Decompression Sickness: Amelioration of Risk Factors

Appropriate manipulation of the depth-time profile as discussed in the preceding section on decompression planning is obviously important in managing the risk of DCS. In addition, certain known or suspected risk factors for DCS, some of which have already been mentioned, can be manipulated or managed to reduce risk further.

Patent foramen ovale

The role of the patent foramen ovale (PFO) in the pathophysiology of DCS is discussed in Chapter 10, in which it was pointed out that PFO appears associated with an increased risk of cerebral, spinal, vestibulocochlear and cutaneous DCS. The most plausible explanation for this increase in risk is that a right-to-left shunt allows VGE to enter the arterial circulation, and these small bubbles can then distribute widely in the body and cause harm, as previously described. The degree of shunt facilitated by the PFO has consistently been found to be significant; with large and spontaneous shunts being important and very small shunts seemingly unimportant. The crucial question is this: ‘How should this knowledge be applied to reducing risk of DCS?’

One obvious strategy would be to screen divers for PFO after an episode of neurological, inner ear or cutaneous DCS and, possibly, to repair large PFOs in divers who wish to continue diving. Another more radical strategy would be to screen all prospective divers before entry to the sport. Many divers have enthusiastically embraced such ideas. When participants on Internet diving discussion forums report an episode of DCS, a chorus of advice to check for a PFO inevitably follows, even if the event involved a form of DCS that has never been associated with a PFO (e.g. musculoskeletal DCS). However, decisions to screen divers for PFO or to repair any lesion that is discovered are not straightforward.

As pointed out in Chapter 10, PFO is very common (around 30 per cent of divers or diving candidates can be expected to have one) and so is the formation of VGE after diving; yet cerebral, spinal and inner ear DCS cases remain rare. There are clearly factors beyond merely having a PFO and producing venous bubbles that are involved in the chain of events leading to the relevant forms of DCS, and at this time we are not certain what they are. Screening all prospective divers by using an expensive invasive test (see Chapter 10), which would detect the target lesion in about 30 per cent of subjects (and potentially exclude them from diving), with the aim of preventing an event that occurs perhaps once in 10 000 dives (even in an unscreened population), is neither sensible nor justified.

In contrast, it may be appropriate to test divers who have had one of the relevant forms of DCS, particularly if there have been multiple events or if the event(s) followed dives that seem unprovocative in terms of decompression stress. It is also inevitable that the diving physician will be approached by enthusiasts who have never had DCS but who are aware of the association of serious DCS with PFO and who wish to be tested for this heart condition. Referring for testing may be appropriate under these circumstances, but the following points should always be explained to the diver before testing is undertaken.

  1. The bubble contrast echocardiographic test is relatively safe, but there are some risks. Transient symptoms of cerebral arterial gas embolism have been reported following tests with strongly positive results for right-to-left shunt.
  2. The test result is likely to be positive in at least 30 per cent of cases (or more depending on the context), and the diver may then have some difficult options to choose from (see later). If the diver does not intend to take one of those options, then there is little practical point in having the test.
  3. A positive test result after an episode of DCS does not guarantee that the PFO was the cause of the DCS.
  4. As a corollary to point 3, repairing a PFO discovered after an episode of DCS does not guarantee that another event will not occur.
  5. A negative test result does not mean that the diver is ‘resistant’ to DCS, as many seem to believe.

If screening for a PFO is undertaken and the result is positive, the response should take account of the size or shunting behaviour of the lesion. There are data suggesting that a grade 1 PFO (see Chapter 10) is of little or no consequence and can be ignored. In contrast, a spontaneously shunting (grade 3) PFO is likely to confer increased risk and merits a response.

To mitigate the risk implied by a large PFO, the diver effectively has three options: cease diving, modify diving practice in an attempt to reduce VGE production or have the PFO repaired. The option to cease diving is self-explanatory and unpalatable to many. Modification of diving practice to reduce VGE production is an imprecise business, but the general aim is to reduce the provocation for bubble formation on arrival at the surface. Options for achieving this include diving well within no decompression limits, ensuring that safety stops are completed, using nitrox (see Chapter 62) but planning the dive as though using air and, if decompression diving using gradient factors, lowering the GF-High to force longer shallow decompression stops at the end of the dive. Breathing oxygen during those stops would also help. In a related vein, advice could also include avoidance of any heavy exercise that could open a pulmonary shunt, or manoeuvres that could encourage right-to-left shunting across a PFO (e.g. lifting or straining), over the typical 2-hour period of maximum VGE formation after a dive.

Having a PFO repaired involves the use of a transvenous catheter technique that leaves an occluder device across the atrial septum. It is an effective treatment, although repair may be incomplete in up to 10 per cent of cases. It is also an invasive procedure, and like many medical procedures considered ‘safe’, it nevertheless has significant risks, some of which are life-threatening. These risks include formation of blood clots on the device, loosening of the occluder from its position, the appearance of new heart rhythm disturbances and new mild aortic regurgitation. Patients are routinely required to take a potent antiplatelet agent for 6 months after placement. Occasionally, open heart surgery is required for explantation of devices that are causing complications. Despite these concerns, most procedures have satisfactory results, and the PFO is closed without complications. It is not known how many divers have taken this option to mitigate the risk of PFO in diving, but anecdotally the numbers are growing. Other than the potential for harm during and after the procedure, one of the concerns about the repair option is that data demonstrating that repair reduces subsequent risk of DCS are incomplete. There is one comparative study that followed divers with large PFOs discovered after DCS who self-selected into groups undergoing repair or not4. The study and its results are summarized in Figure 12.8.

Key features and results of the study by Billinger and associates on the efficacy of repair of patent foramen ovale (PFO) in preventing serious neurological decompression sickness (DCS).
Figure 12.8 Key features and results of the study by Billinger and associates on the efficacy of repair of patent foramen ovale (PFO) in preventing serious neurological decompression sickness (DCS). The final results are based on very small numbers of cases (1 case of DCS in the closure group and 4 cases of DCS in the no closure group). DCI, decompression illness. (Data from Billinger M, Zbinden R, Mordasini R, et al. Patent foramen ovale closure in recreational divers: effect on decompression illness and ischaemic brain lesions during long-term follow-up. Heart 2011;97:1932–1937.)

In this study, divers who continued diving without repair had a markedly higher rate of DCS than those who had a repair, but caution is required in interpreting these data because the numbers of DCS cases arising after the repair decision were so small, and the divers were not randomized. Notwithstanding this concern, the study does provide some reassurance that there is a positive return on the risk exposure associated with having a repair. Many diving enthusiasts may well be prepared to take this risk for the apparent benefit of eliminating their anatomical right-to-left shunt. This may be particularly true of those conducting deep technical dives who may see little practical potential for improving the conservatism of their dives.


The relationship between DCS risk and exercise is a complex and evolving issue, and exercise needs to be considered in multiple contexts, specifically exercise before diving, exercise during diving and exercise after diving.

Until the early 2000s, little attention had been given to the issue of exercise before diving and its relationship with risk of DCS, other than general speculation that being physically fit was probably a good thing. Things changed with the publication of a remarkable series of experiments demonstrating that a single bout of heavy exercise approximately 20 hours before diving markedly reduced mortality in a rodent model of severe DCS. By 48 hours after exercise, the protective effect seemed to wear off. Translation of this finding into human research is incomplete, but there have been several studies demonstrating that heavy exercise between 2 and 20 hours before diving reduces VGE counts after diving. The mechanism for this protective effect is unclear. Early speculation that it was mediated by nitric oxide seemed disproved when protection persisted in the presence of a nitric oxide synthase inhibitor, although as a sidebar to this line of research it was discovered that exogenously administered nitric oxide also appeared to reduce post-dive VGE. It has been suggested that exercise produces some sort of endothelial conditioning effect that results in fewer suitable sites for micronuclei to grow when the surrounding tissue becomes supersaturated. Similarly, exercise may disturb stable micronuclei so that they subsequently involute, thus reducing the population transiently. Restoration of micronuclei numbers by whatever process is responsible for producing them would explain the decay in benefit over time following the exercise episode. There are no widely recommended practical strategies designed to take advantage of this phenomenon. Perhaps the best that can be said is that going for a run (or something similar) between 2 and 24 hours before diving may help reduce the risk of DCS.

The effect of exercise during diving may depend on its timing. The typical pattern is that activity during the bottom time sees the diver exercising moderately, and then ascent and decompression (if any) are largely done at rest. This is probably a disadvantageous pattern of exercise because it will result in increased perfusion and inert gas uptake (in some tissues at least) during the bottom phase of the dive and then decreased perfusion and inert gas elimination during the decompression. It is widely accepted that this explains the perception that dives involving hard work at the bottom are associated with greater risk of DCS. A reduction in risk may therefore be achieved by reducing work at depth and maintaining gentle levels of exercise during decompression. There is some evidence in support of these notions. Although a reduction in work at depth can be impractical in occupational diving, in recreational diving it is afforded by, for example, use of diver propulsion vehicles. Similarly, in a decompression diving situation, to maintain gentle exercise during decompression it is usually possible to fin gently against the resistance of the down line or decompression stage. In diving where hard work at the bottom cannot be avoided, the use of a longer safety stop (for a no decompression dive) or lengthening of the prescribed shallow stops in a decompression dive would be an appropriate precaution. There are no universally accepted guidelines for ‘padding’ decompression in this way.

Exercise after diving has generally been considered unwise, although the timing is unclear. Several concerns are noted, not the least of which is that there are many reports of symptoms of DCS arising during periods of work soon after diving. This, of course, may be coincidental, but there are plausible reasons to believe that exercise may have a causative role in such cases. First, exercise may promote the passage of VGE across pulmonary shunts into the arterial system, where they may be more harmful, as described in Chapter 10. Second (and similarly), exercise (particularly that involving lifting or straining) may promote right-to-left shunting of VGE across a PFO with the same result. Finally, it is speculated that where there are micronuclei in tissues supersaturated with inert gas, exercise may contribute to their excitation into growth, thus producing bubbles. This would be analogous to shaking an open bottle of carbonated drink, but the validity of this concern is unknown. At a practical level, mitigation of this risk involves refraining from exercise or lifting for a period after diving. This ‘period’ should definitely extend for at least several hours because this corresponds to the peak and duration of VGE formation after typical dives. Longer would be better, but how long is unknown.


Hydration (or more correctly, dehydration) is one of the most widely recognized of the alleged risk factors for DCS among divers. For all the attention given to the matter, there is remarkably little proof that dehydration actually imputes increased risk.

There is one study in which pigs deprived of water and administered a diuretic during a saturation pressure exposure had more severe DCS than normally hydrated pigs after decompression. In addition, limited human data have shown that supplemental hydration just before diving reduces VGE numbers after diving, especially in subjects who appear prone to VGE formation. This finding is encouraging but falls short of proving that good hydration is protective in humans. Nevertheless, the proposition makes sense. There is evidence that divers are prone to dehydration through factors such as exposure to hot conditions, poor availability of water on boats, sea sickness and immersion diuresis. There is also evidence that realistic levels of ‘dehydration’ reduce regional tissue perfusion during exercise, and because perfusion is important for inert gas washout, it seems plausible that dehydration could impair this process. It is certainly true to say that no one has ever demonstrated dehydration to be beneficial.

It follows that maintenance of hydration can probably only be good. As a somewhat arbitrary guide, the supplementation of normal fluid intake with a litre of water over the hour before diving would make sense.


It has long been observed that the risk of DCS seems higher when diving is conducted in cold conditions. The potentially dramatic effect of temperature on risk of DCS was demonstrated in a landmark study performed by the US NEDU5. It is a complicated study with multiple arms and profiles, but the most important observation was the comparison of outcomes when divers undertook a 120-foot for 30-minute dive with decompression as prescribed by a US Navy dive table under two different thermal conditions. In one set of dives (referred to as cold/warm), the divers were immersed in water at a temperature of 26°C for the bottom phase of the dive and 36°C for the decompression. In the second set of dives (referred to as warm/cold), the temperature conditions were reversed between the bottom and decompression phases. The divers wore no thermal protection. In the cold/warm series, there were no cases of DCS in 80 dives (0 per cent), whereas in the warm/cold series, there were 7 cases of DCS in 32 dives (22 per cent).

The water temperatures and the lack of exposure protection make the conditions difficult to interpret in real-world terms, but the dramatic change in DCS risk between the cold/warm and warm/cold conditions is highly relevant. It can be argued that the condition most analogous to real diving would be the markedly more hazardous warm/cold situation. Thus, divers tend to start a dive warm and become progressively colder during the dive. If there is a lesson to be learned from the NEDU temperature study it is that becoming cold during a dive should be avoided as much as possible.

Practical strategies to mitigate the risk of diving in cold water include optimizing exposure protection, which would include the use of drysuits with state of the art undergarments and possibly even active heating systems, which are now widely available. The ideal time to turn these heating systems on would be during decompression. Extreme divers in cold water caves have even established underwater habitats where the diver can remain under pressure, but not immersed, thus giving an opportunity to reduce conductive heat loss into the water and to take hot fluids orally. As previously, there is always the option of ‘padding’ or extending decompression for decompression dives conducted in cold water.

Some data suggest that remaining warm after diving (despite a cold environment) may reduce production of VGE and the incidence of DCS. It is therefore probably sensible to avoid becoming cold early after a dive, especially one that was provocative from a decompression point of view. Almost paradoxically, however, there is a report of two cases of DCS arising in temporal relation to exposure to hot water in a shower early after diving. This single report has achieved considerable penetration into the diving community and is the cause of much anxiety about showers after diving. It is plausible that sudden warming of supersaturated superficial tissue could decrease gas solubility and precipitate symptomatic bubble formation. However, many divers take showers early in the post-diving period with no problems, and the risk of such events seems very low.


It has long been believed that obesity is a risk factor for DCS, based largely on the ‘first principle’ belief that because nitrogen is highly soluble in fat, an obese person can absorb more nitrogen. Whether this is a practically relevant consideration is controversial. There is conflict in the literature with some studies (probably the majority of those that have addressed this issue) purporting to show an association between risk of DCS and obesity, whereas others have not. Whatever the truth of this matter, obesity is a condition that is often associated with reduced functional capacity and other health problems. Obese divers would benefit from losing weight for multiple reasons.


There are some data suggesting that older divers are at higher risk of DCS and perhaps at higher risk of an incomplete recovery if they suffer serious event. However, once again, there is conflict in the literature on this subject. The fact that older divers are likely to have a lower functional capacity and a higher risk of cardiac events is probably of greater importance than concern about the risk of DCS.

Dive sequences

As alluded to earlier, multiple dives in a single day are common in recreational diving. Sequential dives conducted while dissolved inert gas in tissue remains after a previous dive are referred to as ‘repetitive dives’. The definition of repetitive diving differs according to which table or decompression algorithm is used because there is variability in assumptions about total outgassing time. For example, the Professional Association of Diving Instructors, Inc. considers that complete outgassing occurs after 6 hours, whereas the Canadian Defence and Civil Institute of Environmental Medicine (DCIEM) table works on a much longer total outgassing time of 18 hours.

Irrespective of the definition, it is clear that if a second dive takes place in the presence of residual dissolved inert gas remaining after a previous one, then tissue gas loading during the second will compound on that remaining from the first. Perhaps for this reason it has frequently been taught that repetitive diving is a risk factor for DCS, although it is not clear why it should be, provided residual inert gas is adequately accounted for in calculation of no decompression limits or decompression protocols for subsequent dives. One argument that is sometimes advanced in this regard is that bubble formation after the first dive alters inert gas kinetics on the second dive, or those bubbles may undergo further growth after the second dive. There are no convincing data that clearly identify repetitive dives per se as being associated with increased risk. Indeed, the situation is made even less clear by the existence of an acclimatization phenomenon reported from occupational environments in which the incidence of DCS among a cohort of workers undertaking diving or compressed air work is reliably noted to fall over a multiday sequence of exposures. These exposures frequently differ (e.g. in being once daily) from the typical repetitive dives undertaken by recreational divers that may involve up to four or more short exposures per day. Nevertheless, the truth relating to risk in these situations is unclear. Part of the problem relates to the fact that so much of the diving undertaken by recreational divers is repetitive, so it is not surprising that many of the DCS cases arise in repetitive diving.

One particular form of repetitive diving that is associated with considerable controversy is so-called ‘reverse profile’ diving. This is the performance of a repetitive dive deeper than the previous dive (or than another dive in the repetitive sequence). In this sense, the term ‘reverse profile’ is a misnomer because what is really being discussed is reverse depth diving. The origins of the edict that reverse profile diving is hazardous are unclear. Cursory manipulation of the repetitive function of common dive tables reveals that avoidance of reverse profiles results in more allowable bottom time over the sequence. That alone could be reason enough to avoid reverse profiles, but as in repetitive diving itself, it is not clear why reverse profile diving should be considered more hazardous provided residual inert gas from the previous shallower dive(s) is adequately accounted for in calculation of no decompression limits or decompression protocols for the subsequent deeper excursion.