How is time away from diving determined?

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islanddream

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I'm interested in understanding how a dive doctor determines how long a person should not dive after the bends. I ask this because I had skin bends about a month ago and was admitted to the chamber (US Navy Table 6 was used). I had no neurological problems, and after coming out of the chamber the itching and much of the mottling was gone. I saw the doctor for two more days and didn't need to go back in the chamber. On the report which was written up and sent to DAN, I'm instructed not to dive for six months, which I will abide by. I know someone will ask......no, my dive computer didn't show I did idiotic diving. I'm a very cautious and safe diver by nature. I do have some thoughts as to why I got skin bends.

Is there a scientific method to determine when a person can start diving again?
 
Islanddream,

There's no scientific method of determining how long a diver should stay away from diving after DCS. The recommendation is based on the individual presentation of symptoms and response to treatment, and can vary between practitioners. What type of skin bends did you have? There's type I that looks like hives and type II that looks streaky or marbled. Type II is considered more serious.

Best regards,
DDM
 
Thanks for your response, DDM. I had type II that itched and looked marbled. I got to the chamber about an hour after the symptoms started.
 
Wow, that's great. The transport time, not the symptoms :)

There is a theory that cutis marmorata is actually mediated by the brain. It's been duplicated in a swine model by injecting air into the cerebral circulation. Six months off of diving is not unheard of for a recommendation after a serious DCS hit.

Best regards,
DDM
 
Hello Islanddream.

I agree with DDM that there is no science behind these decisions.

My personal view is that if all you had was the rash, with no other manifestations, then a 6 month wait to dive is excessively conservative. As DDM has implied, the cutis marmorata form of rash is generally viewed as more "serious" but this perception arises because it is more frequently associated with other more serious symptoms (particularly spinal DCS) than the hive-like rash that he mentions. It is not that the cutis marmorata rash per se will harm you. If all you experienced was the rash with no other symptoms, then we would still view this as a mild episode of DCS. Put another way, the significance of cutis marmorata is that when we see it we are more alert to the possibility that more serious symptoms might arise. If no more serious sumptoms arise then the rash itself is essentially harmless.

We would normally advise divers in the latter situation (cutis marmorata rash but no other symptoms) to have a month off diving. This advice is not based on science, but there is a lot of experience with it, and there is no signal in our experience that it is insufficient time. Having said that, even a diver who waits six months or a year could suffer another event the next time they go diving just on the basis of bad luck. So whenever diving physicians give this sort of advice it is always heavily contextualised with a clear statement that there are NEVER any guarantees that there will not be a repeat event, no matter how long you wait. It follows that the decision to dive again, and when to dive, has to be made by you and you must take responsibility for that decision.

DDM mentioned the study which has shown that pigs may exhibit cutis marmorata after brain arterial gas embolism. Unfortunately this study has led to a fairly uncritical acceptance that cutis marmorata is (or may be) caused in this way in human divers. The truth is that a cutis marmorata appearance of the skin may be caused in many ways, and one of them is a significant adrenergic (think of it as an intense fight or flight) response. This can occur in a variety of medical settings. For example we see a cutis marmorata-like rash in illnesses like septic shock, or shock of any cause for that matter. Non diving brain injury can also cause it - we see it sometimes in brain bleeding events. It is not surprising therefore that cutis marmorata may be seen in severe stroke-like events caused by bubbles (as in the pigs in the study).

Two things get overlooked in conversations about this study. First, the pigs in the study were anaesthetised. Second, the doses of air used to elicit the cutis marmorata response would have produced significant stroke like symptoms if the pigs were awake. But in the vast majority of cases of cutis marmorata in human divers we don't see symptoms of brain injury. Indeed, it is very common to see cases like yours with no other symptoms at all. Thus, it seems that the dose of arterial gas required to elicit the response in pigs is simply not encountered in the vast majority of human cases. It certainly cannot be concluded on the basis of this study that human divers with cutis marmorata must have suffered from arterial gas embolism.

A proponent of the brain embolism hypothesis might argue that maybe you don't need such large doses of gas going to the brain to elicit the response in humans. But this reasoning can also be challenged. Humans undergoing strongly positive bubble contrast echo studies for PFO inevitably have their cerebral circulation showered with bubbles of relevant size to those which "often" enter the arterial circulation from the veins after diving. This happens every day in cardiology suites where PFO tests take place. Sometimes we even see transient cerebral symptoms after such studies, but we NEVER see cutis marmorata. If "sub-clinical" cerebral arterial bubble exposure were the cause of cutis marmorata in human divers, we would expect to see it more often in strongly positive PFO tests, but we never do.

I am not dismissing the study out of hand. It seems likely that cutis marmorata could be seen after serious arterial gas embolism in humans, but this would be accompanied by stroke like brain injuries, and the majority of cutis marmorata cases in divers (who do not exhibit such injuries) do not seem to be caused in that way.

Simon M
 
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Thank you for a very thorough explanation of the pig study, Simon, I really appreciate it. The more I know, the better equipped I will be if I experience another hit. I find it interesting that there's really no science behind the time away from diving. I understand the bubbles will eventually go away but is there some type of scarring that needs to heal after they leave the body?

I totally understand there are no guarantees that I'll not have another hit regardless if I dive tomorrow or wait years. As Dr. Piccolo said, "The only way you won't get bent again is to quit diving." That's definitely not an option I'm taking, but I will abide by his recommendation to wait six months. Heck, I've already paid to go to Bonaire in January with the ScubaBoard Surge but I won't be diving since it will only be about four months since my episode. I'm sure I'll find other things to do in Bonaire that I didn't do the last time I was there because I was too busy diving. Also, I believe since the information was sent to DAN with the recommendation for no diving for six months, and I violated that recommendation and ended up needing the chamber, DAN would probably not pay the expenses. I'm very thankful DAN covered my chamber visit in September. To any divers reading this that don't have DAN or some other medical insurance that covers dive accidents, please get insured. I am probably one of the least expected divers to get bent. It came as a huge surprise to me and my dive buddies.

I'm grateful that there are people like you and DDM that help us better understand DCS. Thanks for all you do!
 
Second, the doses of air used to elicit the cutis marmorata response would have produced significant stroke like symptoms if the pigs were awake. But in the vast majority of cases of cutis marmorata in human divers we don't see symptoms of brain injury. Indeed, it is very common to see cases like yours with no other symptoms at all. Thus, it seems that the dose of arterial gas required to elicit the response in pigs is simply not encountered in the vast majority of human cases. It certainly cannot be concluded on the basis of this study that human divers with cutis marmorata must have suffered from arterial gas embolism.

A proponent of the brain embolism hypothesis might argue that maybe you don't need such large doses of gas going to the brain to elicit the response in humans. But this reasoning can also be challenged. Humans undergoing strongly positive bubble contrast echo studies for PFO inevitably have their cerebral circulation showered with bubbles of relevant size to those which "often" enter the arterial circulation from the veins after diving. This happens every day in cardiology suites where PFO tests take place. Sometimes we even see transient cerebral symptoms after such studies, but we NEVER see cutis marmorata. If "sub-clinical" cerebral arterial bubble exposure were the cause of cutis marmorata in human divers, we would expect to see it more often in strongly positive PFO tests, but we never do.

I am not dismissing the study out of hand. It seems likely that cutis marmorata could be seen after serious arterial gas embolism in humans, but this would be accompanied by stroke like brain injuries, and the majority of cutis marmorata cases in divers (who do not exhibit such injuries) do not seem to be caused in that way.

Simon M

Simon, this steps a little outside the study and gets theoretical, but do you think that rather than the entire bolus of air that the pigs received being responsible for the cutis, some amount of that large bolus managed to land in the correct spot to produce the rash? Is there a comparison between the pig study and many of the animal DCS models we use in that we make certain that their chamber dive profiles are provocative enough to produce the DCS symptoms we're looking for?

Best regards,
DDM
 
Simon, this steps a little outside the study and gets theoretical, but do you think that rather than the entire bolus of air that the pigs received being responsible for the cutis, some amount of that large bolus managed to land in the correct spot to produce the rash? Is there a comparison between the pig study and many of the animal DCS models we use in that we make certain that their chamber dive profiles are provocative enough to produce the DCS symptoms we're looking for?

Best regards,
DDM

Hello DDM,

It doubt it. The gas was injected in what is effectively the carotid artery, so it is unlikely much went peripherally. Moreover, for bubble arriving in cutaneous tissue to cause cutis there probably needs to be a dissolved gas load and these pigs were not dived and decompressed.

Peter Wilmshurst published a very good summary of the concerns about the study that I have articulated above. I have pasted the content of his letter below. It makes very interesting reading.

Diving Hyperb Med. 2015 Dec;45(4):261.
Cutis marmorata and cerebral arterial gas embolism.
Wilmshurst PT.

Dr Kemper and colleagues reported that, when air was injected into the cerebral circulation of pigs, they developed a rash that looked very similar to cutis marmorata of cutaneous decompression illness (DCI) and to livido reticularis. They postulated that cutaneous DCI in divers may be centrally mediated as a result of cerebral gas embolism. It would be helpful if Kemper et al. described the distribution of the rash in their pigs. In divers, cutaneous DCI is generally confined to parts of the body with significant amounts of subcutaneous fat, such as the trunk and thighs, and the rash often crosses the midline. Colleagues and I have reported that cutaneous DCI is commonly associated with significant right-to-left shunts and particularly persistent foramen ovale (PFO). We postulated that the manifestations of shunt-related DCI, whether neurological or cutaneous, are in large part determined by peripheral amplification of embolic bubbles in those tissues that are most supersaturated with dissolved nitrogen (or other inert gas) at the time that emboli arrive. Hence we postulated that cutaneous DCI is the result of amplification of gas emboli that invade cutaneous capillaries. Dr Kemper has kindly sent me a number of the publications from his department on which their report of this skin rash in pigs is based. The aim of their experiments was to produce significant brain injury by means of cerebral air embolism. Their pigs had no tissues supersaturated with inert gas. They were ventilated with a FiO₂ of 0.4 and anaesthetised with ketamine and midazolam. They were also given pancuronium and atropine, before air was injected into their cerebral circulation. If their findings in pigs and the resulting hypothesis were applicable to man, it would mean that one could get cutaneous DCI without decompression: one would only need cerebral gas embolism. During contrast echocardiography, I have produced arterial gas embolism in many hundreds of patients with right-to-left shunts and it is certain that some bubbles went into their cerebral circulations, but I have never seen and no patient has reported getting a rash. Nor am I aware of any reports of gas embolism causing a rash like cutaneous DCI without there being tissue supersaturation following some form of decompression. Kemper and colleagues injected between 0.25 and 1 ml·kg⁻¹ body weight of air into the ascending pharyngeal artery (roughly equivalent to human internal carotid artery) of pigs weighing 30-40kg. That immediately produced significant elevation of blood pressure and heart rate suggesting a 'sympathetic surge'. This is similar to the haemodynamic effects that can occur with subarachnoid haemorrhage and some other catastrophic brain injuries. That effect may have been potentiated by pre-treatment with atropine. There was also a considerable increase in intracranial pressure and major adverse effects on cerebral metabolism. Some pigs died quickly and the survivors were killed at the end of the experiment. I suspect that no pig would have survived the experiments without major neurological injury if they had not been killed. Most people with cutaneous DCI have no detectable neurological manifestations at the time that they have a rash. In those that do have neurological manifestations, it is rarely catastrophic. The increases in heart rate and blood pressure reported in the pigs are similar to the effects of a phaeochromocytoma, which can cause livido reticularis in man. Therefore, I wonder whether an alternative explanation for these observations might be that the cerebral injury in the pigs was so massive that the sympathetic surge was comparable to the effects of catecholamine release from a phaeochromocytoma and caused a rash similar to that seen in patients with a phaeochromocytoma.

Simon M
 
Bonaire..no diving, then hook up with a sail kite school there! Awesome adrenaline rush :)

Heal quickly.
 
https://www.shearwater.com/products/teric/

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