Saturation diving

Abstract: Forty commercial saturation divers, mean age 34.9 (range 24-49) years, were examined one to seven years after their last deep dive (190-500 metres of seawater). Four had by then lost their divers' licence because of neurological problems. Twenty seven (68%) had been selected by neurological examination and electroencephalography before the deep dives. The control group consisted of 100 men, mean age 34.0 (range 22-48) years. The divers reported significantly more symptoms from the nervous system. Concentration difficulties and paraesthesia in feet and hands were common. They had more abnormal neurological findings by neurological examination compatible with dysfunction in the lumbar spinal cord or roots. They also had a larger proportion of abnormal electroencephalograms than the controls. The neurological symptoms and findings were highly significantly correlated with exposure to deep diving (depth included), but even more significantly correlated to air and saturation diving and prevalence of decompression sickness. Visual evoked potentials, brainstem auditory evoked potentials, and magnetic resonance imaging of the brain did not show more abnormal findings in the divers. Four (10%) divers had had episodes of cerebral dysfunction during or after the dives; two had had seizures, one had had transitory cerebral ischaemia and one had had transitory global amnesia. It is concluded that deep diving may have a long term effect on the nervous system of the divers.

Abstract: In saturation diving, divers stay under pressure until most of their tissues are saturated with breathing gas. Divers spend a long time in isolation exposed to increased partial pressure of oxygen, potentially toxic gases, bacteria, and bubble formation during decompression combined with shift work and long periods of relative inactivity. Hyperoxia may lead to the production of reactive oxygen species (ROS) that interact with cell structures, causing damage to proteins, lipids, and nucleic acid. Vascular gas-bubble formation and hyperoxia may lead to dysfunction of the endothelium. The antioxidant status of the diver is an important mechanism in the protection against injury and is influenced both by diet and genetic factors. The factors mentioned above may lead to production of heat shock proteins (HSP) that also may have a negative effect on endothelial function. On the other hand, there is a great deal of evidence that HSPs may also have a "conditioning" effect, thus protecting against injury. As people age, their ability to produce antioxidants decreases. We do not currently know the capacity for antioxidant defense, but it is reasonable to assume that it has a limit. Many studies have linked ROS to disease states such as cancer, insulin resistance, diabetes mellitus, cardiovascular diseases, and atherosclerosis as well as to old age. However, ROS are also involved in a number of protective mechanisms, for instance immune defense, antibacterial action, vascular tone, and signal transduction. Low-grade oxidative stress can increase antioxidant production. While under pressure, divers change depth frequently. After such changes and at the end of the dive, divers must follow procedures to decompress safely. Decompression sickness (DCS) used to be one of the major causes of injury in saturation diving. Improved decompression procedures have significantly reduced the number of reported incidents; however, data indicate considerable underreporting of injuries. Furthermore, divers who are required to return to the surface quickly are under higher risk of serious injury as no adequate decompression procedures for such situations are available. Decompression also leads to the production of endothelial microparticles that may reduce endothelial function. As good endothelial function is a documented indicator of health that can be influenced by regular exercise, regular physical exercise is recommended for saturation divers. Nowadays, saturation diving is a reasonably safe and well controlled method for working under water. Until now, no long-term impact on health due to diving has been documented. However, we still have limited knowledge about the pathophysiologic mechanisms involved. In particular we know little about the effect of long exposure to hyperoxia and microparticles on the endothelium.

Abstract: Deep saturation diving has been shown to have prolonged effects on pulmonary function. We wanted to assess the relative contribution of various factors that could contribute to these effects. Pulmonary function was, therefore, measured before and after 17 different saturation diving operations to depths of 5-450 m of sea water, corresponding to absolute pressures of 0.15-4.6 MPa. Four to fifteen divers participated in each operation. The measurements included static and dynamic lung volumes and flows, transfer factor of the lungs for carbon monoxide (TLCO), and closing volume. The dives were characterized by the cumulative hyperoxic and hyperbaric exposures, and the load of venous gas microemboli encountered during decompression was measured in 41 divers in three dives to 0.25, 1.2 and 3.7 MPa. TLCO was reduced by 8.3 +/- 7.0% mean +/- SD after the dives, this correlated with cumulative hyperoxic exposure and load of venous gas microembolism, independently of each other. Closing volume was increased and forced mid-expiratory flow rate reduced, in correlation with cumulative hyperoxic exposure. An increase in total lung capacity correlated with cumulative hyperbaric exposure. We conclude that hyperoxia, hyperbaria, and venous gas microembolism all contribute to the changes in pulmonary function after a single saturation dive, and all may explain some of the long-term effects of diving on pulmonary function.

Abstract: We recently suggested after laboratory experiments' that undetected hypothermia might account for unexplained casualties during working dives in the North Sea. At depths greater than 50 m in the North Sea water temperature is below 10°C. Heat is usually supplied by flooding the diving suit continuously with warm water pumped from the surface via the diving bell; its temperature is monitored at the bell, but not at the diver, and is regulated mainly on the basis of the diver's report of feeling hot or cold. We found that simulation of this with warm water at 290C around a thin man could produce progressive hypothermia with cardiac irregularities but without any serious sensation of cold. We are now reporting the body temperatures of divers during saturation diving operations using the conventional heating system at a depth of 130-145 m in the North Sea in August-November 1979. The divers breathed helium and oxygen throughout. Their urine tempera-tures2 were measured within eight minutes of their return to the bell after working dives with a maximum-reading Digitron thermistor with a response time of under 10 seconds in at least 50 ml of urine flowing through the outlet of a perforated funnel. This volume had been found with this apparatus to yield readings accurate to within 0 2'C. Skinfold thicknesses were measured with Harpenden callipers.3 The table shows that the thinnest diver in the group developed hypothermia at 34 70C during a dive lasting only 55 minutes. He had felt a little cold and shivered at one point during the dive, but when the temperature of the warm-water supply, measured at the bell, was increased by 4'C he had stopped feeling cold. Two of the other divers cooled to near hypothermia with temperatures below 35 5'C at the end of 4-44 hour dives, in one of which the warm-water system had failed for the last hour. That diver felt cold and shivered, but the other did not. In contrast, one relatively fat diver had a normal body temperature even after a one-hour failure of the warm-water supply; he reported considerable shivering and sensation of cold at that time. Body temperature after other dives was usually normal; in one instance it was a little high at 38 3°C. Physical characteristics and body temperatures of divers, temperatures of warm water, and duration of dives Approximate Body temperature temperature Height Body Skinfold of warm Duration at end of …