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The foramen ovale plays a vital role in sustaining life in-utero; however, a patent foramen ovale (PFO) after birth has been associated with pathologic sequelae in the systemic circulation including stroke/transient ischemic attack (TIA), migraine, high altitude pulmonary edema, decompression illness, platypnea-orthodeoxia syndrome (POS) and worsened severity of obstructive sleep apnea. Importantly, each of these conditions is most commonly observed among specific age groups: migraine in the 20 to 40s, stroke/TIA in the 30-50s and POS in patients >50 years of age. The common and central pathophysiologic mechanism in each of these conditions is PFO-mediated shunting of blood and its contents from the right to the left atrium. PFO-associated pathologies can therefore be divided into (1) paradoxical systemic embolization and (2) right to left shunting (RLS) of blood through the PFO. Missing in the extensive literature on these clinical syndromes are mechanistic explanations for the occurrence of RLS, including timing and the volume of blood shunted, the impact of age on RLS, and the specific anatomical pathway that blood takes from the venous system to the left atrium. Visualization of the flow pattern graphically illustrates the underlying RLS and provides a greater understanding of the critical flow dynamics that determine the frequency, volume, and pathway of flow. In the present review, we describe the important role of foramen ovale in in-utero physiology, flow visualization in patients with PFO, as well as contributing factors that work in concert with PFO to result in the diverse pathophysiological sequelae., Competing Interests: Conflict of Interest Dr. Horlick serves as a consult to Abbott Vascular. Dr. Carroll serves on the Steering Committee of the RESPECT trial and is a consultant to Abbott Vascular and Holistick Medical. Dr. Krasuski reports serving as a consultant to Actelion/Janssen Pharmaceuticals, Bayer Pharmaceuticals, Gore Medical and Neptune Medical. He receives research funding from the Adult Congenital Heart Association, Actelion, Artivion, Corvia, Medtronic and Edwards Lifesciences. Dr. Shah and Dr. Kass report no conflicts., (Copyright © 2024 The Author(s). Published by Elsevier Inc. All rights reserved.)

We report a case of an active-duty diver who developed severe decompression sickness with concomitant patent foramen ovale that was successfully closed contrary to standard guideline recommendations. This case should prompt evaluation of the role of cardiac screening in occupational divers, including tactical athletes, relative to recreational divers., Competing Interests: Funding Support and Author Disclosures Partial support was received from award HU00011920029 from Defense Health Agency to the Military Cardiovascular Outcomes Research program, Uniformed Services University, Bethesda, Maryland. The authors have reported that they have no relationships relevant to the contents of this paper to disclose. The views expressed in this article are those of the authors and do not reflect the official policy of the Department of Defense (DoD) or the U.S. government. The identification of specific products or scientific instrumentation is considered an integral part of the scientific endeavor and does not constitute endorsement or implied endorsement on the part of the author(s), DoD, or any component agency., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

3d Reconnaissance Battalion, a forward-deployed Marine Corps unit in Okinawa, Japan, frequently performs diving operations. Often throughout the year, several reconnaissance teams are diving simultaneously in different locations for training. We present a case of an otherwise healthy 30-year-old-male Reconnaissance Marine who surfaced from a dive with abnormal symptoms and received prompt care from exercise participants who were nonmedical personnel. Studies have demonstrated improved morbidity outcomes in decompression illness patients with shorter times to hyperbaric treatment following the onset of symptoms. High-risk military exercises with diving components have a mandatory safety structure that includes recompression chamber support. All United States Marine Corps Reconnaissance, Marine Corps Special Operations Command, and U.S. Navy dive operations are required to have at least one diving supervisor. To expand the diving capabilities of the unit, Marines are encouraged to attend training and qualify as diving supervisors. This case study demonstrates the efficacy and importance of training Recon Marines to recognize decompression illness as diving supervisors., (Published by Oxford University Press on behalf of the Association of Military Surgeons of the United States 2023. This work is written by (a) US Government employee(s) and is in the public domain in the US.)

A 60-year-old man with hypertension and dyslipidemia complained of chest pain upon ascending from a maximum depth of 27 meters while diving. After reaching the shore, his chest pain persisted, and he called an ambulance. When a physician checked him on the doctor's helicopter, his electrocardiogram (ECG) was normal, and there were no bubbles in his inferior vena cava or heart on a portable ultrasound examination. The physician still suspected that he had acute coronary syndrome instead of decompression illness; therefore, he was transported to our hospital. After arrival at the hospital, standard cardiac echography showed a flap in the ascending aorta. Immediate enhanced computed tomography revealed Stanford type A aortic dissection. The patient obtained a survival outcome after emergency surgery. To our knowledge, this is the first reported case of aortic dissection potentially associated with scuba diving. It highlights the importance of considering aortic dissection in patients with sudden-onset chest pain during physical activity. In addition, this serves as a reminder that symptoms during scuba diving are not always related to decompression. This report also suggests the usefulness of on-site ultrasound for the differential diagnosis of decompression sickness from endogenous diseases that induce chest pain. Further clinical studies of this management approach are warranted., Competing Interests: The authors of this paper declare no conflicts of interest exist with this submission., (Copyright© Undersea and Hyperbaric Medical Society.)

Decompression sickness (DCS) is caused by abrupt changes in extracorporeal pressure with varying severity. Symptoms range from mild musculoskeletal pain to severe organ dysfunction and death, especially among patients with chronic underlying disease. Here, we report an unusual case of a 49-year-old man who experienced DCS after a dive to a depth of 38 meters. The patient's symptoms progressed, starting with mild physical discomfort that progressed to disturbance of consciousness on the second morning. During hospitalization, we identified that in addition to DCS, he had also developed diabetic ketoacidosis, septic shock, and rhabdomyolysis. After carefully balancing the benefits and risks, we decided to provide supportive treatment to sustain vital signs, including ventilation support, sugar-reducing therapy, fluid replacement, and anti-infection medications. We then administered delayed hyperbaric oxygen (HBO 2 ) when his condition was stable. Ultimately, the patient recovered without any sequelae. This is the first case report of a diver suffering from DCS followed by diabetic ketoacidosis and septic shock. We have learned that when DCS and other critical illnesses are highly suspected, it is essential to assess the condition comprehensively and focus on the principal contradiction., Competing Interests: The authors of this paper declare no conflicts of interest exist with this submission., (Copyright© Undersea and Hyperbaric Medical Society.)

McArdle disease is a glycogen storage disease that results in rhabdomyolysis during intense exercise. A number of different triggers have been described. We evaluated a patient with McArdle disease who presented with rhabdomyolysis after recreational scuba diving. There was no concern for barotrauma or decompression sickness. His symptoms resolved with standard-of-care management for non-diving-related rhabdomyolysis. Features of his experience provoked questions about the diving-related factors contributing to his presentation. We present the case and explore possible mechanisms of diving-related injury in patients with McArdle disease, including the possible effects of hyperoxia, hyperbaria, hypothermia and strenuous activity., Competing Interests: Competing interests: None declared., (© BMJ Publishing Group Limited 2023. No commercial re-use. See rights and permissions. Published by BMJ.)

Systemic capillary leak syndrome is a rare derangement of endothelial function characterised by extravasation of plasma and proteins into the interstitial space. Primary capillary leak syndrome is a rare, episodic medical illness of unknown molecular pathology while secondary capillary leak syndrome may be precipitated by any number of inflammatory and infectious syndromes. Decompression sickness, a disorder of depressurisation, has been identified as a very rare trigger. We present a structured case report of systemic capillary leak syndrome secondary to decompression sickness following deep diving, informing physicians of this potential complication. No pharmacological therapy has substantial evidence in the treatment of acute systemic capillary leak syndrome. By review of current recommendations for acute management, we also emphasise an observed positive response to judicious fluid resuscitation and an oral cyclic AMP-elevating agent (ie, terbutaline)., Competing Interests: Competing interests: None declared., (© BMJ Publishing Group Limited 2023. No commercial re-use. See rights and permissions. Published by BMJ.)

Background: In previous studies, the prevalence of patent foramen ovale (PFO) has been reported to be higher in scuba divers who experienced decompression illness (DCI) than in those who did not., Objective: To assess the association between PFO and DCI in scuba divers., Design: Prospective cohort study., Setting: Tertiary cardiac center in South Korea., Participants: One hundred experienced divers from 13 diving organizations who did more than 50 dives per year., Measurements: Participants had transesophageal echocardiography with a saline bubble test to determine the presence of a PFO and were subsequently divided into high- and low-risk groups. They were followed using a self-reported questionnaire while blinded to their PFO status. All of the reported symptoms were adjudicated in a blinded manner. The primary end point of this study was PFO-related DCI. Logistic regression analysis was done to determine the odds ratio of PFO-related DCI., Results: Patent foramen ovale was seen in 68 divers (37 at high risk and 31 at low risk). Patent foramen ovale-related DCI occurred in 12 divers in the PFO group (non-PFO vs. high-risk PFO vs. low-risk PFO: 0 vs. 8.4 vs. 2.0 incidences per 10 000 person-dives; P  = 0.001) during a mean follow-up of 28.7 months. Multivariable analysis showed that high-risk PFO was independently associated with an increased risk for PFO-related DCI (odds ratio, 9.34 [95% CI, 1.95 to 44.88])., Limitation: The sample size was insufficient to assess the association between low-risk PFO and DCI., Conclusion: High-risk PFO was associated with an increased risk for DCI in scuba divers. This finding indicates that divers with high-risk PFO are more susceptible to DCI than what has been previously reported and should consider either refraining from diving or adhering to a conservative diving protocol., Primary Funding Source: Sejong Medical Research Institute., Competing Interests: Disclosures: Disclosures can be viewed at www.acponline.org/authors/icmje/ConflictOfInterestForms.do?msNum=M23-0260.

Introduction: Breath-hold (BH) diving has known risks, for example drowning, pulmonary oedema of immersion and barotrauma. There is also the risk of decompression illness (DCI) from decompression sickness (DCS) and/or arterial gas embolism (AGE). The first report on DCS in repetitive freediving was published in 1958 and from then there have been multiple case reports and a few studies but no prior systematic review or meta-analysis., Methods: We undertook a systematic literature review to identify articles available from PubMed and Google Scholar concerning breath-hold diving and DCI up to August 2021., Results: The present study identified 17 articles (14 case reports, three experimental studies) covering 44 incidences of DCI following BH diving., Conclusions: This review found that the literature supports both DCS and AGE as potential mechanisms for DCI in BH divers; both should be considered a risk for this cohort of divers, just as for those breathing compressed gas while underwater., (Copyright: This article is the copyright of the authors who grant Diving and Hyperbaric Medicine a non-exclusive licence to publish the article in electronic and other forms.)

Background: Dysbaric osteonecrosis (DON) is defined as avascular bone necrosis, usually involving specific parts of the long bones, which is seen in divers or compressed-air workers due to exposure to pressure. We describe a case of DON in an artisanal diving fisherman working underwater for many years. Methods: A 48-year-old male case was admitted to the occupational disease outpatient with left shoulder and arm pain for 1-2 years. Since the age of 20, he has been artisanal diving fishing with a hookah at a depth of 20-25 meters in the sea. In 2011, he received hyperbaric oxygen therapy for widespread pain in the whole body due to decompression sickness (DCS). In the case's left shoulder joint x-ray and magnetic resonance imaging, degenerative changes in the acromioclavicular joint and signal changes consistent with osteonecrosis starting from the subcortical area of the humeral head and extending to the proximal shaft of the humerus were observed. Conclusions: DON is among the most common long-term pathologies in professional divers. In Turkey, as in our case, not applying safe decompression procedures and unsafe diving practices are common among diving fishers. In studies, the frequency of exposure to pressure, duration and depth of dive, insufficient decompression, formation of DCS and increasing age were associated with DON. Today, DON remains an occupational hazard with significant medical and social consequences. Diving fishers should be informed about the sequelae of DCS and trained on the safety measures to be taken.

Objectives: During apnea diving, a patent foramen ovale may function as a pressure relief valve under conditions of high pulmonary pressure, preserving left-ventricular output. Patent foramen ovale prevalence in apneic divers has not been previously reported. We aimed to determine the prevalence of patent foramen ovale in apneic divers compared to non-divers., Design: Cross sectional., Methods: Apnea divers were recruited from a training camp in Cavtat, Croatia and the diving community of Split, Croatia. Controls were recruited from the population of Split, Croatia and Eugene, Oregon, USA. Participants were instrumented with an intravenous catheter and underwent patent foramen ovale screening utilizing transthoracic saline contrast echocardiography. Appearance of microbubbles in the left heart within 3 cardiac cycles indicated the presence of patent foramen ovale. Lung function was measured with spirometry. Comparison of patent foramen ovale prevalence was conducted using chi-square analysis, p < .05., Results: Apnea divers had a significantly higher prevalence of patent foramen ovale (19 of 36, 53%) compared to controls (9 of 36, 25%) (X 2 (1, N = 72) = 5.844, p = .0156)., Conclusions: Why patent foramen ovale prevalence is greater in apnea divers remains unknown, though hyperbaria during an apnea dive results in a translocation of blood volume centrally with a concomitant reduction in lung volume and alveolar hypoxia during ascent results in hypoxic pulmonary vasoconstriction. These conditions increase pulmonary arterial pressure, increasing right-atrial pressure allowing for right-to-left blood flow through a patent foramen ovale which may be beneficial for preserving cardiac output and reducing capillary hydrostatic forces., (Crown Copyright © 2022. Published by Elsevier Ltd. All rights reserved.)

Decompression sickness (DCS) occurs when divers are exposed to reduced barometric pressure during their ascent from depth. We report a case of DCS causing severe acute kidney injury (AKI) after an uneventful dive in which all decompression stops were made as instructed by a dive computer. A 26-year-old man presented with abdominal and bilateral flank pain ~ 24 hours after scuba diving to a depth of 23 m. Vitals and physical exam were unremarkable. Lab results revealed elevated serum creatinine at 2.3 mg/dL from a normal baseline and elevated blood urea nitrogen at 23 mg/dL. The patient was non-oliguric. Other biochemical parameters were unremarkable. Dipstick urinalysis showed presence of blood and 100 mg/dL proteinuria. Urine microscopy revealed hyaline casts and red blood cells ~ 16 - 30/HPF but no acanthocytes. Urine protein-to-creatinine ratio was 340 mg/g. Renal ultrasound showed normal sized kidneys with increased cortical echogenicity, and computed tomography of the abdomen/pelvis showed bilateral striated nephrogram with delayed excretion, both radiographic signs of acute tubular necrosis. The patient received isotonic IV fluids and 5 sessions of hyperbaric oxygen therapy. Symptomatic improvement was observed by day 3 of hospitalization with full recovery of kidney function after discharge. Due to a wide range of associated symptomology, a thorough and prompt evaluation is warranted in suspected cases of DCS, particularly if presentation is more than 24 hours following ascent.

The foramen ovale is an essential component of the fetal circulation contributing to oxygenation and carbon dioxide elimination that remains patent under certain circumstances in ∼30% of the healthy adult population, without major negative sequelae in most. Adults with a patent foramen ovale (PFO) have a greater tendency to develop symptoms of acute mountain sickness and high-altitude pulmonary oedema upon ascent to high altitude, and PFO presence is associated with worse cardiopulmonary function in chronic mountain sickness. This increase in altitude illness prevalence may be related to dysregulated cerebral blood flow associated with altered respiratory chemoreflex sensitivity; however, the mechanisms remain to be elucidated. Interestingly, men with a PFO appear to have a shift in thermoregulatory control to higher internal temperatures, both at rest and during exercise, and they have blunted thermal hyperpnoea. The teleological 'reason' for this thermoregulatory shift is unclear, but the shift of ∼0.5°C in core body temperature does not appear to be sufficient to have any significant negative consequences in terms of risk of heat illness. Further work in this area is needed, particularly in women, to evaluate mechanisms of heat storage and dissipation in these individuals compared to people without a PFO. Consequences of a PFO in SCUBA divers include a greater incidence of unprovoked decompression sickness, but whether PFO is beneficial or detrimental to breath hold diving remains unexplored. Whether PFO presence will explain interindividual variability in responses to, and consequences from, other environmental stressors such as spaceflight remain entirely unknown., (© 2022 The Authors. The Journal of Physiology © 2022 The Physiological Society.)

BACKGROUND Deep sea diving can cause decompression illness which comprises both decompression sickness and arterial gas embolism. Decompression sickness is a clinical diagnosis with symptoms including dizziness, joint pain, rash, and myalgias and is due to nitrogen bubbles that form in tissues during ascent. These gas bubbles can be clinically silent even in the absence of decompression sickness and can rarely predispose a patient to venous thrombus, for which the role of hyperbaric oxygen (HBO) is undefined. The following case describes a male diver who developed portal and mesenteric venous thrombosis secondary to silent nitrogen venous bubbles. CASE REPORT A 48-year-old man developed abdominal pain 1 day after diving to a maximum depth of 13.7 m, without clinical symptoms of decompression sickness after surfacing. He presented to the Emergency Department 10 days later, and magnetic resonance angiogram revealed a diagnosis of gas containing superior mesenteric and portal vein thrombus. Due to the lack of guidelines of HBO with the presence of a thrombus and timing since onset, HBO therapy was not pursued. Oral anticoagulation was initiated, and symptoms resolved. CONCLUSIONS This patient developed gastrointestinal illness 1 day after diving that was later found to be due to thrombosis. Other etiologies were ruled out, making silent nitrogen bubbles within the venous system the most likely etiology. Vascular thrombosis is a rare complication of diving and lacks guidelines for treatment. While HBO is a known treatment for decompression sickness, there are no clinical guidelines for diving-associated thrombi, representing an area for further research.

Introduction: Decompression sickness (DCS) has traditionally been categorized as type I DCS, affecting joints and skin, and type II affecting the nervous system. In the present study, we wanted to examine whether divers with a history of neurological DCS demonstrated a pattern of symptoms and clinical neurological and neurophysiological signs different from divers with other manifestations of DCS or no history of DCS., Methods: Up to 1990, 365 Norwegian offshore divers worked in the North Sea. Two hundred and eight divers who had performed saturation diving, bounce diving or both, were included in this study. They filled in a questionnaire for registration of diving experience and health complaints, and episodes of DCS were registered. All participants had a clinical neurological and neurophysiological examination (ERP- P300)., Results: One hundred and sixty three of the 208 divers (78.4%) reported episodes of DCS. Neurological DCS was reported by 41 (19.7%) divers. Forty-five divers (21.6%) reported no episodes of DCS. Divers who reported episodes of DCS reported significantly more symptoms compared with divers who reported no DCS. Divers who reported neurological DCS had significantly more neurological findings on motility tests, sensory tests and coordination/cerebellar tests. The P300 motor reaction times were significantly longer in divers reporting DCS, but there was no significant difference between divers with neurological DCS and divers with other forms of DCS., Conclusions: This study indicates that DCS is associated with long-term effects on the nervous system independent of the symptomatology in the acute stage., (Copyright © 2022 Elsevier B.V. All rights reserved.)

Dysbarism is a general term which includes the signs and symptoms that can manifest when the body is subject to an increase or a decrease in the atmospheric pressure which occurs either at a rate or duration exceeding the capacity of the body to adapt safely. In the following review, we take dysbarisms into account for our analysis. Starting from the underlying physical laws, we will deal with the pathologies that can develop in the most frequently affected areas of the body, as the atmospheric pressure varies when acclimatization fails. Manifestations of dysbarism range from itching and minor pain to neurological symptoms, cardiac collapse, and death. Overall, four clinical pictures can occur: decompression illness, barotrauma, inert gas narcosis, and oxygen toxicity. We will then review the clinical manifestations and illustrate some hints of therapy. We will first introduce the two forms of decompression sickness. In the next part, we will review the barotrauma, compression, and decompression. The last three parts will be dedicated to gas embolism, inert gas narcosis, and oxygen toxicity. Such an approach is critical for the effective treatment of patients in a hostile environment, or treatment in the emergency room after exposure to extreme physical or environmental factors.

Decompression sickness (DCS) is a known complication of scuba diving. DCS occurs when bubbles are formed as pressure is reduced during and after ascent from a dive, following inert gas uptake during the dive. The bubbles cause inflammation and hypoxia. The definitive treatment for decompression sickness is hyperbaric oxygen therapy. We present a case of a healthy 16-year-old male who presented with decompression sickness and an incidental pulmonary cyst discovered by chest CT, likely congenital. The patient was successfully treated with U.S. Navy Treatment Table 6 (TT6) for his decompression sickness, but he continued to have chest pain, requiring hospitalization and consultation with pediatric pulmonology and cardiothoracic surgery from the cyst. Three years later he complained of chest pain with changes in altitude. Chest CT showed persistence of this cyst, and additional cysts. Case conference with pulmonologists and chest radiologist could not offer a definite etiology without lung biopsy, felt to not be indicated. We believe that the changes in pressure/volumes during the dives and TT6 exacerbated his pulmonary cyst., Competing Interests: The authors of this paper declare no conflicts of interest exist with this submission., (Copyright© Undersea and Hyperbaric Medical Society.)

Introduction: This case report describes an initially overlooked Type II decompression sickness (DCS) occurrence that was confused with a cerebral vascular accident in a patient with chronic atrial fibrillation (AF). The purpose of this case report is to reinforce the maxim that DCS needs to be suspected anytime a scuba diver experiences signs or symptoms compatible with DCS after completing a scuba dive., Methods: A 71-year-old scuba diver with a history of AF and who was taking warfarin made four dives, all with maximum depths less than 60 fsw (20 msw) over a 10-hour interval. Shoulder pain developed before entering the water on the fourth dive and was worse after exiting from the fourth dive. Twenty minutes later the diver collapsed while standing and was unable to make a grip using his left hand. A literature review failed to locate any case reports of divers with AF presenting with strokelike symptoms only to find the cause was Type II DCS.., Findings: Initially the patient's findings were reviewed with a diving medicine team. The recommendation was for the patient to be managed for a stroke. The patient was transferred to a hospital for a computed tomography scan, but no recommendation was made for a hyperbaric oxygen recompression treatment. The scan showed no brain bleed or infarct. The attending neurologist (not diving medicine-trained) was concerned that the patient's findings were diving-related and arranged for transferring the patient to a hyperbaric medicine facility 25 hours later. With hyperbaric oxygen (HBO2) therapy the patient's symptoms remitted over several weeks., Conclusion: The presence of symptoms attributed to a stroke immediately after a scuba dive should not deter a trial of HBO2 therapy. The delay in starting HBO2 therapy is concerning and perhaps the reason recovery was delayed and the need for repetitive HBO2 therapies., Competing Interests: The authors of this paper declare no conflicts of interest exist with this submission., (Copyright© Undersea and Hyperbaric Medical Society.)

Introduction: Dysbaric osteonecrosis, albeit rare, have been reported in patients with decompression sickness. We report a patient with dysbaric osteonecrosis, diagnosed 60 days after presenting with decompression sickness., Case Presentation: A 38-year-old, previously fit and healthy male, noted his tank running out of air at approximately 40-50 m while diving, surfaced rapidly before losing consciousness. Upon gaining consciousness, he noted loss of power on all four limbs. He completed 26 sessions of hyperbaric oxygen treatment. Magnetic resonance (MR) of the spine noted T2 abnormality in the upper cervical spine, with some involvement of the central grey matter and the remainder of the cord. According to the International Standards for Neurological Classification of Spinal Cord Injury, it was noted clinically that the patient had a T9 neurological level with ASIA impairment scale A. MR imaging (MRI) of the shoulder was performed, 60 days since initial presentation, after the patient complained of shoulder pain, noted non-specific subcortical oedema of the humeral head, which suggested early osteonecrosis., Discussion: Dysbaric osteonecrosis is rare but remains extremely important to be recognised as a potential complication from decompressive sickness. The increased risk of pathological fractures with dysbaric osteonecrosis plays an important role as it may alter the rehabilitation prescription. One of the unique features of this case, apart from its rarity, was that it was diagnosed 60 days from his initial presentation, when he has passed his acute phase of illness., (© 2021. Crown.)

Pulmonary barotrauma is a kind of disease caused by the injury of lung tissue or blood vessel when the gas pressure of lung is too high or too lower than the external pressure of the body, which causes the air to enter the blood vessel and adjacent tissue. It could be happened in the escape of the divers with the light diving equipment or the sailors from submarine. Generally, the decompression chamber was used to treating the disease, and the minimum air pressure of 0.5 MPa recompression therapeutic schedule was used to selecting. In November 2019, a patient with pulmonary barotrauma combined with cerebral arterial gas embolism caused by improper underwater escape with light diving equipment was admitted to the General Hospital of Eastern War Zone. He was treated with 0.12 MPa oxygen inhalation recompression scheme in the oxygen chamber pressurized with air. 7 days later, the patient recovered and discharged.

Objective: To discuss the new idea of on-the-spot recompression treatment and multidisciplinary treatment (MDT) for patients with unstable vital signs of type II decompression sickness. To provide reference for the nearby treatment of patients with critical decompression sickness. Methods: The clinical data of a case of a multi-disciplinary collaborative treatment of type II decompression sickness complicated with multiple organ dysfunction syndrome (MODS) admitted to a third-class A hospital in January 2020 were analyzed and summarized. Results: The patient suffered from consciousness disturbance and shock after 3 min of diver's blow-up out of the water. CT examination showed gas accumulation in the systemic multi-organ venous system, and laboratory examination suggested MODS. The oxygen inhalation regimen was given in the session of recompression treatmen by 0.12-0.18 MPa. Intravenous fluid was the total of 8900 ml in the session, and the total recompression treatment time was 9 h 45 min. The patient was still in unconscious when he finished the session. CT re-examination confirmed the elimination of venous bubbles, and laboratory examination indicated multiple organ failure (MOF) . The patient was given comprehensive supporting treatment by mechanical assisted breathing and following by continuons renal replacement therapy (CRRT) and extrocorporeal membrane oxygenation (ECMO) in the intensive care unit, and was discharged after 32 d of hospitalization. Conclusion: Critical decompression sickness patients with unstable vital signs are taken to a local general hospital with hyperbaric oxygen chamber and intensive care unit. The successful treatment can be achieved by organizing diving medicine, hyperbaric oxygen medicine and critical medical personnel for MDT.

Objective: Decompression sickness (DCS) causes serious brain hypoxic-ischemic injury. This experiment was designed to observe whether hyperbaric oxygen (HBO2) pretreatment played a neuroprotective effect in decompression sickness rat models and to explore the mechanism of protective effects., Methods: Sprague-Dawley (SD) male rats were pretreated with HBO2 and then underwent decompression to establish the DCS rat model. Antioxidant capacities were evaluated by detecting peroxides (GPx), superoxide dismutase (SOD), catalase (CAT) activity and malondialdehyde (MDA) content in brains. The levels of metal elements manganese (Mn), zinc (Zn), iron (Fe) and magnesium (Mg) in brain tissues were assessed by flame atomic absorption spectrometry. Necrosis and apoptosis of neurons were assessed by H-E staining and immunohistochemical staining., Results: HBO2 pretreatment reduced the degree of necrosis and apoptosis in brain tissues of decompression sickness rat models. In addition, HBO2 pretreatment increased GPx, SOD and CAT activities and reduced MDA accumulation. It also increased the content of Mn, Zn, Fe and Mg in brain tissue, which are all related to free radical metabolism., Conclusion: These results suggested that HBO2 pretreatment has protective effects on brain injury of rats with decompression sickness. The mechanism of the protective effects may be related to reducing oxidative damage by affecting metal elements in vivo., Competing Interests: The authors of this paper declare no conflicts of interest exist with this submission., (Copyright© Undersea and Hyperbaric Medical Society.)

Sudden decompression can result in bubble formation as the result of nitrogen gas (N2) dissolved in tissue during disabled submarine escape (DISSUB). This may cause dysbaric osteonecrosis (DON), a condition in long bones where bubbles in fatty marrow result in ischemia and necrosis. Previous research has shown that oxygen (O2) pre-breathe of two hours resulted in a reduction of DON; however, effects of shorter O2 pre-breathe remain uncertain. This study's aim was to understand the effect of shorter lengths of O2 pre-breathe. Eight adult Suffolk ewes (89.5± 11.5 kg) were exposed to 33 feet of seawater (fsw) for 24 hours. They were placed randomly into four groups and exposed to either 45, 30 or 15 minutes of O2 (91-88%) pre-breathe; the controls received none. They were then rapidly decompressed. Alizarin complexone was later injected intravenously to visualize the extent of DON in the right and left long bones (radii, tibiae, femur and humeri). The 30- and 15-minute pre-breathe groups saw the greatest deposition. There was significant decrease of variance in the 45-minute group when compared with all other treatments, suggesting that 45 minutes of O2 pre-breathe is required to effectively increase confidence in the reduction of DON. Similar confidence was not reflected in the 30-minute and 15-minute groups: 45 minutes of pre-breathe was the minimum amount needed to effectively prevent against DON in DISSUB escape at 33 fsw. However, future research is needed to determine how to calculate effective dosages of O2 pre-breathe to prevent DON in any given scenario., Competing Interests: The authors of this paper declare no conflicts of interest exist with this submission., (Copyright© Undersea and Hyperbaric Medical Society.)

Background: The treatment of decompression sickness (DCS) with hyperbaric oxygen (HBO2) serves to decrease intravascular bubble size, increase oxygen (O2) delivery to tissue and enhance the elimination of inert gas. Emulsified perfluorocarbons (PFC) combined with breathing O2 have been shown to have similar effects animal models. We studied an ovine model of severe DCS treated with the intravenous PFC Oxycyte™ while breathing O2 compared to saline control also breathing O2., Methods: Juvenile male sheep (N=67; weight 24.4±2.10kg) were compressed to 257 feet of sea water (fsw) in our multiple large-animal chamber where they remained under pressure for 31 minutes. Animals then were decompressed to surface pressure and randomized to receive either Oxycyte at 5mL/kg intravenously (IV) or 5mL/kg saline IV (both receiving 100% O2) 10 minutes after reaching surface pressure. Mortality was recorded at two hours, four hours, and 24 hours after receiving the study drug. Surviving animals underwent perfusion fixation and harvesting of the spinal cord at 24 hours. Spinal cord sections were assessed for volume of lesion area and compared., Results: There was no significant difference in survival at two hours (p=0.2737), four hours (p=0.2101), or 24 hours (p=0.3171). Paralysis at 24 hours was not significantly different. However, spinal cord lesion area was significantly smaller in the Oxycyte group as compared to the saline group, with median spinal cord lesion areas 0.65% vs. 0.94% (p=0.0107)., Conclusion: In this ovine model of severe DCS the intravenous PFC Oxycyte did not reduce mortality but did ameliorate spinal cord injury when used after the onset of DCS., Competing Interests: The authors of this paper declare no conflicts of interest exist with this submission., (Copyright© Undersea and Hyperbaric Medical Society.)

Massive bubble formation after diving can lead to decompression sickness (DCS), which can result in neurological disorders. We demonstrated that hydrogen production from intestinal fermentation could exacerbate DCS in rats fed with a standard diet. The aim of this study is to identify a fecal metabolomic signature that may result from the effects of a provocative hyperbaric exposure. The fecal metabolome was studied in two groups of rats previously fed with maize or soy in order to account for diet effects. 64 animals, weighing 379.0&#95;20.2 g on the day of the dive, were exposed to the hyperbaric protocol. The rats were separated into two groups: 32 fed with maize (Div MAIZE) and 32 fed with soy (Div SOY). Gut fermentation before the dive was estimated by measuring exhaled hydrogen. Following hyperbaric exposure, we assessed for signs of DCS. Blood was analyzed to assay inflammatory cytokines. Conventional and ChemRICH approaches helped the metabolomic interpretation of the cecal content. The effect of the diet is very marked at the metabolomic level, a little less in the blood tests, without this appearing strictly in the clinic status. Nevertheless, 37 of the 184 metabolites analyzed are linked to clinical status. 35 over-expressed compounds let suggest less intestinal absorption, possibly accompanied by an alteration of the gut microbial community, in DCS. The decrease in another metabolite suggests hepatic impairment. This spectral difference of the ceca metabolomes deserves to be studied in order to check if it corresponds to functional microbial particularities.

Massive vascular gas embolism is a feared and often lethal symptom of decompression illness, resulting from diving accidents. The aim of this case report was to correlate post-mortem computed tomography scan (PMCT) findings with autopsy in cases of massive vascular gas embolism. Two cases of fatal diving accidents were retrospectively selected from a forensic radiological pathological database. The PMCT results were initially shared with the forensic pathologist prior to autopsy, enabling a more accurate overall assessment. Both cases were in retrospect thoroughly studied to compare the PMCT findings with the autopsy results. In general, intra- and extra-vascular gas collections are easily detected on PMCT in all body regions. We focused on abundant intravascular gas collections, mainly in the large brain vessels. General autopsy findings are described in both cases, and in one case we elaborate on specific intracerebral changes found at autopsy. Both cases were diagnosed as pulmonary barotrauma with subsequent vascular gas embolisms. We conclude that PMCT excels in the detection of macroscopic gas collections in the body, whereas microscopic gas collections identified at autopsy aid in the differentiation between decompression sickness and pulmonary barotrauma followed by vascular gas embolism. The presented cases highlight the advantages of using both PMCT and autopsy in the post-mortem evaluation of fatal diving accidents.

Introduction: 122,129 dives by 10,358 recreational divers were recorded by dive computers from 11 manufacturers in an exploratory study of how dive profile, breathing gas (air or nitrox [N2/O2] mixes), repetitive diving, gender, age, and dive site conditions influenced observed decompression sickness (DCSobs). Thirty-eight reports were judged as DCS. Overall DCSobs was 3.1 cases/10⁴ dives., Methods: Three dive groups were studied: Basic (live-aboard and shore/dayboat), Cozumel Dive Guides, and Scapa Flow wreck divers. A probabilistic decompression model, BVM(3), controlled dive profile variability. Chi-squared test, t-test, logistic regression, and log-rank tests evaluated statistical associations., Results: (a) DCSobs was 0.7/10⁴ (Basic), 7.6/10⁴ (Guides), and 17.3/104 (Scapa) and differed after control for dive variability (p ≺ 0.001). (b) DCSobs was greater for 22%-29% nitrox (12.6/10⁴) than for 30%-50% nitrox (2.04/10⁴) (p ≤ 0.0064) which did not differ from air (2.97/1010⁴). (c) For daily repetitive dives (≺12-hour surface intervals (SI)), DCS occurred only following one or two dives (4.3/1010⁴ DCSobs; p ≺ 0.001) where SIs were shorter than after three or more dives. (d) For multiday repetitive dives (SIs ≺ 48 hours), DCS was associated with high multiday repetitive dive counts only for Guides (p = 0.0018). (e) DCSobs decreased with age at 3%/year (p ≤ 0.0144). (f) Males dived deeper (p ≺ 0.001) but for less time than females (p ≺ 0.001)., Conclusion: Collecting dive profiles with dive computers and controlling for profile variability by probabilistic modeling was feasible, but analytical results require independent confirmation due to limited observed DCS. Future studies appear promising if more DCS cases are gathered, stakeholders cooperate, and identified data collection problems are corrected., Competing Interests: The authors of this paper declare no conflicts of interest exist with this submission., (Copyright© Undersea and Hyperbaric Medical Society.)

A professional 55-year-old female experienced diver, who surfaced after the second dive, had a lucid interval before dropping Glasgow Coma Scale (GCS) to 3/15. She was admitted to intensive care unit and commenced on hyperbaric oxygen therapy. Her initial computed tomography of the head was normal but her magnetic resonance imaging of the brain at 48 hours showed extensive bilateral cortical watershed territory infarcts. She developed acute respiratory distress syndrome which resolved within a few days. Her GCS gradually improved from 3/15 to 6/15, was repatriated to United Kingdom after about 2 weeks of the insult and admitted to a tertiary care hospital where she had myoclonic seizures and was started on anti-epileptics. Then she was transferred to the Rehabilitation Medicine Ward of Leicester General Hospital, with GCS 14/15 with poor sitting balance, for her management and rehabilitation. She had weakness of right upper and lower limbs, dysarthria, neuropathic bilateral shoulder pains, pressure ulcer of left heel, bladder and bowel incontinence and cognitive issues. She improved to have significant neurological recovery within next 3 months, became ambulant independently and bladder and bowel continent. Her Barthel index (from 4 to 17), Montreal Cognitive Assessment Test, Adembrook Cognitive Examination and Berg Balance scale (from 33/56 to 44/56) improved significantly. Early diagnosis, treatment and rehabilitation can have a significant impact on the recovery of decompression illness.

Gas can enter arteries (arterial gas embolism, AGE) due to alveolar-capillary disruption (caused by pulmonary over-pressurization, e.g. breath-hold ascent by divers) or veins (venous gas embolism, VGE) as a result of tissue bubble formation due to decompression (diving, altitude exposure) or during certain surgical procedures where capillary hydrostatic pressure at the incision site is subatmospheric. Both AGE and VGE can be caused by iatrogenic gas injection. AGE usually produces stroke-like manifestations, such as impaired consciousness, confusion, seizures and focal neurological deficits. Small amounts of VGE are often tolerated due to filtration by pulmonary capillaries; however VGE can cause pulmonary edema, cardiac "vapor lock" and AGE due to transpulmonary passage or right-to-left shunt through a patient foramen ovale. Intravascular gas can cause arterial obstruction or endothelial damage and secondary vasospasm and capillary leak. Vascular gas is frequently not visible with radiographic imaging, which should not be used to exclude the diagnosis of AGE. Isolated VGE usually requires no treatment; AGE treatment is similar to decompression sickness (DCS), with first aid oxygen then hyperbaric oxygen. Although cerebral AGE (CAGE) often causes intracranial hypertension, animal studies have failed to demonstrate a benefit of induced hypocapnia. An evidence based review of adjunctive therapies is presented., Competing Interests: The author of this paper declares no conflicts of interest exist with this submission., (Copyright© Undersea and Hyperbaric Medical Society.)

Background: Decompression sickness (DCS) primarily manifests musculoskeletal pain, cutaneous manifestations, lymphatic symptoms, and neurological symptoms. DCS might affect the central nervous system and induce the stress in the patients, but few studies about the psychiatric morbidity after DCS have been conducted. This study aimed to investigate the association between DCS and the risk of developing psychiatric disorders., Subjects and Methods: This study was a population-based, matched-cohort design. A total of 738 enrolled patients, with 123 study subjects who had suffered from DCS, and 615 controls matched for sex and age, from the Longitudinal Health Insurance Databank from 2000-2010 in Taiwan, and selected from the National Health Insurance Research Database. After adjusting for the confounding factors, Cox proportional hazards analysis was used to compare the risk of developing psychiatric disorders during the 10 years of follow-up period., Results: Of the study subjects, 10 (8.13%) developed psychiatric disorders when compared to 35 (5.69%) in the control group. The study subjects were more likely to develop psychiatric disorders (crude hazard ratio [HR]: 2.79 (95% CI=1.37-5.69, P<0.01). After adjusting for sex, age, monthly income, urbanization level, geographic region, and comorbidities, the adjusted HR was 3.83 (95% CI=1.60-9.16, P<0.01). Sleep disorders was associated with DCS with the adjusted HR as 5.74 (95% CI=1.04-31.56, P<0.01). Hyperbaric oxygenation therapy was not associated with a lower risk of psychiatric disorders., Conclusions: Patients who suffered from DCS have a 3.8-fold risk of developing psychiatric disorders, and a 5.7-fold risk of sleep disorders. This finding is a reminder for the clinicians that a regular psychiatric follow-up might well be needed for these patients.

A 39-year-old male commercial diver developed cutis marmorata after a dive. He had a full recovery after therapy in a hyperbaric oxygen chamber. Transthoracic echocardiography revealed an atrial septal aneurysm and a large shunt during normal respirations. This form of decompression sickness may progress to type II DCS, thus is important to identify and treat. Cutis marmorata as a result of diving is highly associated with an atrial septal defect or a large patent foramen ovale. It is particularly important to assess these patients for a right-to-left shunt as part of a medical evaluation prior to returning to diving., (© 2019 Wiley Periodicals, Inc.)

Diving as a method of fishing is used worldwide in small-scale fisheries. However, one of the main causes of morbidity and mortality among fishermen is decompression sickness (DCS). We report the case of a 46-year-old male fisherman diver who presented with chronic inguinal pain that radiated to the lower left limb. Living and working in a fishing port in Yucatan, he had a prior history of DCS. A diagnosis of avascular necrosis in the left femoral head secondary to DCS was made via analysis of clinical and radiological findings. The necrosis was surgically resolved by a total hip arthroplasty. Dysbaric osteonecrosis is a more probable diagnosis. In this region fishermen undergo significant decompression stress in their daily fishing efforts. Further studies regarding prevalence of dysbaric osteonecrosis among small-scale fisheries divers are needed. In a community where DCS is endemic and has become an epidemic, as of late, the perception of this health risk remains low. Furthermore, training and decompression technique are lacking among the fishing communities., Competing Interests: The authors of this paper declare no conflicts of interest exist with this submission., (Copyright© Undersea and Hyperbaric Medical Society.)

Background: Capillary leak syndrome is a rare type of decompression sickness (DCS) that may be responsible for hypovolemic shock with edema., Clinical Case: A 21-year-old amateur diver suffered from an inner ear DCS following air diving to 96msw. He presented subsequent deterioration with hypovolemia and facial edema secondary to capillary leak syndrome., Discussion: In DCS, bubbles formation alters the wall of blood vessels and activates complex biochemical mechanisms inducing extravascular protein leakage. The clinical expression of this syndrome is variable, ranging from simple hemoconcentration to hypovolemic shock. Close clinical-biological monitoring of patients with elevated hematocrit with or without hypoalbuminemia is advisable. Early vascular filling with albumin infusion may prevent the occurrence of hypovolemic shock and improve the prognosis., (Copyright © 2018 Société Nationale Française de Médecine Interne (SNFMI). Published by Elsevier Masson SAS. All rights reserved.)

Decompression sickness is a disease caused by abrupt pressure change and presents various symptoms. To date, acute kidney injury associated with decompression sickness has been reported frequently, but there is no report of hepatic infarction associated with decompression sickness. We report a case of acute kidney injury and acute hepatic infarction treated with hyperbaric oxygen (HBO2) therapy and dialysis in a patient with severe decompression sickness after work diving., Competing Interests: The authors of this paper declare no conflicts of interest exist with this submission., (Copyright© Undersea and Hyperbaric Medical Society.)

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.

Severe decompression illness (DCI) is an uncommon medical issue affecting divers and results mainly from rapid surfacing using inadequate decompression protocols. Massive gas embolism with central nervous system involvement often leads to a poor prognosis, with permanent residual neurologic defects. Moreover, DCI complicated with multiple organ dysfunction syndrome (MODS) is tremendously rare and difficult to cure, although hyperbaric oxygen (HBO2) therapy following the U.S. Navy Treatment Tables is a consensus. We report a case of severe DCI with profound shock and MODS after an initial treatment with HBO2 therapy using U.S. Navy Treatment Table 6A. Following the Surviving Sepsis Campaign Guidelines, low-dose hydrocortisone was administered. Although this treatment went against recommendation of the U.S. Navy Diving Manual, it resulted in a dramatic clinical improvement. After a second round of HBO2 treatments, the patient was discharged from hospital two weeks after the diving accident., Competing Interests: The authors of this paper declare no conflicts of interest exist with this submission., (Copyright© Undersea and Hyperbaric Medical Society.)