Clinical Presentations and Significance of Decompression Sickness: an Analysis of Incidents from Commercial Diving Operations 1977–87

Abstract

A review of the symptomatology of decompression sickness must make reference to present understanding of the cause of the condition. Since Boyle^1,2 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 1863.³ 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.