Sunday, July 23, 2006

Should All Divers be Screened for PFO?

An increased prevalence of brain lesions has been found in divers even in the absence of recognized decompression illness. Permanent neuropsychological changes such as memory disturbances and depression have been found in professional divers, even in those who have never had decompression sickness. The changes are probably the result of intravascular gas bubbles insufficient to cause acute symptoms. A study examined amateur divers with long histories of self-contained underwater breathing apparatus diving by magnetic resonance imaging and compared them with normal controls. Hyperintense lesions of the subcortical cerebral white matter and degenerative changes of the cervical disks were significantly more common in the divers. 27 of 52 divers had a total of 86 focal hyperintensities versus 10 of 50 controls with 14 focal hyperintensities (p < 0.01). [Reul J, Weis J, Jung A, Willmes K, Thron A. Department of Neuroradiology, Technical University, Aachen, Germany.]

In a seminal study, transcranial Doppler ultrasonography detected a right-to-left shunt in all divers with multiple brain lesions. Multiple brain lesions in sport divers were associated with presence of a large patent foramen ovale. This association suggests paradoxical gas embolism as the pathological mechanism. A patent foramen ovale of high haemodynamic relevance seems to be an important risk factor for developing multiple brain lesions in sport divers.[Michael Knauth et al, Department of Neuroradiology University of Heidelberg Klinikum Heidelberg Im Neuenheimer Feld 400 D 69120 Heidelberg Germany, b Department of Neurology, University of Heidelberg, Klinikum Mannheim, Germany, c Department of Biology, University of Frankfurt, Klinikum Frankfurt, Germany]

A foramen ovale no doubt accounted for most of these cases. A comparative investigation regarding brain lesions and the presence of a foramen ovale in sport divers and non-diving controls showed that brain lesions were more common in individuals with a foramen ovale, although divers had more brain lesions than non-divers, irrespective of the presence of a PFO. In a Swiss University and dive club study, the risk for decompression illness events was 4.5-fold greater in divers with patent foramen ovale than in divers without patent foramen ovale (risk ratio, 4.5 [95% CI, 1.2 to 18.0]; P = 0.03). Among divers, 1.23 ± 2.0 and 0.64 ± 1.22 ischemic brain lesions per person (mean ± SD) were detected in those with and those without patent foramen ovale, respectively. Among controls, 0.22 ± 0.44 and 0.12 ± 0.63 lesion per person were detected (P < 0.001 for all groups). Conclusions: Regardless of whether a diver has a patent foramen ovale, diving is associated with ischemic brain lesions. [Schwerzmann et al]

This has led some diving schools to recommend screening for the presence of a PFO for professional divers or avid amateurs. In such divers, PFO closure would make sense. If a non-invasive, inexpensive, valid method for determining the presence or absence of a PFO could be found - would it be protective for decompression illness, or better yet protective for brain lesions in the absence of decompression illness.

There is a study that was done in 2001 in Finland that found that ear oximetry fit the bill for all of these factors. As reported in Stroke. 2001;32:448, "Ear Oximetry: A Noninvasive Method for Detection of Patent Foramen Ovale", the following results were noted:—Dye dilution curves were obtained from 67 patients. Dye dilution correctly diagnosed 35 of the 46 patients who had PFO in TEE and all the 21 patients without PFO. Thus, the sensitivity (95% CI) of the dye dilution method was 76% (61% to 87%) and its specificity 100% (84% to 100%). Ear oximetry was done on 83 patients. Oximetry correctly diagnosed 45 of the 53 patients who had PFO in TEE and all of the 30 patients without PFO. Thus, the sensitivity of ear oximetry was 85% (72% to 93%) and its specificity 100% (88% to 100%). When only the largest shunts were included, oximetry had a sensitivity of 93% (38 of 41).The interrater agreement was excellent ({kappa} value 0.94 for dye dilution and 0.90 for oximetry).

Conclusions—Dye dilution and oximetry are both sensitive and specific methods for the detection of PFO. Oximetry has the following primary advantages over the currently available diagnostic methods: it is noninvasive, safe, and inexpensive and causes no discomfort for the patient. We suggest that oximetry could be used as a first-line screening method for PFO in patients with cryptogenic stroke. Ear oximetry also has potential use in epidemiological studies. [Vesa Karttunen, MD et al from the Department of Neurology (V.K., M.H.) and the Department of Cardiology (M.I., M.N.), Oulu (Finland) University Hospital; and the Department of Cardiology (M.V.), Helsinki (Finland) University Central Hospital. ] Full Text at .

Scientists in Switzerland have also found that those with PFOs more than 9mm in diameter had a much higher risk of DCI. They were up to 13 times more likely to have ended up in a chamber for treatment and five times more likely to have had major DCI than divers without a PFO or divers with a small PFO.

Research by Dr Peter Wilmshurst, a British expert in this field, has confirmed the importance of PFO size. He says: ‘There is no doubt that here, as in most things, size really does matter. The bigger your PFO, the greater your chance of getting bent. But to put this into perspective, only 1.3 per cent of the population have PFOs that are 10mm in diameter or larger and these people suffer between 30 and 40 per cent of all bends.’

Dr. Avi Shupak, Haifa, Israel writes :
I have read with great interest your excellent summary on PFO as a risk factor for DCI and long term neurological effects in divers.

I would like to draw your attention to a recent article published in Mayo Clin Proc 2006;81:602-8 (Petty GW, et al. Population-based study of the relationship between PFO and cerebrovascular ischemic event.). The study results showed that PFO is not an independent risk factor for cryptogenic ischemic stroke or TIA. The data analysis also included separate evaluation of large PFO as a risk factor that reach identical conclusion.

Although the damage mechanism of paradoxical gas emboli (anticipated during a dive) might differ from the pathogenesis of cerebrovascular event by solid emboli, the remarks of the authors about possible methodology flaws in previous studies reporting PFO to be a risk factor for cryptogenic CVA might be of relevance to parallel studies in divers.

Best Regards,

Avi Shupak, MD

Haifa, Israel

We posted this article May 30, 2006 without very much comment. See

See also:
Patent Foramen Ovale

B. Meier and J. E. Lock
Contemporary Management of Patent Foramen Ovale
Circulation, January 7, 2003; 107(1): 5 - 9.
[Full Text] [PDF]