Undeserved Hit, Question for Dr. D

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As a DMT, I'd like to make a couple of points if I may. The first being that the folks at the ER are just NOT going to be real familiar with DCS problems. It is not their fault. It is the fault of the system. The only education they get about it will be a few minutes of one lecture, mas o menos. They are not going to understand it. They are also not going to listen to the patient telling them how to do their job.

Sorry, but that is reality. The ONLY answer is to have someone call DAN's emergency hot-line, like ASAP!!

We are trying to get away from calling DCS hits "undeserved" or "deserved". We don't want people put in the position of feeling guilty because they may be deserving of DCS!:11: The new term for DCS incidents that seem to have occurred in a diving regime that would otherwise not explain it is "unexpected".

As for the possibility of a PFO, a certain percentage of the populace have them. Given the circumstances, and the patient's expressed desire to keep diving, it might be wise to check. At that point, the results could either rule out that particular worry, or lead to a GO-NO GO decision on repairing it or not.

I hope your girlfriend will recover completely and continue a long, and happy life with lots of diving!:D
 
Rick Inman:
Because I had called DAN, the hyperbolic Doctor met me at the door. ..., Deaconess Medical Center ER.
I too had called DAN and even spoke directly to the Hyperbaric doctor at Long Beach Memorial in Long Beach CA. But proceedures said I had to be admitted through the emergency room. The chamber called down 4 times looking for me, but that did not help the emergency room folks connect the dots and get me out of there. The just forgot about me. If there ever is a next time I will make all kinds of noise.
 
As Dr. D has not replied, I'll assist.

Her symptoms (shoulder pain, tingling and numbness in the arm) are all but gone, but she occasionally gets bursts of pain in her left arm.


Neural recovery often manifest with paresthesias. Further recompression will not alter sensations.

Additionally, he heard a very faint heart murmur that in her 24 years no other doctor has mentioned. He recommended a bubble tracking EKG to determine if she has a PFO. What are your thoughts about diving with PFO (assuming she has one)?

Bubble tracking echocardiogram as a TEE, not EKG. She would benefit from a TEE if she wishes to continue to dive and wants an explanation for the unexpected DCS.

In the future, she plans to limit herself to 60FSW max (doctor’s recommendation) diving air tables on Nitrox, no more twice a day, observing conservative surface intervals. Do you have any input? Should she seek rec TriMix?

Until the TEE, this are prudent. The size of a PFO many help plan what exactly she should do during dives, moreso if there is no PFO. No diving with helium containing gases because He bubbles more, and injuries can be most severe for errors in buoyancy or decompression.

Triox requires absolute buoyancy control, which pretty much requires technical diving skills.
 
Saturation:
The size of a PFO many help plan what exactly she should do during dives, moreso if there is no PFO.
Hmmmm -- I've read that sentence several times, and am still having trouble parsing it. If it turns out there isn't a PFO, what is it that's more so?
 
Blackwood:
My girlfriend took an undeserved (type-II, I believe) hit this Sunday.

Catalina Island: three dives (max depths of 72, 73 and 49, with surface intervals of 1:50 and 1:30, respectively), slow ascents (less than 30fpm). Average depths in the 35, 40 and 25 foot range. Only foul was dehydration.

She underwent two chamber treatments at Long Beach Memorial (90 minutes each, the consisting of a 30 minute dive to 3ATA followed by 60 minutes at 2ATA, and the second at 2ATA for the entire 90 minutes).

Her symptoms (shoulder pain, tingling and numbness in the arm) are all but gone, but she occasionally gets bursts of pain in her left arm.

She's wondering if this is normal or whether she should seek a third treatment. The Hyperbaric Doctor quoted 1.5 rides as average, and said her symptoms should subside within a few weeks. Would you agree with that?




Additionally, he heard a very faint heart murmur that in her 24 years no other doctor has mentioned. He recommended a bubble tracking EKG to determine if she has a PFO. What are your thoughts about diving with PFO (assuming she has one)?



In the future, she plans to limit herself to 60FSW max (doctor’s recommendation) diving air tables on Nitrox, no more twice a day, observing conservative surface intervals. Do you have any input? Should she seek rec TriMix?



Thanks!


The trimix is not any benefit with regards to DCI. The benefit of trimix is to reduce nitrogen narcosis on deep dives, but the decompression repercussions are far greater - Helium is much less dense than nitrogen, so it goes faster in, but comes faster out again.

This means that should you have a fast ascent, or be sloppy with your deco stops, you will bubble much faster, and hence make the effect of DCI much more severe. In other words, if you ascend fast on air, you might get DCI - Ascend fast on trimix, and you will almost certainly die.

I would suggest diving on a high nitrox mix instead. As long as dives are kept short, (As in 45 minutes dive time) , your body can probably handle a pp02 of 1.6 for most of the dive - So planning with a pp02 of 1.5 would be fairly safe. (The lowest recorded instance of o2 tox within the o2 exposure limits (According to the NOAA tables (I believe)) was on a partial pressure of 1.72)

Even better, have a look at the v-planner deco planning software, use conservatism of 5+ and plan recreational dives as deco dives, adding a few minutes of deco even on the no-stop times - This would only serve to increase safety.
 
Hello Blackwood:

Dr D. was away from the JSC office for a while on NASA business. We were discussing decompression on the Moon. This is definitely cool!

Many thanks to Saturation for his comments.

- - -


There is always the possibility of a PFO when neurological DCS presents itself. As mentions, the test that she needs is cardiocardiogram with bubble contrast. This is best performed with a transesophageal probe rather than a simple transthoracic echo.

In all cases where arterialization is expected as the case, one can avoid future situations by diving with small nitrogen doses, that is, limit the time/depth exposure. Little nitrogen uptake will mean no tissue load. In tern, no loading results in no bubbles and no embolizing entities.

Dr Deco :doctor:
 
Alex in L.A.:
Hmmmm -- I've read that sentence several times, and am still having trouble parsing it. If it turns out there isn't a PFO, what is it that's more so?

Sorry for being terse.

I did a search and found little is discussed about this item elsewhere. So here is a summary.

The sources for shunts to cause AGE or DCS2 that are treatable to an extent are: PFOs and "lung shunts". Shunts are various sized arterial to venous connections, commonly as fistulas, and these can occur in any organ. As blood from all organs converge to the lungs, lung fistulas are more severe, as they are basically large defects in the lung as a bubble filter. Note, bubbles can also squeeze passed the lung if the volume of bubbles is large after a dive or the lung has defects in its structure due to acquired disease, such as damage from smoking. Thus, the generic name of 'lung shunt,' its a term for all bypasses of the lung as bubble filter.

http://www.yorkshire-divers.co.uk/forums/showthread.php?t=17827

Severity depends on the size of shunts.

PFO are least risky if 4mm or less in diameter.

Lung shunts and large PFOs offer a higher risk, but its not quantitative at this time. There is a theoretical risk for intra-dive AGE in these situations, and potential drowning at worse case.

To enter arterial circulation via a PFO, bubbles need to traverse the right atrium to the left atrium via an increase in right atrial pressure usually caused by coughing or lifting. Lung shunts push bubbles to the arterial side without such action. Therefore, sources for lung shunts are much worse, and are not evaluated very thoroughly after an unexpected hit on patients.

'More so if there is no PFO...' is because if the PFO evaluation is negative and one had an unexpected hit, it could need more workup and more bubble reducing measures to dive safely.

Without knowing the source of emboli, its not possible to logically plan a protective action, unless we blanketly take ALL possible steps to minimize bubbling. If diver cannot cope with all these added issues, diving is over for them or they dive in very risky conditions for simple recreational dives.

The approach most dive docs are using is simply to forego the workup and just do the conservative measure and see what happens. Typically that is dive to P02 of 1.2 or 1.3 with nitrox, reduce bottom time and longer safety stops both mid depth and 20' variety.

Additional actions are: reducing intra-dive motion as much as possible, and breath 40% or more 02 at the safety stops as a kind of 'deco' stop to wash out as much N2 as possible, increasing fitness, and weight at BMI <= 25.

Diving deeper is a problem for high risk folks as more inert gas is uptaken, and there is a risk of bubbling with long ascent alone as large shunts do not allow bubbles to be decompressed during stops, a worse case scenario is embolization in-water leading to unconsciousness and drowning, such as in the case of Paul Thomas, M.D. who embolized while on ascent possibly through a PFO. His story is all over Scubaboard.

To diagnose these issues requires a TCD and a TEE. TCDs are positive in arterial to venous shunts of any type. TEE is for PFO only. If the TEE is negative and TCD positive, then the patient has a non-PFO shunt which is presumed from the lungs. Shunts in other organs may not pass enough bubbles fast enough to be heard, but it can be the source too. For large PFOs, there is the option of repair for to continue to dive. If fistulas are found, the treatment is a specialized.

Shunts of small dimension that cause diving problems often do not cause other problems, but fistulas can be life threatening as a source of bleeding. They can occur anywhere, and if the TCD is positive the difficult step finding the fistula. And alas, there is still much more to it.

Thus, the "more so" if a PFO is negative as a source for gas emboli: lung shunts that aren't a PFO are the most risky and undefined.

Finally, lung shunts are not static structures, they can be acquired or grow as one ages or worsen from other diseases: a pneumonia can create a lung defect that is otherwise not an issue unless you dive. Its another reason PFO screening for diving is not warranted, even if you are negative, you can still develop another shunt elsewhere that is just waiting for an opportunity to open up. This is often the case when one has dove for years without issue then suddenly gets an unexpected hit.

Luckily, the vast majority of emboli from unexpected hits are not fatal, as note here and elsewhere, the symptoms are startling, obvious, gets the diver to see a dive doctor and trigger a need to decide whether to do something about it or stop diving.
 
Hello readers:

Curiously enough, bubble arterialization though a PFO was almost never discussedprior to 1990. Most researchers targeted transpulmonic passage. This was associated with numerous gas bubbles in the venous return, a blockade of lung capillaries, and a rise of pulmonary artery pressure.

In the last decade and a half, we have seen a concentration on the PFO and a forgetfulness/neglect of the other mechanisms. Some references are provided below

Dr Deco :doctor:



References :book3:

One can note the dates to see a shift in interest in Lungs versus PFO. [The references are not in chronological order.]

PFO

Wijman CA; Babikian VL; Winter MR; Pochay VE (2000). Distribution of cerebral microembolism in the anterior and middle cerebral arteries. Acta Neurol Scand 101(2):122-7

Wilmshurst P (1992). Patent foramen ovale and subaqua diving. BMJ, 304, 1312.

Albert A, Muller HR, Hetzel A (1997). Optimized transcranial Doppler technique for the diagnosis of cardiac right-to-left shunts. J Neuroimaging; 7(3): 159-63

Balestra C; Germonpre P; Marroni A (1998). Intrathoracic pressure changes after Valsalva strain and other maneuvers: implications for divers with patent foramen ovale. Undersea Hyperb Med; 25(3):171-4

Chimowitz, M. I.; J. J. Nemec; T. H. Marwick; R. J. Lorig; A. J. Furlan; and E. E. Salcedo (1991). Trans¬cranial Doppler ultrasound identifies patients with right to left cardiac of pulmonary shunts. Neurology, 41, 1902.

Droste DW; Kriete JU; Stypmann J; Castrucci M; Wichter T; Tietje R; Weltermann B; Young P; Ringelstein EB (1999). Contrast transcranial Doppler ultrasound in the detection of right-to-left shunts: comparison of different procedures and different contrast agents. Stroke;30(9):1827-32

Droste DW; Reisener M; Kemeny V; Dittrich R; Schulte-Altedorneburg G; Stypmann J; Wichter T; Ringelstein EB. (1999). Contrast transcranial Doppler ultrasound in the detection of right-to-left shunts. Reproducibility, comparison of 2 agents, and distribution of microemboli. Stroke 30(5):1014-8

Germonpré P, P Dendale, P Unger, and C Balestra (1998). Patent foramen ovale and decompression sickness in sports divers. J. Appl. Physiol., 84 (5), 1622 - 1626.

Georgiadis D, Grosset DG. Kelman A, Faichney A. Lees KR. (1994). Prevalence and characteristics of intracranial microemboli signals hi patients with different types of prosthetic cardiac valves. Stroke; 25: 587 592.

Horner S; Ni XS; Weihs W; Harb S; Augustin M; Duft M; Niederkorn K (1997). Simultaneous bilateral contrast transcranial Doppler monitoring in patients with intracardiac and intrapulmonary shunts. J Neurol Sci; 150(1):49-57

Kerut EK; Truax WD; Borreson TE; Van Meter KW; Given MB; Giles TD (1997). Detection of right to left shunts in decompression sickness in divers. Am J Cardiol. 1; 79(3):377-8

Klotzsch C; Janssen G; Berlit P (1994). Transesophageal echocardiography and contrast-TCD in the detection of a patent foramen ovale: experiences with 111 patients. Neurology 1994 Sep;44(9):1603-6

Moon RE; Camporesi EM; Kisslo JA (1989). Patent foramen ovale and decompression sickness in divers. Lancet ;1(8637):513-4

Moon, R. E.; J. A. Kisslo; E. W. Massed, T. A. Fawcett; and D. R. Theil (1991). Patent foremen ovate (PFO) and decompression illness. Undersea Biomed. Res., 18 (Suppl.), IS.

Powell, M. R., K. V. Kumar, W. Norfleet, and J. Waligora, B. Butler (1995). Patent foramen ovale and hypobaric decompression. Aviat Space Environ Med. 66(3):273-5

Ries S; Knauth M; Kern R; Klingmann C; Daffertshofer M; Sartor K; Hennerici M (1999). Arterial gas embolism after decompression: correlation with right-to- left shunting. Neurology; 52 (2):401-4

Ringelstein EB; Droste DW; Babikian VL; Evans DH; Grosset DG; Kaps M; Markus HS; Russell D; Siebler M 1998. Consensus on microembolus detection by TCD. International Consensus Group on Microembolus Detection. Stroke ;29(3):725-9



LUNG

Brubakk, A. O.; R. Peterson; A. Grip; B. Holand; J. Onarheim; K Segadal; T. K Kunlde; and S. T¢njum (1986). Gas bubbles in the circulation of divers after ascending excursions from 300 to 250 msw. J. Appl. Physiol., 60(1), 45.

Butler, B. D. and B. A. Hills (1979). The lung as a filter for microbubbles. J. Appl. Physiol. Respirat. Envi¬ron. Exercise Physiol., 47 (3).

Butler, B. D. and B. A. Hills (1980). Transpulmonary passage of venous air emboli. J. Appl Physiol., 56, S43.

Butler BD; Robinson R; Sutton T; Kemper GB (1995). Cardiovascular pressures with venous gas embolism and decompression. Aviat Space Environ Med; 66(5):408-14

Emerson, L.V.; H. V. Hempleman; and R. G. Lentel (1967). The passage of gaseous emboli through the pulmonary vasculature. Resp. Physiol., 3, 219.

Masurel, G., Gutierrez, N., and Colas, C. (1989). Considerations on the pulmonary removal of circulating bubbles. Undersea Biomed. Res. 16 (Suppl.), 90.

Meltzer, R. S.; E. G. Tickner, and R. L. Popp (1980). Why do the lungs clear ultrasonic contrast? Ultra¬sound Biol. Med., 6, 23S.

Powell, M. R.; M. P. Spencer and O. van Ramm (1982). Ultrasonic Surveillance of Decompression. In: The Physiology and Medicine of Diving, Eds.: P. Bennett and D. H. Elliott. Bailliere Tindall, London.

Vim A.; A. O. Brubakk; T. R. Hennessy, B. M. Jenssen; and M. Ekker; and S. A. Slordahl (1990). Venous air embolism in swine: transport of gas bubbles through the pulmonary circulation. J. Appl. Physiol., 69,

Vik, A.; B. M. Jenssen; and A. O. Brubakk (1992). Paradoxical air embolism in pigs with a patent fora¬men ovate. Undersea Biomed. Res., 19, 361.
 
Thanks Dr. D for probably the most comprehensive reference list in regards to lung shunts I think to date, in any publication!

Did workers ever try to find the shunts in experimental animals or humans and attempt to repair them in those days?

I think part of the interest in PFO is that it is repairable and the controversy is whether a PFO is actually a shunt for fat or thrombotic emboli that cause strokes in the non-diving population. Thus, this work has broader application than just divers.


Dr Deco:
Hello readers:

Curiously enough, bubble arterialization though a PFO was almost never discussedprior to 1990. Most researchers targeted transpulmonic passage. This was associated with numerous gas bubbles in the venous return, a blockade of lung capillaries, and a rise of pulmonary artery pressure.

In the last decade and a half, we have seen a concentration on the PFO and a forgetfulness/neglect of the other mechanisms. Some references are provided below

Dr Deco :doctor:
 
Hello readers:

Vein-to-artery Stroke

As Saturation has indicated, a majority of the interest in the medical field over the PFO question arises from what is termed &#8220;paradoxical stroke.&#8221; This is also known as vein-to-artery stroke. Much information concerning diving has come from a &#8220;reverse spin-off&#8221; of medicine to the dive arena.

Considerably more interest - and money - is available when it concerns stoke in the general population. Divers are a recipient of this legacy.

PFO Repair in Animals

To my knowledge, there never was any attempt made to repair, or investigate, the arterialization pathway. Concepts/methods such as TCD and the number of heartbeats between contrast injection and the appearance of bubbles was not recognized in the 1970s and 80s.

Dr Deco :doctor:
 
https://www.shearwater.com/products/teric/

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