A novel method for tracking nitrogen kinetics in vivo under hyperbaric conditions using radioactive nitrogen-13 gas and positron emission tomography.

Decompression sickness (DCS) is caused by gaseous nitrogen dissolved in tissues forming bubbles during decompression. To date, no method exists to identify nitrogen within tissues, but with advances in positron-emission tomography (PET) technology, it may be possible to track gaseous radionuclides into tissues. We aimed to develop a method to track nitrogen movement in vivo and under hyperbaric pressure that could then be used to further our understanding of DCS using nitrogen-13 (13N2). A single anesthetized female Sprague-Dawley rat was exposed to 625 kPa, composed of air, isoflurane, and 13N2 for 10 min. The PET scanner recorded 13N2 during the hyperbaric exposure with energy windows of 250-750 keV. The PET showed an increase in 13N2 concentration in the lung, heart, and abdominal regions, which all reached a plateau after ∼4 min. This showed that it is possible to gain noninvasive in vivo measurements of nitrogen kinetics through the body while at hyperbaric pressures. Tissue samples showed radioactivity above background levels in the blood, brain, liver, femur, and thigh muscle when assessed using a γ counter. The method can be used to evaluate an array of challenges to our understanding of decompression physiology by quantifying nitrogen load through γ counts of 13N2, and signal intensity of the PET. Further development of the method will improve the specificity of the measured outcomes, and enable it to be used with larger mammals, including humans.NEW & NOTEWORTHY This article describes a method for the in vivo quantification and tracking of nitrogen through the mammalian body whilst exposed to hyperbaric pressure. The method has the potential to further our understanding of decompression sickness, and quantitatively evaluate the effectiveness of both the treatment and prevention of decompression sickness.

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.

Hyperbaric treatment deviations for U.S. Navy divers: Spinal DCS.

Introduction: The United States Navy (USN) developed and refined standardized oxygen treatment tables for diving injuries, but USN tables may not address all situations of spinal decompression sickness (DCS). We describe a detailed recompression treatment regimen that deviated from standard USN protocol for an active-duty USN diver with a severe, delayed presentation of spinal cord DCS. Case Report: A USN diver surfaced from his second of three dives on a standard Navy 'no-Decompression' Air SCUBA dive (Max depth 101 fsw utilizing a Navy Dive Computer) and developed mid-thoracic back pain, intense nausea, paresthesias of bilateral feet, and penile erection. Either not recognizing the con- stellation of symptoms as DCS and after resolution of the aforementioned symptoms, he completed the third planned dive (essentially an in-water recompression). Several hours later, he developed paresthesias and numbness of bilateral feet and legs and bowel incontinence. He presented for hyperbaric treatment twenty hours after surfacing from the final dive and was diagnosed with severe spinal DCS. Based on the severity of clinical presentation and delay to treatment, the initial and follow-on treatments were modified from standard USN protocol. MRI of the spine four days after initial presentation demonstrated a 2.2 cm lesion at the T4 vertebral level extending caudally. Follow-up examinations over two years demonstrated almost complete return of motor and sensory function; however, the patient continued to suffer fecal incontinence and demonstrated an abnormal post-void residual urinary volume. An atypical presenting symptom, a discussion of MRI findings, and clinical correlations to the syndrome of spinal DCS are discussed throughout treatment and long-term recovery of the patient.

A retrospective review of divers treated for inner ear decompression sickness at Fiona Stanley Hospital hyperbaric medicine unit 2014-2020.

Introduction: Inner ear decompression sickness (IEDCS) is increasingly recognised in recreational diving, with the inner ear particularly vulnerable to decompression sickness in divers with a right-to-left shunt, such as is possible through a persistent (patent) foramen ovale (PFO). A review of patients treated for IEDCS at Fiona Stanley Hospital Hyperbaric Medicine Unit (FSH HMU) in Western Australia was performed to examine the epidemiology, risk factors for developing this condition, the treatment administered and the outcomes of this patient population. Methods: A retrospective review of all divers treated for IEDCS from the opening of the FSH HMU on 17 November 2014 to 31 December 2020 was performed. Patients were included if presenting with vestibular or cochlear dysfunction within 24 hours of surfacing from a dive, and excluded if demonstrating features of inner ear barotrauma. Results: There were a total of 23 IEDCS patients and 24 cases of IEDCS included for analysis, with 88% experiencing vestibular manifestations and 38% cochlear. Median dive time was 40 minutes and median maximum depth was 24.5 metres. The median time from surfacing to hyperbaric oxygen treatment (HBOT) was 22 hours. Vestibulocochlear symptoms fully resolved in 67% and complete symptom recovery was achieved in 58%. A PFO was found in 6 of 10 patients who subsequently underwent investigation with bubble contrast echocardiography upon follow-up. Conclusions: IEDCS occurred predominantly after non-technical repetitive air dives and ongoing symptoms and signs were often observed after HBOT. Appropriate follow-up is required given the high prevalence of PFO in these patients.

Aviation Decompression Sickness in Aerospace and Hyperbaric Medicine.

INTRODUCTION: The U.S. Navy experienced a series of physiological events in aircrew involving primarily the F/A-18 airframe related to rapid decompression of cabin pressures, of which aviation decompression sickness (DCS) was felt to contribute. The underlying pathophysiology of aviation DCS is the same as that of diving-related. However, based on the innate multifactorial circumstances surrounding hypobaric DCS, in clinical practice it continues to be unpredictable and less familiar as it falls at the intersect of aerospace and hyperbaric medicine. This retrospective study aimed to review the case series diagnosed as aviation DCS in a collaborative effort between aerospace specialists and hyperbaricists to increase appropriate identification and treatment of hypobaric DCS.METHODS: We identified 18 cases involving high-performance aircraft emergently treated as aviation DCS at a civilian hyperbaric chamber. Four reviewers with dual training in aviation and hyperbaric medicine retrospectively reviewed cases and categorized presentations as "DCS" or "Alternative Diagnosis".RESULTS: Reviewers identified over half of presenting cases could be attributed to an alternative diagnosis. In events that occurred at flight altitudes below 17,000 ft (5182 m) or with rapid decompression pressure changes under 0.3 atm, DCS was less likely to be the etiology of the presenting symptoms.CONCLUSIONS: Aviation physiological events continue to be difficult to diagnose. This study aimed to better understand this phenomenon and provide additional insight and key characteristics for both flight physicians and hyperbaric physicians. As human exploration continues to challenge the limits of sustainable physiology, the incidence of aerospace DCS may increase and underscores our need to recognize and appropriately treat it.Kutz CJ, Kirby IJ, Grover IR, Tanaka HL. Aviation decompression sickness in aerospace and hyperbaric medicine. Aerosp Med Hum Perform. 2023; 94(1):11-17.

Delayed treatment for decompression illness: factors associated with long treatment delays and treatment outcome.

INTRODUCTION: Effectiveness of delayed hyperbaric oxygen treatment (HBOT) for decompression illness (DCI) and factors affecting treatment delays have not been studied in large groups of patients. METHODS: This retrospective study included 546 DCI patients treated in Finland in the years 1999-2018 and investigated factors associated with recompression delay and outcome. Treatment outcome was defined as fully recovered or presence of residual symptoms on completion of HBOT. The symptoms, use of first aid oxygen, number of recompression treatments needed and characteristics of the study cohort were also addressed. RESULTS: Delayed HBOT (> 48 h) remained effective with final outcomes similar to those treated within 48 h. Cardio-pulmonary symptoms were associated with a shorter treatment delay (median 15 h vs 28 h without cardiopulmonary symptoms, P < 0.001), whereas mild sensory symptoms were associated with a longer delay (48 vs 24 h, P < 0.001). A shorter delay was also associated with only one required HBOT treatment (median 24 h vs 34 h for those requiring multiple recompressions) ( P = 0.002). Tinnitus and hearing impairment were associated with a higher proportion of incomplete recoveries (78 and 73% respectively, P < 0.001), whereas a smaller proportion of cases with tingling/itching (15%, P = 0.03), nausea (27%, P = 0.03), motor weakness (33%, P = 0.05) and visual disturbances (36%, P = 0.04) exhibited residual symptoms. Patients with severe symptoms had a significantly shorter delay than those with mild symptoms (median 24 h vs 36 h respectively, P < 0.001), and a lower incidence of complete recovery. CONCLUSIONS: Delayed HBOT remains an effective and useful intervention. A shorter delay to recompression is associated with fewer recompressions required to achieve recovery or recovery plateau.

Descriptive study of decompression illness in a hyperbaric medicine centre in Bangkok, Thailand from 2015 to 2021.

INTRODUCTION: This study aimed to determine the characteristics of decompression illness patients and their treatment outcomes, at the Center of Hyperbaric Medicine, Somdech Phra Pinklao Hospital, one of the largest centres in Thailand. METHODS: Past medical records of patients with decompression illness from 2015 to 2021 were retrieved and analysed. RESULTS: Ninety-eight records of diving-related illness from 97 divers were reviewed. Most of the divers were male (n = 50), Thai (n = 86), and were certified at least open water or equivalent (n = 88). On-site first aid oxygen inhalation was provided to 17 divers. Decompression sickness (DCS) cases were characterised according to organ systems involved. The most prominent organ system involved was neurological (57%), followed by mixed organs (28%), musculoskeletal (13%), and pulmonary (2%). There were three cases of arterial gas embolism (AGE). Median presentation delay was three days. Ninety patients were treated with US Navy Treatment Table 6. At the end of their hyperbaric oxygen treatment, most divers (65%) recovered completely. CONCLUSIONS: Despite oxygen first aid being given infrequently and long delays before definitive treatment, treatment outcome was satisfactory. Basic knowledge and awareness of diving-related illnesses should be promoted among divers and related personnel in Thailand along with further studies.

Comparison of treatment recompression tables for neurologic decompression illness in swine model.

BACKGROUND: Significant reductions in ambient pressure subject an individual to risk of decompression illness (DCI); with incidence up to 35 per 10,000 dives. In severe cases, the central nervous system is often compromised (>80%), making DCI among the most morbid of diving related injuries. While hyperbaric specialists suggest initiating recompression therapy with either a Treatment Table 6 (TT6) or 6A (TT6A), the optimal initial recompression treatment for severe DCI is unknown. METHODS: Swine were exposed to an insult dive breathing air at 7.06 ATA (715.35 kPa) for 24 min followed by rapid decompression at a rate of 1.82 ATA/min (184.41 kPa/min). Swine that developed neurologic DCI within 1 hour of surfacing were block randomized to one of four United States Navy Treatment Tables (USN TT): TT6, TT6A-air (21% oxygen, 79% nitrogen), TT6A-nitrox (50% oxygen, 50% nitrogen), and TT6A-heliox (50% oxygen, 50% helium). The primary outcome was the mean number of spinal cord lesions, which was analyzed following cord harvest 24 hours after successful recompression treatment. Secondary outcomes included spinal cord lesion incidence and gross neurologic outcomes based on a pre- and post- modified Tarlov assessment. We compared outcomes among these four groups and between the two treatment profiles (i.e. TT6 and TT6A). RESULTS: One-hundred and forty-one swine underwent the insult dive, with 61 swine meeting inclusion criteria (43%). We found no differences in baseline characteristics among the groups. We found no significant differences in functional neurologic outcomes (p = 0.77 and 0.33), spinal cord lesion incidence (p = 0.09 and 0.07), or spinal cord lesion area (p = 0.51 and 0.17) among the four treatment groups or between the two treatment profiles, respectively. While the trends were not statistically significant, animals treated with TT6 had the lowest rates of functional deficits and the fewest spinal cord lesions. Moreover, across all animals, functional neurologic deficit had strong correlation with lesion area pathology (Logistic Regression, p < 0.01, Somers' D = 0.74). CONCLUSIONS: TT6 performed as well as the other treatment tables and is the least resource intensive. TT6 is the most appropriate initial treatment for neurologic DCI in swine, among the tables that we compared.

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.

A prospective single-blind randomised clinical trial comparing two treatment tables for the initial management of mild decompression sickness.

INTRODUCTION: Limited evidence suggests that shorter recompression schedules may be as efficacious as the US Navy Treatment Table 6 (USN TT6) for treatment of milder presentations of decompression sickness (DCS). This study aimed to determine if divers with mild DCS could be effectively treated with a shorter chamber treatment table. METHODS: All patients presenting to the Fremantle Hospital Hyperbaric Medicine Unit with suspected DCS were assessed for inclusion. Participants with mild DCS were randomly allocated to receive recompression in a monoplace chamber via either a modified USN TT6 (TT6m) or a shorter, custom treatment table (FH01). The primary outcome was the number of treatments required until resolution or no further improvement (plateau). RESULTS: Forty-one DCS cases were included, 21 TT6m and 20 FH01. Two patients allocated to FH01 were moved to TT6m mid-treatment due to failure to significantly improve (as per protocol), and two TT6m required extensions. The median total number of treatments till symptom resolution was 1 (IQR 1-1) for FH01 and 2 (IQR 1-2) for TT6m (P = 0.01). More patients in the FH01 arm (17/20, 85%) showed complete symptom resolution after the initial treatment, versus 8/21 (38%) for TT6m (P = 0.003). Both FH01 and TT6m had similar overall outcomes, with 19/20 and 20/21 respectively asymptomatic at the completion of their final treatment (P = 0.97). In all cases where two-week follow-up contact was made, (n = 14 FH01 and n = 12 TT6m), patients reported maintaining full symptom resolution. CONCLUSIONS: The median total number of treatments till symptom resolution was meaningfully fewer with FH01 and the shorter treatment more frequently resulted in complete symptom resolution after the initial treatment. There were similar patient outcomes at treatment completion, and at follow-up. We conclude that FH01 appears superior to TT6m for the treatment of mild decompression sickness.

Decompression Illness Treated with the Hart-Kindwall Protocol in a Monoplace Chamber.

BACKGROUND Hyperbaric oxygen (HBO2) therapy in a multiplace chamber is the standard treatment for severe altitude decompression illness (DCI). However, some hospitals may only have a monoplace chamber. Herein, we present the case of a patient with severe altitude DCI caused by rapid decompression during an actual flight operation that was successfully treated through emergency HBO2 therapy with the Hart-Kindwall protocol, a no-air-break tables with the minimal-pressure oxygen approach in a monoplace chamber due to unavailability of rapid access to a multiplace chamber. CASE REPORT A 34-year-old male aviator presented with chest pain, paresthesia, and mild cognitive impairment following rapid decompression 20 minutes after take-off, which comprised 10 minutes of reaching a height of 10 058 m (33 000 feet) and 10 minutes of cruising at that altitude. He then initiated flight descent and landing. He visited a primary clinic, and severe DCI was suggested clinically. However, since the closest hospital with a multiplace chamber was a 3-hour drive away, we provided emergency HBO2 therapy with the Hart-Kindwall protocol in a monoplace chamber at a nearby hospital 4 hours after the initial decompression. He recovered fully and returned to flight duty 2 weeks later. CONCLUSIONS Emergency HBO2 therapy with the Hart-Kindwall protocol in a monoplace chamber may be a suitable option for severe DCI, especially in remote locations with no access to facilities with a multiplace chamber. However, prior logistical coordination must be established to transfer patients to hospitals with multiplace chambers if their symptoms do not resolve.

Exceptional survival of an airplane stowaway, treated successfully with hyperbaric oxygen.

Survival of airplane stowaways is rare. Here we report an exceptional case of successful treatment and full recovery. After a transcontinental flight an unconscious stowaway was discovered in a wheel well of a Boeing 747-400F. Airport paramedics confirmed regular respiration and achieved 100% oxygen saturation (pulse oximetry) by high-flow oxygen. Rectal body temperature was 35.5 °C. On arrival at the emergency department, the patient's vital signs were stable. He did not respond to verbal stimuli. He localized to painful stimuli with both arms, however, there was no reaction to stimuli to both legs. We suspected his neurological deficits were caused by posthypoxic encephalopathy or altitude decompression sickness (DCS), the latter amenable to hyperbaric oxygen therapy (HBOT). HBOT was performed for 5 h (US Navy Treatment Table 6) and afterwards, full neurological recovery was documented. About 24 h after admission a new proximal paresis of the left leg was noted. Assuming recurrence of DCS, daily HBOT was scheduled for three days, after which motor function had again returned to normal. Stowaways travelling in airplane wheel wells experience extreme environmental circumstances. The presented patient survived an eight-hour exposure to calculated barometric pressures as low as 190 mmHg and ambient PO2 of 40 mmHg. Apart from creating awareness of this rare patient category, we want to stress the risk of altitude DCS in unpressurized flights. When DCS is suspected, immediate high-flow oxygen therapy should be initiated, followed by HBOT at the earliest opportunity.

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.

Dysbarism: An Overview of an Unusual Medical Emergency.

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.

Inner ear decompression sickness in a hyperbaric chamber inside tender: a case report.

Inner ear decompression sickness (IEDCS) is a rare diving complication that presents with vestibular dysfunction, cochlear dysfunction, or a combination of both. While scuba diving is a known cause, no cases have been reported in the occupational hyperbaric setting. We present the case of a 55-year-old man who developed IEDCS after working as a hyperbaric multiplace chamber inside tender. The patient was treated with seven sessions of hyperbaric oxygen therapy, resulting in resolution of the majority of his symptoms. This case illustrates a potential occupational hazard of working in a hyperbaric chamber and demonstrates successful treatment with hyperbaric oxygen therapy.

Effects of hyperbaric oxygen pretreatment on brain antioxidant capacity in rats with decompression sickness.

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.

Pulmonary barotrauma with cerebral arterial gas embolism from a depth of 0.75-1.2 metres of fresh water or less: A case report.

During underwater vehicle escape training with compressed air, a fit 26-year-old soldier suffered pulmonary barotrauma with cerebral arterial gas embolism after surfacing from a depth of 0.75-1.2 metres of freshwater or less. She presented with an altered level of consciousness. Rapid neurological examination noted slurred speech, a sensory deficit and right hemiparesis. Eleven hours after the accident, hyperbaric oxygen treatment was initiated using US Navy Treatment Table 6. The soldier almost completely recovered after repeated hyperbaric oxygen treatment. Given the very shallow depth this is an unusual case with only two similar case reports published previously.

[What is the Best Therapeutic Strategy for Decompression Illness? First Aid Oxygen Inhalation and Hyperbaric Oxygen Therapy].

Decompression illness (DCI), a syndrome following inadequate reduction in environmental pressure, has two forms: decompression sickness and arterial gas embolism after pulmonary barotrauma. Recompression therapy using oxygen, a kind of hyperbaric oxygen therapy, has been considered the gold standard treatment for DCI, although there is no randomized controlled trial evidence for its use. We evaluated the effectiveness of recompression therapy in treating DCI by reviewing the reported therapeutic results of serious DCI, especially neurological disorders. Early or ultra-early recompression therapy did not dramatically improve clinical recovery from DCI symptoms, including spinal cord disorders. In contrast, early first aid normobaric oxygen inhalation highly improved or stabilized clinical conditions of DCI. Based on these clinical results, the international committee for hyperbaric and diving medicine has stated that cases of mild DCI may be managed without recompression therapy. Further work is needed to clarify the clinical utility of recompression therapy for spinal injury as a common symptom of DCI. We also point out that the Japanese decree "Ordinance on Safety and Health of Work under High Pressure", which describes work under hyperbaric environments, has some serious issues and should be amended on the basis of scientific evidence.

[A case of decompression sickness complicated with multiple organ failure treated by hyperbaric oxygen therapy sequential with continuous renal replacement therapy and extracorporeal membrane oxygenation].

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.