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Patent Foramen Ovale and Decompression Sickness Douglas Ebersole, MDIntroductionPatent

Patent Foramen Ovale and Decompression Sickness

 

Douglas Ebersole, MD

Introduction

Patent foramen ovale (PFO) is a very popular topic in scuba diving as the appreciation of its relationship to decompression sickness (DCS) becomes more widespread in the diving community.  Though the incidence of DCS in recreational diving is only about 2 episodes per 10,000 dives, decompression sickness affects approximately 1000 divers per year.  The presence of a PFO is felt to increase the risk 5- to 13-fold (1-3).  An understanding of the link between PFO and DCS as well as various treatment options is vitally important to health professionals who treat these patients.

Incidence and Anatomy

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The patent foramen ovale is an integral part of the normal fetal circulation.  Normally, a portion of the blood from the inferior vena cava passes from the right atrium to the left atrium through the PFO during fetal life, bypassing the lungs.  At birth, pulmonary blood flow increases greatly, increasing left atrial pressure.  The resulting atrial pressure differences compress the septum primum against the septum secundum, functionally closing the PFO.  Anatomic closure of the PFO occurs later in infancy in most people but is incomplete in approximately 25% of the population (4,5), leaving these individuals at risk for right to left shunting.  PFO diameters are quite variable in size ranging from 1-19 mm with the average size being larger in older adults (4), suggesting PFOs my continue to enlarge during life.

Relationship of PFO to DCS

2It was first suggested in 1986 that a cardiac right to left shunt may be important for paradoxical gasembolism in scuba divers (6). Subsequently, the importance of PFO for DCS in divers has been further investigated (1,7-10).  As mentioned above, the risk of DCS in sport divers is quite low but is increased by at least 5-fold in the presence of a PFO (1-3).  Additionally, the average number of ischemic brain lesions as seen on MRI in experienced divers with PFO has been reported to be twice as high as in divers without PFO (11).  The etiology and clinical significance of these findings are unclear but may represent multiple subclinical paradoxic embolic events across the PFO.

Diagnosis

Both transthoracic echo (TTE) and transesophageal echo (TEE) have been used for the diagnosis and assessment of PFO.  TEE is the preferred diagnostic test of choice, however, given its better visualization of the atrial septum resulting in greater sensitivity in making the diagnosis.

The injection of agitated saline increases the diagnostic sensitivity by enhancing echocardiographic detection of the trivial intermittent right-to-left shunting across a typical PFO.  Agitated saline contrast injected intravenously during Valsalva maneuver with release of straining when contrast is visualized in the right atrium increases sensitivity.  Visualization of contrast microbubbles passing from the right to left atrium through the visualized foramen ovale during the release phase is diagnostic of an interatrial communication.  In clinical practice, the actual site of right-to-left shunting may not be convincingly visualized or recorded for technical reasons.  If a recording co

nvincingly demonstrates microbubbles appearing in the left atrium immediately after arriving in the right atrium, then the presence of a PFO can be presumed.  If bubbles appear in the left atrium before or > 5 beats after they appear in the right atrium, then the possibility of anomalous pulmonary arteriovenous connection to the left atrium or pulmonary arteriovenous malformations must be considered.

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Contrast injected through an upper extremity vein may be washed away by contrast-free blood flow from the inferior vena cava directed by the Eustachian valve, creating a false-negative result (12).  Injection of contrast via the femoral vein has been proposed to enhance detection by TEE, with the streaming effect of directed inferior vena cava flow to the region of the fossa ovalis and through a patent foramen (13).

Therapeutic Options

No specific guidelines exist for PFO closure in people who have decompression illness, but the options are to stop scuba diving, decrease the depth and/or time of dives to limit the inert gas load, or undergo percutaneous PFO closure.  Some divers decide that they have many other interests and diving is not that important to them.  These divers will frequently give up the sport.  Other divers who enjoy the sport but dive infrequently often opt for diving “conservatively” to limit their bubble-load.  This would involve no-decompression diving, limiting depths to < 100 feet, diving nitrox on air profiles, prolonged (> than the usually recommended 3-5 min) safety stops at approximately 15-20 feet at the end of their dives, and limiting the number of dives per day to one or two.  People who make their living through scuba diving (instructors, divemasters, etc) and divers who enjoy more aggressive types of diving such as deep wrecks, cave diving, rebreather diving, and mixed gas diving often elect percutaneous closure of the PFO.  This also holds true for divers who have had recurrent “unexpected” DCS events despite diving conservatively as defined above.

Treatment Results

A recent study reported the results of conservative diving practices after an episode of DCS (14).  Eighteen divers in this study had a right-to-left shunt, nine were small and nine were large.  Mean follow-up was 5.3 years (range 0-11 years).  Four of these divers had undergone PFO closure and had no episodes of DCS in follow-up.  The absolute risk of suffering DCS before examination for the remaining 14 divers with right-to-left shunt and no closure was 23.5 DCS events per 10,000 dives for those with a small shunt compared to 71.6 for those with a large shunt.  After recommendation for conservative diving practices, the DCS risk at follow-up fell to 6.0 per 10,000 dives in the small shunt group and zero in divers with the large shunt.  The major limitation to this study is its small sample size, but the results suggest a need for more studies of conservative diving practices for divers with right to left shunts.

When DCS has occurred, especially after so called “undeserved” cases of DCS, divers are often encouraged to seek screening for a shunt and some diving medical societies classify these divers as ineligible to return to diving (15).   There are also several diving medical specialists who recommend divers with a history of DCS and a positive right-to-left shunt to undergo closure if it turns out to be a PFO, even though there is no clear evidence to indicate that this intervention reduces the risk of DCS or neurologic events (16-19).

However, in a 2011 study of 83 scuba divers with a history of DCS and a follow-up of 5.3 years, 28 divers had no PFO, 25 had a PFO closure, and 30 continued diving with a PFO without closure (20).   At the beginning of the study, there were no significant differences between the groups in the number of dives, dive profiles, diving depth, or cumulative dives to more than 40 meters of salt water (msw).  After follow-up, while there were no differences between the groups with respect to minor DCS events, the risk for major DCS was significantly higher in the divers with PFO and no closure than in divers with PFO and closure or divers without PFO.  Although this offers new evidence that PFO closure reduces the risk for major DCS, the authors do not recommend closure in all divers with a history of DCS but rather recommend further studies to confirm these results.

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Percutaneous PFO Closure

The closure procedure for a patent foramen ovale is relatively painless and is done percutaneously through a femoral vein.  Imaging during the procedure is done with a combination of fluoroscopy and ultrasound imaging, either TEE or intracardiac echo.  The most common device in use in the United States is the Amplatzer Cribriform Occluder .  This is a wire mesh made out of nickel and a titanium alloy.  The device is filled with securely sewn polyester fabric to help close the defect.  It is deployed through a small catheter which has been placed across the PFO.  The procedure takes about an hour and patients are usually discharged home the same day or the following morning.

Ongoing Studies

In 2010, Divers Alert Network (DAN) began a five year prospective non-randomized study following divers with a history of decompression sickness and a PFO, whether or not the diver had chosen to have the PFOclosed.  At this time there are 60 of the planned 120 participants enrolled.   Divers interested in participation can find more information at http://www.diversalertnetwork.org/research/studies/risk_benefit_of_pfo_closure.

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Conclusions and Recommendations

  1. Should all divers be screened for a PFO? No. There is approximately a 5-fold increased relative-risk of DCS in patients with PFO, but the absolute risk is still quite small.
  2. Should all divers with DCS be screened for a PFO? No.  Twenty five percent of the population has a PFO so one would expect a similar percentage of divers with DCS to have a PFO.  Not all scuba dives have the same risk of DCS.  To paraphrase James Carville’s famous quote from the first Clinton presidential campaign, “it’s the bubble, stupid”.  The issue with decompression sickness is the inert gas “bubble load”, not the PFO.  However, episodes of DCS in “low-risk” dives, especially neurologic events, or multiple “undeserved” DCS events should prompt investigation for PFO.
  3. Should all divers with DCS and PFO have a PFO closure? No. Options for divers with PFO and DCS include discontinuing diving, conservative diving practices, or PFO closure.  Recommendations should be made on a case-by-case basis based on the DCS event(s), the type of diving being performed by the diver involved, and the risks of PFO closure.

 

Dr. Douglas Ebersole, MD is a cardiologist specializing in coronary and structural heart interventions at the Watson Clinic LLP in Lakeland, Florida.  He is also an avid technical, cave, and rebreather diver and instructor.  He can be reached at debersole@watsonclinic.com.

References:

  1. Wilmshurst, PT, Byrne JC, Webb-Peploe MM. Relation between interatrial shunts and decompression sickness in divers.  Lancet. 1989;334:1302-1306
  2. Torti SR, Billinger M, Schwerzmann M. Risk of decompression illness among 230 divers in relation to the presence and size of patent foramen ovale. Eur Heart J 2004;25:1014-1020
  3. Bove AA. Risk of decompression sickness with patent foramen ovale. Undersea Hyperb Med 1998;25:175-8.
  4. Hagan PT, Scholz DG, Edwards WD. Incidence and size of patent foramen ovale during the first 10 decades of life: an autopsy study of 965 normal hearts. Mayo Clin Proc 1984;59:17-20.
  5. Kerut EK, Norfleet WT, Plotnick GD, Giles TD. Patent foramen ovale: a review of associated conditions and the impact of physiological size. J Am Coll Cardiol 2001;38 (3): 613-623.
  6. Wilmhurst PK, Ellis BG, Jenkins BS. Paradoxical gas embolism in a scuba diver with an atrial septal defect. Br Med J (Clin Res Ed) 1986;293:1277
  7. Moon RE, Camporesi EM, Kisslo JA. Patent foramen ovale and decompression sickness in divers. Lancet 1989;1:513-14.
  8. Germonpre P, Dendale P, Unger P, et al. Patent foramen ovale and decompression sickness in sport divers. J Appl Physiol 1998;84:1622-6.
  9. Germonpre P, Hastir F, Dendale P, et al. Evidence for increasing patency of the patent foramen ovale in divers. Am J Cardiol 2005;95;912-15.
  10. Gempp E, Blattearu J, Stephant E, et al. Relation between right-to-left shunts and spinal cord decompression sickness in divers. Int J Sports Med 2009;30:150-3.
  11. Schwerzmann M, Seiler C, LippE, et al.  Relation between directly detected patent foramen ovale and ischemic brain lesions in sport divers.  Ann Intern Med 2001:134:21-4.
  12. Schuchlenz HW, Weihs W, Hackl E, Rehak P. A large Eustachian valve is a confounder of contrast but not of color Doppler transesophageal echocardiography in detecting a right-to-left shunt across a patent foramen ovale.  Int J Cardiol 2006;109:375-80.
  13. Gin KG, Huckell VF, Pollick C. Femoral vein delivery of contrast medium enhances transthoracic echocardiographic detection of patent foramen ovale. J Am Coll Cardiol 1993;22:1994-2000.
  14. Klingmann, C, Rathmann N, Hausmann D, et al.  Lower risk of decompression sickness after recommendation of conservative decompression practices in divers with and without vascular right-to-left shunt.  Diving and Hyperbaric Medicine 2012;42(3):146-150.
  15. [Swiss Underwater and Hyperbaric Medical Society. Empfehlungen 2007. Der Schwiezerischen Gesellschaft Fur Unterwasser-und Hyperbarmedizin Zum Tauchen Mit Einem Offenen Foramen Ovale]
    [cited 2012 June11]. Available from: http://www.suhms.org/downloads/SUHMS%20PFO%20Flyer%20d.pdf(German)
  16. Scott P, Wilson N, Veldtman G. Fracture of a GORE HELEX septal occluder following PFO closure in a diver. Catheter Cardiovasc Interv 2009;73:828-31.
  17. Wahl A, Praz F, Stinimann J, Windecker S, Seiler C, Nedeltchev K, et al. Safety and feasibility of percutaneous closure of patent foramen ovale without intra-procedural echocardiography in 825 patients. Swiss Med Wkly. 2008:138:567-72.
  18. Saguner AM, Wahl A, Praz F, et al. Figulla PFO occlude versus Amplatzer PFO occlude for percutaneous closure of patent foramen ovale. Catheter Cardiovasc Interv 2011;77:709-14
  19. Furlan AJ, ReismanM, Massaro J, et al. Closure or medical therapy for cryptogenic stroke with patent foramen ovale. N Engl J Med. 2012;366:991-9.
  20. 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;97:1932-7.