Prevention and Treatment of DI

Prevention of DI could only follow an understanding of its cause. Accordingly, the first measures were aimed at merely alleviating the symptoms. Triger himself advocated "rubbing with spirits of wine" which, he reported, "soon relieved this pain in both men and they kept working on the following days". Two years later, Pol and Watelle wrote that they felt "justified in hoping that a sure and prompt means of relief would be to recompress immediately, then decompress very carefully" 6.

By the turn of the 19th century civil engineering had achieved proportions of depth and complexity that DI became more than a trivial concern: On 15th May 1896 the Journal of the Society of Art described the landmark work of E. W. Moir during the digging of the Hudson river tunnel in 1889 7. Facing a DI fatality rate of over 25% of the employed workers, Moir installed a recompression chamber at the worksite. The result was a dramatic reduction in mortality - only two deaths were recorded during the next 15 months out of a workforce of more than 120. Moir, who seemed almost apologetic about this empirical therapy, wrote: "With a view to remedying the state of things an air compartment like a boiler was made in which the men could be treated homeopathically, or reimmersed in compressed air. It was erected near the top of the shaft, and when a man was overcome or paralyzed, as I have seen them often, completely unconscious and unable to use their limbs, they were carried into the compartment and the air pressure raised to about 1/2 or 2/3 of that in which they had been working, with immediate improvement. The pressure was then lowered at the very slow rate of one pound per minute or even less. The time allowed for equalization being from 25 to 30 minutes, and even in severe cases the men went away quite cured".

Ironically Paul Bert in 1878 had already validated this concept 8. He had demonstrated that the cause of DI was nitrogen going into gas phase in the tissues and that this bubble formation was responsible for symptoms. Bert understood that prompt recompression was the key to effective treatment. Remarkably, he already highlighted the existence of "silent bubbles" in the venous blood; used oxygen at one atmosphere following very rapid decompression; and observed that cardiopulmonary symptoms, but not spinal cord paralysis, were relieved by normobaric oxygen breathing.

Since that time, prompt recompression followed by slow decompression has been universally considered the standard of care in the treatment of DI. Further developments delineated the best combinations of pressure, time, gas composition and decompression rates as well as the addition of resuscitation and adjunctive therapy (Fig. 2.2.1-1).

Treatment of DI

Simple resuscitation Hyperbaric air

Hyperbaric O2


1900 1925 1950 1975 2000


Figure 2.2.1-1. Developments in the Treatment for DI over the past century (Courtesy of

Richard Moon, MD)

However, even though we are now gaining a better understanding of the tools of therapy, we remain challenged by inconsistency and confusion in terminology for DI and uncertainty of diagnosis. Clearly there is little uncertainty in the case of severe neurological DI. However, minor forms may manifest in very subtle ways. These are likely to be ignored or denied by the affected diver unless there is an appropriate level of awareness. Indeed, there is reason to believe that there is widespread underreporting of symptoms that may cause an unquantified amount of morbidity. On the other hand over-emphasis of risks and hazards may cause hypochondriacal responses or deter pursuit of the activity altogether. It remains, therefore, an ongoing challenge to achieve the correct balance between denial and hysteria in the face of untoward symptoms following diving.

As far as prevention is concerned, the definitive contribution in the context of diving was made by Boycott, Damant and Haldane in 1908 9. Their work, although based on speculative mechanisms, forever changed the fate of those facing decompression after breathing compressed gas. For the next 60 years refinements in modeling theory, mathematics and statistics have suggested a variety of depth-time combinations followed by various decompression stops strung together by empirical ascent rates. Unfortunately the fundamental principles on which all of these systems are based are empirical as are their progeny of tables and decompression algorithms. Their limitations have become particularly evident in recreational diving where one half of DI cases do not appear to be the consequence of overt dive profile violations. These observations have led to a search for unique physiological factors and other unique risk factors. Possibilities have included pulmonary-systemic shunts (e.g., patent foramen ovale, atrial septal defects, intra pulmonary shunts, etc.); endothelial morphological anomalies and reactivity; activation of complement; and many more. The search for these elusive risk factors continues, as does their ambiguity 2'10'11.

The introduction of precordial Doppler in the 1970's promised a solution to the mystery of DI 12. Unfortunately the association between recordable bubbles and DI symptoms did not prove to be particularly strong: high grade bubbles correlated more closely with DI than lower grades, but DI has even been observed in the absence of any detectable bubbles. Nevertheless, this modality may again enjoy greater utility in the years to come: Recently there has been an increasing emphasis on paradoxical embolism of venous gas and a growing body of experimental and clinical evidence suggesting that large quantities of asymptomatic or "silent" venous bubbles may in fact be causing cellular and biological reactions and be releasing potentially damaging biochemical substances in the blood 13-16.

Current prevention theory for DI recommends that participants: (1) possess and maintain an appropriate level of dive medical fitness (including controlling daily physiological variables such as body temperature and hydration status); (2) avoid / prevent air trapping with gas expansion (e.g., not diving with respiratory infections and untreated reactive airway problems); and (3) observe appropriate decompression procedures for their exposure (i.e., following the recommended combination of pressure and time for their planned diving activities). Violation of one or more of these parameters increases the risk of DI

In the future our improved ability to detect bubbles and - more recently -to detect the biochemical injuries they cause, may ultimately generate more physiological approaches to decompression. Accordingly, future decompression safety is likely to focus on three areas of intervention: (1) manipulating decompression (ascent) to reduce the appearance, quantities and size of venous gas emboli; (2) reducing the propensity of the body to form bubbles; and (3) preconditioning the body biochemically and/or physically to reduce the pathophysiological impact of such bubbles 17-25.

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