Suba diving is a popular sport in many countries. While the general risk of death or major injury during scuba diving is small (<0.001% per dive), one of the notable risks include decompression sickness.
Decompression sickness, also known as divers’ disease, is caused by nitrogen bubbles forming in the diver’s tissues during his ascent. These bubbles can form in or migrate to any part of the body, causing varied levels of symptoms, ranging from simple symptoms involving skin rashes and pain in the joints to more serious symptoms which can lead to paralysis or even death when the other organs such as the central nervous system (including brain), are involved.
The connection between Patent Foramen Ovale (PFO) and decompression sickness was first described in the 1980s. Foramen ovale is a hole between the top chambers of the heart in the fetus which is normally closed by a flap within the first breaths at birth. However, in about 27% of the adults, the flap does not seal the gap causing it to remain open (patent), hence allowing blood to travel from the right to the left heart chambers during occasions when the chest pressure is raised. In the event of decompression sickness in divers, the bubbles in the venous system can by pass the lungs where they were supposed to be filtered out, and travel directly to the arterial system through the PFO and left side of the heart. The arterial system includes arteries to the brain, spinal cord and heart. Blood formation in the arterial system also known as arterial gas embolism, is far more dangerous as it can result in blockage in the blood supply to the brain or spinal cord, leading to stroke or paralysis.
Currently, in most countries, routine screening for PFO in divers is not recommended. Suggested recommendations for divers with diagnosed PFO and a history of decompression sickness include cessation of diving, a conservative approach to diving, and PFO closure.
Transcatheter Device Closure of the PFO is the implantation of an occluder device across the PFO through a catheter (plastic tube) inserted via the leg vein in the groin. The device acts like a double-sided umbrella that opens on each side of the atrial wall between the top chambers of the heart to seal the PFO. This helps to eliminate the chance of arterial embolization, allowing the diver to return to unrestricted diving. It is a minimally invasive procedure, which can be performed with mild sedation, and takes less than one hour, with one night stay in the hospital. Most patients can return to normal activity in two days, but they must take anti-coagulation medication and blood thinners for three to six months. Other restrictions include: no elective dental care (such as cleanings) for three months, no contact sports for three months, and no heavy lifting for one week. After implantation, divers must abstain from the sport for three to six months.
Before proceeding to do the transcatheter PFO closure, the patient has to undergo a transthoracic echocardiogram or a heart scan, with an ‘agitated bubble saline study’ to see if there is any possible sign of PFO. After which, a transoesophageal echocardiogram (similar to a scope), will be performed to help confirm the diagnosis.
Although there are no consensus criteria for PFO closure in divers currently, several studies have established that the incidence of PFO is two to six times greater in divers who experience a neurological decompression; and that catheter-based PFO closure is shown to lead to complete elimination of arterial bubbles after simulated dives, suggesting that PFO closure in continuing divers have a relevance in preventing symptomatic (major decompression sickness) and asymptomatic (ischaemic brain lesions) neurological events. There is a small risk of complications with PFO closure which should be discussed with the cardiologist.