Acute aortic dissection during scuba diving.

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.

Decompression sickness followed by diabetic ketoacidosis and sepsis shock: an unusual case report.

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 (HBO2) 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.

The Influence of Advanced Hyperbaric Medical Training on Arterial Gas Embolism Treatment.

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.

Rhabdomyolysis in McArdle disease caused by scuba diving.

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.

Atypical distally distributed cutis marmorata decompression sickness associated with unconventional use of thermal protection in a diver with persistent foramen ovale.

Cutis marmorata is a mottled, marbling, livedoid rash caused by vascular inflammation and congestion in cutaneous decompression sickness. It may occur during or after ascent due to the formation of bubbles from dissolved nitrogen accumulated throughout the dive. It is strongly associated with the presence of right to left shunts, particularly persistent (patent) foramen ovale (PFO). We report a case of cutis marmorata decompression sickness of an unusual pattern associated with unconventional use of thermal protection (a 'shorty' wetsuit worn over full suit) by a diver with a PFO. The patient also had neurological manifestations of decompression sickness. The distal lower limb pattern of involvement favours the hypothesis that cutis marmorata in humans is likely to be due to bubbles in the skin itself and/or adjacent tissues rather than cerebrally mediated.

Decompression Illness in Divers With or Without Patent Foramen Ovale : A Cohort Study.

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.

Systemic capillary leak syndrome secondary to decompression sickness.

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).

The risk of decompression illness in breath-hold divers: a systematic review.

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.

Dysbaric osteonecrosis in diving fisherman: a case report.

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.

Decompression sickness with incidental pulmonary cyst.

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.

Breath-Hold Diving-Related Decompression Sickness with Brain Involvement: From Neuroimaging to Pathophysiology.

Central nervous system involvement related to decompression sickness (DCS) is a very rare complication of breath-hold diving. So far, it has been postulated that repeated dives with short surface intervals represent a key factor in the development of breath-holding-related DCS. We report the case of a breath-hold diver who, after repeated immersion, developed DCS with brain involvement. After treatment in a hyperbaric chamber, there was a clinical improvement in the symptoms. Magnetic resonance imaging of the brain showed hyperintense lesions in long-time repetition sequences (FLAIR, T2WI) in the left frontal and right temporal lobes. Diffusion-weighted imaging (DWI) sequences and the apparent diffusion coefficient (ADC) map were characteristic of vasogenic edema, allowing us to exclude the ischemic nature of the process. These findings, together with the acute clinical presentation, the resolution of lesions in evolutionary radiological controls and the possible involvement of blood-brain barrier/endothelial dysfunction in DCS, could suggest a new form of posterior reversible encephalopathy syndrome (PRES)-like presentation of DCS. This would represent a novel mechanism to explain the pathophysiology of this entity. We conducted a literature review, analyzing the pathophysiological and neuroimaging characteristics of DCS in breath-hold diving based on a case of this rare disease.

Delayed recognition of Type II decompression sickness in a diver with chronic atrial fibrillation.

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.

High prevalence of patent foramen ovale in recreational to elite breath hold divers.

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%) (X2 (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.

Portal and Mesenteric Vein Thrombosis Associated with Decompression Sickness in a 48-Year-Old Deep Sea Self-Contained Underwater Breathing Apparatus (SCUBA) Diver.

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.

Long-term neurological sequelae after decompression sickness in retired professional divers.

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.

Implications of a patent foramen ovale for environmental physiology and pathophysiology: do we know the 'hole' story?

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.