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Patent Foramen Ovale in Diving
Introduction
Patent foramen ovale (PFO), also known as persistent foramen ovale, is a condition in which the foramen ovale, a naturally occurring opening in the atrial septum of the developing fetus, fails to close after birth. Among individuals who participate in aquatic diving, this condition has been associated with severe, sudden-onset neurological decompression sickness, inner ear decompression sickness, and cutis marmorata.[1][2][3]
Etiology
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Etiology
During fetal development, the foramen ovale enables blood to flow from the right atrium to the left atrium, bypassing the fetal lungs. This opening typically closes within a few years after birth. If it fails to close, venous blood will continue to be shunted into the left heart without passing through the lungs.[4] The shunt is not clinically significant in most individuals.
Epidemiology
The foramen ovale remains open, or patent, in approximately 20% to 34% of adults, with detectable shunting occurring in 8% to 10% of cases.[5] The incidence of decompression sickness in the general diving population is relatively low, ranging from 0.01% to 0.095%, depending on the diving environment and type of diving performed.[6] In relatively small cohorts of divers with a known patent foramen ovale, the incidence of decompression sickness ranges from 0.5% to 1.8%.[7][8]
Pathophysiology
Seawater weighs approximately 64 lb/ft3 or 1024 kg/cm3. Freshwater weighs slightly less but is considered equivalent to seawater when determining the diving depth and calculating decompression schedules. During a diver's descent, the ambient pressure increases as a function of the weight of the surrounding water. For example, at 33 feet of seawater (FSW) or 10 meters of seawater (MSW), the pressure is double that at sea level (2 atmospheres absolute (ATA), where 1 ATA = 1.01325 bar = 760 mm Hg). At 66 FSW (20 MSW), the pressure is triple that at sea level (3 ATA), and at 99 FSW (30 MSW), it is 4 times (4 ATA), and so on. For the diver to inflate their lungs, breathing gas must be supplied at a pressure equivalent to the ambient water pressure. This is one of the critical functions of diving life support equipment, which may be a self-contained underwater breathing apparatus (SCUBA) or surface-supplied.
Most divers breathe compressed air, which is roughly 78% nitrogen. However, nitrogen produces measurable decrements in cognitive performance beginning at a depth of about 3 ATA, or 66 FSW (20 MSW). This "nitrogen narcosis" effect becomes debilitating beyond 200 FSW (60 MSW).[9][10] Dives deeper than that are typically performed using a mixture of helium and oxygen, as helium has almost no narcotic effects. Many technical divers use a combination of helium, nitrogen, and oxygen (trimix) at shallower depths to help offset the effects of nitrogen narcosis and the considerable cost of using helium alone as a diluent. Although nitrogen is not chemically inert, divers commonly label it an inert gas.
At atmospheric pressure, the dissolved inert gas in the body is in equilibrium with that of the atmosphere. As the pressure of the diver's breathing gas increases with increasing depth, the partial pressure of inert gas in the breathing mix also rises. This elevation creates a positive pressure gradient between the inert gas in the lungs and the gas dissolved in the blood and body tissues. Inert gas molecules in the lungs then pass through the alveolar-capillary interface and dissolve in the body as a function of partial pressure and time. In other words, the farther a diver descends and the longer they stay at depth, the more inert gas dissolves in the blood and is distributed throughout the body.
As a diver ascends towards the surface, the inert gas pressure in the lungs decreases, and the pressure gradient between the lungs and the body equilibrates and eventually reverses. When the partial pressure of dissolved inert gas in the body is greater than that in the lungs, the tissues become supersaturated. Gas molecules within the body then pass through the alveolar-capillary membrane into the lungs and are exhaled. This simplified overview of the process is known as decompression. Detailed decompression algorithms are designed to control this process and allow the diver to return safely to the surface.
Bubbles can form in supersaturated body tissues. The physical process of bubble formation is similar to what occurs in a carbonated beverage after removing the lid. Decompression sickness occurs when these bubbles produce symptoms. Asymptomatic, or "silent," bubbles may form in the venous blood even after a standard and uneventful decompression. Silent venous bubbles typically travel through the right heart and lodge in the pulmonary circulation, where they are slowly eliminated during respiration.
Upon reaching the right atrium, bubbles within the venous circulation may be shunted through a patent foramen ovale. They subsequently become arterialized, where they may produce symptoms of DCS if they obstruct arterial blood flow to a tissue. There is not a 1:1 correlation between patent foramen ovale and decompression sickness, and the exact relationship between them remains unclear.
Intrapulmonary shunts are commonly found in the general population, particularly after vigorous exercise, suggesting that patent foramen ovale is not the only mechanism of arteriovenous shunting of bubbles in divers without other abnormalities of the cardiac septum.[11][12]
History and Physical
Patent foramen ovale is typically asymptomatic but has been associated with migraine with aura and cryptogenic stroke, though the evidence supporting these associations is inconsistent.[13][14][15][16][17]
General risk factors for decompression sickness include long and deep dives, aggressive decompression protocols, omitted decompression, rapid ascent, heavy work at depth, exposure to cold during decompression, and repetitive dives, especially over multiple days.
Right-to-left shunting of bubbles is most commonly implicated in decompression sickness episodes that arise during dives that provoke silent venous gas emboli, uneventfully follow an established decompression protocol, are without other known risk factors, and produce sudden-onset severe decompression sickness symptoms. More than one such episode should raise the index of suspicion that a right-to-left shunt exists.
Evaluation
Routine screening for patent foramen ovale in the general diving population is not recommended. However, it is reasonable to screen high-risk individuals such as those who have experienced migraine with aura or congenital heart disease or who have a family history of patent foramen ovale.[2]
When recommending patent foramen ovale testing and interpreting test results, the practitioner should remember that patent foramen ovale is not the only source of arteriovenous shunting, as previously mentioned. Patent foramen ovale testing is not indicated in divers who have experienced only minor decompression sickness symptoms (ie, joint pain, swelling, and type 1 skin rash).
Echocardiography with bubble contrast is the standard method for detecting patent foramen ovale. Studies should be performed at rest and during provocative maneuvers like the Valsalva maneuver. Transcranial Doppler is an inexpensive and noninvasive screening tool for patients with a suspected right-to-left shunt, but it cannot determine intracardiac shunt morphology.[18][19] Transthoracic echocardiography with bubble contrast is sensitive enough to detect a clinically significant patent foramen ovale, but some practitioners may choose to perform transesophageal echocardiography with bubble contrast.[2][20]
Treatment / Management
Divers experiencing acute decompression sickness should undergo hyperbaric oxygen therapy following established protocols. The United States Navy's treatment tables in the US Navy Diving Manual are available for download.
Testing for PFO is reasonable in a diver who has experienced unexplained severe sudden-onset neurological decompression sickness (DCS), inner ear decompression sickness, or cutis marmorata. If a PFO is discovered, the diver should be cautioned against returning to diving. More than one episode of DCS increases the gravity of this recommendation. However, clearance to dive is based partly on the judgment of a qualified and experienced practitioner. Some divers may safely return to diving with preventive measures, which can include diving using nitrox with air tables or the air setting on a dive computer, avoiding decompression diving, and not diving to the no-decompression limits of their computer's decompression algorithm.[2] Military and commercial divers are typically subject to more stringent requirements. Any diver with residual neurological symptoms should refrain from diving until those symptoms are fully resolved.
Divers with PFO may inquire about percutaneous closure. This decision should be made in consultation with a cardiologist and a clinician trained in diving medicine. PFO closure is not without risk, and this risk must be balanced against the individual's risk of decompression sickness. A 2024 literature review by Foreman et al found an incidence of complications related to PFO device closure of 6.9% (N=48,348).[21] Mas et al (2017) reported a major device and procedural complication rate of 5.9% using 11 different devices (N=238), and Saver et al (2017) reported a combined procedural (2.4%) and device-related (2.6%) complication rate of 5.0% using the Amplatzer™ patent foramen ovale occluder (N=499).[22][23] Turner et al (2017) reported an adverse event rate associated with the Amplatzer™ septal occluder or delivery system of 6.56% at a 2-year follow-up after atrial septal defect closure (N=930).[24] Pearman et al (2015) reported a serious complication rate of 2.9% in 105 divers who had a patent foramen ovale closure performed by a single cardiologist.[25] Verna and Tobis (2011) cite a closure device explantation rate of 0.28% (N=13,736).[26] Bissessor et al reported zero residual shunts at 1 year with only one in-hospital complication using both the available devices (N=70).[27] Lee et al (2018) reported closure complications in 2 of the 60 patients studied (3.3%).[28](B3)
Torti et al (2004) reported an incidence of serious decompression sickness of 5 per 10,000 dives (0.05%) in divers with patent foramen ovale (N=63).[7] Liou et al (2015) reported an incidence of serious decompression sickness of 18 per 1000 (1.8%) divers with patent foramen ovale (N=39); their incidence of serious decompression sickness in divers without patent foramen ovale was 1.3% (N=36), which is significantly higher compared to 0.01% to 0.095% cited by other authorities based on much larger cohorts.[8][6] Some evidence suggests a correlation between patent foramen ovale size and decompression sickness risk. A retrospective study found that the mean patent foramen ovale size in divers who had experienced decompression sickness was 5 mm larger than the mean patent foramen ovale size in the general population.[29](B2)
Closure should not be routinely considered in divers with asymptomatic PFO who have not experienced decompression sickness. These divers should instead be counseled to dive conservatively using preventive measures, as previously discussed.[30] Rarely, a diver with a known patent foramen ovale and no history of decompression sickness who plans to participate in expedition-level dives involving extensive decompression may request closure before these dives. The risk of device and procedural complications must be weighed against the best estimate of the individual diver's risk of decompression sickness.(B2)
A diver who has undergone patent foramen ovale closure may return to diving after they are cleared for full activity by the cardiologist and a clinician trained and experienced in the examination of divers. Post-closure echocardiography should show adequate reduction or abolition of the patent foramen ovale, and the diver should be off all anticoagulants other than aspirin.[2] Evidence suggests that closure of a patent foramen ovale may decrease the risk of decompression illness in divers with patent foramen ovale who have previously experienced decompression sickness.[20][31][32]
Differential Diagnosis
Differential diagnoses of patent foramen ovale include atrial septal defect and small patent ductus arteriosus.[33] Differential diagnosis of decompression illness is beyond the scope of this article and is well-described in the published literature.[6][34]
Enhancing Healthcare Team Outcomes
The paradox of PFO and diving is that it is seldom discovered in a diver until they experience a DCS incident that suggests right-to-left bubble shunting; the diver is then tested for PFO. Counseling about future diving is based on the presumption that the PFO or other source of shunting is the root cause of the DCS episode.
Educating divers with patent foramen ovale is crucial to enhancing their safety and reducing the risk of decompression illness. By providing thorough and informative guidance, healthcare providers can help divers better understand the potential implications of their condition and make informed decisions about their diving activities.
Using a collaborative and descriptive approach is vital in this educational process. Rather than dictating strict rules or prohibitions, healthcare professionals should engage divers in open dialogue, discussing the nature of their condition, the associated risks, and strategies for minimizing those risks during diving activities. This approach fosters a partnership between healthcare professionals and divers, empowering the latter to actively manage their health while diving.
References
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