Patent foramen ovale and diving
Section snippets
History of diving accidents related to patent foramen ovale
Although paradoxical embolism through a patent foramen ovale (PFO) had been described as early as in 1877 [14], and paradoxical gas embolism was described in 1979 [15], the first reports of a possible relationship between decompression sickness and patency of the foramen ovale date only from 1989 [16]. Since then, considerable controversy has arisen concerning the real importance of PFO as a risk factor for diving. This controversy is related to several factors.
First, the diagnosis of
Retrospective evidence of increased risk with patent foramen ovale
Retrospective studies compare divers who have suffered from DCS with healthy volunteers, both divers or nondivers. Divers with neurologic DCS were found to have a significantly higher prevalence of PFO (Table 1). From these retrospective studies, the odds ratio (OR) can be calculated for the probability of suffering DCS when diving with a PFO. From a combined analysis of the c-TTE studies, an OR of 2.6 has been calculated. The c-TEE and c-TCD studies yielded ORs of 5.6 [25], 4.3 [36], and 4.8
Nature of decompression pathology related to patent foramen ovale
PFO-related decompression sickness is presumed to be caused by paradoxical nitrogen bubble embolization through the interatrial septum. After many long, deep (25 msw or more) dives, large numbers of nitrogen microbubbles (19–700 microns in diameter) [4] can be detected in the central venous circulation. If about 25% of all divers have a PFO, why does this condition not lead to decompression sickness more often?
It is a popular misconception that a PFO allows the continuous passage of blood
Prospective evaluation of increased risk
One reason why not more of the divers with PFO are affected by neurologic DCS may be the “fast-tissue” nature of the brain; that is, the brain has a sufficiently high and constant blood supply so that it can desaturate quickly after a dive [45]. By the time nitrogen bubbles actually are embolized into the brain (20 to 30 minutes after surfacing from the dive), the partial nitrogen pressure in brain tissue would probably be sufficiently low for nitrogen to diffuse out of the bubble rapidly.
Changing patency over time
Finally, when making statements about the risk of PFO for divers, one must take into account the possibility that a PFO may evolve over time and possibly become more patent after some years.
In the classical autopsy studies performed in 1931 and 1984 [22], [23], different age cohorts seemed to have different patency prevalence (Table 2). This finding suggests that PFOs tend to close with advancing age unless they are large or unless something keeps them open.
Anecdotal observations of divers who,
Summary
Patency of the foramen ovale is a risk factor for DCS in SCUBA divers, even if they adhere to the currently accepted and used decompression tables. The primary cause of DCS, however, is the nitrogen bubble, not the PFO. There are a number of techniques any diver can use to minimize the occurrence of nitrogen bubbles after a dive.
The authors current practice is to inform civilian sports divers of the increased risk and to advise them to adopt conservative dive profiles. This can be achieved by
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Cutis Marmorata skin decompression sickness is a manifestation of brainstem bubble embolization, not of local skin bubbles
2015, Medical HypothesesCitation Excerpt :It constitutes a pathway for a right-to-left intracardial blood shunts. When, in the course of the normal cardiac contraction–relaxation cycle or, more commonly, provoked by certain “straining” (Valsalva-like) maneuvers performed by the diver, a pressure reversal takes place with right atrial pressure exceeding left, venous gas emboli may be swept into the arterial circulation and become so-called paradoxical arterial gas emboli [12,13]. The association between PFO and certain forms of DCS has been well established.
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