Cutaneous decompression sickness (DCS), or “skin bends,” most often manifests as skin mottling on the torso, upper arms and buttocks to various degrees. An associated marbled look to the skin is sometimes referred to as cutis marmorata. While cutaneous DCS is most likely related to gas occurring in body — after decompression or due to lung barotrauma or some medical procedures — there generally is no accepted explanation how the free gas is related to skin changes.
Possible explanations include the occurrence of gas bubbles in subcutaneous tissues, occlusion of subcutaneous arteries with circulating bubbles bypassing the lung filter (as with a patent foramen ovale), inflammatory reaction bubbles present locally or bubbles causing endothelial injury at remote locations.
Are some divers prone — or resistant — to gas bubbles after diving?
Decompression sickness (DCS), which may occur in divers after decompression from a dive, is dependent on the combined dose of gas saturation during the dive and the rate and magnitude of decompression. However, there is a great variability of outcomes in subjects exposed to the same dive profiles. The variability decreases as the severity of exposure increases.
DCS is correlated with the degree of venous gas emboli (VGE), or “bubbles”, in circulation after a dive. Generally, the higher the VGE grade (more bubbles) the greater the probability of DCS, and vice versa. Similar to DCS, there is a great variance in the probability of VGE appearing postdive. Some researchers who practice VGE detection have hinted that some divers bubble after most dives and may exhibit a high bubble grade (HBG) and others tend not to bubble at all or rarely exhibit HBG. The former are often labeled as bubblers (or high bubblers), while the latter are labeled as nonbubblers (or low bubblers).
Phosphodiesterase type 5 (PDE5) inhibitors — such as Viagra, Cialis, Levitra, Vivanza, Mvix and Lodenafil — are a class of popular drugs prescribed to treat erectile dysfunction and are often sold on the black market as sexual-function enhancers. It is reasonable to assume that many divers use PDE5 inhibitors while on a diving vacation, although the drugs’ possible effects on decompression safety have not been studied previously. In a recent paper, Blatteau et al.1 presented the results of a study on rats treated with sildenafil (Viagra) and then exposed to a simulated dive.
Venous gas embolism (VGE), or bubbles, in divers postdive indicates that their decompression was too fast, their bodies became supersaturated and free gas emerged from solution in tissues. The occurrence of free gas is considered a necessary condition for decompression sickness (DCS), which can happen even without VGE. However, the presence of VGE increases the number and types of possible harms to the body and thus the probability of DCS.
A number of studies indicate variability in proneness to DCS among divers; however, the question of whether divers who have suffered DCS produce bubbles more readily in general has not been answered yet. To answer this question, researchers would need to identify “bubblers” and “nonbubblers” and observe the outcomes of their dives over some period of time, which would require a lot of resources and time. (more…)
Biological organisms maintain their functional integrity in varying environmental conditions through the activity of the innate immune system and controlled inflammation. During scuba diving, divers are exposed to greater than usual environmental changes, which challenges the entire body. The circulatory system is specifically stressed with an elevated partial pressure of oxygen and by decompression-induced gas bubbles on ascent to the surface. When the stress caused by the pressure changes exceeds a certain threshold, a variety of symptoms may occur after return to the surface — this is usually called decompression sickness (DCS).
DCS has been associated with the presence of a free gas phase in blood and tissues but we know little about the biological pathways and processes involved. While involvement of immune and inflammation cells and processes has been indicated previously, measurable changes are rarely present in asymptomatic divers, making it difficult to study the transition of physiological adaptive stress response into maladaptive or pathological reactions leading to loss of organ functions. We have reported in this blog about recent microparticle studies that may potentially shed more light on this gray area.
During the ONR-NAVSEA Progress Review Meeting that took place in Durham from July 15-17 this summer, Stephen Thom summarized the current status of his research on circulating microparticles (MPs), which are small fragments shed by various cells that have been exposed to stress. These MPs can be found in subjects with inflammation or injury and in divers after diving.
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.