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Iatrogenic air embolism is a rare and potentially fatal complication of gastrointestinal endoscopy. We present a 66-year-old male patient who developed cerebral arterial gas embolism shortly after therapeutic endoscopic retrograde cholangiopancreatography (ERCP) for acute biliary pancreatitis, which is the first case reported in Hong Kong according to latest literature search. Some risk factors of iatrogenic air embolism in this patient include cholangitis with intraductal stones, sphincterotomy and bleeding at papillotomy site which required haemostasis with balloon tamponade. Early diagnosis and timely treatment with hyperbaric oxygen therapy resulted in full neurological recovery of our patient.

Air embolism (a result of direct communication with the vasculature and an external pressure gradient from the gastrointestinal or the biliary tract), although rare, is a potentially devastating adverse event seen in endoscopic retrograde cholangiopancreatography (ERCP) procedures. Whether venous, arterial, or paradoxical, the clinical presentation ranges from asymptomatic patients to cardiorespiratory arrest. This is of particular importance because it makes the diagnosis of air embolism even more difficult in an already sedated patient. Since early recognition increases the chances of patients’ survival, endoscopists should be highly motivated and trained to recognize this complication as early as possible. With only 60 cases of air embolism reported (and even fewer related to paradoxical air embolism), we aimed to report a case of paradoxical cerebral air embolism in a patient undergoing ERCP due to a common bile duct stricture and to provide a mini-review of this clinical entity that can serve as a bedside quick reference guide for endoscopists worldwide.

Only a few clinical cases of cerebral arterial gas embolism during spinal surgery are published. It seems important not to overlook this diagnosis in order to initiate rapid appropriate treatment. This was a suspected case of paradoxical gas embolism revealed postoperatively by neurological deficits and whose recovery was noted during hyperbaric oxygen treatment. Unfortunately, no complementary examination showed gas embolism and only the context, the clinical picture and the case evolution evoke this diagnosis. The diagnostic difficulty in the immediate postoperative period is highlighted.

Background: Hyperbaric oxygen (HBO2) therapy is a safe and well-tolerated treatment modality. Seizures, one of the most severe central nervous system side effects of HBO2 therapy, can occur. Episodes of seizures during HBO2 therapy have not yet been reported in countries such as Korea, where hyperbaric medicine is still in the developmental stage. Methods: The registry data of all patients treated with HBO2 therapy in a tertiary academic hospital in Korea were prospectively collected, and patients who developed seizures during HBO2 therapy between October 2016 and December 2019 were evaluated. In addition, we reviewed previous studies on occurrence of seizures during HBO2 therapy. Results: During the study period, a total of 10,425 treatments were provided to 1,308 patients. The most frequently treated indication was carbon monoxide (CO) poisoning (n=547, 41.8%). During the HBO2 therapy sessions (total: 10,425), five seizure episodes occurred (patients with CO poisoning: n=4; patients with arterial gas embolism [AGE]: n=1). The frequency of seizures in patients with CO poisoning (0.148%) and AGE (3.448%) was significantly higher than that in patients with all indications (0.048%) (p=0.001). None of the patients had lasting effects due to the seizures. Conclusion: Our study revealed a similar frequency rate in terms of all indications and CO poisoning, and a slightly higher rate in AGE. Seizures were observed in patients with CO poisoning and AGE. Therefore, if clinicians plan to operate a hyperbaric center in a country like Korea, where there are several patients with acute CO poisoning, they should be prepared to handle seizures that may occur during HBO2 therapy

(Thaler J, Pignel R, Magnan M-A, Pellegrini M, Louge P. Decompression illness treated at the Geneva hyperbaric facility 2010–2016: A retrospective analysis of local cases. Diving and Hyperbaric Medicine. 2020 December 20;50(4):370–376. doi: 10.28920/dhm50.4.370-376. PMID: 33325018.) Introduction: The Geneva hyperbaric chamber is the main treatment centre for decompression illness (DCI) in Switzerland. The characteristics, symptomatology, treatment and short-term outcome of divers treated at this chamber have not previously been investigated. Methods: This was a retrospective study of patients treated with hyperbaric oxygen (HBO) for DCI from 2010 to 2016. Data were analysed to provide a description of the cases and statistical analysis for possible factors associated with an unfavourable outcome. Results: One hundred and thirty-five patients were treated for DCI. Ninety-two were included in the study. Sixty-four presented with neurological and 28 with mild DCI. One hundred and thirty-five patients were treated for DCI. Ninety-two were included in the study. Sixty-four presented with neurological and 28 with mild DCI. Patients with mild DCI mainly had musculoskeletal symptoms (79%). Patients with neurological DCI mainly had spinal (55%), followed by vestibular (36%) symptoms. Arterial gas embolism was diagnosed in 30% of cases. Diving depths ranged between 15 and 142 metres, and dive times between two and 241 min. Median time to treatment was 6 h. Patients with neurological DCI had a high rate (25%) of persisting deficits after treatment. Older age was associated with an unfavourable outcome in univariate but not in multivariate analysis. No adverse effects of HBO were observed. For spinal DCI, a high Boussuges score was associated with persisting deficits after treatment. Conclusions: Our findings are consistent with other series. Severe DCI was associated with a high rate of persisting deficits. No single factor was associated with a negative outcome. A Boussuges score > 7 had sensitivity of 90% and positive predictive value 53% for predicting an unfavourable outcome in spinal DCI.

Cerebral arterial gas embolism is a serious and often iatrogenic fatal event associated with invasive procedures. It is a possible cause of a cardiac arrest and the diagnosis is challenging. We report a case of a cardiac arrest after a cerebral arterial gas embolism, in a 63-year-old male subjected to a Computed Tomography-guided Transthoracic Needle Aspiration Biopsy, which was successfully managed with hyperbaric oxygen therapy.

During underwater vehicle escape training with compressed air, a fit 26-year-old soldier suffered pulmonary barotrauma with cerebral arterial gas embolism after surfacing from a depth of 0.75–1.2 metres of freshwater or less. She presented with an altered level of consciousness. Rapid neurological examination noted slurred speech, a sensory deficit and right hemiparesis. Eleven hours after the accident, hyperbaric oxygen treatment was initiated using US Navy Treatment Table 6. The soldier almost completely recovered after repeated hyperbaric oxygen treatment. Given the very shallow depth this is an unusual case with only two similar case reports published previously.

Arterial gas embolism is a well-described and frequently seen injury encountered in both civilian and military diving operations. It is becoming increasingly reported and potentially increasingly more common in the hospital environment as a complication of more frequent gastroenterology procedures. We present a case of a 49-year-old, active-duty female who developed significant left-sided neurological deficits manifesting as diffuse left-sided weakness, subjective confusion, and severe headache following esophagogastroduodenoscopy. With increased clinical suspicion for arterial gas embolism, the patient was evaluated by the hyperbaric medicine team at our facility and subsequently treated to near-resolution of symptoms by multiple hyperbaric oxygen treatments. This case highlights the importance of considering this rare complication during or following common invasive procedures. Furthermore, the unique training and experience of physicians with expertise in diving medicine and their ability to recognize these types of injury in the hospital setting highlights the importance of continued training in these fields within Military Medicine in addition to civilian Undersea and Hyperbaric Medicine fellowships.

Introduction: We aimed to identify the possible chain of events leading to fatal scuba diving incidents in Australia from 2001–2013 to inform appropriate countermeasures. Methods: The National Coronial Information System was searched to identify scuba diving-related deaths from 2001–2013, inclusive. Coronial findings, witness and police reports, medical histories and autopsies, toxicology and equipment reports were scrutinised. These were analysed for predisposing factors, triggers, disabling agents, disabling injuries and causes of death using a validated template. Results: There were 126 known scuba diving fatalities and 189 predisposing factors were identified, the major being health conditions (59; 47%), organisational/training/experience/skills issues (46; 37%), planning shortcomings (29; 23%) and equipment inadequacies (24; 19%). The 138 suspected triggers included environmental (68; 54%), exertion (23; 18%) and gas supply problems (15; 12%) among others. The 121 identified disabling agents included medical-related (48; 38%), ascent-related (21; 17%), poor buoyancy control (18; 14%), gas supply (17; 13%), environmental (13; 10%) and equipment (4; 3%). The main disabling injuries were asphyxia (37%), cardiac (25%) and cerebral arterial gas embolism/pulmonary barotrauma (15%). Conclusions: Chronic medical conditions, predominantly cardiac-related, are a major contributor to diving incidents. Divers with such conditions and/or older divers should undergo thorough fitness-to-dive assessments. Appropriate local knowledge, planning and monitoring are important to minimise the potential for incidents triggered by adverse environmental conditions, most of which involve inexperienced divers. Chain of events analysis should increase understanding of diving incidents and has the potential to reduce morbidity and mortality in divers.

Decompression illness in breath‐hold diving is a rare dysbaric disease mainly characterized by stroke‐like neurological disorders. The early use of DWI‐MRI combined with ADC map in suspected cases can help in the early diagnosis and treatment.

Supplemental Digital Content is available in the text., Objectives: Iatrogenic cerebral arterial gas embolism occurs when gas enters the cerebral arterial circulation during a medical procedure and is considered a severe complication. Seizures have been described in these patients, but information on clinical characteristics, treatment, and outcome is lacking in current literature. The aim of the study was to explore seizures in patients with iatrogenic cerebral arterial gas embolism and to evaluate management strategies. Design: Retrospective single-center observational study. Setting: The only university hospital in the Netherlands with a hyperbaric oxygen therapy facility. Patients: All patients presenting at or referred to our center with iatrogenic cerebral arterial gas embolism between May 2016 and December 2020. Interventions: Not applicable. Measurements and Main Results: Fifteen patients with iatrogenic cerebral arterial gas embolism were identified, of whom 11 (73%) developed seizures. Five patients developed their first seizure prior to hyperbaric oxygen therapy, three during hyperbaric oxygen therapy, and three after hyperbaric oxygen therapy. Of the 11 patients with seizures, all but one were treated with anti-epileptic drugs. With a median follow-up time of 5 months (range, 1–54 mo), five patients showed complete neurologic recovery, five had minor neurologic deficit, two had moderate to severe neurologic deficit, and three had died. Four patients still used anti-epileptic drugs at follow-up. No patients had recurrent seizures after hospital discharge. Conclusions: `Seizures are a common symptom in iatrogenic cerebral arterial gas embolism. They are often treated with anti-epileptic drugs and do not seem to lead to chronic epilepsy.

Arterial gas embolism (AGE) may result when diving while breathing compressed gas and ascending rapidly or with a closed glottis. Pulmonary over-pressurisation can result in lung stretch injury with entry of bubbles into the pulmonary venous circulation and subsequently the systemic arterial circulation. We present the case of an individual who suffered AGE while breathing compressed air at 1.2 metres’ fresh water (mfw) in a swimming pool and discuss the factors determining the depth at which this form of injury may occur. This case serves to underscore the fact that risk of AGE exists at shallow depths.

We present the case of a 42-year-old female who was critically ill due to an arterial gas embolism (AGE) she experienced while diving in Maui, Hawaii. She presented with shortness of breath and dizziness shortly after surfacing from a scuba dive and then rapidly lost consciousness. The diver then had a complicated hospital course: persistent hypoxemia (likely secondary to aspiration) requiring intubation; markedly elevated creatine kinase; atrial fibrillation requiring cardioversion; and slow neurologic improvement. She had encountered significant delay in treatment due to lack of availability of local hyperbaric oxygen (HBO2) therapy. Our case illustrates many of the complications that can occur when a patient suffers a severe AGE. These cases may occur even without a history of rapid ascent or risk factors for pulmonary barotrauma, and it is imperative that they be recognized and treated as quickly as possible with HBO2. Unfortunately, our case also highlights the challenges in treating critically ill divers, particularly with the growing shortage of 24/7 hyperbaric chambers able to treat these ICU-level patients.

Middle ear barotrauma is common in diving. However, facial nerve baroparesis is a relatively rare complication. A dehiscent facial nerve canal may be a predisposing factor to developing this complication. Although there is an increasing number of facial baroparesis cases in the literature, they are likely still under-reported. In order to avoid unnecessary recompression treatments or detrimental effects to a professional diver’s career, it is important to consider this in the differential diagnosis while evaluating dive injuries. This case report describes recurrent facial baroparesis in a military diver, which manifested on contralateral sides of his face. His initial presentation was misdiagnosed as an arterial gas embolism, which led to recompression treatment and a cardiac procedure. Upon recurrence about one year later, a complete work-up was done, which included an ENT evaluation and a CT scan. Imaging demonstrated a predisposing anatomic variant bilaterally. His symptoms resolved quickly and spontaneously both times, and he has been able to return to diving.

BACKGROUND: Systemic arterial gas embolism (SAGE) is a rare yet serious and underrecognized complication of bronchoscopic procedures. A recent case of presumed SAGE after transbronchial needle aspiration prompted a systematic literature review of SAGE after biopsy procedures during flexible bronchoscopy. METHODS: We performed a systematic database search for case reports and case series pertaining to SAGE after bronchoscopic lung biopsy; reports or series involving only bronchoscopic laser therapy or argon plasma coagulation (APC) were excluded. Patient data were extracted directly from published reports. RESULTS: A total of 29 unique patient reports were assessed for patient demographics, specifics of the procedure, clinical manifestations, diagnostic findings, and clinical outcomes. Cases of SAGE occurred after multiple types of bronchoscopic biopsy and under both positive and negative pressure ventilation. The most common clinical findings were neurologic, followed by cardiac manifestations; temporal patterns included acute onset of cardiac or neurologic emergencies immediately after biopsy, or delayed awakening post-procedure. There was a high mortality rate among cases (28%), with residual neurologic deficits also common (24%). DISCUSSION: SAGE is an underrecognized but severe adverse effect of bronchoscopic lung biopsy, which often presents with acute coronary or cerebral ischemia or delayed awakening from sedation. It is important for all physicians who perform bronchoscopic biopsies to be aware of the clinical manifestations and therapeutic management of SAGE in order to mitigate morbidity and mortality among patients undergoing these procedures.

A diver practicing controlled emergency ascent training on the island of Guam suffered bilateral pneumothorax, pneumomediastinum, coronary arterial gas embolism, and developed multiple organ dysfunction syndrome. Due to limitations of available resources he was medically managed in the intensive care unit until he could be transferred to University of California San Diego for definitive management. We provide an account of our management of the patient, the pathophysiology of injury as well as a review of the safety of recreational diving skills training, current standards of practice and potential pitfalls when considering proper management of a critically injured diver.

A 75 year-old male developed features of an acute stroke following bubble contrast echocardiography, which was shown on emergent computed tomography scanning to be a result of cerebral arterial gas embolism (CAGE) to the left middle cerebral artery. Ischaemic stroke symptoms have previously been reported as a rare complication of bubble contrast echocardiography. Radiologically proven CAGE from bubble contrast echocardiography had not been reported at the time this case occurred. Immediate provision of 100% oxygen and administration of hyperbaric oxygen are recommended treatments for CAGE and were associated with a substantial recovery for this patient.

Vascular air embolism (VAE) is an important complication of some routine medical procedures, particularly intravenous access for the administration of fluids or medications. The capillary bed of the pulmonary circulatory system is capable of compensating for small amounts of air entrained into a vein. However, large amounts of air can overwhelm that system and lead to complications ranging from cough, chest pain, or shortness of breath to cardiopulmonary collapse. Additionally, air entrained directly into the arterial system, or that which crosses from the venous system to the arterial system through a shunt can cause the acute coronary syndrome, loss of consciousness, arrhythmias, altered mental status, stroke, or limb ischemia. We present a case in which a patient with a known atrial septal defect had a moderate volume of air entrained through an intravenous catheter requiring hyperbaric oxygen therapy.

Pulmonary barotrauma (PBT) is a common type of decompressing injury (DCI), which occurs during diving and submarine escape. Pulmonary tissue damages with secondary emphysema, pneumothorax, and arterial gas embolism (AGE) are the primary pathological changes. The pathophysiology, predisposing factors, clinical manifestations, differential diagnosis, and therapeutic principles of PBT are discussed here. Management on site and prevention by medical fitness and diving training are emphasized. Sufferers returning to diving after PBT needed diving medical assessment.

The purpose of this study was to suggest modifications of autopsy techniques in order to improve post-mortem diagnosis of arterial gas embolism (AGE) based on multidisciplinary investigation of SCUBA diving fatalities. Five adult human cadavers from the voluntary donation program of the Human Anatomy Laboratory, and eight judicial autopsied bodies of SCUBA divers from the Forensic Pathology Service were assessed. Before performing any autopsies, we accessed the diving plan and the divers' profiles for each case. We then introduced a new dissection procedure that included identification, isolation, and manipulation of carotid, vertebral and thoracic arterial systems. The dissected vascular structures that allowed optimall isolation of the systemic arterial circulation were identified and ligated. In three of the eight judicial cases, we had a strongly suggestive history of arterial gas embolism following pulmonary barotrauma (PBt/AGE). In these cases, the additional arterial dissection allowed us to clearly diagnose AGE in one of them. The autopsy of the rest of the cases showed other causes of death such as asphyxia by drowning and heart attack. In all cases we were able to reject decompression sickness, and in some of them we showed the presence of artefacts secondary to decomposition and resuscitation maneuvers. These results allow us to suggest a specific autopsy technique divided into four steps, aimed at confirming or excluding some evidence of dysbaric disorders according to a re-enactment of the incident. We have demonstrated the presence of large volumes of intravascular air, which is typical of PBt/AGE.

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.

Introduction Arterial gas embolism (AGE) is a rare but severe complication of scuba diving. While AGE is most commonly encountered in coastal areas with high volumes of recreational divers, at-risk populations exist throughout the United States, making basic knowledge of the disease important for all emergency medicine (EM) physicians. Methods We used a hypothetical simulation case to train EM residents on diagnosis and management of AGE. A 32-year-old male presented with shortness of breath and unilateral neurologic deficits immediately after scuba diving. Residents were challenged to emergently diagnose and treat tension pneumothorax followed by diagnosis and treatment of AGE. A resident, attending, and simulation technician ran the case for four separate simulation teams in the simulation center with the addition of chest tube supplies to the basic resuscitation bay setup. Teams were allowed to use the internet in real time as a reference tool. Results Most teams arrived at the correct diagnosis using real-time internet searches, but none found the Divers Alert Network Emergency Hotline. Learners were debriefed both immediately and in a formal lecture. A follow-up survey showed good retention of knowledge. Discussion This case fills a significant knowledge and training gap for many EM physicians. AGE is a rare but highly morbid complication of diving, and EM residents should have knowledge of the disease and available consultation resources. Most EM residents will not have the opportunity to treat a diver during training, and the simulation environment provides a means to teach and practice this skill set.

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 .

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.

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.

Introduccion. El embolismo arterial gaseoso se define como la presencia de aire en la circulacion arterial. Se trata de una causa extremadamente rara de ictus que se ha descrito en multitud de escenarios clinicos, generalmente relacionados con procesos yatrogenos. Se aporta un caso clinico en el que el embolismo arterial gaseoso sucedio tras un traumatismo craneoencefalico, y se revisan los aspectos mas relevantes del diagnostico y la etiopatogenia. Caso clinico. Mujer de 52 anos que presentaba herida incisa craneofacial tras una agresion con un hacha. La tomografia computarizada inicial objetivo fractura en los arcos cigomatico, esfenoidal y maxilar izquierdos, asi como neumoencefalo en los senos cavernosos y el canal carotideo derecho. Una hora mas tarde, la paciente mostro un deficit neurologico hemisferico derecho, por lo que se solicito de forma urgente una nueva tomografia computarizada craneal con estudio vascular multimodal, que objetivo la movilizacion del neumoencefalo y descarto una oclusion arterial de gran vaso. Un estudio de shunt mediante Doppler transcraneal y ecocardiografia comprobo la presencia de un foramen oval permeable como causa de comunicacion arteriovenosa que justificaba un embolismo arterial gaseoso. La tomografia computarizada de control a las 48 horas confirmo la aparicion de una lesion isquemica parietal derecha. Conclusion. En este caso queda reflejada la presencia simultanea de aire en la circulacion cerebral arterial y venosa y la comunicacion periferica a traves de un foramen oval permeable. Este mecanismo de produccion esta escasamente documentado en la bibliografia.

Drowning deaths are commonly seen in most forensic pathology practices. Experienced forensic pathologists perform autopsies and assign a cause and manner of death in such cases as a matter of routine. Deaths due to pulmonary overexpansion injury and subsequent air embolism are far less common and typically involve individuals who have been breathing compressed gas at depth, generally SCUBA (self-contained underwater breathing apparatus) divers. This review outlines the pathophysiological basis of these two forensic pulmonary issues and recommends an approach to performing and interpreting the results of a forensic autopsy when faced with such cases.

Arterialization of gas bubbles after decompression from scuba diving has traditionally been associated with pulmonary barotraumas or cardiac defects, such as the patent foramen ovale. Recent studies have demonstrated the right-to-left passage of bubbles through intrapulmonary arterial-venous anastamoses (IPAVA) that allow blood to bypass the pulmonary microcirculation. These passages open up during exercise, and the aim of this study is to see if exercise in a postdiving period increases the incidence of arterialization. After completing a dive to 18 m for 47 min, patent foramen ovale-negative subjects were monitored via transthoracic echocardiography, within 10 min after surfacing, for bubble score at rest. Subjects then completed an incremental cycle ergometry test to exhaustion under continuous transthoracic echocardiography observation. Exercise was suspended if arterialization was observed and resumed when the arterialization cleared. If arterialization was observed a second time, exercise was terminated, and oxygen was administered. Out of 23 subjects, 3 arterialized at rest, 12 arterialized with exercise, and 8 did not arterialize at all even during maximal exercise. The time for arterialization to clear with oxygen was significantly shorter than without. Exercise after diving increased the incidence of arterialization from 13% at rest to 52%. This study shows that individuals are capable of arterializing through IPAVA, and that the intensity at which these open varies by individual. Basic activities associated with SCUBA diving, such as surface swimming or walking with heavy equipment, may be enough to allow the passage of venous gas emboli through IPAVA.

Introduction Decompression sickness (DCS) is a rare and dangerous complication from a rapid decrease in environmental pressure, commonly seen in patients leaving a compressed-air environment, such as scuba divers, aviators, and deep tunnel workers. Failure to clinically diagnose and adequately treat DCS with hydration and supplemental oxygen before bridging to hyperbaric oxygen (HBO) therapy can result in permanent residual symptoms or, in rare cases, death. Despite the increasing incidence of DCS, there are limited published simulation case studies discussing this perilous environmental exposure. Methods This fictional simulation case is written for emergency medicine residents to diagnose and manage DCS from a live-actor patient presenting with unilateral neurologic symptoms and concealed cyanotic mottling (cutis marmorata). This case ran for four separate iterations at a simulation center, with a resident, fellow, and attending acting as specific confederates for their respective roles. Following each case, the learners were debriefed at bedside, discussed a PowerPoint presentation, and underwent a question-and-answer session. Results Based on postsimulation qualitative assessments, junior and senior residents correctly identified DCS, but junior residents alone were less likely to elicit pertinent social history or to fully physically examine the patient without the presence of senior residents. Both resident groups were able to verbally explain the fundamental DCS pathophysiology to the patient, but junior residents were unable to specifically direct oxygenation, hydration, and HBO protocols for DCS. After case completion and debriefing, all learners demonstrated achievement of primary learning objectives. Discussion Overall, we noted this case worked well for junior EM residents with senior-resident backup. Both learner groups appreciated the concealed elements of case, including scuba diving history and exposed dermatologic findings, and reported that these were invaluable learning moments for all future patient encounters, not just those limited to DCS.

The diagnosis of drowning is often established by an authority who lacks medicolegal training only on the basis that the body was found in water. However, a thorough evaluation of the circumstances, the victim’s characteristics, and autopsy findings is necessary to establish the etiology of such a death. Natural conditions, injuries, and intoxication can cause death in water or can be factors contributing to drowning. Drowning can be accidental or the result of an intentional action, either suicide or homicide. A multidisciplinary approach has a greater success rate than police and medicolegal investigations alone, and this is particularly evident in diving-related incidents.

Recent computational investigations have shed light into the various hydrodynamic mechanisms at play during arterial gas embolism that may result in endothelial cell (EC) injury. Other recent studies have suggested that variations in hematocrit level may play an important role in determining the severity of neurological complications due to decompression sickness associated with gas embolism.To develop a comprehensive picture, we computationally modeled the effect of hematocrit variations on the motion of a nearly occluding gas bubble in arterial blood vessels of various sizes. The computational methodology is based on an axisymmetric finite difference immersed boundary numerical method to precisely track the blood-bubble dynamics of the interface. Hematocrit variations are taken to be in the range of 0.2-0.6. The chosen blood vessel sizes correspond to small arteries and small and large arterioles in normal humans.Relevant hydrodynamic interactions between the gas bubble and EC-lined vessel lumen have been characterized and quantified as a function of hematocrit levels. In particular, the variations in shear stress, spatial and temporal shear stress gradients, and the gap between bubble and vascular endothelium surfaces that contribute to EC injury have been computed.The results suggest that in small arteries, the deleterious hydrodynamic effects of the gas embolism on an EC-lined cell wall are significantly amplified as the hematocrit levels increase. However, such pronounced variations with hematocrit levels are not observed in the arterioles.

Post-mortem radiology and autopsy findings in a series of six diving-related deaths are presented. The cases had different causes of death but essentially similar radiological findings. We propose that the so-called classical radiological features of cerebral arterial gas embolism more likely represent “off-gassing” (gas coming out of solution into intra-vascular spaces due to pressure changes). As such, we suggest that post-mortem radiology, when accompanying a competent autopsy examination, be limited to the chest, whereby it may be useful in the demonstration of pneumothoraces which might not be demonstrated at autopsy, thereby providing supporting evidence for barotrauma in the context of appropriate clinical and autopsy findings.

Interest in scuba (self-contained underwater breathing apparatus) diving increased in the 1970s, and undersea diving continues to be a popular sport early in the 21st century, with approximately 3 million certified divers in the United States. The Divers Alert Network (DAN), an institution created in 1981 by the Commerce Department, National Oceanic and Atmospheric Administration, has collected diving injury data for US and Canadian divers since 1987 that can be studied to suggest the epidemiologic characteristics of diving. This article examines neurologic injuries resulting from scuba diving.

We report the case of a 50-year-old woman undergoing elective endoscopic retrograde cholangiopancreatography, who developed coma and hemiparesis secondary to severe cerebral artery gas embolism. Despite prompt diagnosis and early hyperbaric oxygen therapy (HBO 2 ) she developed severe cerebral edema and died within 24 h.

Arterial gas embolism may occur as a complication of diving or certain medical procedures. Although relatively rare, the consequences may be disastrous. Recent articles in the critical care literature suggest the non-hyperbaric medical community may not be aware of the role for hyperbaric oxygen therapy in non-diving related gas embolism. This review is part of an Australian appraisal of experience in the management of arterial gas embolism over the last 10 years. We identified all patients referred to Prince of Wales Hospital Department of Diving and Hyperbaric Medicine with a diagnosis of arterial gas embolism from 1996 to 2006. Twenty-six patient records met our selection criteria, eight iatrogenic and 18 diving related. All patients were treated initially with a 280 kPa compression schedule. At discharge six patients were left with residual symptoms. Four were left with minor symptoms that did not significantly impact quality of life. Two remained severely affected with major neurological injury. Both had non-diving-related arterial gas embolism. There was a good outcome in the majority of patients who presented with arterial gas embolism and were treated with compression.

SUMMARY Computed tomography scan findings are described in cerebral arterial gas embolism in two patients with right to left intracardiac shunts by accidental injection of air during intravenous therapy. Although imaging may not be necessary to diagnose the condition, the patient may be referred to CT scan as a case of stroke. Cerebral arterial gas embolism should be considered in the differential diagnosis of stroke, particularly in case of right-to-left shunts. CT findings described are classical and diagnostic of the condition.

Fibrobronchoscopy is commonly considered a safe procedure with a low major complication rate not including cerebral arterial gas embolism (CAGE) a severe life threatening iatrogenic complication. Several cases of transbronchial needle aspiration (TBNA) has been related with CAGE when patient happens to have the high airway pressure that exceeds the pressure of the pulmonary veins allowing the air to enter the systemic circulation through the left heart. HBOT is the only effective treatment available for CAGE that provides 100% oxygen at high pressure, which accelerates nitrogen reabsorption and improves oxygenation of ischemic tissue. We reported a case of successful treatment with full recovery after early Hyperbaric Oxygen therapy of CAGE induced by an uneventful transbronchial biopsy during fibrobronchoscopy.