Thanks, I like your suggestion!Bonaire..no diving, then hook up with a sail kite school there! Awesome adrenaline rush
Heal quickly.
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Thanks, I like your suggestion!Bonaire..no diving, then hook up with a sail kite school there! Awesome adrenaline rush
Heal quickly.
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
As you might imagine, I've searched my soul for what could have caused the hit. Here are a few thoughts: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)
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.
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
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".