ABSTRACT
We and others have reported that decompression of divers is accompanied by changes in cellular and chemical components of the blood. Some of these have been seen following surfacing from as little as 3 ATA. While some may be regarded as laboratory curiosities, others have the potential to influence the progression of decompression sickness (DCS) and perhaps dysbaric osteonecrosis (aseptic bone necrosis); namely, those changes which indicate an acceleration of the blood clotting process and which appear to be triggered by the presence of intravascular bubbles, even ‘silent’ ones that do not lead to DCS. They include: (1) a loss of blood platelets of about 25% over 48-h post decompression, (2) an increase in levels of fibrinogen/fibrin split products, (3) changes in complement levels, and (4) other trends suggesting a mild hypercoagulable state. These changes could contribute to the formation of tiny thrombi which, in conjunction with vascular bubbles, might occlude small blood vessels to delay nitrogen washout, and interrupt the blood supply to critical areas of the longbones, leading to bone death. Increases in circulating enzyme levels, indicative of tissue damage, have been seen in divers in the absence of overt DCS. Human studies to determine whether intervention with drugs can prevent these changes, have been equivocal. Most of these have been conducted in divers. Similar investigations in compressed air workers could be instructive.
