, sustaining massive PBt and CAGE with a fatal outcome. BH and scuba divers, especially those with less experience, need to be well-informed about this potential risk.

Introduction This study identified pre-existing medical conditions among scuba diving fatalities in Australia from 2001 to 2013, inclusive, and assessed whether these conditions likely contributed to the deaths. Methods The National Coronial Information System (NCIS) was searched for scuba diving-related cases during 2001-2013, inclusive. Coronial findings, witness and police reports, medical histories, and autopsy and toxicology reports were scrutinised for pre-existing medical conditions and autopsy findings. Predisposing factors, triggers, disabling agents, disabling injuries and causes of death were analysed using a validated template. Results There were 126 scuba diving-related fatalities identified during the study period. Forty-six (37%) divers were identified as having a significant medical condition which may have contributed to their incident. The most common condition was ischaemic heart disease (IHD) which had been diagnosed in 15 of the divers. Thirty-two (25%) deaths were attributed to cardiac disabling injuries (DI) such as ischaemic heart disease and arrhythmias, although a cardiac DI was thought likely in another six. Respiratory conditions were implicated in eight (6%) deaths, at least four associated with cerebral arterial gas embolism. At least 14 (11%) divers who had contributory pre-existing medical conditions had been cleared to dive by a medical practitioner within the year prior. Conclusions Chronic health-related factors played a major role in almost half of these deaths; primarily cardiac conditions such as IHD and cardiac arrhythmias. Although fitness-to-dive (FTD) assessments have limitations, the high incidence of cardiac-related deaths indicates a need for 'older' divers to be medically assessed for FTD.

Divers, pneumatic construction workers, aviators, and astronauts sometimes suffer decompression illness (DCI). DCI includes decompression sickness (DCS) and arterial gas embolism (AGE) and is treated with recompression therapy. Etiology of DCS is highly related with micro bubbles formed in the body fluid. AGE is caused by pulmonary over inflation-induced rupture of the alveoli. Recompression therapy is a kind of hyperbaric oxygen therapy, for which U.S. Navy treatment tables are widely used. The purposes of recompression therapy are (1) to reduce volume of the bubbles in the body, (2) to increase absorption of the bubbles in the body fluid and exhalation of inert gases from the lung, and (3) to increase oxygen supply via plasma to the cells in peripheral tissues. Recompression therapy has other beneficial effects, such as anti-inflammatory, wound healing, and anti-infectious effects. During the evacuation of the DCI patient to an appropriate facility, to continue administration of 100% oxygen and not to decrease environmental pressure are both critical for stabilizing the patients’ condition. It is important for all physicians who have a chance to treat DCI patients to be versed in mechanisms of recompression therapy and handling the treatment tables.

A 43-year-old female scuba diver was retrieved and treated following a rapid ascent and presumed cerebral arterial gas embolism (CAGE). She subsequently developed respiratory distress and was found to have Takotsubo cardiomyopathy, with transient left ventricular dysfunction, elevated cardiac enzymes, and normal CT coronary angiography. We believe this to be the first report of CAGE associated with Takotsubo cardiomyopathy.

Primary lung bullae have been reported to cause pulmonary barotrauma and lead to cerebral arterial gas embolism (CAGE) in the context of diving; however, a lack of symptoms and often minimal radiographic findings often preclude a diagnosis of lung bullae prior to undertaking diving activity. We present the case of a healthy 27-year-old Caucasian male who presented following the second of two introductory resort dives with neurological symptoms attributable to CAGE. Investigations revealed a previously undiagnosed large primary lung bulla. This case highlights the clinical sequelae of primary lung bullae in the context of pulmonary barotrauma related to recreational diving activity.

Decompression illness (DCI) is a complex clinical syndrome caused by supersaturation of respiratory gases in blood and tissues after abrupt reduction in ambient pressure. The resulting formation of gas bubbles combined with pulmonary barotrauma leads to venous and arterial gas embolism. Severity of DCI depends on the degree of direct tissue damage caused by growing bubbles or indirect cell injury by impaired oxygen transport, coagulopathy, endothelial dysfunction, and subsequent inflammatory processes. The standard therapy of DCI requires expensive and not ubiquitously accessible hyperbaric chambers, so there is an ongoing search for alternatives. In theory, perfluorocarbons (PFC) are ideal non-recompressive therapeutics, characterized by high solubility of gases. A dual mechanism allows capturing of excess nitrogen and delivery of additional oxygen. Since the 1980s, numerous animal studies have proven significant benefits concerning survival and reduction in DCI symptoms by intravenous application of emulsion-based PFC preparations. However, limited shelf-life, extended organ retention and severe side effects have prevented approval for human usage by regulatory authorities. These negative characteristics are mainly due to emulsifiers, which provide compatibility of PFC to the aqueous medium blood. The encapsulation of PFC with amphiphilic biopolymers, such as albumin, offers a new option to achieve the required biocompatibility avoiding toxic emulsifiers. Recent studies with PFC nanocapsules, which can also be used as artificial oxygen carriers, show promising results. This review summarizes the current state of research concerning DCI pathology and the therapeutic use of PFC including the new generation of non-emulsified formulations based on nanocapsules.

Cerebral arterial gas embolism is a recognised complication of endovascular intervention with an estimated incidence of 0.08%. Its diagnosis is predominantly clinical, supported by neuroimaging. The treatment relies on alleviating mechanical obstruction and reversing the proinflammatory processes that contribute to tissue ischaemia. Hyperbaric oxygen therapy is an effective treatment and has multiple mechanisms to reverse the pathological processes involved in cerebral arterial gas embolism. Symptomatic cerebral arterial gas embolism is a rare complication of endovascular intervention for acute ischaemic stroke. Although there are no previous descriptions of its successful treatment with hyperbaric oxygen therapy following mechanical thrombectomy, this is likely to become more common as mechanical thrombectomy is increasingly used worldwide to treat acute ischaemic stroke.

Guidelines for the pre-hospital management of decompression illness (DCI) had not been formally revised since the 2004 Divers Alert Network/Undersea and Hyperbaric Medical Society workshop held in Sydney, entitled "Management of mild or marginal decompression illness in remote locations". A contemporary review was initiated by the Diver's Alert Network and undertaken by a multinational committee with members from Australasia, the USA and Europe. The process began with literature reviews by designated committee members on: the diagnosis of DCI; first aid strategies for DCI; remote triage of possible DCI victims by diving medicine experts; evacuation of DCI victims; effect of delay to recompression in DCI; pitfalls in management when DCI victims present at hospitals without diving medicine expertise and in-water recompression. This was followed by presentation of those reviews at a dedicated workshop at the 2017 UHMS Annual Meeting, discussion by registrants at that workshop and finally several committee meetings to formulate statements addressing points considered of prime importance to the management of DCI in the field. The committee placed particular emphasis on resolving controversies around the definition of "mild DCI" arising over 12 years of practical application of the 2004 workshop's findings, and on the controversial issue of in-water recompression. The guideline statements are promulgated in this paper. The full workshop proceedings are in preparation for publication.

Cerebral arterial gas embolism (CAGE) is a dramatic event with a very rapid onset of symptoms and occurs in diving and in a variety of medical procedures without the requirement for preceding supersaturation of tissues with inert gas. Decompression sickness (DCS) occurs only when there is prior accumulation of a gas-load in tissues (supersaturation) followed by subsequent depressurization, and bubbles mainly occur in the tissues and the venous side of the circulation. There is increasing evidence that microparticles, microbubbles, inflammatory mediators and ischemia-reperfusion injury all play important roles in CAGE and DCS. Gas embolism in the spinal cord is very rare, but a majority of DCS cases involve the spinal cord and this is often also accompanied by cerebral effects. The anatomy of the blood supply of the brain and spinal cord has important influences on CAGE and spinal DCS. The effects of bubbles occurring in cardiopulmonary bypass (CPB) are compared and contrasted with those seen in CAGE and DCS. Nine clinical case examples of CAGE and DCS are very briefly described and the outcomes are described in Chapter 9 .

Understanding the anatomy and physiology of the cardiovascular and pulmonary systems is essential to appreciate the dynamics of bubbles in the body, including the structure of arterial and venous vessels, cell membranes and the transport of gases. Bubbles may be spherical, but if larger than the diameter of an enclosing vessel will become “sausage-shaped” (cylindrical with hemispherical end-caps). Microbubbles and microparticles play important roles in decompression sickness (DCS) and arterial gas embolism (AGE). Bubbles may be stabilized by a surrounding skin of molecules and thereby persist much longer than would be expected otherwise. The pulmonary bubble filter is a crucial defense against venous bubbles entering the arterial circulation, but may be bypassed by a patent foramen ovale and other mechanisms. The uptake and elimination of inert gases may be described by “washin” and “washout” exponentials. The appendix describes fundamental concepts of gas pressures in the body.

Although prompt treatment of decompression sickness (DCS) and arterial gas embolism (AGE) is best, diffusion of gases through bubbles and streaming around bubbles likely contributes to better than expected outcomes even after prolonged delays. Quantitative analysis within the limits of the best available model (LHV3) is provided for the application of normobaric oxygen, pressure, and both combined (hyperbaric oxygen) on bubble size. This demonstrates that breathing oxygen before commencing hyperbaric treatment is very effective in shrinking “uncovered” or “bare” bubbles. The analysis further demonstrates that helium bubbles will extinguish faster than the same size nitrogen bubbles. Further, treatment with the USN Table 6 would be expected to eliminate even the largest likely sizes of uncovered bubbles. No model of bubble dynamics presently available accurately predicts the duration of persistence of any size of bubble surrounded by a skin of phospholipids or protein molecules, but it is clear that such bubbles could survive for very prolonged periods. Whether covered or not, the diffusion characteristics of elongated vascular bubbles are not known, but these survive for a longer period than spherical bubbles and first shrink in a linear manner until they become spherical, at which time they will release from contact with vessel walls and then move in the direction of blood flow. Microparticles and microbubbles play an important role in the overall effects of DCS and AGE. The chapter demonstrates how medicine and mathematics can collaborate in approaches to gas-bubble disease.

Ein 17-Jahriger wird nach einem Tauchgang im Krankenhaus vorstellig. Alle Zeichen deuten auf einen Tauchunfall hin: Kraftlosigkeit in beiden Beinen, Kribbelparasthesien am ganzen Korper, Sehstorungen und Kopfschmerzen. Wie gehen Sie vor? Bestatigt sich die Diagnose?

Die hyperbare Oxygenierung (HBO) ist eine wissenschaftlich begrundete und international etablierte, in Deutschland aber wenig bekannte und zu selten eingesetzte Behandlungsmethode. Bei einer HBO wird unter Atmung von 100% O2 und durch die Erhohung des Umgebungsdrucks der Gewebepartialdruck von Sauerstoff (ptO2) deutlich erhoht. Dies setzt verschiedene druck- und O2-assoziierte Mechanismen in Gang. Drei Fallbeispiele beschreiben die Wirkungsweise und Einsatzbereiche der HBO.

The cardiac effects of aquatic sports have increased in interest with the experience of cardiac responses to swimming and diving. The syndrome of swimming-induced pulmonary edema is likely caused by a combination of central blood shifts, sudden onset of high exercise demands, and impaired diastolic relaxation of the left ventricle. Divers also develop venous gas emboli caused by nitrogen supersaturation in blood and tissues during ascent from depth. The physiology and physics of water immersion and diving are unique. Knowledge of pressure effects, gas solubility, and changes in gas volumes with depth is needed to understand the disorders related to these activities.

Scuba diving is an increasingly common recreational activity. We describe the physiopathology of barotrauma in two cases where death was caused by pulmonary barotrauma while diving. An inspection and autopsy were carried out in both cases. The autopsy data were supported by post-mortem radiological investigation. Histological and toxicological analyses were also carried out, and dive computer and tank manometer analysis performed. In both cases, the cause of death was attributable to arterial gas embolism, resulting from pulmonary barotrauma subsequent to pulmonary over-distension. The dive computer analysis and the tank manometer allowed us to understand what happened underwater. In our opinion, a multidisciplinary approach is crucial in order to clarify the cause of death. Some pathological conditions and risk factors should be considered before diving.

Arterial gas embolism (AGE) can be clinically devastating, and is most often associated with exposure to changes in ambient pressure, medical procedure or congenital malformation. Here we report a case of AGE in a 78-year-old male without these traditional risk factors. Rather, the patient's history included chronic obstructive pulmonary disease, necrotizing pneumonia, bullous disease and coughing. He was safely treated with hyperbaric oxygen (HBO₂) therapy for AGE, with initial clinical improvement, but ultimately died from his underlying condition. Pathophysiology is discussed. This case illustrates the possibility that AGE can occur due to rupture of lung tissue in the absence of traditional risk factors. HBO₂ therapy should be considered in the management of such patients.

Important developments in the diagnosis of scuba diving fatalities have been made thanks to forensic imaging tool improvements. Multi-detector computed tomography (MDCT) permits reliable interpretation of the overall gaseous distribution in the cadaver. However, due to post-mortem delay, the radiological interpretation is often doubtful because the distinction between gas related to the dive and post-mortem decomposition artifactual gases becomes less obvious. We present six cases of fatal scuba diving showing gas in the heart and other vasculature. Carbon dioxide (CO₂) in cardiac gas measured by gas chromatography coupled to thermal conductivity detection were employed to distinguish decomposition from embolism based on the detection of decomposition gases (hydrogen, hydrogen sulfide and methane) and to confirm arterial gas embolism (AGE) or post-mortem offgasing diagnoses. A Radiological Alteration Index (RAI) was calculated from the scan. Based on the dive history, the intra-cadaveric gas was diagnosed as deriving from decomposition (one case, minimal RAI of 61), post-mortem decompression artifacts (two cases, intermediate RAI between 60 and 85) and barotrauma/AGE (three cases, maximal RAI between 85 and 100), illustrating a large distribution inside the bodies. MDCT scans should be interpreted simultaneously with compositional analysis of intra-cadaveric gases. Intra-cadaveric gas sampling and analysis may become useful tools for understanding and diagnosing scuba diving fatalities. In cases with short post-mortem delays, the CO₂ concentration of the cardiac gas provides relevant information about the circumstances and cause of death when this parameter is interpreted in combination with the diving profile.

Decompression sickness and arterial gas embolism, collectively known as decompression illness (DCI), are rare but serious afflictions that can result from compressed gas diving exposures. Risk is primarily determined by the pressure-time profile but is influenced by several factors. DCI can present idiosyncratically but with a wide range of neurologic symptoms. Examination is critical for assessment in the absence of diagnostic indicators. Many conditions must be considered in the differential diagnosis. High-fraction oxygen breathing provides first aid but definitive treatment of DCI is hyperbaric oxygen.