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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.

Diving is a popular activity, largely practiced worldwide. Diving fatalities are not rare events, with drowning being the most common cause of death, followed by cardiac-related natural causes, immersion pulmonary edema and arterial gas embolism. In such cases, positive signs of drowning are not specific, depending also on the time of submersion of corpses. Moreover, drowning can be the terminal event. Over the years, measures to perform appropriate post-mortem examination in cases of diving fatalities were suggested, including the execution of post-mortem CT-scan, the use of a decompression chamber and the adoption of specific autoptic techniques. Although a multidisciplinary approach in forensic investigations concerning diving fatalities is discussed, poor cases focus on how the analysis of diving computer records and equipment can contribute to determining the cause of death. The present study shows how the cooperation between a forensic underwater expert and a forensic pathologist played a crucial role in interpreting radiological findings, guiding the autopsy and confirming/denying circumstantial data emerging from the investigations. Technical analysis of dive computer records and diving equipment is a fundamental step in the definition of the cause of death in diving fatalities. All diving computer data, not only those related to maximum depth and ascent’s profile, should be considered in detail, and the immersion graph carefully studied by both the forensic pathologist and the forensic underwater experts. The diving technical data can often play a crucial role in explaining any legal issue related to the circumstances of death, possibly leading the prosecutor to further investigation. •Diving fatalities are not rare events.•In those cases, autoptic diagnosis can be challenging.•PMCT-scan can steer the forensic pathologist to perform a proper examination.•Forensic underwater experts have a pivotal role in diving fatalities.•Technical analysis of dive computer records and equipment are fundamental.

PurposeUnderwater divers face several potential neurological hazards when breathing compressed gas mixtures including nitrogen narcosis which can impact diver’s safety. Various human studies have clearly demonstrated brain impairment due to nitrogen narcosis in divers at 4 ATA using critical flicker fusion frequency (CFFF) as a cortical performance indicator. However, recently some authors have proposed a probable adaptive phenomenon during repetitive exposure to high nitrogen pressure in rats, where they found a reversal effect on dopamine release.MethodsSixty experienced divers breathing Air, Trimix or Heliox, were studied during an open water dive to a depth of 6 ATA with a square profile testing CFFF measurement before (T0), during the dive upon arriving at the bottom (6 ATA) (T1), 20 min of bottom time (T2), and at 5 m (1.5 ATA) (T3).ResultsCFFF results showed a slight increase in alertness and arousal during the deep dive regardless of the gas mixture breathed. The percent change in CFFF values at T1 and T2 differed among the three groups being lower in the air group than in the other groups. All CFFF values returned to basal values 5 min before the final ascent at 5 m (T3), but the Trimix measurements were still slightly better than those at T0.ConclusionsOur results highlight that nitrogen and oxygen alone and in combination can produce neuronal excitability or depression in a dose-related response.

This letter addresses errors in the statistical analysis found in a paper addressing pulmonary diffusing capacity and decompression sickness. Our re-analysis could not confirm any of the significant statistical contrasts described for the bubble data, invalidating the speculation on the relationships between bubble scores and decompression sickness.

PurposeDivers can experience cognitive impairment due to inert gas narcosis (IGN) at depth. Brain-derived neurotrophic factor (BDNF) rules neuronal connectivity/metabolism to maintain cognitive function and protect tissues against oxidative stress (OxS). Dopamine and glutamate enhance BDNF bioavailability. Thus, we hypothesized that lower circulating BDNF levels (via lessened dopamine and/or glutamate release) underpin IGN in divers, while testing if BDNF loss is associated with increased OxS.MethodsTo mimic IGN, we administered a deep narcosis test via a dry dive test (DDT) at 48 msw in a multiplace hyperbaric chamber to six well-trained divers. We collected: (1) saliva samples before DDT (T0), 25 msw (descending, T1), 48 msw (depth, T2), 25 msw (ascending, T3), 10 min after decompression (T4) to dopamine and/or reactive oxygen species (ROS) levels; (2) blood and urine samples at T0 and T4 for OxS too. We administered cognitive tests at T0, T2, and re-evaluated the divers at T4.ResultsAt 48 msw, all subjects experienced IGN, as revealed by the cognitive test failure. Dopamine and total antioxidant capacity (TAC) reached a nadir at T2 when ROS emission was maximal. At decompression (T4), a marked drop of BDNF/glutamate content was evidenced, coinciding with a persisting decline in dopamine and cognitive capacity.ConclusionsDivers encounter IGN at – 48 msw, exhibiting a marked loss in circulating dopamine levels, likely accounting for BDNF-dependent impairment of mental capacity and heightened OxS. The decline in dopamine and BDNF appears to persist at decompression; thus, boosting dopamine/BDNF signaling via pharmacological or other intervention types might attenuate IGN in deep dives.

As snorkelling and breath-hold diving are conducted in a potentially hostile environment by participants with varying skills and health, fatalities occur. In this study, snorkelling and breath-hold diving fatalities were investigated in Australia from 2000 to 2021 to identify causes and countermeasures. The Australasian Diving Safety Foundation database and the National Coronial Information System were searched to identify snorkelling/breath-hold diving deaths from 2000 to 2021. Relevant data were extracted, recorded, and analysed. The median age of the 317 victims was 48 years, two-thirds were overweight or obese, and almost half had health conditions, including ischaemic heart disease (IHD) and left ventricular hypertrophy (LVH), predisposing them to an arrhythmia-related snorkelling incident. One-third of victims were likely disabled by cardiac arrhythmias and at least 137 deaths were from primary drowning, with 34 following apnoeic hypoxia. Pre-existing health conditions, particularly IHD and LVH, predispose to many snorkelling deaths in older participants and may be somewhat mitigated by targeted health screening. Drownings from apnoeic hypoxia persist in younger breath-hold divers who should avoid pushing their limits without close monitoring. Skills practice in a controlled environment, increased focus on the importance of an effective buddy, and improved supervision are necessary to mitigate risk in the inexperienced.

Long-term alterations of pulmonary function (mainly decreased airway conductance and capacity of the lungs to diffuse carbon monoxide (DLCO)) have been described after hyperbaric exposures. However, whether these alterations convey a higher risk for divers’ safety has never been investigated before. The purpose of the present pilot study was to assess whether decreased DLCO is associated with modifications of the physiological response to diving. In this case–control observational study, 15 “fit-to-dive” occupational divers were split into two groups according to their DLCO measurements compared to references values, either normal (control) or reduced (DLCO group). After a standardized 20 m/40 min dive in a sea water pool, the peak-flow, vascular gas emboli (VGE) grade, micro-circulatory reactivity, inflammatory biomarkers, thrombotic factors, and plasmatic aldosterone concentration were assessed at different times post-dive. Although VGE were recorded in all divers, no cases of decompression sickness (DCS) occurred. Compared to the control, the latency to VGE peak was increased in the DLCO group (60 vs. 30 min) along with a higher maximal VGE grade (p < 0.0001). P-selectin was higher in the DLCO group, both pre- and post-dive. The plasmatic aldosterone concentration was significantly decreased in the control group (−30.4 ± 24.6%) but not in the DLCO group. Apart from a state of hypocoagulability in all divers, other measured parameters remained unchanged. Our results suggest that divers with decreased DLCO might have a higher risk of DCS. Further studies are required to confirm these preliminary results.

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.

A field study was conducted to examine the vulnerability of military divers to non-freezing cold injury (NFCI) during Arctic ice-diving operations. Participants were instrumented with temperature sensors on the back of their hands and on the bottom of their big toe for each dive to measure cooling of their extremities. While NFCI was not diagnosed in any of the participants during this field study, the data indicate that the feet were particularly vulnerable during the dives given that they were mostly in a temperature zone that could cause pain and performance decrements. The data also show that for short term dives, the dry and wet suits with wet gloves in both configurations were thermally more comfortable for the hands than the dry suit with dry glove configuration; however, the latter would be more protective against potential NFCI during longer dives. Features such as hydrostatic pressure and repetitive diving that are unique to diving but not previously considered as risk factors for NFCI are examined herein and warrant deeper investigation given that symptoms of NFCI might be mistaken as decompression sickness.

[1] which highlights the potential diagnostic value of histomorphometric digital analysis in cases of diving-related fatalities with pulmonary barotrauma. [...]although the research is original and interesting, it has some weaknesses, including a small sample size, a narrow age range, and a lack of information on potential confounding factors that may influence the results. [...]diving technical data often play a crucial role in explaining any legal issues related to the circumstances of death, leading the prosecutor to further investigations.