Bubbles formed during or after an ascent can have their origin in two different mechanisms; either evolving from any dissolved inert gas (most often nitrogen) or they can originate through pulmonary barotrauma. Inert gases are not involved in the manifestation of barotraumas, since barotrauma can be generated from ascents from only 1 to 2 msw. As such, the present review will not focus on the formation of bubbles from barotrauma, but rather on the formation of bubbles from dissolved, inert gas.
If the ambient pressure is reduced sufficiently below the partial pressure of the dissolved gas in the tissue and blood, formation of bubbles can lead to DCS. Gas bubbles may form at any site in the body and can be categorized in two groups; stationary or circulating bubbles. Stationary bubbles are formed in the tissues and may produce local damage and intravascular blockage, which gives rise to a variety of symptoms and signs. While there exists no method to measure stationary bubbles, Doppler and echocardiography are commonly used to measure VGE in the central venous pools. The lungs filter and remove the nitrogen bubbles formed in the veins, whereas arterial bubbles can block and/or damage the blood vessels in vital organs such as the brain and heart. Thus it seems that venous bubbles are less dangerous compared to arterial bubbles. However, venous bubbles can become arterial bubbles through shunts in the lungs and/or the heart. Recent studies have reported high incidences of VGE with subsequent arterialization after trimix diving and after no-decompression air dives (Ljubkovic et al. 2010a
). Both the studies with trimix dives and with no-decompression dives used standardized protocols without any violations, and without any clinical signs of adverse effects of decompression. These two recent studies have again raised the question of possible long-term adverse effects of diving due to the unknown effect of repeated exposures to arterialization of VGE.
Traditionally, DCS is divided into type I or type II, depending on the symptoms and manifestations. Type I concerns only the symptoms of musculoskeletal pain, while type II are the more serious manifestations mainly related to the CNS. It has been suggested that there has been a shift from type I to type II DCS in the recent past, as type II is now more common (Francis and Mitchell 2003
). In as many as 77% of the cases of DCS, the UK Institute of Naval Medicine showed prevalence of neurological manifestations. Limb pain was found in 49% of the cases. The shift in manifestation may be explained by the introduction of dive computers, leading to increased bottom time and deeper dives (Andric et al. 2003
). On the other hand, an alternative explanation is the increased focus on neurological damage to divers.
Involvement of VGE in CNS DCS has been discussed for several years. Clinical observations showing that the spinal cord is more involved in DCS compared to the brain made Hallenbeck et al. (1975
) suggest that gas embolism is not a mechanism for spinal cord DCS. If VGE is the main mechanism, one would rather suspect higher perfused organs to be more involved in CNS DCS than actually observed in the clinical setting. However, it is well documented by using ultrasound contrast media that small gas bubbles will lodge in small vessels and that the distribution of these bubbles is critically dependent on size (Talu et al. 2007
; Klibanov 2006
). Other studies have shown that vascular gas bubbles can be located in the spinal cord in DCS (Sparacia et al. 1997
). Several investigators have shown that the brain might be more involved in CNS DCS than previously believed. Moon et al. (1989
) showed by contrast echocardiography that gas emboli play an important role in CNS DCS. They observed a higher incidence of atrial septal defects in cases with neurologic DCS. Such defects would allow VGE to be transported from the right to the left side of the circulation.
Involvement of VGE in neurologic DCS has been showed both in animals and in men (Wilmshurst et al. 1994
; Vik et al. 1993
; Germonpre et al. 1998
). However, several other researchers are not convinced about this role of VGE in relation to DCS (Smith et al. 1990
; Cross et al. 1992
; Langton 1996
). In addition to the blood flow argument cited above, the observation of a patent foramen ovale (PFO) in approximately 30% of the population does not fit with the numbers developing DCS. The relevance of shunting is questioned since many divers with detectable shunts have no history of DCS (Wilmshurst et al. 1989
; Cross et al. 1992
). On the other hand, Wilmshurst and Bryson (2000
) showed that individuals with right to left shunting had higher risk of neurological decompression illness than individuals without shunts. They also pointed out that individuals with smaller shunts would have intermediate risk, but other factors like individual susceptibility to venous bubble formation would affect the risk as well. Another implication for divers with a PFO to take into consideration is the change in intrathoracic pressure that takes place during a Valsalva maneuver (Balestra et al. 1998
). A Valsalva is used during descent to equalize pressure in the middle ear with the ambient pressure, and can cause an increase in right arterial pressure which will open a PFO (if present). Balestra et al.
concluded that movements other than the Valsalva also can increase the intrathoracic pressure, such as sustained isometric exercise or abdominal strains. These other maneuvers were more likely to cause post-release central blood shifts, which made them recommend that divers with PFO should avoid any exercise that is likely to increase the intrathoracic pressure for prolonged periods of time. A more recent study also showed that over a period of seven years the permeability of PFO in a group of sports divers had changed (Germonpre et al. 2005
). For the first time, an increase in PFO size was documented in humans, an increase that might imply that divers could develop more susceptibility for serious DCS over time. Additionally, an important point made by Wilmshurst and Bryson was that CNS DCS could also be related to lung disease and unsafe dive profiles, not only to bubbles shunting from the venous to the arterial side. Symptoms from the joints and muscles were not correlated with shunts.