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PFO and Inner Ear DCS

May 27, 2014 By Petar Denoble, MD, D.Sc.

Does the selective vulnerability of the inner ear to DCS help explain the disconnect between a prevalent risk factor and a rare disease?

In his presentation at SPUMS 2014, Dr. Simon Mitchell has summarized the work he and Dr. David Doolette have done regarding the pathophysiology of inner ear decompression sickness (IEDCS) as well as some recent publications from other authors.

Mitchell addressed the reservations some experts have when it comes to the causal relationship of patent foramen ovale (PFO) and decompression sickness (DCS). Some experts say there is a disconnect; PFO must be present in many divers (one quarter), but DCS occurs only in few. Wilmshurst responds to this disconnect asserting that only divers with a large PFO are at risk and this is generally in line with the DCS statistics.

Mitchell goes further and provides theoretical explanation for the disconnect.  The saturation and desaturation of the inner ear with inert gas shows that during relatively rapid ascents (due to slow wash out of nitrogen from the inner ear spaces containing liquid) these spaces remain supersaturated for about 30 minutes postdive, and that DCS may occur even without PFO. In case of PFO, some bubbles end up in an artery feeding the inner ear. The bubble trapped in inner ear circulation continues to grow as gas comes out of the supersaturated ear liquids. Their growth injures the fragile inner ear structures and causes vertigo, nausea and loss of balance. Although most of the bubbles transgressing through the PFO end up in the brain, they rarely cause symptoms of brain injury; when this occurs most of the nitrogen in the brain has already cleared so the bubbles quickly dissipate.

In summary, Mitchell lists the conditions necessary for DCS to occur in divers with PFO:

  1. Diver must have a functional PFO.
  2. Venous gas bubbles must form.
  3. Something must provoke opening of PFO and the passage of blood to the left side (arterialization).
  4. Arterialization (and embolization) must occur while the embolized tissue is still supersaturated.

Thus, there is no disconnect.