Gas in Joints After Diving: Computed Tomography May Be Useful for Diagnosing Decompression Sickness.

A 26-y-old experienced scotoma scintillans after 59 min of scuba diving at a maximum depth of 26 m. After the patient smoked a cigarette, the scotoma scintillans ceased. However, he then developed a headache, general fatigue, and shoulder and elbow pain. He therefore called an ambulance. Based on the rules of the medical cooperative system for decompression sickness in Izu Peninsula, the fire department called a physician-staffed helicopter. After a physician checked the patient, his complaints remained aside from a low-grade fever. A portable ultrasound revealed bubbles in his inferior vena cava. Because of the risk of his being infected with COVID-19, he was transported to our hospital not by air evacuation but via ground ambulance staff while receiving a drip infusion of fluid and oxygen. After arriving at the hospital, his symptoms had almost subsided. Whole-body computed tomography revealed gas around the bladder, left hip, right knee, bilateral shoulder, joints, and right intramedullary humerus. The patient received high-concentration oxygen, infusion therapy, and observational admission. On the second day of admission, his symptoms had completely disappeared, and he was discharged. To our knowledge, this is the first report that computed tomography might be useful for detecting gas in multiple joints, suggesting the onset of decompression sickness after diving. This might be the first report of gas in an intramedullary space after diving as a potential cause of dysbaric osteonecrosis.

Massive gas embolisms in diving fatalities visualized by radiology and neuropathology.

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.

MRI of the central nervous system in rats following heliox saturation decompression.

AIMS: The main objectives of the present study was to establish an animal model of decompression sickness (DCS) after heliox saturation diving, and to use this model to evaluate possible morphological changes in the CNS induced by DCS using structural MRI. METHODS: Two groups of rats were pressurized with heliox to 5 bar (pO2 = 50 kPa). The saturation time was three hours; decompression rate was 1 bar/10 seconds or 1 bar/20 seconds. A 7.0 Tesla small animal MRI scanner was used for detection of possible morphological changes in the brain and spinal cord, two hours and one week after the dive, compared to one week prior to the dive. RESULTS: Neurological symptoms of DCS were observed in seven out of 10 animals. MRI of the brain and spinal cord did not reveal any morphological CNS injuries. CONCLUSION: This diving procedure was successful in causing DCS in a large proportion of the animals. However, despite massive neurological signs of DCS, no visible CNS injuries were observed in the MRI scans.

Expression changes of inflammatory factors in the rat lung of decompression sickness induced by fast buoyancy ascent escape.

Fast buoyancy ascent escape is one of the major naval submarine escape maneuvers. Decompression sickness (DCS) is the major bottleneck to increase the depth of fast buoyancy ascent escape. Rapid decompression induces the release of inflammatory mediators and results in tissue inflammation cascades and a protective anti-inflammatory response. In our previous study, we found that DCS caused by simulated fast buoyancy ascent escape could induce acute lung injury (ALI) and the expression changes of the proinflammatory cytokines: tumor necrosis factor alpha (TNF-α), interleukin (IL)-1ß and IL-6 in rat lung tissue. In order to study the expression change characteristics of TNF-α, IL-1ß, IL-6, IL-10 and IL-13 in the rat lung of DCS caused by simulated fast buoyancy ascent escape, we detected the rat lung mRNA and protein levels of TNF-α, IL-1ß, IL-6, IL-10 and IL-13 at 0.5 hour after DCS caused by simulated fast buoyancy ascent escape (fast escape group), compared with the normal control group (control group) and diving DCS (decompression group). We observed that DCS caused by simulated fast buoyancy ascent escape could increase the mRNA levels of TNF-α, IL-1ß, IL-6, IL-10, and the protein levels of TNF-α, IL-10 in rat lung tissue. At the same time, we found that the protein level of IL-13 was also downregulated in rat lung tissue. TNF-α, IL-10 and IL-13 may be involved in the process of the rat lung injury of DCS caused by simulated fast buoyancy ascent escape. In conclusion, the expression changes of inflammatory factors in the rat lung of DCS caused by simulated fast buoyancy ascent escape were probably different from that in the rat lung of diving DCS, which indicated that the pathological mechanism of DCS caused by simulated fast buoyancy ascent escape might be different from that of diving DCS.

Expression changes of TNF-α, IL-1ß and IL-6 in the rat lung of decompression sickness induced by fast buoyancy ascent escape.

Fast buoyancy ascent escape is the general submarine escape manner adopted by the majority of naval forces all over the world. However, if hyperbaric exposure time exceeds the time limit, fast buoyancy ascent escape has a high risk to result in decompression sickness (DCS). Tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß) and IL-6 have been all implicated in the process of inflammation associated with acute lung injury (ALI). Our work demonstrated that DCS caused by simulated fast buoyancy ascent escape could induce ALß in the rat model. The purpose of the present work was to study the expression changes of TNF-α, IL-1ß and IL-6 in the rat lung affected by DCS caused by simulated fast buoyancy ascent escape. The lung tissue mRNA levels of TNF-α, Il-1ß and Il-6 were significantly increased at 0.5 hour after DCS caused by simulated fast buoyancy ascent escape. The lung contents of TNF-α, IL-1ß and IL-6 were at an expression peak at 0.5 hour, although showing no statistical difference when compared with the normal control group. In conclusion, the rat lung expression variations of TNF-α, IL-1ß and IL-6 are the most obvious at 0.5 hour within 24 hours after the lung injury by DCS caused by simulated fast buoyancy ascent escape.

[Role of tumor necrosis factor-alpha in spinal cord injury of rabbits with decompression sickness].

OBJECTIVE: To observe the pathological changes in rabbits with spinal cord injury induced by decompression sickness (DCS), and to investigate the role of tumor necrosis factor-alpha (TNF-α) in spinal cord injury induced by DCS. METHODS: Rabbits were randomly divided into normal control group, DCS group, and safe decompression group. The rabbit model of DCS was established. Light microscopy, real-time PCR, and immunohistochemical method were used to observe the pathomorphological changes in the thoracolumbar spinal cord and the mRNA and protein expression of TNF-α, respectively. The terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) was used to observe the apoptosis in the spinal cord. RESULTS: In the DCS group, cavities formed in the white matter of spinal cord and gliosis occurred around necrotic areas. Moreover, the mRNA and protein expression of TNF-α was significantly higher in the DCS group than in the normal control group and the safe decompression group (P<0.01). The results of TUNEL showed that the number of positive apoptotic cells was significantly larger in the DCS group than in the normal control group and the safe decompression group (P<0.05). CONCLUSION: Apoptosis plays an important role in spinal cord injury induced by DCS. In the early stage of DCS, the massive release of TNF-α initiates apoptosis and contributes to the pathological changes in spinal cord injury induced by DCS.

Relation between cervical and thoracic spinal canal stenosis and the development of spinal cord decompression sickness in recreational scuba divers.

STUDY DESIGN: Retrospective case-control study. OBJECTIVES: The intent of this study was to investigate the relationships between vertebral degenerative changes resulting in spinal canal stenosis, spinal cord lesions and the development of spinal cord decompression sickness (DCS) in scuba divers. SETTING: Referral hyperbaric facility, Toulon, France. METHODS: We examined 33 injured divers less than 50 years old by cervical and thoracic MRI and compared them with 34 matched control divers. The number of intervertebral disk abnormalities and the degree of canal compression were analyzed on T2-weighted sagittal images using a validated grading system developed recently. The presence and the distribution of hyperintense cord lesions in relation with the accident and the recovery status at 6 months were also assessed. RESULTS: Canal spinal narrowing was more common in injured divers than in controls (79% vs. 50%, OR=3.7 [95% CI, 1.3-10.8], P=0.021). We found a significant linear association between the extent of canal stenosis, multisegmental findings and the development of spinal cord decompression sickness. MRI intramedullary lesions were significantly more frequent in divers with incomplete recovery (OR=16 [95% CI, 2.6-99], P=0.0014), but statistical analysis failed to demonstrate a significant relationship between canal compression, signal cord abnormalities and a negative clinical outcome. CONCLUSIONS: These results suggest that divers with cervical and thoracic spinal canal stenosis, mainly due to disk degeneration, are at increased risk for the occurrence of spinal cord decompression sickness.

Decompression sickness ('the bends') in sea turtles.

Decompression sickness (DCS), as clinically diagnosed by reversal of symptoms with recompression, has never been reported in aquatic breath-hold diving vertebrates despite the occurrence of tissue gas tensions sufficient for bubble formation and injury in terrestrial animals. Similarly to diving mammals, sea turtles manage gas exchange and decompression through anatomical, physiological, and behavioral adaptations. In the former group, DCS-like lesions have been observed on necropsies following behavioral disturbance such as high-powered acoustic sources (e.g. active sonar) and in bycaught animals. In sea turtles, in spite of abundant literature on diving physiology and bycatch interference, this is the first report of DCS-like symptoms and lesions. We diagnosed a clinico-pathological condition consistent with DCS in 29 gas-embolized loggerhead sea turtles Caretta caretta from a sample of 67. Fifty-nine were recovered alive and 8 had recently died following bycatch in trawls and gillnets of local fisheries from the east coast of Spain. Gas embolization and distribution in vital organs were evaluated through conventional radiography, computed tomography, and ultrasound. Additionally, positive response following repressurization was clinically observed in 2 live affected turtles. Gas embolism was also observed postmortem in carcasses and tissues as described in cetaceans and human divers. Compositional gas analysis of intravascular bubbles was consistent with DCS. Definitive diagnosis of DCS in sea turtles opens a new era for research in sea turtle diving physiology, conservation, and bycatch impact mitigation, as well as for comparative studies in other air-breathing marine vertebrates and human divers.

Recent modifications to the investigation of diving related deaths.

The investigation of deaths that involve diving using a compressed breathing gas (SCUBA diving) is a specialized area of forensic pathology. Diving related deaths occur more frequently in certain jurisdictions, but any medical examiner or coroner's office may be faced with performing this type of investigation. In order to arrive at the correct conclusion regarding the cause and manner of death, forensic pathologists and investigators need to have a basic understanding of diving physiology, and should also utilize more recently developed technology and ancillary techniques. In the majority of diving related deaths, the cause of death is drowning, but this more often represents a final common pathway due to a water environment. The chain of events leading to the death is just as important to elucidate if similar deaths are to be minimized in the future. Re-enactment of accident scenarios, interrogation of dive computers, postmortem radiographic imaging, and slight alterations in autopsy technique may allow some of these diving related deaths to the better characterized. The amount and location of gas present in the body at the time of autopsy may be very meaningful or may simply represent a postmortem artifact. Medical examiners, coroners, and forensic investigators should consider employing select ancillary techniques to more thoroughly investigate the factors contributing a death associated with SCUBA diving.

Simulated dive in rats lead to acute changes in cerebral blood flow on MRI, but no cerebral injuries to grey or white matter.

In this study, the effect of a simulated dive on rat brain was investigated using several magnetic resonance imaging (MRI)-methods and immunohistochemistry. Rats were randomly assigned to a dive- or a control group. The dive group was exposed to a simulated air dive to 600 kPa for 45 min. Pulmonary artery was monitored for vascular gas bubbles by ultrasound. MRI was performed 1 h after decompression and at one and 2 weeks after the dive with a different combination of MRI sequences at each time point. Two weeks after decompression, rats were sacrificed and brains were prepared for histology. Dived rats had a different time-curve for the dynamic contrast-enhanced MRI signal than controls with higher relative signal intensity, a tendency towards longer time to peak and a larger area under the curve for the whole brain on the acute MRI scan. On MRI, 1 and 2 weeks after dive, T2-maps showed no signal abnormalities or morphological changes. However, region of interest based measurements of T2 showed higher T2 in the brain stem among decompressed animals than controls after one and 2 weeks. Microscopical examination including immunohistochemistry did not reveal apparent structural or cellular injuries in any part of the rat brains. These observations indicate that severe decompression does not seem to cause any structural or cellular injury to the brain tissue of the rat, but may cause circulatory changes in the brain perfusion in the acute phase.

Exercise-induced myofibrillar disruption with sarcolemmal integrity prior to simulated diving has no effect on vascular bubble formation in rats.

Decompression sickness is initiated by gas bubbles formed during decompression, and it has been generally accepted that exercise before decompression causes increased bubble formation. There are indications that exercise-induced muscle injury seems to be involved. Trauma-induced skeletal muscle injury and vigorous exercise that could theoretically injure muscle tissues before decompression have each been shown to result in profuse bubble formation. Based on these findings, we hypothesized that exercise-induced skeletal muscle injury prior to decompression from diving would cause increase of vascular bubbles and lower survival rates after decompression. In this study, we examined muscle injury caused by eccentric exercise in rats prior to simulated diving and we observed the resulting bubble formation. Female Sprague-Dawley rats (n = 42) ran downhill (-16º) for 100 min on a treadmill followed by 90 min rest before a 50-min simulated saturation dive (709 kPa) in a pressure chamber. Muscle injury was evaluated by immunohistochemistry and qPCR, and vascular bubbles after diving were detected by ultrasonic imaging. The exercise protocol resulted in increased mRNA expression of markers of muscle injury; αB-crystallin, NF-κB, and TNF-α, and myofibrillar disruption with preserved sarcolemmal integrity. Despite evident myofibrillar disruption after eccentric exercise, no differences in bubble amounts or survival rates were observed in the exercised animals as compared to non-exercised animals after diving, a novel finding that may be applicable to humans.

The emulsified perfluorocarbon Oxycyte improves spinal cord injury in a swine model of decompression sickness.

STUDY DESIGN: A prospective, animal model for pharmacological intervention of decompression sickness (DCS), including spinal cord (SC) injury. BACKGROUND: Signs and symptoms of DCS can include joint pain, skin discoloration, cardiopulmonary congestion and SC injury; severity ranges from trivial to fatal. Non-recompressive therapy for DCS may improve time-to-treatment and therefore impact mortality and morbidity. OBJECTIVES: Oxycyte at 5 cc kg(-1) provides both SC protection and statistically significant survival benefit in a swine model of DCS. The purpose of this study was to test whether a reduced dose of Oxycyte (3 cc kg(-1)) would provide similar benefit. SETTING: Silver Spring, MD, USA METHODS: Male Yorkshire swine (N=50) underwent a non-linear compression profile to 200 fsw (feet of sea water), which was identical to previous work using the 5 cc kg(-1) dose of Oxycyte. After 31 min of bottom time, decompression was initiated at 30 fsw per minute until surface pressure was reached. Following decompression and the onset of DCS, intravenous Oxycyte or saline was administered with concurrent 100% O(2) for 1 h. The primary end point was DCS-induced mortality, with Tarlov score and SC histopathology as secondary end points. RESULTS: Oxycyte administration of 3 cc kg(-1) following surfacing produced no significant detectable survival benefit. Animals that received Oxycyte, however, had reduced SC lesion area. CONCLUSION: Further studies to determine the lowest fully efficacious dose of Oxycyte for the adjunct treatment of DCS are warranted.

Diving under a microscope--a new simple and versatile in vitro diving device for fluorescence and confocal microscopy allowing the controls of hydrostatic pressure, gas pressures, and kinetics of gas saturation.

How underwater diving effects the function of the arterial wall and the activities of endothelial cells is the focus of recent studies on decompression sickness. Here we describe an in vitro diving system constructed to achieve real-time monitoring of cell activity during simulated dives under fluorescent microscopy and confocal microscopy. A 1-mL chamber with sapphire windows on both sides and located on the stage of an inverted microscope was built to allow in vitro diving simulation of isolated cells or arteries in which activities during diving are monitored in real-time via fluorescent microscopy and confocal microscopy. Speed of compression and decompression can range from 20 to 2000 kPa/min, allowing systemic pressure to range up to 6500 kPa. Diving temperature is controlled at 37°C. During air dive simulation oxygen partial pressure is optically monitored. Perfusion speed can range from 0.05 to 10 mL/min. The system can support physiological viability of in vitro samples for real-time monitoring of cellular activity during diving. It allows regulations of pressure, speeds of compression and decompression, temperature, gas saturation, and perfusion speed. It will be a valuable tool for hyperbaric research.

Brain magnetic resonance imaging anomalies in U-2 pilots with neurological decompression sickness.

INTRODUCTION: This was a retrospective observational study of imaging used to evaluate and treat 13 U-2 pilots with neurological decompression sickness (DCS). Magnetic resonance imaging (MRI) and computed tomography (CT) provided data for screening, diagnosis, and determinations of fitness to fly after recovery. While small series and case reports described the role of imaging in diving DCS, none addressed radiology's role in aviation DCS. METHODS: We performed a literature review of altitude DCS radiology studies. We then reviewed radiology images at our institution on U-2 pilots with neurological DCS between January 2002 and August 2010. We retrospectively analyzed MRI data for white matter hyper-intensities (WMHs), defined as hyperintense lesions > or = 3 mm on T2 and FLAIR. All studies occurred after hyperbaric oxygen (HBO) treatment. RESULTS: There were 17 pilots who reported 20 neurological DCS incidents. Of these 17 pilots, 13 underwent imaging. Two (15%) demonstrated acute subcortical lesions on MRI, seven (54%) had asymptomatic WMHs, and six (46%) were normal. The clinical significance of the lesions is unknown. Consistent with diving DCS, imaging played no role in acute diagnosis. However, imaging was vital for determining fitness for return to flying. Additionally, CT identified a potentially predisposing sinus condition in one pilot which may enable return to flying after treatment. CONCLUSIONS: Modern imaging has unique findings for altitude DCS patients. The high incidence of WMHs in this series is a matter of ongoing research to determine potential clinical consequences. Emerging techniques such as functional MRI may play important roles in future aeromedical decisions.

Pathophysiology, prevention, and treatment of ebullism.

INTRODUCTION: Ebullism is the spontaneous evolution of liquid water in tissues to water vapor at body temperature when the ambient pressure is 47 mmHg or less. While injuries secondary to ebullism are generally considered fatal, some reports have described recovery after exposure to near vacuum for several minutes. The objectives of this article are to review the current literature on ebullism and to present prevention and treatment recommendations that can be used to enhance the safety of high altitude activities and space operations. METHODS: A systematic review was conducted on currently available information and published literature of human and animal studies involving rapid decompression to vacuum and ebullism, with subsequent development of an applicable treatment protocol. RESULTS: Available research on ebullism in human and animal subjects is extremely limited. Literature available identified key pathophysiologic processes and mitigation strategies that were used for treatment protocol design and outlining appropriate interventions using current best medical practices and technologies. DISCUSSION: Available literature suggests that the pathophysiology of ebullism leads to predictable and often treatable injuries, and that many exposures may be survivable. With the growing number of high altitude and space-related activities, more individuals will be at risk for ebullism. An integrated medical protocol can provide guidance for the prevention and treatment of ebullism and help to mitigate this risk in the future.

Diffusion tensor MRI of spinal decompression sickness.

In order to develop more sensitive imaging tools for clinical use and basic research of spinal decompression sickness (DCS), we used diffusion tensor MRI (DTI) validated by histology to assess DCS-related tissue injury in sheep spinal cords. DTI is based on the measurement of water diffusion indices, including fractional anisotropy (FA) and mean diffusion (MD) to detect tissue microstructural abnormalities. In this study, we measured FA and MD in white and gray matter spinal cord regions in samples taken from sheep following hyperbaric exposure to 60-132 fsw and 0-180 minutes of oxygen pre-breathing treatment before rapid decompression. The main finding of the study was that decompression from >60 fsw resulted in reduced FA that was associated with cell death and disrupted tissue microstructure in spinal cord white matter tracts. Additionally, animals exposed to prolonged oxygen pre-breathing prior to decompression demonstrated reduced MD in spinal cord gray matter regions regardless of dive depth. To our knowledge, this is the first study to demonstrate the utility of DTI for the investigation of DCS-related injury and to define DTI biomarkers of spinal DCS.

Adaptations for marine habitat and the effect of Triassic and Jurassic predator pressure on development of decompression syndrome in ichthyosaurs.

Decompression syndrome (caisson disease or the "the bends") resulting in avascular necrosis has been documented in mosasaurs, sauropterygians, ichthyosaurs, and turtles from the Middle Jurassic to Late Cretaceous, but it was unclear that this disease occurred as far back as the Triassic. We have examined a large Triassic sample of ichthyosaurs and compared it with an equally large post-Triassic sample. Avascular necrosis was observed in over 15% of Late Middle Jurassic to Cretaceous ichthyosaurs with the highest occurrence (18%) in the Early Cretaceous, but was rare or absent in geologically older specimens. Triassic reptiles that dive were either physiologically protected, or rapid changes of their position in the water column rare and insignificant enough to prevent being recorded in the skeleton. Emergency surfacing due to a threat from an underwater predator may be the most important cause of avascular necrosis for air-breathing divers, with relative frequency of such events documented in the skeleton. Diving in the Triassic appears to have been a "leisurely" behavior until the evolution of large predators in the Late Jurassic that forced sudden depth alterations contributed to a higher occurrence of bends.

Hyperintense white matter lesions in 50 high-altitude pilots with neurologic decompression sickness.

INTRODUCTION: Neurologic decompression sickness (NDCS) can affect high-altitude pilots, causing variable central nervous system symptoms. Five recent severe episodes prompted further investigation. METHODS: We report the hyperintense white matter (HWM) lesion imaging findings in 50 U-2 pilot volunteers, and compare 12 U-2 pilots who experienced clinical NDCS to 38 U-2 pilots who did not. The imaging data were collected using a 3T magnetic resonance imaging scanner and high-resolution (1-mm isotropic) three-dimensional fluid-attenuated inversion recovery sequence. Whole-brain and regional lesion volume and number were compared between groups. RESULTS: The NDCS group had significantly increased whole brain and insular volumes of HWM lesions. The intergroup difference in lesion numbers was not significant. CONCLUSION: A clinical episode of NDCS was associated with a significant increase in HWM lesion volume, especially in the insula. We postulate this to be due to hypobaric exposure rather than hypoxia since all pilots were maintained on 100% oxygen throughout the flight. Further studies will be necessary to better understand the pathophysiology underlying these lesions.

[Case report: fatal diving-accident. Or: accident while diving?]. / Tödlicher Tauchunfall. Oder: Unfall während des Tauchens mit Todesfolge?

This example of a fatal diving accident shows how challenging such cases can be in pre-hospital and clinical care. There is no common mechanism in diving fatalities and more than one group of disorders coming along with decompression sickness. Diving medicine is not an element of medical education, which results in insecurity and hampers adequate therapy of diving incidents. This is aggravated by an insufficient availability of hyperbaric chambers in Germany.