A review of the symptomatology of decompression sickness must make reference to present understanding of the cause of the condition Since Boyle1,2 was able to produce decompression sickness (DCS) in animals by changes in ambient pressure, it has been held that at least the initial stimulus to the development of the condition is the formation of bubbles of inert gas within tissues and small blood vessels The converse of this process, achieving elimination of these bubbles by recompression, was first realized in 1863 The mechanical effects of undissolved gas liberated from solution within tissues and the bloodstream are not, however, sufficient to explain the variable symptomatology, and cannot account for variations in individual susceptibility, time of onset, duration, and the nature of the response to treatment Explanations of the pathophysiology of decompression sickness are not complete, but it has been known since 19374 that activity at the surface of undissolved gas has the potential in plasma for causing alterations in the structure and reactivity of substances within the plasma It is currently thought5 that these alterations may lead to the denaturing of plasma proteins and the formation of lipid micelles from triglycerides, sterols and fatty acids normally contained within blood lipoproteins These changes in the macromolecular constitution of blood will lead to changes in the flow characteristics of blood, 5 with increased viscosity and decreased local flow It is suggested that there will then be intravascular aggregation followed by microembolism, platelet involvement and impaired tissue perfusion, leading to pulmonary and central nervous system damage5–7Other changes thought to occur in blood following exposure to a gas surface, as would occur around bubbles, are many and will affect the coagulation, complement and fibrinolytic systems, and it is suggested5 that minor pre-dive abnormalities in the levels of inhibitors may allow the alterations in coagulation, fibrinolytic and complement activities to overwhelm any available inhibitors Extensive local propagation or dissemination of an otherwise well-contained process may then occur.
A satisfactory clinical description which matches this interpretation of the cause of decompression sickness has not yet been achieved Golding et al8 used the terms ‘Type I’ and ‘Type II’ decompression sickness in 1960 as a means of distinguishing between what they described as ‘simple’, and ‘more serious and more complicated’ cases Opinion has varied since then about the validity of these two categories9 and clinical experience suggests that the terms do not accurately indicate the clinical nature and significance of symptoms they are used to describe Further, differences in the syndrome related to the nature of the precipitating dive9 and use of the same terms to describe the condition at stages varying from immediate post-decompression to some hours or days later do not take into account differences in the pathology of the condition which may have occurred because of the progression between initial bubble appearance and the sequence of intravascular and extravascular events outlined above.
