Introduction: Previous research identified a trend for increasing numbers of injuries sustained while rock climbing. This study investigates whether that trend continued and describes characteristics of climbing injuries. Methods: The National Electronic Injury Surveillance System registry was searched for rock climbing injuries in US emergency departments in 2008 through 2016 among patients aged ≥7 y. Variables included each patient's age, diagnosis, injured body part, mechanism of injury, and disposition. Injuries were graded using International Mountaineering and Climbing Federation injury grades. National estimates were generated using sample weighting. Results: An estimated 34,785 rock climbing injuries were seen in emergency departments nationally, a mean of 3816 per year (SD 854). The median age of injured climbers was 24 y (range 7–77), with those aged 20 to 39 y accounting for 60% and males for 66%, respectively. Fractures (27%) and sprains and strains (26%) were the most common types of injuries. The most frequently injured body parts were lower extremities (47%), followed by upper extremities (25%). The most commonly fractured body part (27%) was the ankle. The knee and lower leg accounted for 42% of all lacerations and were 5.8 times as likely as lacerations to other body parts. Falls were the most common mechanism, accounting for 60% of all injuries. Conclusions: This study reports continued increase in annual numbers of climbing injuries. Whether this is based on a higher injury rate or on a higher number of climbers overall cannot be stated with certainty because no denominator is presented to estimate the injury rate among climbers.

Excessive reactive oxygen species (ROS) is considered a consequence of hyperoxia and a major contributor to diving-derived vascular endothelial damage and decompression sickness. The aims of this work were: 1) to directly observe endothelial ROS production during simulated air dives as well as its relation with both mitochondrial activity and cell survival; and 2) to determine which ambient factor during air diving (hydrostatic pressure or oxygen and/or nitrogen partial pressure) is responsible for the observed modifications. In vitro diving simulation was performed with bovine arterial endothelial cells under real-time observation. The effects of air diving, hydrostatic, oxygen and nitrogen pressures, and N-acetylcysteine (NAC) treatment on mitochondrial ROS generation, mitochondrial membrane potential and cellular survival during simulation were investigated. Vascular endothelial cells performing air diving simulation suffered excessive mitochondrial ROS, mitochondrial depolarization, and cell death. These effects were prevented by NAC: after NAC treatment, the cells presented no difference in damage from nondiving cells. Oxygen diving showed a higher effect on ROS generation but lower impacts on mitochondrial depolarization and cell death than hydrostatic or nitrogen diving. Nitrogen diving had no effect on the inductions of ROS, mito-depolarization, or cell death. This study is the first direct observation of mitochondrial ROS production, mitochondrial membrane potential and cell survival during diving. Simulated air SCUBA diving induces excessive ROS production, which leads to mitochondrial depolarization and endothelial cell death. Oxygen partial pressure plays a crucial role in the production of ROS. Deleterious effects of hyperoxia-induced ROS are potentiated by hydrostatic pressure. These findings hold new implications for the pathogenesis of diving-derived endothelial dysfunction.

Reactive oxygen species (ROS) production is a well-known effect in individuals after an undersea dive. This study aimed to delineate the links between ROS, endothelial dysfunction, and decompression sickness (DCS) through the use of antioxidants in vitro and in vivo. The effect of N-acetylcysteine (NAC) on superoxide and peroxynitrite, nitric oxide (NO) generation, and cell viability during in vitro diving simulation were analyzed. Also analyzed was the effect of vitamin C and NAC on plasma glutathione thiol and thiobarbituric acid reactive substances (TBARS), plasma angiotensin-converting enzyme (ACE) activity, and angiotensin-II and DCS morbidity during in vivo diving simulation. During an in vitro diving simulation, vascular endothelial cells showed overproduction of superoxide and peroxynitrite, obvious attenuation of NO generation, and promotion of cell death, all of which were reversed by NAC treatment. After in vivo diving simulation, plasma ACE activity and angiotensin-II level were not affected. The plasma level of glutathione thiol was downregulated after the dive, which was attenuated partially by NAC treatment. Plasma TBARS level was upregulated; however, either NAC or vitamin C treatment failed to prevent DCS morbidity. During in vitro simulation, endothelial superoxide and peroxynitrite-mediated oxidative stress were involved in the attenuation of NO availability and cell death. This study is the first attempt to link oxidative stress and DCS occurrence, and the link could not be confirmed in vivo. Even in the presence of antioxidants, ROS and bubbles generated during diving and/or decompression might lead to embolic or biochemical stress and DCS. Diving-induced oxidative stress might not be the only trigger of DCS morbidity.

Previous studies have documented that decompression led to endothelial dysfunction with controversial results. This study aimed to clarify the relationship between endothelial dysfunction, bubble formation and decompression rate. Rats were subjected to simulated air dives with one of four decompression rates: one slow and three rapid. Bubble formation was detected ultrasonically following decompression for two hours, before measurement of endothelial related indices. Bubbles were found in only rapid-decompressed rats and the amount correlated with decompression rate with significant variability. Serum levels of ET-1, 6-keto-PGF1α, ICAM-1, VCAM-1 and MDA, lung Wet/Dry weight ratio and histological score increased, serum NO decreased following rapid decompression. Endothelial-dependent vasodilatation to Ach was reduced in pulmonary artery rings among rapid-decompressed rats. Near all the above changes correlated significantly with bubble amounts. The results suggest that bubbles may be the causative agent of decompression–induced endothelial damage and bubble amount is of clinical significance in assessing decompression stress. Furthermore, serum levels of ET-1 and MDA may serve as sensitive biomarkers with the capacity to indicate endothelial dysfunction and decompression stress following dives.

The epidemiology of injury associated with recreational scuba diving is reviewed. A search of electronic databases and reference lists identified pertinent research. Barotrauma, decompression sickness and drowning-related injuries were the most common morbidities associated with recreational scuba diving. The prevalence of incidents ranged from 7 to 35 injuries per 10,000 divers and from 5 to 152 injuries per 100,000 dives. Recreational scuba diving fatalities account for 0.013% of all-cause mortality aged ≥ 15 years. Drowning was the most common cause of death. Among treated injuries, recovery was complete in the majority of cases. Dive injuries were associated with diver-specific factors such as insufficient training and preexisting medical conditions. Environmental factors included air temperature and flying after diving. Dive-specific factors included loss of buoyancy control, rapid ascent and repetitive deep diving. The most common event to precede drowning was running out of gas (compressed air). Though diving injuries are relatively rare prospective, longitudinal studies are needed to quantify the effects of known risk factors and, indeed, asymptomatic injuries (e.g. brain lesions). Dive injury health economics data also remains wanting. Meanwhile, health promotion initiatives should continue to reinforce adherence to established safe diving practices such as observing depth/time limits, safety stops and conservative ascent rates. However, there is an obvious lack of evaluated diving safety interventions.