Although DI is causally related to bubbles, there are a multitude of pathophysiological mysteries between the physical appearance of bubbles and the onset of biological injury or clinical illness. Various unknown individual physical and physiological factors may contribute towards individual variability in the production of, and response to, bubbles 37,38. Venous bubbles are commonly observed following routine and even relatively shallow dives and appear to be largely asymptomatic. On the other hand, the appearance of left ventricular or arterial bubbles are thought to be of greater clinical importance; however these have rarely been observed, even in a laboratory setting. Recently, ocular tear film bubbles have generated some interest, but their persistence following decompression has limited their reliability as a predictor of decompression stress 3'39.

When it comes to actually diagnosing DI, we presently rely almost exclusively on the diver's history and an estimation of clinical probability from an enormously divergent spectrum of signs and symptoms following decompression. As yet, there are no specific biochemical markers for bubble related injury 40-42. Also, the sensitivity of radiological and nuclear medical examinations does not exceed that of clinical observation and, in the absence of diagnostic uncertainty, these rarely affect management. We must therefore accept that the best scientific case definition we have for DI at present is one of exclusion, i.e. the appearance of unexplained pain, cutaneous, cardiovascular or neurological abnormalities - chronologically associated with compressed gas diving - upon the exclusion of other etiologies. In a clinical setting, our index of suspicion should be high to avoid under-treatment. Fortunately, the risk of injury remains relatively small: in recreational diving, for example, DI occurs with an incidence of one to three per 10,000 dives 43.

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