How is time away from diving determined?

[islanddream]

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

Heal quickly.

Thanks, I like your suggestion!

 

[Rred]

islanddream-
Have you found any environmental factors (meds, booze, short sleep, running marathons?) that might have played a role in your incident? Or are you certain you stayed within (someone's) tables? Any clues at all to a possible cause for the incident?

And if not, have you considered that you might "need" to simply dive even more conservatively in the future, to prevent a re-occurrence? (i.e. add a PF or two in the computer, or an extra stop/s on the tables)

 

[uncfnp]

I am absolutely not encouraging you to do anything you are uncomfortable with but in Bonaire you could strap on a tank of 32 Nitrox and dive in the 15 to 30 feet range and see tons of stuff and it would be little more risk then snorkeling. Bari reef and the foundation come to mind as well as many of the southern sites where there can be lots of life in the sandy areas before the reef even starts.

 

[Duke Dive Medicine]

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

Thanks Simon. What meant was, is it possible that the large bolus of air that was introduced in the pig obstructed the area of the brain that was responsible for mediating the rash (along with a lot of other brain tissue), and with that, would it not be possible that shunted bubbles could produce the same effect? The bubble contrast argument is a good point, but those bubbles are minute and not subject to growth from dissolved nitrogen the way shunted bubbles in a diver are.

Best regards,
DDM

 

[islanddream]

islanddream-
Have you found any environmental factors (meds, booze, short sleep, running marathons?) that might have played a role in your incident? Or are you certain you stayed within (someone's) tables? Any clues at all to a possible cause for the incident?

And if not, have you considered that you might "need" to simply dive even more conservatively in the future, to prevent a re-occurrence? (i.e. add a PF or two in the computer, or an extra stop/s on the tables)

As you might imagine, I've searched my soul for what could have caused the hit. Here are a few thoughts:

• We had just experienced Hurricane Irma before we left for Cozumel. Even though the storm wasn't as bad as it could have been, there was still a fair amount of stress getting the house ready for the storm, cleaning up after the storm, and then getting everything ready for travel. Stress.
• We missed our flight to Cancun out of Fort Lauderdale due to bumper to bumper traffic. Many of the people were returning to Miami after having evacuated, therefore, the roads were a mess. We left in plenty of time to get to the airport but had no idea how bad the traffic was going to be. I had to search for another airline to get us to Cancun in time to do the bag drag and not miss the last ferry to Coz. I had to stay in contact with the condo owner and keep her in the loop so that we could get the condo keys when we arrived later than planned. Lots of stress.
• We dived five days in a row and the dives averaged about 80 minutes. The day before my hit we did three dives with the first two being a bit deep (107 ft. was the deepest) and the third dive was around 70 feet. (The other days we did two dives a day.) I never went into deco and paid close attention to my nitrogen loading. All of us were on nitrox. We ascended from each dive slowly, stay longer at the safety stops, and had more than an hour surface intervals.
• The day of the hit we did two dives, went back to the condo and cleaned up, and walked into town for dinner and back to the condo. It was probably a 2 miles round trip walk. It was hot and humid. At dinner I began to have symptoms.

I truly believe the stress, multiple dives each day with some being deep and all being long, diving five days in a row, and walking two miles on "hit" day all contributed to the episode.

My dive buddies and I all agreed on the following:

• In the future we will take a whole day off from diving in the middle of the trip. That would give us time to off-gas even more.
• We plan on going back to Coz next September and renting the same condo. It will be hot and humid that time a year so we should will consider taking a taxi to dinner if the walk is a bit far.
• I will definitely not dive as deep on future trips. Hanging above the crowd is OK with me.
• We are going to do eight minute safety stops in the future.
• Before I book a trip I'm going to find out where the nearest chamber is located.

A few other facts:

• When I downloaded my computer after I got home, there were no violations, nothing looked suspicious, and it appeared I didn't do anything stupid.
• I don't drink, smoke, or do drugs.
• I'm in good health and fairly fit. I could be more fit........
• During the trip I slept well and usually got 7-8 hours of sleep a night.
• I stay hydrated before, during, and after diving.

If you've never experience DCS, it really isn't much fun. It's uncomfortable (the skin bends), it's embarrassing, and it's scary. It's depressing to know I can't dive for six months....well, five months now, but I'm definitely going to follow the doctor's orders. I was so fortunate to have Dr. Piccolo (Clinic of San Miguel) as my dive doc. He's an amazing and interesting man and he doesn't suffer fools easily. My kind of doctor! I entered the chamber at 10 PM and exited at 3:45 AM. The chamber attendant was a really nice guy. We watched Netflix together in the chamber which made the time pass quickly. I'm happy to say I have no lasting affects of the hit....I feel very blessed. It could've been much worse.

Please, please, please.....if you suspect you might be bent, call DAN immediately and describe your symptoms. They will tell you what to do next. Follow their advice. If you don't have dive insurance, please get it. My episode cost several thousand dollars and DAN covered all of it.

No matter how safe a diver you are, DSC can happen to you.

Thanks to everyone for your well-wishes. I'll be back in the water on March 25, 2018.

 

[Dr Simon Mitchell]

Thanks Simon. What meant was, is it possible that the large bolus of air that was introduced in the pig obstructed the area of the brain that was responsible for mediating the rash (along with a lot of other brain tissue),

Yes, absolutely, that is the cause of the rash.... probably as a result of a substantial brain injury causing a massive sympathetic response, thus mediating the rash (which we also see in other non-diving brain injury scenarios).

and with that, would it not be possible that shunted bubbles could produce the same effect? The bubble contrast argument is a good point, but those bubbles are minute and not subject to growth from dissolved nitrogen the way shunted bubbles in a diver are.

Bubble contrast used in PFO tests are actually almost identical in size to the bubbles that form in the veins and cross a PFO after a dive (both have been measured). There is no way that these tiny bubbles after a dive would produce the sort of brain injury arising from having a massive gas bolus like those the pigs were exposed to (which was the equivalent of a 70kg human having 35 - 70 ml of air injected into the carotid artery!). Moreover, we have previously demonstrated that the brain does not remain supersaturated with dissolved nitrogen after a dive because it is such a fast tissue. So the tiny nitrogen bubbles crossing a PFO after diving will not grow in the cerebral circulation.

Thus, we return to the point, while a massive arterial gas embolism from pulmonary barotrauma might produce the sort of rash the pigs had (along with serious stroke-like symptoms), this is not a plausible explanation for the rash seen in most divers who exhibit the rash but without any neurological symptoms. It seems more likely that other mechanisms (like that discussed by Wilmshurst above) are responsible for the rash in the majority of cases.

All the relevant references to bubble sizes and the brain's rapid outgassing during decompression are discussed in this paper:

Mitchell SJ, Doolette DJ. Selective vulnerability of the inner ear to decompression sickness in divers with right to left shunt: the role of tissue gas supersaturation. J Appl Physiol 2009;106:298-301.

Simon

 

[Duke Dive Medicine]

Thanks for indulging me Simon. I appreciate the detail you put into your posts.

Back to the original post - it's interesting that cutis seems to be treated with more gravity here, at least in my experience. Have you noticed that as well?

Thanks,
DDM

 

[Dr Simon Mitchell]

Thanks for indulging me Simon. I appreciate the detail you put into your posts.

Back to the original post - it's interesting that cutis seems to be treated with more gravity here, at least in my experience. Have you noticed that as well?

Thanks,
DDM

Definitely,

This actually came up when I was teaching on the NOAA course in Seattle last week when I referred to rash as part of the 'mild' spectrum of DCI. One of the course participants objected to characterization of cutis marmorata as 'mild'. My point then, as it is now, was that the rash per se is not a serious problem. It will not of itself cause you any harm, and if it is the only manifestation present then it can regarded as mild. However, the significance of cutis is that there is a recognized (but not invariable) association with more serious symptoms. So if we see cutis, we should be alert to the possibility that there may be other manifestations present or on the way. This is the basis of confusion about how it should be viewed as a symptom. It certainly gets my attention when I see it and I would make sure there is nothing else going on, but if it turns out to be the ONLY thing going on (as in the OP's case), then I would still regard that as a mild case. IIRC this is how the remote DCI workshop saw it in 2004 when trying to define mild DCI.

Let me illustrate with 3 hypothetical cases that draw on many of the points made in this thread.

Case 1. A diver is at 40' for 30 minutes then panics and comes rocketing to the surface. He holds his breath and suffers pulmonary barotrauma. At the surface he rapidly becomes weak down his left side, and then unconscious. Shortly after, whilst managing his airway and administering oxygen the rescuers notice he has a cutis marmorata-like rash on his chest.

In this case it is almost certain that large bubbles introduced to the arterial circulation by pulmonary barotrauma have gone to the brain. These bubbles have caused a stroke-like syndrome, and the rash may well have arisen through the same brain-related mechanism as in the Kemper pig experiment. Obviously this is not a mild case, but it is serious because of the serious neurological manifestations, not because of the rash.

Case 2. A diver is a 90' for 25 minutes and makes an appropriate ascent and safety stop. Thirty minutes after the dive they notice an itch over the abdomen. Initially there is a pink rash but over the next 15 minutes it develops a blotchy appearance like cutis marmorata. Around this time they also develop tingling in both feet that slowly ascends up the legs, and there is an increasing sense that it is harder to stand and walk. The dive master is informed and the diver is given 100% oxygen. A doctor on board performs a neurological examination and finds weakness in both legs, with some reduction in sensation to pain up to the lower abdomen. The diver is evacuated on 100% oxygen and the rash slowly fades whereas the weakness remains.

This symptoms (rash and neurological symptoms) could not be caused by large bubbles going to the brain. The neurological symptoms are serious, but are localized to the spinal cord, not the brain. It is likely that tiny bubbles have crossed a PFO or pulmonary shunt, been carried to the skin and spinal cord in the arterial blood, and grown from inward diffusion of dissolved nitrogen from the surrounding tissue. Alternatively the bubbles might have formed in the skin or spinal cord tissue itself. Whatever the pathophysiological mechanism, this is obviously not a mild case, but it is serious because of the spinal manifestations, not because of the rash.

Case 3. A diver is a 90' for 25 minutes and makes an appropriate ascent and safety stop. Thirty minutes after the dive they notice an itch over the abdomen. Initially there is a pink rash but over the next 15 minutes it develops a blotchy appearance like cutis marmorata. They feel a little tired (as usual after diving) but otherwise completely well. In particular, there are no neurological manifestations. The dive master is informed and the diver is given 100% oxygen. Over the next hour the rash gradually fades away and diver continues to feel well. A doctor on board performs a neurological examination and can find no abnormalities.

It is virtually certain that this case could not be caused by large bubbles going to the brain (because if large bubbles had gone to the brain there would be other serious symptoms). It is much more likely that tiny bubbles have crossed a PFO or pulmonary shunt, been carried to the skin in the arterial blood, and grown from inward diffusion of dissolved nitrogen from the surrounding skin tissue. Alternatively the bubbles might have formed in the skin tissue itself. Whatever the pathophysiological mechanism, the rash itself will cause no harm, and in the absence of any other more serious symptoms, the case can be considered "mild".

Hope this makes sense.

Simon

 

[MargaritaMike]

Case 3. A diver is a 90' for 25 minutes and makes an appropriate ascent and safety stop. Thirty minutes after the dive they notice an itch over the abdomen. Initially there is a pink rash but over the next 15 minutes it develops a blotchy appearance like cutis marmorata. They feel a little tired (as usual after diving) but otherwise completely well. In particular, there are no neurological manifestations. The dive master is informed and the diver is given 100% oxygen. Over the next hour the rash gradually fades away and diver continues to feel well. A doctor on board performs a neurological examination and can find no abnormalities.

It is virtually certain that this case could not be caused by large bubbles going to the brain (because if large bubbles had gone to the brain there would be other serious symptoms). It is much more likely that tiny bubbles have crossed a PFO or pulmonary shunt, been carried to the skin in the arterial blood, and grown from inward diffusion of dissolved nitrogen from the surrounding skin tissue. Alternatively the bubbles might have formed in the skin tissue itself. Whatever the pathophysiological mechanism, the rash itself will cause no harm, and in the absence of any other more serious symptoms, the case can be considered "mild".

As a completely non-medical person Case 3 gives rise to this question, "Since the rash itself will cause no harm, and in the absence of any other more serious symptoms, the case can be considered "mild" how is extended treatment / observation (and extended abstinence from diving) called for if the rash disappears? That is to say, if the external symptoms are not present in this type of case, what would cause them to reappear or not reappear by not diving for an arbitrary period of time (1 week, 1 month, 3 months, 6 months, forever, etc.)? Please forgive my lay ignorance.

Thank you - M²

 

[uncfnp]

I was about to ask that same question.

For the hypothetical diver # 3. Would not his risk be the same once the nitrogen has been eliminated from the body, day 1 or day 180? Or is there a risk for some duration of time from tissues that have been sensitized by the previous event?

BTW. I want to expression my appreciation for both Dr Mitchell’s and DDM’s willingness to participate and share their respective insights into decompress injury and risks.