Decompression illness is a systematic affliction that can lead to critical neurological problems. The disease had its first occurrence in the 1840s when deep-sea divers were unable to bend their joints. Still, researchers agree the disease was not entirely comprehended until 1878 when Paul Bert theorized that the disease is induced by nitrogen bubbles within the body (Moon et al., 1995; Jallul et al., 2007). Decompression illness is a result of bubbles in the tissue during or after a decrease in environmental pressure. It is accepted that decompression illness includes “two pathophysiological syndromes: arterial gas embolism and decompression sickness” (Jallul et al., 2007; Vann et al., 2011). When gas expands and breaks alveolar capillaries, the gas can move into the arterial circulation; this is termed as arterial gas embolism. (Moon et al., 1995; Jallul et al., 2007; Vann et al., 2011). Decompression sickness (DCS) is a result of the emergence and growth of extravascular and intravascular bubbles after the total dissolved gas tensions surpass the absolute pressure (Moon et al., 1995; Jallul et al., 2007; Vann et al., 2011).
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According to Jallul et al. and Vann et al., DCS has traditionally been classified as either Type I or Type II. Type I DCS is collectively classified by pain in or around the joint (Jallul et al., 2007; Vann et al., 2009). Type II DCS is the more critical of the two types. It is known to result in injury of the central nervous system, particularly to the spinal cord. 20-50% of people who develop Type II DCS have injury to their spinal cord (Jallul et al., 2007). Like with Type I DCS, scientists are in agreement with the symptoms of Type II DCS which are “numbness, tingling, paranesthesia, muscle weakness, paralysis, and mental or motor abnormalities” (Jallul et al., 2007; Vann et al., 2011). Vann et al. further states that other classification systems have been developed. These systems are severity indices which might be useful with treatment. The severity indices are on a scale, with ten being the maximum score, to determine in how many regions of the body the patient is exhibiting symptoms (Vann et al., 2011) . These indices play an important role in assessing a patient’s condition, but the two main categories of DCS are still fundamental.
When the pressure of dissolved gases in the tissues exceeds the ambient pressure, the tissues are supersaturated. During this time of supersaturation, bubbles can form, but there is contradiction of where the bubbles form. Vann et al. states that these bubbles can form in both the tissues and the blood (Vann et al., 2011). On the other hand, Moon et al. states these bubbles do not form within the blood itself. He states that when sealed within a blood vessel and isolated from circulation, blood does not form bubbles even when severely decompressed (Moon et al., 1995). While Moon states bubbles do not form within the blood, they can form within pockets of gas in the joints and in and around the spine (Moon et al., 1995). The residual gas from these pockets can act as nuclei from which the bubbles form (Moon et al., 1995). Even though Moon et al. states bubbles cannot form within the blood, they indicate that the nuclei may expand and rupture capillaries, causing bubbles to enter the circulating blood (Moon et al., 1995), thus coinciding with Vann et al.’s definition of the disease.
Scientists have studied cases of DCS in a variety of ways. Jallul et al. used MRI to observe abnormalities within the brain and the spinal cord (Jallul et al., 2007). Vann et al. believes these imaging methods are not useful in detecting abnormalities. These methods are rarely successful in imaging bubbles (Vann et al. 2011), which are the main component of DCS. Therefore, scanning methods, including MRI and CT scans may be unreliable. Vann et al. use the symptoms of the disease to identify, study, and treat it (Vann et al., 2011). With the differential methodology, cases of DCS have led to three different theories about Type II DCS. The current leading theory, according to Jallul et al., states that myelopathy occurs due to the “congestion of the spinal epidural venous plexus”, followed by spinal cord ischemia (Jallul et al., 2007). The second theory is the autochthonous theory. It proposes that “decompression causes gas bubbles to nucleate within the tissues themselves” (Jallul et al., 2007). Gas bubbles act as space-occupying lesions, disrupting blood flow and causing damage to the myelin sheath (Jallul et al., 2007). While Jallul et al. states that the first hypothesis is the leading hypothesis, most researchers, including Vann and Moon, still believe the second hypothesis to hold true. The third theory, which has become unwelcomed, implies that gas bubbles from the tissues leak into the arterial system and fuse to block the arterial circulation (Jallul et al., 2007).
Research states that marine mammals are not recognized to endure decompression sickness because of the various anatomical, physiological, and behavioral adaptations which stop bubble formation (de Quiros et al., 2012; Hooker et al., 2012). According to research, one of the most critical adaptations is alveolar collapse (de Quiros et al., 2012; Hooker et al., 2012). With alveolar collapse gas uptake by the blood is stopped once a certain critical depth of lung collapse is reached (de Quiros et al., 2012; Hooker et al., 2012). Specifically, compression of the respiratory system combined with blood flow changes during dives would limit the amount of nitrogen absorbed (de Quiros et al., 2012). Compression of the respiratory system is proposed to push the air into the upper airways where there is no gas exchange, therefore it is presumed that the small volume of available gas in the lungs would not be sufficient to raise the tissue and blood inert gas tension. Hooker et al. further mentions that marine mammals have stiffened upper airways, with lungs that lack “smaller branching respiratory bronchi”, that obtain air from more compressible airways during a dive (Hooker et al., 2012). These mammals additionally possess a well-developed diving response which allows them to conserve oxygen stores, extend maximum dive times, and limit nitrogen uptake (Hooker et al., 2012). While this dive response is important in a cetacean’s diving ability, alveolar collapse is still the most crucial in prevention of DCS.
However, an growing number of studies have described lesions related to in vivo bubbles in marine mammals. Macroscopic bubbles within the cardiovascular system have been reported in necropsied stranded mammals. Researchers agree that due to putrefaction, bubbles can be found within animals with decomposition codes 4 and 5. Yet, it is strange to observe gas bubbles within the cardiovascular system in fresh necropsied animals (de Quiros et al., 2012). The intravascular bubbles in fresh stranded and necropsied cetaceans are most likely a result from gas embolism rather than putrefaction, since the process of putrefaction has yet to begin.
It has further been suggested that DCS is related to acoustic naval exercises. Lesions coinciding with intravascular and major organ gas emboli have been observed in beaked whales associated with military exercises utilizing sonar (Jepson et al., 2003; Fernandez et al., 2005; Hooker et al., 2012). While there have been multiple occurrences of these types of standings, the most notorious was in 2002 when fourteen beaked whales stranded in the Canary Islands after naval exercises. The stranding began approximately four hours after the start of midfrequency sonar activity (Fernandez et al., 2005). Like with other strandings, necropsies of the animals were performed. These necropsies showed “gas-bubble associated lesions and fat emboli in the vessels and parenchyma of vital organs” (Fernandez et al., 2005). Fernandez et al. proposed two different hypotheses for these lesions. The first states that nitrogen supersaturation higher than a threshold value resulted due to in vivo bubble formation related to the sonar exposure (Fernandez et al., 2005). This hypothesis is the more likely of the two because it corresponds with what normally happens in DCS. Conversely, the second hypothesis states that sonar may lower the threshold for expansion of gas nuclei in tissues that have been supersaturated with nitrogen gas (Fernandez et al., 2005).
Other researchers have proposed hypotheses of how bubbles result from naval sonar activity. One hypothesis, from Houser et al., is that bubble formation caused by acoustic exposure may be a result of rectified diffusion. Rectified diffusion occurs when a bubble is exposed to sound and it experiences expansion and compression. As the radius of the bubble grows, the amount of gas inside the bubble drops, gas spreads into the bubble, and raises the bubble volume (Houser et al., 2001). As the bubble shrinks, the reverse will occur and gas leaves the bubble (Houser et al., 2001). More gas enters the bubble than leaves due to diffusion being proportional to the bubble surface area (Houser et al., 2001). Bubble growth happens over the entirety of the acoustic cycle (Houser et al., 2001).
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A second hypothesis has support from numerous authors, including Crum, Mao, and Potter. It states that continuous sound exposure may not be required for the growth of bubbles if the tissues are sufficiently supersaturated (Potter, 2004). This occurs via a process termed static diffusion. Static diffusion is defined as gas bubbles diffusing while they are not being exposed to sound (Crum & Mao, 1996). Once bubble growth begins, it can be supported by static diffusion and the growth will continue without sound exposure (Crum & Mao, 1996). With static diffusion in supersaturated tissues, there is no limit to bubble growth (Crum & Mao, 1996). Based on the research and support of the hypotheses of rectified and static diffusion, both are highly likely to play a role in bubble formation in marine mammals.
Crum, Mao, and Potter have another hypothesis which states that due to sound exposure, previously stabilized, preexisting gas micro-bubbles are triggered (Crum et al., 2005). Micro-bubbles are stabilized to defend them from collapse under Laplace pressure (Potter, 2004). It is proposed that stabilization occurs by the same mechanism which avoids expansion with static diffusion (Potter, 2004). The stabilization mechanism is interrupted, and supersaturation of the body fluids allows destabilized nuclei to form bubbles (Crum et al., 2005). The micro-bubble will be able to exchange gas across its walls (Potter, 2004). This hypothesis has also been suggested by Fernandez et al., after their work with the strandings in the Canary Islands, but it was the least likely of their proposed hypotheses.
Decompression sickness is a severe disease, but all research agrees that it can be prevented if proper dive regulations are followed (Moon et al., 1995; Jallul et al., 2007; Vann et al., 2011). Research is generally consistent with the methodology used to assess DCS and the symptoms of it. Many agree that marine mammals are unaffected by this disease due to their physiological adaptations. However, cases of gas-related lesions in marine mammals are becoming more prominent. Future research is necessary to determine how this disease inflicts marine mammals. Many agree that this research will delve into the molecular, cellular, and organ level impacts of gas bubbles (Fernandez et al., 2005; Hooker et al., 2012).
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