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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.

We report a randomized trial examining adjunctive administration of the NSAID, tenoxicam, to divers suffering with DCI. 180 subjects were graded for severity on admission and randomized according to a stratified random number schedule. Subjects were recompressed and treatment continued daily until symptom stabilization or complete resolution. Tenoxicam 20 mg or a placebo preparation was administered at the first air break during the initial recompression and continued daily for seven days. The subjects were assessed using a recovery status score at the completion of treatment and at 4-6 weeks. The proportion of patients with mild residual symptoms at discharge and final follow-up was not significantly different (discharge placebo 30% versus tenoxicam 37%, P=0.41; six weeks placebo 20% versus tenoxicam 17%, P=0.58). There was a significant reduction in the number of treatments required to achieve discharge (median treatments placebo 3, tenoxicam 2, P=0.01). 61% of patients in the tenoxicam group required less than 3 compressions, versus 40% in the placebo group (P=0.01, RRR 33 % [95%CI 9%-56%], NNT=5 [95%CI 3-18]). There was no evidence of increased complications of treatment in the tenoxicam group. When given this NSAID, patients with DCI require fewer hyperbaric oxygen (HBO2) sessions to achieve a standard clinical end-point and there is likely to be an associated cost saving.

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.

Hyperbaric oxygen therapy refers to inhalation of pure oxygen in a closed chamber. Hyperbaric oxygen has a therapeutic effect in numerous pathological conditions, such as decompression sickness, arterial gas embolism, carbon monoxide poisoning and smoke inhalation, osteomylitis, osteoradionecrosis and wound healing. Hyperbaric oxygen therapy is used for treating underlying hypoxia. This review indicates the action of hyperbaric oxygen on biochemical and various physiological changes in cellular level. Narrative review covers the current indications and contraindications of hyperbaric oxygen therapy. The review also focuses on the therapeutic effects of hyperbaric oxygen pretreatment and precondition in different pathological conditions. The complications and side effects of hyperbaric oxygen therapy are discussed.

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.

Most cases of decompression sickness (DCS) occur soon after surfacing, with 98% within 24 hours. Recompression using hyperbaric chamber should be administrated as soon as feasible in order to decrease bubble size and avoid further tissue injury. Unfortunately, there may be a significant time delay from surfacing to recompression. The time beyond which hyperbaric treatment is non effective is unclear. The aims of the study were first to evaluate the effect of delayed hyperbaric treatment, initiated more than 48 h after surfacing for DCS and second, to evaluate the different treatment protocols. From January 2000 to February 2014, 76 divers had delayed hyperbaric treatment (≥48 h) for DCS in the Sagol center for Hyperbaric medicine and Research, Assaf-Harofeh Medical Center, Israel. Data were collected from their medical records and compared to data of 128 patients treated earlier than 48 h after surfacing at the same hyperbaric institute. There was no significant difference, as to any of the baseline characteristics, between the delayed and early treatment groups. With respect to treatment results, at the delayed treatment divers, complete recovery was achieved in 76% of the divers, partial recovery in 17.1% and no improvement in 6.6%. Similar results were achieved when treatment started early, where 78% of the divers had complete recovery, 15.6% partial recovery and 6.2% no recovery. Delayed hyperbaric treatment using US Navy Table 6 protocol trended toward a better clinical outcome yet not statistically significant (OR=2.786, CI95%[0.896-8.66], p=0.07) compared to standard hyperbaric oxygen therapy of 90 minutes at 2 ATA, irrespective of the symptoms severity at presentation. Late recompression for DCS, 48 hours or more after surfacing, has clinical value and when applied can achieve complete recovery in 76% of the divers. It seems that the preferred hyperbaric treatment protocol should be based on US Navy Table 6.

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.

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.

Background Extracorporeal membrane oxygenation (ECMO) is increasingly being used for critically ill patients with cardiopulmonary failure. Air in the ECMO circuit is an emergency, a rare but fatal complication. Case presentation We introduce a case of a 76-year-old female who suffered from cardiac arrest complicated with severe trauma and was administered veno-arterial extracorporeal membrane oxygenation. In managing the patient with ECMO, air entered the ECMO circuit, which had not come out nor was folded or broken. Although the ECMO flow was quickly re-established, the patient died 6 h after initiating ECMO therapy. Conclusions In this case report, the reason for the complication is drainage insufficiency. This phenomenon is similar to decompression sickness. Understanding this complication is very helpful for educating the ECMO team for preventing this rare but devastating complication of fatal decompression sickness in patients on ECMO.