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Decompression illness is caused by intravascular or extravascular bubbles that are formed as a result of reduction in environmental pressure (decompression). The term covers both arterial gas embolism, in which alveolar gas or venous gas emboli (via cardiac shunts or via pulmonary vessels) are introduced into the arterial circulation, and decompression sickness, which is caused by in-situ bubble formation from dissolved inert gas. Both syndromes can occur in divers, compressed air workers, aviators, and astronauts, but arterial gas embolism also arises from iatrogenic causes unrelated to decompression. Risk of decompression illness is affected by immersion, exercise, and heat or cold. Manifestations range from itching and minor pain to neurological symptoms, cardiac collapse, and death. First-aid treatment is 100% oxygen and definitive treatment is recompression to increased pressure, breathing 100% oxygen. Adjunctive treatment, including fluid administration and prophylaxis against venous thromboembolism in paralysed patients, is also recommended. Treatment is, in most cases, effective although residual deficits can remain in serious cases, even after several recompressions.

Decompression sickness is a fatal disease worldwide. Therefore, to find a prophylactic modality for decompression sickness is urgently required. Bone marrow derived mesenchymal stem cells exhibit effectiveness in antioxidant, anti-inflammation, and decrease cell death; while its effects on decompression sickness remains unclear. This study aimed to further investigate the mechanisms of decompression sickness induced lung injury, as well as effects of bone marrow derived mesenchymal stem cells on decompression sickness induced lung injury and explore the role of oxidative stress, inflammation and cell death play in this disease. The study involved Sprague-Dawley rats age at 8−10 weeks weighting 350 ± 10g. Acute lung injury was induced by decompression hyperbaric chamber. A dose of bone marrow derived mesenchymal stem cells (2 × 10 6 cells) was given to rats one day prior to the start of decompression. Lung injury severity was estimated by determining lung damage scores, pulmonary oxidative, inflammatory factors and cell death. In bone marrow derived mesenchymal stem cells treated rats, the morbidity and mortality of decompression markedly decreased. The increases of protein IL-1 and IL-6 in BALF and lung wet/dry ratio and lung injury score were alleviated. The ROS, CAT, SOD, and MDA activities and GSH levels were significant attenuated (P < 0.05). The pyroptosis and nerroptosis were significant mitigate (P < 0.05). Based on the results, bone marrow derived mesenchymal stem cells is an potential efficient and safe prophylactic modality protect rats from decompression induced acute lung injury.

SCUBA diving poses risks due to pressure changes during descent (compression) and ascent (decompression). Decompression sickness (DCS) occurs due to gas bubble formation as the pressure decreases, causing joint pain, numbness, dizziness, or even paralysis and death. Immediate treatment involves 100% oxygen to help eliminate inert gases and hyperbaric oxygen therapy (HBOT), which is essential to reduce gas emboli formation and inflammation, thus improving symptoms. We evaluated oxy-inflammation biomarkers in the saliva and urine of nine subjects pre- and post-technical dive on the Haven wreck (GE, Italy). A case of DCS occurred during the dive. The injured diver was treated immediately with O2 and transported to the hyperbaric center of “ASST Ospedale Ca Granda” in Milan. He was treated following the U.S. Navy Treatment Table 5 at 2.8 ATA and the day after with Table 15 at 2.4 ATA. Venous blood and urine samples were collected before and after each HBO treatment. Our study shows that dive increased oxy-inflammation biomarkers (ROS +126%; lipid peroxidation +23%; interleukins-6 +81%, -1β +19%, and TNFα +84%) and nitric oxide metabolites levels (+36%). HBOT after a DCS episode reduced oxidative stress, lowering the very high marker of lipid peroxidation (8-iso-PGF2α), and inhibited inflammatory interleukins. Overall, HBOT improved physiological responses in the diver affected by DCS.

Hydrostatic lung compression in diving marine mammals, with collapsing alveoli blocking gas exchange at depth, has been the main theoretical basis for limiting N2 uptake and avoiding gas emboli (GE) as they ascend. However, studies of beached and bycaught cetaceans and sea turtles imply that air-breathing marine vertebrates may, under unusual circumstances, develop GE that result in decompression sickness (DCS) symptoms. Theoretical modelling of tissue and blood gas dynamics of breath-hold divers suggests that changes in perfusion and blood flow distribution may also play a significant role. The results from the modelling work suggest that our current understanding of diving physiology in many species is poor, as the models predict blood and tissue N2 levels that would result in severe DCS symptoms (chokes, paralysis and death) in a large fraction of natural dive profiles. In this review, we combine published results from marine mammals and turtles to propose alternative mechanisms for how marine vertebrates control gas exchange in the lung, through management of the pulmonary distribution of alveolar ventilation () and cardiac output/lung perfusion (), varying the level of in different regions of the lung. Man-made disturbances, causing stress, could alter the mismatch level in the lung, resulting in an abnormally elevated uptake of N2, increasing the risk for GE. Our hypothesis provides avenues for new areas of research, offers an explanation for how sonar exposure may alter physiology causing GE and provides a new mechanism for how air-breathing marine vertebrates usually avoid the diving-related problems observed in human divers.

Abstract Exposure to the undersea environment has unique effects on normal physiology and can result in unique disorders that require an understanding of the effects of pressure and inert gas supersaturation on organ function and knowledge of the appropriate therapies, which can include recompression in a hyperbaric chamber. The effects of Boyle’s law result in changes in volume of gas-containing spaces when exposed to the increased pressure underwater. These effects can cause middle ear and sinus injury and lung barotrauma due to lung overexpansion during ascent from depth. Disorders related to diving have unique presentations, and an understanding of the high-pressure environment is needed to properly diagnose and manage these disorders. Breathing compressed air underwater results in increased dissolved inert gas in tissues and organs. On ascent after a diving exposure, the dissolved gas can achieve a supersaturated state and can form gas bubbles in blood and tissues, with resulting tissue and organ damage. Decompression sickness can involve the musculoskeletal system, skin, inner ear, brain, and spinal cord, with characteristic signs and symptoms. Usual therapy is recompression in a hyperbaric chamber following well-established protocols. Many recreational diving candidates seek medical clearance for diving, and healthcare providers must be knowledgeable of the environmental exposure and its effects on physiologic function to properly assess individuals for fitness to dive. This review provides a basis for understanding the diving environment and its accompanying disorders and provides a basis for assessment of fitness for diving.

To test the hypothesis whether enriched air nitrox (EAN) breathing during simulated diving reduces decompression stress when compared to compressed air breathing as assessed by intravascular bubble formation after decompression. Human volunteers underwent a first simulated dive breathing compressed air to include subjects prone to post-decompression venous gas bubbling. Twelve subjects prone to bubbling underwent a double-blind, randomized, cross-over trial including one simulated dive breathing compressed air, and one dive breathing EAN (36% O2) in a hyperbaric chamber, with identical diving profiles (28 msw for 55 minutes). Intravascular bubble formation was assessed after decompression using pulmonary artery pulsed Doppler. Twelve subjects showing high bubble production were included for the cross-over trial, and all completed the experimental protocol. In the randomized protocol, EAN significantly reduced the bubble score at all time points (cumulative bubble scores: 1 [0-3.5] vs. 8 [4.5-10]; P < 0.001). Three decompression incidents, all presenting as cutaneous itching, occurred in the air versus zero in the EAN group (P = 0.217). Weak correlations were observed between bubble scores and age or body mass index, respectively. EAN breathing markedly reduces venous gas bubble emboli after decompression in volunteers selected for susceptibility for intravascular bubble formation. When using similar diving profiles and avoiding oxygen toxicity limits, EAN increases safety of diving as compared to compressed air breathing. ISRCTN 31681480.

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.

Decompression illness (DCI) is a major concern in pressure-related activities. Due to its specific prerequisite conditions, DCI is rare in comparison with other illnesses and most physicians are inexperienced in treatment. In a fishery area in northern China, during the past decade, tens of thousands of divers engaged in seafood harvesting and thousands suffered from DCI. We established a hyperbaric facility there and treated the majority of the cases. A total of 5,278 DCI cases were admitted in our facility from February 2000 through December 2010 and treated using our recompression schedules. Cutaneous abnormalities, joint and muscular pain and neurological manifestations were three most common symptoms. The initial symptom occurred within 6 h after surfacing in 98.9% of cases, with an overall median latency of 62 min. The shorter the latent time, the more serious the symptoms would be (P<0.0001). Nine cases died before recompression and 5,269 were treated using four recompression schedules, with an overall effectiveness rate of 99.3%. The full recovery rate decreased with the increase of the delay from the onset of symptoms to the treatment (P<0.0001). DCI presents specific occurrence rules. Recompression should be administered as soon as possible and should never be abandoned irrespective of the delay. The recompression schedules used were effective and flexible for variety conditions of DCI.

Recent observations suggest that development of venous gas emboli (VGE) during high-altitude flying whilst breathing hyperoxic gas will be reduced by intermittent excursions to moderate altitude. The present study aimed to investigate if an early, single excursion from high to moderate altitude can be used as an in-flight means to reduce high-altitude decompression strain. Ten healthy men were investigated whilst breathing oxygen in a hypobaric chamber under two conditions, once during a 90-min continuous exposure to a simulated cabin altitude of 24,000 ft (High; H) and once during 10 min at 24,000 ft, followed by 30 min at 15,000 ft and by 80 min at 24,000 ft (high–low–high; H–L–H). VGE scores were assessed by cardiac ultrasound, using a 6-graded scale. In H, VGE increased throughout the course of the sojourn at 24,000 ft to attain peak value [median (range)] of 3 (2–4) at min 90, just prior to descent. In H–L–H, median VGE scores were 0 throughout the trial, except for at min 10, just prior to the excursion to 15,000 ft, whence the VGE score was 1.5 (0–3). Thus, an early, single excursion from high to moderate cabin altitude holds promise as an in-flight means to reduce the risk of altitude decompression sickness during long-duration high-altitude flying in aircraft with limited cabin pressurization. Presumably, such excursion acts by facilitating the gas exchange in decompression bubbles from a predomination of nitrogen to that of oxygen.

Medical hyperbaric sessions for Hyperbaric Oxygen Therapy, conducted at 2.4-2.5 ATA for 80 to 120 minutes, expose staff to increased risk of DCS due to the inhalation of compressed air, which increases gas solubility in body fluids as per Henry's Law. This study evaluates the incidence and risk factors of decompression sickness (DCS) among medical personnel in a hyperbaric centre over a 25-year period. Decompression sickness, characterized by gas bubble formation in tissues during planned decompression, was documented in 6 cases among 41,507 sessions. Symptoms varied from mild cutaneous to severe neurological manifestations, dependent on bubble size and location. Risk factors identified include age, physical condition, dehydration, and BMI. Preventative measures included adherence to decompression protocols, hydration, oxygen pre-breathing, and physical fitness maintenance. Despite these precautions, the occurrence of DCS underscores the inherent occupational risk faced by hyperbaric medical staff. The study advocates for stringent safety protocols and continuous monitoring to mitigate this risk.