Thanks Ayisha but the link doesn't work for me I get a 404 message
Pulmonary Oedema incident
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Ayisha
Contributor
Sorry about that. Let me try again: http://www.underwatercouncil.com/downloads/newsletters/current_newsletter.pdf
If that doesn't work, just scroll down to the "Ontario Diver Newsletter" link on the right at Ontario Underwater Council
Thanks for looking!
If that doesn't work, just scroll down to the "Ontario Diver Newsletter" link on the right at Ontario Underwater Council
Thanks for looking!
Aisha your posts are always worth looking at 
Thanks for the info... I have forwarded it to the group of friends we dive with here in OZ.
Thanks for the info... I have forwarded it to the group of friends we dive with here in OZ.Ashleyallen0524
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It's good to hear that you saved your life from that incident. As long as you have life insurance with you, there's nothing to be worry about, because you know your safe and secured.
I hope this is tongue-in-cheek..? No amount of insurance can compensate for death or a debilitating injury.
OP
InTheDrink
Contributor
Sorry about that. Let me try again: http://www.underwatercouncil.com/downloads/newsletters/current_newsletter.pdf
If that doesn't work, just scroll down to the "Ontario Diver Newsletter" link on the right at Ontario Underwater Council
Thanks for looking!
Thanks for that Ayisha, very informative
- out of curiousity, you mention rebreathers a fair amount including ADVs.... this on the back of my experience or are you referencing other incidents too?Thanks,
John
---------- Post added December 11th, 2012 at 11:00 AM ----------
Bizarro!
Ayisha
Contributor
Hi John, the ways rb's can contribute to IPE came primarily from the research articles I read, but I also took note of some vetted medical opinions expressed in your thread. It may seem there was a fair bit on rb's, but I think that was just due to trying to simplify some complex processes that many readers would be unfamiliar with.
OP
InTheDrink
Contributor
O'K cool and interesting. If you've got any other references wrt ADVs in particular I'd be interested to read. FYI, in the latest version of my unit apparently the ADV is now very generous/sensitive.
Thanks,
John
Thanks,
John
retendokid
Registered
Ayisha- Nice job with this article on immersion pulmonary edema. (Post # 90)
If I may, a few further thoughts on this subject.
The more I think about IPE, the more I suspect it is a multifactorial event or process with relative contributions of various factors that likely differ from diver to diver. As an anesthesiologist who deals with pulmonary physiology on a daily basis, but also as a diver constantly thinking about the impact of underwater environments on our bodies, I've started to put pieces of the puzzle together in my own mind. Anyway, there is fairly good scientific evidence for most of the individual components listed below, but the cumulative and compounding effects that ultimately lead to life threating pulmonary edema are still incompletely understood due to the rarity of reported cases and likelihood of events attributed to other etiologies (eg drowning). In the absence of solid medical/scientific data, we are left to rationally consider probable causes. It is, at least in my mind, extremely unlikely that IPE results from a SINGLE identifiable trigger or cause. Rather, several of the following, in varying degrees and with different susceptibilities in individuals, contribute to flash pulmonary edema while diving:
1) Exercise: inevitably, this results in large increases in pulmonary blood flow. Its important that the pulmonary circulation be capable of rapidly expanding for increased oxygen loading capacity in response to physical exertion. Many of the articles/cases on pulmonary edema describe a considerable physical exertion immediately prior to a serious event. The result of exertion, (eg. long surface swim, swimming against current ,or even just anxiety) is a large increase in cardiac output and a large increase in pulmonary blood flow .and with that, pulmonary fluid volume. Another factor may be the lack of adequate cardiopulmonary health and fitness among divers, although this is a fasttrack to a separate and lengthy discussion which Ill avoid for now.
2) Immersion: even the simplest form of water immersion (sitting in a bath) leads to increased hydrostatic pressures that force fluid from the periphery to central vascular compartments. Consequently, normovolemic persons on the surface become hypervolemic underwater. For nearly all divers, this excess circulating volume presents no real risk, as most possess the cardiopulmonary reserve to handle it. This fluid shifting during immersion explains why we all have to pee in our wetsuits while diving......the bodys sensing mechanisms detect volume overload and tell the kidneys to start dumping fluid. The typical volumes shunted from periphery to central compartments are well defined. Studies done submersing patients in lithotripsy tanks show an average of approximately 700 ml increase in central compartment volume during water immersion. This is simply a direct consequence of changing from ambient air pressure to hydrostatic pressure surrounding the body.
3) Cold: cold water immersion further contributes to rapid shifts in body fluid volumes via peripheral vasoconstriction and the body's natural attempt to preserve heat. Case reports of IPE have been sometimes associated with diving in cold water. This becomes problematic for two reasons-vasoconstriction shunts body fluid from the periphery, exacerbating #2 above, but cold water also necessitates heavier thermal protection (thicker tighter wetsuits) further squeezing peripheral volumes toward intrathoracic circulation. And lets face it, unless you are diving in the Keys in August (86 F), all ocean water is probably cold enough to induce some loss in body heat and induce vasoconstriction. Moreover, the vasoconstrictive responses to cold are highly individualized-some people develop Raynauds and develop cold, white, ischemic hands from the slightest drop in temperature, while other people seem to be immune to cold.
4) Pressure: There are many studies examining cardiopulmonary effects of scuba diving, and breath hold diving. We have a hyperbaric chamber at my institution and I have colleagues regularly conducting research with it. Needlesss to say, the effects of pressure on human physiology represents a vast body of medical science and can in no way be addressed here. However, there are several salient features for this topic that include a 15-20% reduction in lung volumes, increase work of breathing due to increased gas density, and respiratory muscle fatigue because of increased WOB. This is a complicated set of factors but all probably play a role. Here's one example--when lungs function at reduced volumes there are areas of regional collapse, and as partially collapsed alveoli open and close, there are shear forces from the normally open alveoli now rubbing against one another. This leads to inflammation, injury, and fluid collection. Furthermore, the work of breathing is increased during partial lung collapse for the following unavoidable reason--the pressure required to inflate a partially collapsed alveoli, compared to a properly inflated one, is much higher and leads to increased work of breathing, and greater inspiratory effort. (the analogy is blowing up a balloon-the greatest effort is required to start the balloon expanding, but the pressure required to further inflate the balloon decreases as it inflates) At any rate, diving puts the lungs under a variety of abnormal physiologic pressures and conditions with complicated implications, some of which may be harmful or benign, but certainly none of which are protective.
5. Negative Pressure Pulmonary Edema: - see description of this in the thread posts above. In short, sudden or even gradual resistance to airflow causes an imbalance in pulmonary capillary transmural pressure (difference in pressures across the wall of the capillary) and that favors fluid collection in the alveoli. Ironically, the bigger and stronger the person, the greater inspiratory forces they can generate, and the greater the risk of developing injury/edema from breathing against high resistance or any direct obstruction to airflow. (take a big breath off of a regulator without the air turned for a good illustration of this) The result of these high pressures/forces, is endothelial damage and disruption of the capillary-alveolar membrane which results in fluid collection. In and of itself, acute episodes of NPPE have produced enough fluid collection and lung injury to be fatal in otherwise healthy patients--a phenomenon well described in critical care medicine and anesthesiology. Despite these in-hospital events, the exact pathophysiology is still poorly understood, so it should hardly be surprising that IPE remains a mystery.
6. Tight restrictive wetsuits/bcds/weight belts: -as mentioned above, these contribute to further external squeeze forcing peripheral fluid volumes centrally. This should not be surprising as support hose (compression stocking) are frequently recommended for patients with peripheral edema, and they function simply by squeezing fluid out of the extremity which is then eliminated by the kidneys. But pulling on a whole body wetsuit must force considerable fluid content from the extremities to the central compartments. I think the hemodynamic and fluid shift phenomenon of donning a wetsuit has yet to be properly studied. I did a brief literature review and cannot find anything published about this. If anyone knows of such research please let me know.
At any rate, one can easily imagine the following scenario: a diver gains considerable weight, heads out on a dive trip, and now that 5 or 7 mm wetsuit that fit well two years ago has become one gigantic compression stocking, pushing fluid from the legs, arms, and all outer layer soft tissues. The volume of fluid now forced into the restricted cardiopulmonary circulation is anybody's guess....just remember that the average water content of a 70 kg person is about 40 liters!
But restrictive/protective gear may also pose direct mechanical obstruction to proper lung inflation. Anything tight across the chest and abdomen, can impose restrictive forces for breathing and/or limit diaphragmatic excursion, thereby reducing functional respiratory volumes and increasing the work of breathing.
7. Alcohol: -This is pure speculation but in several of the cases I've read about, reports of alcohol ingestion the night before diving were mentioned. The diverse effects of alcohol are widely known, including the fact that alcohol produces dehydration. But what if the problem was not from the alcohol itself, but from a prudent divers attempts to compensate for their nightly libations by large fluid intakes the next morning before going diving. This is certainly how I would think: "was out drinking last night, now Im going diving in salt water, tend to urinate while diving....better replace a bunch of fluid". Again, guesswork, but possibly it was not the alcohol per se that caused the problem, but smart people attempting to compensate for indulgences.
8. Hypoxic pulmonary vasoconstriction: This is another well known phenomenon in anesthesia, wherein the pulmonary vasculature vasoconstricts, thereby increasing resistive forces and making it more likely for increased transmural capillary pressures to force fluid into the interstitial space (result=pulmonary edema). There are two known causes of HPV-hypoxia and acidosis. While most divers will never breath hypoxic gases, and that is unlikely to be an issue until fluid begins to prevent capillaries from sensing adequate oxygen tension, the acidosis is another story. Nearly every diver I know tries to stretch out their air supply by slowing breathing. Divers sometimes surface with headaches from hypercarbia as a result of conscious ventilatory control. Slowing breathing limits ventilation and lets CO2 build up, which causes acidemia this can lead to HPV: the bodys natural response to match blood flow with the areas of the lungs where optimal gas exchange is occurring. In fact, patients with COPD rely upon their HPV to prevent unnecessary pulmonary circulation to areas of the lungs which are diseased and poorly oxygenated. This process, however, occurs in all of us. But while this common mechanism is usually helpful, it becomes harmful when fluid begins to collect, because as alveoli become poorly oxygenated, vasoconstriction will simply worsen the problem. I'm doubtful that this is truly a significant player in IPE, but once a downward spiral gets rolling, factors such as this may continue to push things in the wrong direction.
9. Sodium load/water retention: Congestive heart failure patients can acutely decompensate and develop pulmonary edema simply from the sodium load of eating a can of Campbells Soup. In these people, excess sodium intake, and the water retention that follows, will lead to circulatory overload and a buildup of fluid in the lungs. Many divers go on vacation, go out for big dinners, and consume amounts of sodium far beyond their usual and daily recommended intake. Again, while most divers are relatively fit, in terms of cardiovascular health, and will NOT rapidly develop pulmonary edema from a high salt meal, it may precipitate problems by leading to a higher than normal body water content in the pre-dive period . excess volume that is just waiting to be squeezed into the thoracic circulation by factors listed above. This is another area of speculation, but the steady stream of hospital readmissions for volume overloaded CHF patients is a big lesson regarding the role that dietary sodium plays in fluid management and pulmonary edema.
10. Repetitive Dives: Both John's account above, as well as several others on SB (see thread links below for similar accounts) noted that the events occurred on repetitive diving training or dive trips.
http://www.scubaboard.com/forums/ne...rned/408252-pulmonary-barotrauma-age-hit.html
http://www.scubaboard.com/forums/ac...eniseggs-incident-near-miss-jackson-blue.html
Its difficult to pin down anything specific here, but these associations may prove to have a greater role than imagined. In my field, it is becoming increasingly clear that minor lung injury occurs during most general anesthetics, where positive pressure ventilation and hyperinflation occurs. Examination of inflammatory markers, in healthy people, suggests that even a well controlled general anesthetic and reasonable ventilatory management may produce mild forms of lung injury. Again, the vast majority of the time, this is clinically insignificant. But in conjunction with other confounding factors, it may contribute to a problem. The latest thinking is that repetitive hyperinflation may be the precipitating cause of ventilator-associated lung injury (VALI). Essentially, over stretching of the alveoli leads to injury, edema, blood collection, and then alveolar collapse. When diving, we are at significant risk of hyperinflation and barotrauma of this nature and thus the cardinal rule taught during basic training: never hold your breath underwater. However, the lungs may not always follow our voluntary control-that is, anyplace where air-trapping can occur (very common in asthmatics, COPD etc), segments which were filled under pressure during descent or at the bottom of a profile, may be unable to vent during ascent and suffer hyperinflation injury or barotrauma. (personal note-I've had two ruptured ear drums while diving, both were from air trapping and occurred on ascent after being able to equalize fine on the way down)
And the truth is that entities like asthma (reactive airway disease) are not bimodal-either you have it or you don't-but rather exist in many subclinical forms that may be unrecognized by the individuals themselves and escape medical detection. Personally, I've never had any asthmatic symptoms, but a few years ago a combination of an upper respiratory infection and a trip to high altitude left me with a six week struggle with post-viral reactive airways needing inhalers and steroids. My point is that the potential is there for all of us, you just need to incur the right insults.
Moreover, I'm probably guilty of minor barotrauma every time I dive with my underwater photography rig. The first lesson in shooting shy creatures is that bubbles scare them away. So I know that I've very frequently used breath holding to adjust my buoyancy to position for a shot. Even if its just ascending a few feet, this repetitive process is likely causing minor problems. I'm frequently aware that my lungs kind of ache several days into a dive trip and I've often wondered if this is the cause. Its also difficult to predict the pulmonary implications of repetitive diving from breathing dry tank air or micro aspirations of seawater, but these may pose additional insults to the lungs.
Undoubtedly, some of this is incomplete, and other suggestions may not play a role or be flat out wrong. Medical science continues to chip away at the unknown, but one lesson is clear, the more rare the event or disease, the longer it takes to develop a full understanding. But what is clear to me is that the lungs are sometimes precarious organs with the potential to fail us above or below the water. For example, in susceptible individuals, a relatively mild insult (infection, trauma) can lead to acute lung injury and even full blown adult respiratory distress syndrome necessitating extensive ventilatory support in an ICU. The million dollar question is: why did that persons lungs get so sick from an otherwise non life-threatening insult? At this point, modern medicine is at a loss to predict who may be susceptible to these pulmonary injuries and who is resistant. But I think similarly, the question facing us as divers who will be susceptible to IPE, when others remain unaffected? It is likely the insults and physiologic challenges alluded to above conjoin to trigger lung injury and rapid accumulation of pulmonary edema....which if it occurs underwater, at the surface, or even a long boat ride away from medical services, can prove fatal.
My own plan to avoid problems-attention to factors above and only diving in gin clear warm water (kidding)
If others can clarify, expand, or correct any information I've provided, we'd all benefit from this. And again, I'll simply remind Scubaboard readers that this post does not constitute medical facts about IPE. Rather, these are the observations and logic from one standing at a crossroads where pulmonary pathophysiology and diving intersect.
I know if I were reading the freewheeling speculations included above, I would want to know the credentials of the author, so for those who are curious
Hugh M Smith MD PhD
Assistant Professor, Mayo Clinic
Department of Anesthesiology
Rochester, Minnesota
Dive Certification: Rescue Diver
Sent from my iPad using Tapatalk HD
If I may, a few further thoughts on this subject.
The more I think about IPE, the more I suspect it is a multifactorial event or process with relative contributions of various factors that likely differ from diver to diver. As an anesthesiologist who deals with pulmonary physiology on a daily basis, but also as a diver constantly thinking about the impact of underwater environments on our bodies, I've started to put pieces of the puzzle together in my own mind. Anyway, there is fairly good scientific evidence for most of the individual components listed below, but the cumulative and compounding effects that ultimately lead to life threating pulmonary edema are still incompletely understood due to the rarity of reported cases and likelihood of events attributed to other etiologies (eg drowning). In the absence of solid medical/scientific data, we are left to rationally consider probable causes. It is, at least in my mind, extremely unlikely that IPE results from a SINGLE identifiable trigger or cause. Rather, several of the following, in varying degrees and with different susceptibilities in individuals, contribute to flash pulmonary edema while diving:
1) Exercise: inevitably, this results in large increases in pulmonary blood flow. Its important that the pulmonary circulation be capable of rapidly expanding for increased oxygen loading capacity in response to physical exertion. Many of the articles/cases on pulmonary edema describe a considerable physical exertion immediately prior to a serious event. The result of exertion, (eg. long surface swim, swimming against current ,or even just anxiety) is a large increase in cardiac output and a large increase in pulmonary blood flow .and with that, pulmonary fluid volume. Another factor may be the lack of adequate cardiopulmonary health and fitness among divers, although this is a fasttrack to a separate and lengthy discussion which Ill avoid for now.
2) Immersion: even the simplest form of water immersion (sitting in a bath) leads to increased hydrostatic pressures that force fluid from the periphery to central vascular compartments. Consequently, normovolemic persons on the surface become hypervolemic underwater. For nearly all divers, this excess circulating volume presents no real risk, as most possess the cardiopulmonary reserve to handle it. This fluid shifting during immersion explains why we all have to pee in our wetsuits while diving......the bodys sensing mechanisms detect volume overload and tell the kidneys to start dumping fluid. The typical volumes shunted from periphery to central compartments are well defined. Studies done submersing patients in lithotripsy tanks show an average of approximately 700 ml increase in central compartment volume during water immersion. This is simply a direct consequence of changing from ambient air pressure to hydrostatic pressure surrounding the body.
3) Cold: cold water immersion further contributes to rapid shifts in body fluid volumes via peripheral vasoconstriction and the body's natural attempt to preserve heat. Case reports of IPE have been sometimes associated with diving in cold water. This becomes problematic for two reasons-vasoconstriction shunts body fluid from the periphery, exacerbating #2 above, but cold water also necessitates heavier thermal protection (thicker tighter wetsuits) further squeezing peripheral volumes toward intrathoracic circulation. And lets face it, unless you are diving in the Keys in August (86 F), all ocean water is probably cold enough to induce some loss in body heat and induce vasoconstriction. Moreover, the vasoconstrictive responses to cold are highly individualized-some people develop Raynauds and develop cold, white, ischemic hands from the slightest drop in temperature, while other people seem to be immune to cold.
4) Pressure: There are many studies examining cardiopulmonary effects of scuba diving, and breath hold diving. We have a hyperbaric chamber at my institution and I have colleagues regularly conducting research with it. Needlesss to say, the effects of pressure on human physiology represents a vast body of medical science and can in no way be addressed here. However, there are several salient features for this topic that include a 15-20% reduction in lung volumes, increase work of breathing due to increased gas density, and respiratory muscle fatigue because of increased WOB. This is a complicated set of factors but all probably play a role. Here's one example--when lungs function at reduced volumes there are areas of regional collapse, and as partially collapsed alveoli open and close, there are shear forces from the normally open alveoli now rubbing against one another. This leads to inflammation, injury, and fluid collection. Furthermore, the work of breathing is increased during partial lung collapse for the following unavoidable reason--the pressure required to inflate a partially collapsed alveoli, compared to a properly inflated one, is much higher and leads to increased work of breathing, and greater inspiratory effort. (the analogy is blowing up a balloon-the greatest effort is required to start the balloon expanding, but the pressure required to further inflate the balloon decreases as it inflates) At any rate, diving puts the lungs under a variety of abnormal physiologic pressures and conditions with complicated implications, some of which may be harmful or benign, but certainly none of which are protective.
5. Negative Pressure Pulmonary Edema: - see description of this in the thread posts above. In short, sudden or even gradual resistance to airflow causes an imbalance in pulmonary capillary transmural pressure (difference in pressures across the wall of the capillary) and that favors fluid collection in the alveoli. Ironically, the bigger and stronger the person, the greater inspiratory forces they can generate, and the greater the risk of developing injury/edema from breathing against high resistance or any direct obstruction to airflow. (take a big breath off of a regulator without the air turned for a good illustration of this) The result of these high pressures/forces, is endothelial damage and disruption of the capillary-alveolar membrane which results in fluid collection. In and of itself, acute episodes of NPPE have produced enough fluid collection and lung injury to be fatal in otherwise healthy patients--a phenomenon well described in critical care medicine and anesthesiology. Despite these in-hospital events, the exact pathophysiology is still poorly understood, so it should hardly be surprising that IPE remains a mystery.
6. Tight restrictive wetsuits/bcds/weight belts: -as mentioned above, these contribute to further external squeeze forcing peripheral fluid volumes centrally. This should not be surprising as support hose (compression stocking) are frequently recommended for patients with peripheral edema, and they function simply by squeezing fluid out of the extremity which is then eliminated by the kidneys. But pulling on a whole body wetsuit must force considerable fluid content from the extremities to the central compartments. I think the hemodynamic and fluid shift phenomenon of donning a wetsuit has yet to be properly studied. I did a brief literature review and cannot find anything published about this. If anyone knows of such research please let me know.
At any rate, one can easily imagine the following scenario: a diver gains considerable weight, heads out on a dive trip, and now that 5 or 7 mm wetsuit that fit well two years ago has become one gigantic compression stocking, pushing fluid from the legs, arms, and all outer layer soft tissues. The volume of fluid now forced into the restricted cardiopulmonary circulation is anybody's guess....just remember that the average water content of a 70 kg person is about 40 liters!
But restrictive/protective gear may also pose direct mechanical obstruction to proper lung inflation. Anything tight across the chest and abdomen, can impose restrictive forces for breathing and/or limit diaphragmatic excursion, thereby reducing functional respiratory volumes and increasing the work of breathing.
7. Alcohol: -This is pure speculation but in several of the cases I've read about, reports of alcohol ingestion the night before diving were mentioned. The diverse effects of alcohol are widely known, including the fact that alcohol produces dehydration. But what if the problem was not from the alcohol itself, but from a prudent divers attempts to compensate for their nightly libations by large fluid intakes the next morning before going diving. This is certainly how I would think: "was out drinking last night, now Im going diving in salt water, tend to urinate while diving....better replace a bunch of fluid". Again, guesswork, but possibly it was not the alcohol per se that caused the problem, but smart people attempting to compensate for indulgences.
8. Hypoxic pulmonary vasoconstriction: This is another well known phenomenon in anesthesia, wherein the pulmonary vasculature vasoconstricts, thereby increasing resistive forces and making it more likely for increased transmural capillary pressures to force fluid into the interstitial space (result=pulmonary edema). There are two known causes of HPV-hypoxia and acidosis. While most divers will never breath hypoxic gases, and that is unlikely to be an issue until fluid begins to prevent capillaries from sensing adequate oxygen tension, the acidosis is another story. Nearly every diver I know tries to stretch out their air supply by slowing breathing. Divers sometimes surface with headaches from hypercarbia as a result of conscious ventilatory control. Slowing breathing limits ventilation and lets CO2 build up, which causes acidemia this can lead to HPV: the bodys natural response to match blood flow with the areas of the lungs where optimal gas exchange is occurring. In fact, patients with COPD rely upon their HPV to prevent unnecessary pulmonary circulation to areas of the lungs which are diseased and poorly oxygenated. This process, however, occurs in all of us. But while this common mechanism is usually helpful, it becomes harmful when fluid begins to collect, because as alveoli become poorly oxygenated, vasoconstriction will simply worsen the problem. I'm doubtful that this is truly a significant player in IPE, but once a downward spiral gets rolling, factors such as this may continue to push things in the wrong direction.
9. Sodium load/water retention: Congestive heart failure patients can acutely decompensate and develop pulmonary edema simply from the sodium load of eating a can of Campbells Soup. In these people, excess sodium intake, and the water retention that follows, will lead to circulatory overload and a buildup of fluid in the lungs. Many divers go on vacation, go out for big dinners, and consume amounts of sodium far beyond their usual and daily recommended intake. Again, while most divers are relatively fit, in terms of cardiovascular health, and will NOT rapidly develop pulmonary edema from a high salt meal, it may precipitate problems by leading to a higher than normal body water content in the pre-dive period . excess volume that is just waiting to be squeezed into the thoracic circulation by factors listed above. This is another area of speculation, but the steady stream of hospital readmissions for volume overloaded CHF patients is a big lesson regarding the role that dietary sodium plays in fluid management and pulmonary edema.
10. Repetitive Dives: Both John's account above, as well as several others on SB (see thread links below for similar accounts) noted that the events occurred on repetitive diving training or dive trips.
http://www.scubaboard.com/forums/ne...rned/408252-pulmonary-barotrauma-age-hit.html
http://www.scubaboard.com/forums/ac...eniseggs-incident-near-miss-jackson-blue.html
Its difficult to pin down anything specific here, but these associations may prove to have a greater role than imagined. In my field, it is becoming increasingly clear that minor lung injury occurs during most general anesthetics, where positive pressure ventilation and hyperinflation occurs. Examination of inflammatory markers, in healthy people, suggests that even a well controlled general anesthetic and reasonable ventilatory management may produce mild forms of lung injury. Again, the vast majority of the time, this is clinically insignificant. But in conjunction with other confounding factors, it may contribute to a problem. The latest thinking is that repetitive hyperinflation may be the precipitating cause of ventilator-associated lung injury (VALI). Essentially, over stretching of the alveoli leads to injury, edema, blood collection, and then alveolar collapse. When diving, we are at significant risk of hyperinflation and barotrauma of this nature and thus the cardinal rule taught during basic training: never hold your breath underwater. However, the lungs may not always follow our voluntary control-that is, anyplace where air-trapping can occur (very common in asthmatics, COPD etc), segments which were filled under pressure during descent or at the bottom of a profile, may be unable to vent during ascent and suffer hyperinflation injury or barotrauma. (personal note-I've had two ruptured ear drums while diving, both were from air trapping and occurred on ascent after being able to equalize fine on the way down)
And the truth is that entities like asthma (reactive airway disease) are not bimodal-either you have it or you don't-but rather exist in many subclinical forms that may be unrecognized by the individuals themselves and escape medical detection. Personally, I've never had any asthmatic symptoms, but a few years ago a combination of an upper respiratory infection and a trip to high altitude left me with a six week struggle with post-viral reactive airways needing inhalers and steroids. My point is that the potential is there for all of us, you just need to incur the right insults.
Moreover, I'm probably guilty of minor barotrauma every time I dive with my underwater photography rig. The first lesson in shooting shy creatures is that bubbles scare them away. So I know that I've very frequently used breath holding to adjust my buoyancy to position for a shot. Even if its just ascending a few feet, this repetitive process is likely causing minor problems. I'm frequently aware that my lungs kind of ache several days into a dive trip and I've often wondered if this is the cause. Its also difficult to predict the pulmonary implications of repetitive diving from breathing dry tank air or micro aspirations of seawater, but these may pose additional insults to the lungs.
Undoubtedly, some of this is incomplete, and other suggestions may not play a role or be flat out wrong. Medical science continues to chip away at the unknown, but one lesson is clear, the more rare the event or disease, the longer it takes to develop a full understanding. But what is clear to me is that the lungs are sometimes precarious organs with the potential to fail us above or below the water. For example, in susceptible individuals, a relatively mild insult (infection, trauma) can lead to acute lung injury and even full blown adult respiratory distress syndrome necessitating extensive ventilatory support in an ICU. The million dollar question is: why did that persons lungs get so sick from an otherwise non life-threatening insult? At this point, modern medicine is at a loss to predict who may be susceptible to these pulmonary injuries and who is resistant. But I think similarly, the question facing us as divers who will be susceptible to IPE, when others remain unaffected? It is likely the insults and physiologic challenges alluded to above conjoin to trigger lung injury and rapid accumulation of pulmonary edema....which if it occurs underwater, at the surface, or even a long boat ride away from medical services, can prove fatal.
My own plan to avoid problems-attention to factors above and only diving in gin clear warm water (kidding)
If others can clarify, expand, or correct any information I've provided, we'd all benefit from this. And again, I'll simply remind Scubaboard readers that this post does not constitute medical facts about IPE. Rather, these are the observations and logic from one standing at a crossroads where pulmonary pathophysiology and diving intersect.
I know if I were reading the freewheeling speculations included above, I would want to know the credentials of the author, so for those who are curious
Hugh M Smith MD PhD
Assistant Professor, Mayo Clinic
Department of Anesthesiology
Rochester, Minnesota
Dive Certification: Rescue Diver
Sent from my iPad using Tapatalk HD
Ayisha
Contributor
Wow, thanks Dr Smith. Very insightful. Some of the medical professionals that have posted here have stated that it tends to be extremely difficult to pinpoint one cause that triggered the IPE in an individual case because there are multiple factors that could have contributed in many cases. I guess if we try to reduce the contributing factors that we can, like not wearing overly restrictive gear, not working too hard, maintaining trim, keeping our equipment maintained, keeping blood pressure under control, not over-hydrating, etc., we decrease our chances of getting IPE. Knowing when to call a dive is also very important.
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