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Sarah Milton

It has long been a tenet of diving physiology that deep-diving whales and dolphins are essentially immune to decompression sickness, or `the bends'. The bends can severely affect human divers (SCUBA divers, for example) who surface too quickly, causing nitrogen gas to rapidly bubble out of solution from the blood into blood vessels and joints. Diving marine mammals, however, have a variety of anatomical and physiological adaptations that help prevent the bends. The amount of respiratory gas available to a diving mammal is limited to that present in its lungs at the beginning of the dive, and as increasing pressures at depth collapse the lungs this gas is driven into non-respiratory conducting airways, where it is sequestered from the circulatory system, preventing gas bubbles from entering the animal's bloodstream. There has been much controversy of late in the literature, though, as to whether dolphins and whales may in fact be susceptible to decompression sickness; correlations have been reported between military sonar use and cetaceans stranding with decompression sickness-like symptoms, perhaps because acoustic exposure causes the animals to surface too quickly. Michael Moore and Greg Early's recent contribution to this discussion suggests that whales really do suffer from the bends.

Moore and Early investigated osteonecrosis, bone tissue death, in sperm whale bones collected from carcasses from the Atlantic and Pacific oceans. Dysbaric osteonecrosis is generally associated with large ambient pressure changes, such as those that also induce the bends, which result in the formation of gas bubbles that block blood vessels. This leads to decreased blood supply to the bones, causing necrotic lesions in the fatty marrow-containing shafts of the long bones as well as in ball and socket joints. Moore and Early reasoned that if sperm whales suffer from dysbaric osteonecrosis, this would suggest that these creatures are indeed susceptible to the bends.

Moore and Early's histological post-mortem examination of the bones of a 14.7m adult male sperm whale revealed pitted and eroded bones and joints, the erosion of cartilage, and extensive remodelling of cartilage and bone, all signs of dysbaric osteonecrosis. There was no indication of infectious diseases that might otherwise be responsible for the damage. The investigators also examined 16 other sperm whale skeletons of varied age and size, collected over a 111-year time span. They found that as body length increased, the severity of bone erosion and bone remodelling increased. So older animals that had presumably experienced the bends more frequently than younger animals had suffered greater bone damage. Similar correlations between dysbaric osteonecrosis and human diver age, experience and decompression sickness have also been reported in the literature.

Osteonecrosis that is indistinguishable from dysbaric osteonecrosis can be caused by other factors, including blood disorders, irradiation and thermal injuries. As it is unlikely that all of Moore and Early's whales suffered from adrenal or blood disorders, or experienced irradiation or thermal stress, the authors hypothesize that the most likely cause of the bone damage they observed was the bends. They conclude that, despite the dogma, sperm whales may be neither physiologically nor anatomically immune to the pathological effects of deep diving.