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Cardiomyopathy is a known but rare sequelae of diving-related cerebral arterial gas embolism (CAGE). In previously reported cases, patient findings have been consistent with takotsubo cardiomyopathy (TCM) per the revised Mayo Clinic's diagnostic criteria. A lesser-known variant of stress-related cardiomyopathy is neurogenic stunned myocardium (NSM), which occurs after a neurological event such as subarachnoid hemorrhage and typically presents in younger patients. Presentation tends to differ slightly to TCM with non-specific left ventricular dysfunction and T wave inversions. This case adds to the rare numbers of reported cardiomyopathy from diving and is the first reported case of suspected NSM associated with CAGE.

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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.

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INTRODUCTION: Hyperbaric oxygen treatment (HBOT) may be complicated by oxygen toxicity seizures, which typically occur with hyperbaric partial pressures of oxygen exceeding 203 kPa (2 atmospheres absolute). All other hyperbaric units in Australia exclusively use a multiplace chamber when treating with United States Navy Treatment Table 6 (USN TT6) due to this perceived risk. The purpose of this study was to determine the safety of a monoplace chamber when treating decompression illness (DCI) with USN TT6. METHODS: A retrospective review of the medical records of all patients treated at Fiona Stanley Hospital Hyperbaric Medicine Unit with USN TT6 between November 2014 and June 2020 was undertaken. These data were combined with previous results from studies performed at our hyperbaric unit at Fremantle Hospital from 1989 to 2014, creating a data set covering a 30-year period. RESULTS: One thousand treatments with USN TT6 were performed between 1989 and 2020; 331 in a monoplace chamber and 669 in a multiplace chamber. Four seizures occurred: a rate of 0.59% (1/167) in a multiplace chamber; and none in a monoplace chamber, indicating no statistically significant difference between seizures in a monoplace versus multiplace chamber (P = 0.31). CONCLUSIONS: The rate of oxygen toxicity seizures in a monoplace chamber is not significantly higher than for treatment in the multiplace chamber. We conclude that using the monoplace chamber for USN TT6 in selected patients poses an acceptably low seizure risk.

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This paper summarises the history and capabilities of monoplace chambers in treatment of decompression illness (DCI); both in support of diving operations and in the hospital setting. In the field, monoplace hyperbaric chambers provide victims of DCI immediate access to recompression in settings where traditional multiplace chambers are not available. Alternatively, they may facilitate pressurised transport to a multiplace chamber for continued management. Recently, collapsible lightweight versions have improved suitability for field deployment aboard small vessels in remote settings, and for use by less technically capable military, occupational and civilian operators. The resulting elimination of treatment delays may prove lifesaving and central nervous system sparing, and avoid subsequent diving fitness disqualification. Monoplace chambers thus facilitate diving operations that would otherwise be difficult to condone on health and safety grounds. The 1960s saw the introduction of multiplace hyperbaric chambers into the hospital setting, as a number of non-diving conditions appeared to benefit from hyperbaric oxygen. This coincided with interest in hyperbaric oxygen as a solid tumour radiation sensitiser. Development of a novel acrylic-hulled single occupancy chamber enabled patients to undergo radiotherapy while pressurised within its oxygen atmosphere. Increasing numbers of health care facilities adopted this chamber type as a more economical, less complex alternative to the multiplace chamber. Incorporation of relevant biomedical technologies have allowed monoplace chambers to support increasingly complex patients in a safe, effective manner. Despite these advances, criticism of medical centre-based monoplace chamber treatment of DCI exists. This paper evaluates this controversy and presents relevant counter-arguments.

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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.

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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.

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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.

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In 2018, the Medical Panel of the NATO Underwater Diving Working Group (UDWG) discussed the question of the rescue and management of a submerged unresponsive compressed-gas diver. The Panel reviewed the 2012 recommendation by the UHMS Diving Committee with respect to the specific recommendation in a convulsing diver using a half-face mask and separate mouthpiece, to delay surfacing until the clonic phase had subsided if the mouthpiece was in place. There is a paucity of scientific, epidemiological, experimental and observational human studies to substantiate this guidance. Experimental animal studies suggest that the likelihood of a complete airway obstruction during an ongoing seizure is low and that there is a high likelihood of surviving pulmonary barotrauma caused by complete airway closure. Airway management and control is an essential step in the management of the unresponsive diver and would be challenging to achieve in the underwater environment. Even in the military setting, it will be difficult to provide sufficient training to enable divers to handle such a situation. In this very rare scenario it is considered that emergency guidelines should be clear, concise and easy to follow. The UDWG therefore recommends that all unconscious military divers in this situation should be rescued to surface without waiting for clonic seizures to subside. Training organizations for recreational and occupational divers should consider whether this guidance should be applied for civilian divers as well.

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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.

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Cerebral air embolism should be considered in case of stroke symptoms during any invasive procedure. Transport to a hospital with neurosurgical/hyperbaric oxygen treatment (HBOT) facility could improve the outcome for the patient. Absence of air on computed tomography (CT) scan should not disqualify a patient from HBOT if air embolism is suspected.

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Cerebral arterial gas embolism (CAGE) shows various manifestations according to the quantity of gas and the brain areas affected. The symptoms range from minor motor weakness, headache, and confusion to disorientation, convulsions, hemiparesis, unconsciousness, and coma. A 46-year-old man was transferred to our emergency department due to altered sensorium. Immediately after a controlled ascent from 33 m of seawater, he complained of shortness of breath and rigid extremities, lapsing into unconsciousness. He was intubated at another medical center, where a brain computerized axial tomography scan showed no definitive abnormal findings. Pneumothorax and obstructing lesions were apparent in the left thorax of the computed tomography scan. Following closed thoracostomy, we provided hyperbaric oxygen therapy (HBOT) using U.S. Navy Treatment Table (USN TT) 6A. A brain magnetic resonance imaging diffusion image taken after HBOT showed acute infarction in both middle and posterior cerebral arteries. We implemented targeted temperature management (TTM) to prevent worsening of cerebral function in the intensive care unit. After completing TTM, we repeated HBOT using USN TT5 and started rehabilitation therapy. He fully recovered from the neurological deficits. This is the first case of CAGE treated with TTM and consecutive HBOTs suggesting that TTM might facilitate salvage of the penumbra in severe CAGE.

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A diver presented with total loss of vision in the left eye and right hemiparesis following a routine no-stop scuba dive to 20 metres' depth. A diagnosis of decompression illness (DCI) with acute ophthalmic artery air embolism and left carotid artery insult causing acute anterior circulatory ischaemia was made. He underwent seven hyperbaric treatments leading to a full recovery. Magnetic resonance angiography revealed an underlying left anterior cerebral artery A1 segment hypoplasia. Making a prompt diagnosis and early hyperbaric oxygen treatment are crucial to halt further tissue damage from ischaemia in central nervous system DCI. In this case, the finding of a left A1 anterior cerebral artery segment hypoplasia variant may have increased the severity of DCI due to deficient collateral circulation.

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Arterial gas embolism is a catastrophic event. Bubbles in the arterial circulation may lodge in the brain and cause infarction in the affected area and/or in a coronary vessel causing acute myocardial ischaemia. There is no well-defined window of time beyond which a response to hyperbaric oxygen is not expected. Major improvement may occur if the patient is treated as soon as possible, but is less likely in divers with severe decompression illness who have delayed intervention. We report on a 51-year-old, male rebreather diver who suffered loss of consciousness and cardiovascular collapse within minutes of a 30-metre deep dive at a remote Micronesian dive site. Recompression treatment did not start for six days for reasons to be presented, during which time he remained deeply comatose, cardiovascularly unstable and intubated on ventilator support. Despite this, following aggressive hyperbaric treatment over many days he made a functional recovery. At one year post injury, he is leading a functional life but has not returned to his previous occupation as a diver and suffers from moderately severe tinnitus and impaired right ear hearing and occasional mild speech problems. He is undertaking a number of on-line courses with a view to re-employment.

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INTRODUCTION: Owing to the scarcity of randomized controlled trials to guide treatment for decompression illness (DCI), there are many unanswered questions about its management. Apart from reviews and expert opinion, surveys that report practice patterns provide information about useful management strategies. Hence, this study aimed to identify current treatment preferences for DCI amongst diving physicians in Singapore. METHODS: An anonymous web-based questionnaire was sent to known diving physicians in Singapore. The demographics of the respondents were captured. Respondents were asked about their preferred management for five different DCI scenarios. RESULTS: The response rate was 74% (17 of 23 responses). All respondents chose to recompress patients described in the five scenarios. Regarding the number of recompression sessions, "one additional session after no further improvement in signs and symptoms" was the most common end point of treatment across all the scenarios (47 of 85 responses). Analgesics would be used by five physicians, three would use lidocaine and two steroids as adjuvant therapies. CONCLUSIONS: Apart from the general agreement that recompression is indicated for DCI, there was no strong consensus regarding other aspects of management. This survey reinforces the need for robust RCTs to validate the existing recommendations for DCI treatment.

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INTRODUCTION: The aim of this study was to review patients with iatrogenic cerebral gas embolism (CGE) referred to The Alfred Hospital hyperbaric unit to determine whether hyperbaric oxygen treatment (HBOT) reduced morbidity and mortality. METHODS: This is a retrospective cohort study with a contemporaneous comparison group of patients referred between January 1998 and December 2014. The primary end point was good neurological outcome at the time of discharge from hospital or rehabilitation facility as assessed by the Glasgow Outcome Scale (GOS-E). RESULTS: Thirty-six patients were treated with HBOT for CGE and nine patients were diagnosed with CGE but did not receive HBOT. Thirty-two patients developed CGE from an arterial source and 13 from a venous source. The mean time from recognition of the event to institution of HBOT was 15 hours. Four of 45 patients (8.9%) died. Good neurological outcomes (defined as GOS-E 7 or 8) occurred in 27 patients and moderate disability in 13. The only independent factor that was associated with good neurological outcome was time to first HBOT (OR 0.94, 0.89-0.99; P = 0.05). Hemiplegia as the first presenting sign, however, was associated with poor outcome (OR 0.27, 0.06-1.08; P = 0.05). The source of embolus (arterial versus venous), hyperbaric treatment table used and patient age did not affect outcome. CONCLUSION: Appropriate treatment of CGE with hyperbaric oxygen was found to be impeded by delays in diagnosis and subsequent transfer of patients. Better neurological outcome was associated with HBOT within eight hours of CGE.

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Dr Kemper and colleagues reported that, when air was injected into the cerebral circulation of pigs, they developed a rash that looked very similar to cutis marmorata of cutaneous decompression illness (DCI) and to livido reticularis. They postulated that cutaneous DCI in divers may be centrally mediated as a result of cerebral gas embolism. It would be helpful if Kemper et al. described the distribution of the rash in their pigs. In divers, cutaneous DCI is generally confined to parts of the body with significant amounts of subcutaneous fat, such as the trunk and thighs, and the rash often crosses the midline. Colleagues and I have reported that cutaneous DCI is commonly associated with significant right-to-left shunts and particularly persistent foramen ovale (PFO). We postulated that the manifestations of shunt-related DCI, whether neurological or cutaneous, are in large part determined by peripheral amplification of embolic bubbles in those tissues that are most supersaturated with dissolved nitrogen (or other inert gas) at the time that emboli arrive. Hence we postulated that cutaneous DCI is the result of amplification of gas emboli that invade cutaneous capillaries. Dr Kemper has kindly sent me a number of the publications from his department on which their report of this skin rash in pigs is based. The aim of their experiments was to produce significant brain injury by means of cerebral air embolism. Their pigs had no tissues supersaturated with inert gas. They were ventilated with a FiO2 of 0.4 and anaesthetised with ketamine and midazolam. They were also given pancuronium and atropine, before air was injected into their cerebral circulation. If their findings in pigs and the resulting hypothesis were applicable to man, it would mean that one could get cutaneous DCI without decompression: one would only need cerebral gas embolism. During contrast echocardiography, I have produced arterial gas embolism in many hundreds of patients with right-to-left shunts and it is certain that some bubbles went into their cerebral circulations, but I have never seen and no patient has reported getting a rash. Nor am I aware of any reports of gas embolism causing a rash like cutaneous DCI without there being tissue supersaturation following some form of decompression. Kemper and colleagues injected between 0.25 and 1 ml·kg⁻¹ body weight of air into the ascending pharyngeal artery (roughly equivalent to human internal carotid artery) of pigs weighing 30-40kg. That immediately produced significant elevation of blood pressure and heart rate suggesting a 'sympathetic surge'. This is similar to the haemodynamic effects that can occur with subarachnoid haemorrhage and some other catastrophic brain injuries. That effect may have been potentiated by pre-treatment with atropine. There was also a considerable increase in intracranial pressure and major adverse effects on cerebral metabolism. Some pigs died quickly and the survivors were killed at the end of the experiment. I suspect that no pig would have survived the experiments without major neurological injury if they had not been killed. Most people with cutaneous DCI have no detectable neurological manifestations at the time that they have a rash. In those that do have neurological manifestations, it is rarely catastrophic. The increases in heart rate and blood pressure reported in the pigs are similar to the effects of a phaeochromocytoma, which can cause livido reticularis in man. Therefore, I wonder whether an alternative explanation for these observations might be that the cerebral injury in the pigs was so massive that the sympathetic surge was comparable to the effects of catecholamine release from a phaeochromocytoma and caused a rash similar to that seen in patients with a phaeochromocytoma.

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