© Springer-Verlag London 2015
Zahid Amin, Jonathan M. Tobis, Horst Sievert and John D. Carroll (eds.)Patent Foramen Ovale10.1007/978-1-4471-4987-3_1212. Patent Foramen Ovale and Divers
(1)
Cardiology Department, The Mater Misericordiae Hospital, Eccles Street, Dublin 7, Ireland
Abstract
A patent foramen ovale (PFO) occurs in approximately 27–30 % of the population (Thompson and Evans, Q J Med 23:135–52, 1930; Hagen et al. Mayo Clin Proc 59:17–20, 1984) and has been linked to paradoxical embolism, cryptogenic stroke, migraine and an increased risk of decompression illness (DCI) in divers.
Recent estimates have suggested that over 15 million people worldwide are participating in recreational diving, with greater than 250,000 dives per year (UN atlas of the Oceans. 2006. http://www.oceanaltas.org). Decompression sickness is estimated to occur in one per every 6,369 dives deeper than 30 m of sea water (St Leger Dowse et al., Aviat Space Environ Med 73:743–9, 2002). However, those with PFOs have been shown to have a fivefold increase in the risk of experiencing decompression illness (Torti et al., Eur Heart J 25:1014–20, 2004). This, and recent studies describing a higher incidence of subclinical cerebral damage in divers with PFOs has led to increasing numbers of divers seeking out screening for the presence of a PFO and elective PFO closure.
In the absence of definitive practice guidelines, the clinical management of such patients remains challenging. In this chapter we review the pathophysiology of diving and PFOs, the potential risks associated with the presence of a PFO in divers, as well as some proposed methods of screening and managing this patient group.
Keywords
Patent foramen ovaleDeep sea divingDecompression illnessAbbreviations
ACC
American College of Cardiology
DCI
Decompression illness
ESC
European Society of Cardiology
MRI
Magnetic resonance imaging
NHS
National Health Service
PFO
Patent foramen ovale
TCD
Transcranial doppler
TOE
Transoesophageal echocardiogram
TTE
Transthoracic echocardiogram
Pathophysiology
Decompression illness occurs when a reduction in surrounding pressure allows inert gas, typically nitrogen, to come out of solution and form bubbles. This is associated with diving as the combination of breathing compressed air and the extremes of environmental pressure on diving descent and ascent can result in inert gases coming out of solution.
When a diver descends they are exposed to increased environmental pressure and increased amounts of inert gas dissolving in the tissues [1–5]. The amount of gas dissolved is proportional to the ambient pressure (depth of the dive), duration of the dive, and individual factors such as percentage body fat, cardiac output and pulmonary diffusion coefficient [6]. On ascent, if an inadequate amount of time is taken to reduce the ambient pressure, the inert gas exceeds solubility and forms bubbles in tissues and venous blood.
Decompression illness is typically categorised into two types. The type of DCI experienced is thought to be related to the size and the quantity of bubble formation. Type I/ Minor (musculoskeletal) is typically characterised by pain in joints and limbs (‘the bends’), generalised itching and a characteristic skin rash (cutis marmorata) and occasionally localised ischaemia. It is associated with small gas loads. Type II/ Major (neurological/ cardiorespiratory) is characterised by predominantly neurological symptoms- the thoracic spinal cord is usually affected, with cerebral involvement occurring in up to 30 % of cases. This may manifest as limb weakness or paralysis, bowel and bladder dysfunction, as well as confusion, visual disturbances and vertigo. In order for the bubbles to pass into the systemic circulation there must be a large bubble load, as otherwise the pulmonary capillary bed would successfully diffuse the nitrogen.
The presence of a PFO, increases the risk of type II DCI as it allows nitrogen bubbles that may otherwise have diffused out in the lung tissue, to pass into the systemic circulation. The likelihood of paradoxical gas embolism in the presence of a PFO is increased in divers as they have been shown to reproduce physiological conditions favourable for right to left shunting. Pulmonary embolisation of nitrogen bubbles causes an increase in pulmonary vascular resistance and consequently augmented right atrial pressures [7]. Whilst some of the respiratory manoeuvres associated with deep sea diving have been shown to alter intrathoracic pressures and facilitate a transient reversal in the interatrial pressure gradient [8, 9].
However not all divers with PFOs experience DCI, and plenty of divers without PFOs do experience an episode of DCI. So although there are strong physiological arguments for the association of PFOs with DCI in divers, there are other factors to consider.
Risks Associated with Diving and PFOs
Decompression Sickness
The estimated risk of DCI in divers is reported to be 2.5 per 104 dives. However, this risk has been shown to be five times higher in those with PFOs compared to those without a PFO.
One issue with DCI for the clinician is that a retrospective definitive diagnosis of DCI in divers can prove difficult. Patients may present months or even years after their event. Although some cases may have a documented abnormal neurological examination ± neuroimaging, many divers report transient non-specific neurological symptoms that may or may not represent DCI.
Another factor to consider with reported DCI events is whether the episode is considered ‘undeserved’. In other words, if a diver misses decompression stops or ascends too rapidly then some degree of decompression sickness would be expected, regardless of whether or not the diver has a PFO.
For those that present with a convincing history of DCI, despite taking the appropriate precautions with their diving schedule, the presence of a PFO would be considered a risk factor for the event and for the possibility of a recurrent event.
Divers with a history of migraine with aura have also been shown to have an increased risk of neurological DCI. Wilmshurst et al. demonstrated that 26.5 % of their diving population had a history of migraine with aura, with 41.7 % of these patients having anatomically larger shunts on transthoracic echocardiography (TTE) with contrast [10].
Some studies have looked at particular characteristics of PFOs that may be associated with an increased risk of DCI. One group reported a high incidence of larger diameter flap valve PFOs in a diving population, and suggested that this type of PFO is more likely to be related to DCI type II compared to other anatomical variants and those of smaller diameter [11]. Cartoni et al. demonstrated in a group of divers with PFOs, that those with a larger PFO diameter and increased mobility of the interatrial septum had an increased risk of DCI [12].
Divers with a PFO who experience DCI are also more likely to develop type II DCI or Major DCI than type I DCI. Wilmshurst et al. showed that 66 % of divers with type II DCI had PFOs compared to only 24 % of control group divers having PFOs [13]. The same group also demonstrated the link between cutaneous DCI and PFOs, finding that 77 % of those with cutaneous DCI had a PFO compared to 27.6 % of a control diver group [14].
Ischaemic Brain Lesions
Several groups have reported an increase prevalence of hyperintense white matter brain lesions in divers compared to non-divers [15]. These lesions were initially described in divers presenting with DCI but follow up studies noted that even divers without a history of neurological signs or symptoms were still found to have lesions on neuro-imaging.
The frequency of such asymptomatic lesions on magnetic resonance imaging (MRI) has been reported to be between 44 and 52 % in the diving population, and although there appears to be a relatively high prevalence of such lesions in control groups (20 %), these studies demonstrated that the presence of multiple brain lesions was found only in the divers [16, 17].
Schwerzmann et al. demonstrated 41 ischaemic lesions in 19 divers compared to 7 lesions in 6 controls, and almost twice as many lesions in divers with PFOs compared to those without (p = 0.07). These lesions were not found to be associated with a history of DCI [16].
However Koch et al. were unable to find a significant correlation between the presence or quantity of cerebral hyperintensities and the presence of a PFO in a group of divers with no history of DCI [18].
The long-term significance of such lesions remains unclear. The mean age of divers in the literature that reports hyperintense brain lesions ranges between 35 and 51 years [16, 17, 19]. Moen et al. probably report on the oldest cohort of divers (mean age 51 years) with the longest follow up since their last dive (median 12 years)- they described widespread diffusion and localised perfusion pattern abnormalities in divers compared to controls. It should be noted that these findings were reported in a group of symptomatic divers (mostly neurological symptoms) and thus there is a degree of selection bias in their diver group, compared to their asymptomatic controls.
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