Article about decompression sickness

[markmantei]

A full text of the article can be found here: USC Dornsife Scientific Diving: New Methods to Avoid Decompression Sickness

To quote the relevant section:

"As the bubbles course through our body, an inflammatory signal is activated, and the nitrogen bubbles are easily trapped in the pathways through which they travel ... One possibility of decompression sickness risk reduction, as explored by the NMRC, involves blocking the immune system’s inflammatory response to intravascular bubbles with the use of anti-inflammatory drugs. This technique is regarded as one of the safest and most effective ways of avoiding decompression sickness."

So, my question is, are there specific over-the-counter anti-inflammatories that "may" lessen the risk for DCS in a otherwise healthy person, that could potentially be taken pre-dive as an additional safety measure?

 

[Duke Dive Medicine]

It appears that the author of the article misinterpreted a phrase in one of the citations (the NMRC publication from 2000). The 2009 Lang/Brubakk paper that she cites states, "It may thus be possible to reduce the risk of DCS by oral treatments of anti-inflammatory medications. However, highly successful pharmaceuticals of this nature have yet to be identified."

To the best of my knowledge, there isn't any evidence that using anti-inflammatory medications prior to diving can prevent or decrease the risk of DCS.

 

[Kevrumbo]

Yeah . . .a lot of articles & studies of adjunctive treatment for DCS with NSAIDS (i.g. prescription Tenoxicam, see Bennett, Dominguez) --but nothing about any over-the-counter NSAID prophylaxis.

Kind of off-topic, but endurance exercise could play a role in reducing susceptibility to DCS, or the severity of DCS. . .

On Diving acclimatization and DCS:
In summary, our results show that DCS induces a stress response, as confirmed by the expression of heat-shock protein in lung, liver, and heart tissue. DCS preconditioning reduced the neurological impairment caused by subsequent rapid decompression from exposure to high pressure. We conclude that bubble formation in tissues after decompression can activate a stress response and that the protective effects derived from this stress response may be the mechanism responsible for the phenomenon of diving acclimatization. . .
Diving acclimatization has been described as an adaptive response to decompression stress after repetitive exposure to pressure (7). This adaptation reduces a diver's susceptibility to DCS or the severity of DCS. The mechanism contributing to diving acclimatization, however, remains obscure. We proposed an "induction hypothesis," speculating that repetitive compression-decompression is a form of preconditioning that generates protective factors and reduces the severity of acute tissue injury during subsequent bubble formation. In the present study, our results further demonstrate that DCS induces a stress response and that this DCS preconditioning significantly alleviates the neurological impairment induced by subsequent exposure to high pressure. These results strengthen our induction hypothesis by explaining the mechanism underlying diving acclimatization. . .
DCS is a disease caused by gas bubble formation in tissues. Air bubbles produce their effects by mechanical obstruction, by altering the biochemical environment, or both. Bubble formation interrupts blood flow and compresses or disrupts tissues (22). Air bubbles can also initiate an air-liquid interface reaction in tissues, which activates plasma proteins, including clotting factors, enzymes, and immunoglobulins (15). The complement system, polymorphonuclear leukocytes, and oxygen metabolites are proven factors that mediate air-bubble-induced tissue injury (22). Protection from air-bubble-induced tissue injury may result from a smaller number of bubbles or from less tissue reaction to air bubbles. Wisloff and Brubakk (31) reported that endurance exercise reduces bubble formation and increases survival in rats exposed to hyperbaric pressure. It is not known whether DCS preconditioning reduces bubble formation after the next episode of decompression from a hyperbaric environment. Nevertheless, endurance exercise is a stressor that increases the expression of HSP70 and may represent a powerful preventative agent against tissue injury in several models (8, 23). These reports suggest that stresses such as endurance exercise can activate bioprotective mechanisms. Compatible with these reports, our results show that prior DCS is also a stress inducer, which may activate a bioprotective mechanism similar to that induced by endurance exercise. This suggests that this protection involves mechanisms more complex than a reduction in bubble formation. . .
Acclimatization to neurological decompression sickness in rabbits

 

[TSandM]

I just ran a PubMed search and could find nothing supporting the use of any immunomodulator in the treatment of DCS.

 

[DocVikingo]

It appears that the author of the article misinterpreted a phrase in one of the citations (the NMRC publication from 2000). The 2009 Lang/Brubakk paper that she cites states, "It may thus be possible to reduce the risk of DCS by oral treatments of anti-inflammatory medications. However, highly successful pharmaceuticals of this nature have yet to be identified."

To the best of my knowledge, there isn't any evidence that using anti-inflammatory medications prior to diving can prevent or decrease the risk of DCS.

Nor mine, e.g.:

“J Appl Physiol. 2011 Jan 6.

Pharmacological intervention against bubble-induced platelet aggregation in a rat model of decompression sickness.

Pontier JM, Vallée N, Ignatescu M, Bourdon L.

1 Naval Medical Institute.

Abstract

Decompression sickness (DCS) with alterations in coagulation system and formation of platelet thrombi occurs when a subject is subjected to a reduction in environmental pressure. Blood platelet consumption after decompression is clearly linked to bubble formation in humans and offers an index for evaluating DCS severity in animal models. Previous studies highlighted a predominant involvement of platelet activation and thrombin generation in bubble-induced platelet aggregation. In order to study the mechanism of the bubble-induced platelet aggregation in DCS, we examined the effect of acetylsalicylic acid (ASA), heparin (Hep) and clopidogrel (Clo), with anti-thrombotic dose pre-treatment in a rat model of decompression sickness. Male Sprague-Dawley rats were first compressed to 1000 kPa for 45 min then decompressed to surface in 38 min. In a control experiment, rats were treated with ASA, Clo, or Hep, and maintained at atmospheric pressure for an equivalent period of time. Onset of DCS symptoms and death were recorded during a 60-min observation period after surfacing. DCS evaluation included pulmonary and neurological signs. Blood samples for platelet count (PC) were taken before hyperbaric exposure and after surfacing. Clopidogrel reduces the DCS mortality risk and DCS severity. Clopidogrel reduced fall in platelet count and bubble-induced platelet aggregation (-4,5% with Clo, - 19.5% with ASA, -19,9% with Hep and -29,6% in the untreated group). ASA which inhibits the thromboxane A2 pathway and Hep which inhibits thrombin generation have no protective effect on DCS incidence. Clopidogrel, a specific ADP-receptor antagonist, reduces post-decompression platelet consumption. These results point to the predominant involvement of the ADP release in bubble-induced platelet aggregation but cannot differentiate definitively between bubble-induced vessel wall injury and bubble-blood component interactions in DCS.”

Expert opinion:

- Dive Training, September 2008 Volume 18 Number 9, statement by Joel Dovenbarger, recently retired Vice President for Medical Services at DAN: "There is no benefit to taking aspirin before a dive any way you look at it. Aspirin will no more prevent DCS than it will prevent pain if you fall down while taking it. There is no anti-bubble-formula aspirin or nitrogen off-gassing dosage that will make any difference, at least none that has ever been reported. In studies, there was no change in outcome for people who took aspirin versus those who did not, and researchers have pretty much stopped looking at aspirin in DCS. So, no matter what you do, the outcome is pretty much the same. By the way, the same is true for oral steroids. Even after you have symptoms, there is no outcome change with or without steroids and it will not prevent DCS. There is also at least one circumstance where aspirin could be problematic, and that's if someone takes so much aspirin that it causes hearing issues or impedes blood clotting. Aspirin is toxic to the eight cranial nerve in high doses, and may prolong bleeding, which is something you don't want to have happen if you've ruptured a small vessel in the spinal cord or brain from AGE [arterial gas embolism] or DCS."

- See post #31 (by a noted diving medicine cardiologist) in the following thread --> Aspirin and Diving

Regards,

DocVikingo

 

[w ripley]

The only thing medically proven - more or less - that can be taken orally after a dive to prevent decompression injuries are Cathy Lesh's (Dive Outpost, Live Oak, FL) chocolate-chip cookies. Don't know what she puts in them but to date they have worked for many hundreds of divers. If DAN decides to look into this phenomenon, I will gladly volunteer to be a test subject, assuming there will be an unlimited supply of those delicious goodies, LOL.

---------- Post added ----------

Oh, forgot to mention they are called "Deco Cookies."

 

[NAUIWOWI]

Interesting stuff. Thanks for posting/discussing.


Now I'm craving a cookie..........

 

[Kevrumbo]

Chocolate Chip Cookies, endurance training and nominal diving profiles --and since my bends hit in Oct '08 --figure I've got a pretty good working DCS preconditioning factor per the model's hypothesis (post #3 above), should I incur another decompression accident/incident in the future. . .

 

[Dr Deco]

Hello markmantei :

Immediate and Late DCS

This is anarticle that contains considerable material, but much of it is old. The use of compounds blocking platelet aggregation was first examined in the early 1970s and was the first of many compounds examining what I call “biochemical hypotheses” of DCS. Bubbles were considered a “mechanical trigger,”and the harm was attributed to physiological responses and not to bubblegrowth.

While there is no doubt that as time elapses following decompression, many things can occur– most appear to be bad. However, the argument for bubbles per se initially causing joint-pain DCS [bends] and neurological problems is simple. Pressurization causes immediate reversal and relief. Furthermore, the gas phase does not appear tomove [i.e., it is extravascular] since dropping the pressure will result in the reappearance of the pain or paralysis in the same location. After a couple of hours, however, other events happen such as fluid shifts and swelling, that is, edema. This edema is not shrunk by pressure and recompression has little effect.

The administration of oxygen under pressure is another matter and is VERY helpful, as itcan aid in the reversal of the edema and oxygenate hypoxic nerve cells. This latter is important since neurons have a low tolerance for oxygen deprivation. [This deprivation process is more complicated than this, but the result of cell death is easy to understand.]

These “late onset” effects are what the researchers are talking about, but it can appear to SCUBA divers that they are talking about a simple pain in the knee right after surfacing.

Testing

What has been done, and still is done to some extent, is to use a small animal model for DCS and use death as the endpoint. This is actually massive pulmonary gas embolism and is not related to joint-pain DCS [the bends]. Small animals are simple to use and the endpoint very clear. Haldane also was uncertain whether DCS in his goats was the same as that seen in the human divers.

When humans were used, the results are not the same. Aspirin was not found useful, for example, for DCS in humans.

Gas Exchange

The idea ofusing bacteria to “digest” hydrogen gas was investigated a couple of decades ago. While novel in concept, the hydrogen used [digested] by the bacteria was not large. Furthermore, we are talking about exchange is the wrong direction. Dissolve hydrogen is excreted by cells and eliminated at the lungs. The dissolved gas then in the arterial system is small. Hydrogen digested in the gut will not help you with joint pain. But barophysiologists loved it – initially – because of its novelty.

Microparticles are the latest in a long line of novelties over the decades. Each one found is the new “key.” They are more for severe DCS in the central nervous system. Bends is considered a simple bubble growth problem and not very interesting. Barophysiologists want something more exciting involving the CNS.


What we still need to find is why some people produce bubbles in the first place. We need to know why some divers have more micronuclei than do others. This is a difficult problem and will probably go uninvestigated for a long time. I have retired and my time is gone.

The cookies are a good idea, though!:cool2:

Dr Deco :doctor: