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"Michael J. Black" wrote:
>
> ... <snip>
>
> As for ibuprofen while diving, 800 mg every 4 hours or even as a
> pre-dive ritual seems excessive, as you probably only need one 200 mg
> tablet in a 24-hour period. God almighty you guys must bleed like
> hell if you ever cut yourself (ibuprofen prolongs bleeding time just
> like aspirin, not to mention the effects it has on your stomach).
Your uncivil rantings sir, are a waste of time. Open factual
discussion, not ill-toned rhetoric may be more appropriate. It's next
to impossible to give any hard line "best effect dose" which attains the
best of ibuprofins benefits with the least amount of side affects. I
would submit that it's part science, and part 'art' on behalf of the
diver. High doses are definitely required to gain benefit mind you, and
it would appear that at least a few others on this list are unaware of
its use and benefit. For the moment, I wish to address aspirin
specifically and not ibuprofen. Although both are used for the same
purpose, aspirin's use has been widely documented with respect to
decompression diving. I submit the following to whomever for the sake
of further discussion and intelligent hypothesis.
Aspirin is a powerful medication and is actually an analgesic and
an anti-inflammatory drug. Aspirin is a brand name in Canada;
acetylsalicylic acid is the generic name. ASA, a commonly used
designation for aspirin (or acetylsalicylic acid) in both the U.S. and
Canada, is the term used in Canadian product labeling. Aspirin is an
over-the-counter (OTC) medicine, and because it is so common and so
readily available, many people do not consider it a "real medication."
This is a common misconception and aspirin is a very "real drug." Its
use in staged decompression diving has been extrapolated from other
benefits that aspirin has been prescribed for (1).
Aspirin's main use in diving is to prevent blood clotting and
platelet aggregation. Although aspirin is referred to as a "blood
thinner," it does not actually "thin" the blood. Instead,
anticoagulants alter proteins in the blood that are responsible for
clotting while antiplatelet drugs prevent platelets from clumping and
forming clots. Aspirin functions to make the platelets less 'sticky',
thereby acting as an anti-coagulant. Aspirin is an aid; not a
substitute for proper hydration, even though its main benefit to the
diver is to allow improved blood flow and gas transport by increasing
tissue gas perfusion.
In vitro and in vivo studies have shown that hyperbaric pressure
increases red blood cell (RBC) aggregation (2). Enhanced RBC
aggregation in pathologic states can cause increased clotting. Both
aggregation and clotting hamper the transport of gas which may lead to
any number of hyperbaric related injuries. It is known that the
hyper-aggregability of platelets is remarkably important in the
pathogenesis of decompression sickness (3).
One investigation (2) examined the effects of pressure on RBC
aggregation in human volunteers. The hypothesis tested was that RBC
aggregation is increased during hyperbaric exposure. Subjects
participated in dives to 300 fsw in a chamber. Blood samples were taken
at the surface, at 66 fsw, and at 300 fsw. The median aggregate size
(number of RBC/aggregate) of RBCs was significantly increased at depth.
The deeper one goes, the greater the aggregate size. These results show
that even mild pressure increases RBC aggregation in the human
circulation. Therefore, aspirin is used as a preventive measure to a
known prohibitor of gas transport, which may lead to symptomatic DCS.
There are some controversial lines within the diving community
concerning the use of aspirin. All groups are aware of the later; the
segregation comes from discussion of aspirins effect on blood
viscosity. There are some who contend that aspirin will reduce blood
viscosity and therefore do more harm than good. Reduced blood viscosity
would reduce gas tensions and therefore contribute to micro bubble
formation.
It is unproven however, that aspirin will decrease the viscosity of
blood and contribute to micro bubble formation. Decreases in systemic
hematocrit (blood count of red cells) tend to decrease blood viscosity
and promote microvascular vasomotion and tissue perfusion (4,5), whereas
an abnormally high hematocrit increases blood viscosity and results in
clumping and aggregation of the erythrocytes, capillary occlusion and
regional redistribution of the circulation.
One study (6) examined the effects of aspirin and dipyridamole
(pronounced dye-peer-id-a-mole -- its a powerful platelet aggregation
inhibitor; antithrombotic adjunct) on platelet function, hematology, and
blood chemistry of saturation divers. 24 divers were assigned randomly
to 4 treatment groups. Group I received aspirin (325
mg) t.i.d. (ter in die, Latin meaning 3 times a day); Group II received
dipyridamole (75 mg) t.i.d.; and Group III received both drug regimens;
while group IV received matching placebo.
Double-blind procedures were followed. Treatment began 24-h prior
to a 48-h saturation dive (inclusive of 17 hour decompression) and
continued throughout and for 3 days after the dive. A post-dive
reduction in circulating platelet count was observed in all groups,
except the group that received aspirin only. Platelet survival was
shortened in all treatment groups. Five cases of Type I DCS occurred
and were treated by recompression, two in the aspirin plus dipyridamole
group, two in the dipyridamole group, and one in the placebo group; none
in the aspirin only group. Blood chemistry and hematology profiles
showed that divers with decompression sickness had elevated GOT
(glutamic oxaloacetic transaminase), GPT (glutamic pyruvic
transaminase), and CPK (creatinine phosphokinase is one of several
chemicals usually released in the blood after a heart attack, an
increase of this form of isoenzyme in the blood is a diagnostic clue to
tissue damage). Divers with DCS had more elevated cholesterol and
triglyceride levels, and greater reductions in platelet count, platelet
factor 4 and thrombin (an enzyme formed in the clotting) clotting time
than most other subjects. Subjects receiving either aspirin or aspirin
plus dipyridamole had fewer changes in these parameters. Failure of
aspirin to potentiate, or add to, dipyridamole may be due to other
actions of aspirin such as inhibition of prostacyclin (PGI2 )
synthesis.
(PGI2 , a prostaglandin, is formed mainly in the blood vessel walls and
slows blood platelet clumping. Aspirin, in doses as little as 4 mg/kg
of body weight, inhibits prostacyclin as well as thromboxane formation.
Prostaglandins may induce or inhibit platelet aggregation and constrict
or dilate blood vessels. For an in-depth overview on prostaglandin and
thromboxane biosynthesis; the role of steroidal and non- steroidal
anti-inflammatory drugs; the reader is referred to an excellent review
by Smith et al (7) )
This particular study (6) seems to favour the use of aspirin in a
hyperbaric environment, however further studies of the role of
antiplatelet drugs such as dipyridamole in decompression sickness may be
warranted. These results indicate that the combination of aspirin and
dipyridamole offers no measurable advantage over aspirin alone. This
study also suggests that antiplatelet drugs such as dipyridamole may
actually be a contra-indication for a hyperbaric environment.
Yet another study examined the hematology and blood chemistry in
saturation diving using antiplatelet drugs, aspirin, and VK744. Blood
chemistry and cellular parameters were studied before, during, and after
saturation dives in a habitat, on two separate occasions. The results
confirm previous observations and indicate that
post-decompression loss of platelets may be related to sequestering of
reactive platelets, possibly by microbubbles, and that the phenomenon
can be inhibited by some antiplatelet drugs.
Lastly, it should be stated that in vitro and in vivo research
clearly demonstrates the influence of nutrition on platelet aggregation
and clumping ie. eating fatty foods compounds the problematic blood
chemistry situation (8-11).
Aspirin is effectively used by many staged decompression divers who
can tolerate the drugs side effects. In general, sustained release
doses by divers, range from 325 mg to 600 mg, (single one time dose)
taken 60 to 120 minutes before a dive. There does not appear to be a
specific or "magic" dose to provide for the best protection with the
least amount of side effects. The anti-aggregating therapy usually
associated with hyperbaric treatment involves administration of
acetylsalicylic acid in low doses; 3.5 ~ 5 mg/kg of body weight (3).
During one study (12), platelet functions were studied after
various single doses of aspirin (75 mg, 150 mg, 300 mg, and 600 mg) in
20 males. Clotting time and platelet counts remained unchanged.
Significant de-aggregation of platelets occurred only with 600 mg of
aspirin. Another study (13) by Heavey et al, reports that an oral dose
of aspirin (600 mg) causes rapid and substantial inhibition of
bradykinin-stimulated PGI2 production, but recovery occurs within 6
hours; this implies that endothelial PGI2 synthesis would be spared most
of the time during dosing once daily with even this relatively large
dose of aspirin (13).
Yet another study (14), examined the effect of chronic
administration of variable low doses of aspirin on platelet
adhesiveness, platelet count, bleeding time and clotting time to find
out, as to how low the dose of aspirin needs to be in order to have an
effective antiplatelet effect in individuals who require such therapy
(meaning over a longer period of time). A statistically significant
reduction in the platelet adhesiveness was observed in all the groups,
but the best effect was exhibited by 50 mg of aspirin dose. Bleeding
time was also increased in all the groups but statistically significant
difference were observed with 50, 75 and 100 mg doses.
So far we have doses somewhere between 50 mg/day, minium for long
term chronic dosing; 325 mg t.i.d. for up to 5 days dosing (15); to 600
mg/day one time minimum effective dosage. If one cares to search, they
will find a myriad of studies for aspirin and effective dosages.
Therefore it is next to impossible to give any hard line "best effect
dose" which attains the best of aspirins benefits with the least amount
of aspirin's side affects. There are several brands of coated aspirin
such as 'Entrophen 10', an enteric coated tablet of ASA, which are
dissolved in the gut instead of the stomach (650 mg effective for up to
six hours or so). What is known however, is that antacids can decrease
the effectiveness of aspirin.
Since aspirin is an analgesic and an anti-inflammatory, where high
doses are used, it may mask mild symptoms of DCS. Many antihystamines
and corticosteriods used by divers for certain conditions, to aid in
ease of equalization, can have the same effect. Excessive bleeding may
also be a concern from an acquired injury such as cuts, bruises, broken
bones etc. Bleeding into the middle ear or sinus from a squeeze may
require special precaution as well. Every diver has minor trauma that
is usually of little consequence. This can become a major problem if
the diver is on perscription anticoagulants, however most authorities
(Bove, Davis, DAN, etc.) agree that divers taking coumadin or other
anticoagulants is either a relative contra-indication or an absolute
contraindication to diving and therefore not an issue (16). As well,
aspirin may have more benefits to the decompression diver, with less
side effects than those of anticoagulant drugs such as coumadin,
dipyridamole, heparin etc.
The added side bonus of aspirin in deep diving is of course, that
it helps prevent pain associated with CO2 headaches commonly attributed
to hard work and/or improper breathing techniques underwater. In short,
headache is a sign that something is not right, however it's
not a sure sign of CO2 buildup. The need for proper, slow,
moderate-sized deep breathing technique during extreme depth diving
cannot be overstated mind you.
--
Randy F. Milak
(1) Popovic P, et al. Levodopa and aspirin pretreatment beneficial in
experimental decompression sickness. Proc Soc Exp Biol Med. 1982
Jan;169(1):140-3.
(2) Taylor WF., Chen S, Barshtein G, Hyde DE, Yedgar S. Enhanced
aggregability of human red blood cells by diving. Undersea Hyper Med
1998; 25(3)167-170.
(3) Reggiani E, et al. Blood coagulation processes in decompression
sickness and hyperbaric therapy. Minerva Med. 1981 May
31;72(22):1383-90.
(4) Messmer K. Blood rheology factors and capillary blood flow, in
Gutierrez G, Vincent JL (eds). Update in Intensive Care and Emergency
Medicine, Vol 12, Tissue Oxygen Utilization. New York, Springer-Verlag,
1991, pp 103-113.
(5) Restorff WV, Hofling B, Holtz J, et al. Effect of increased blood
fluidity through hemodilution on general circulation at rest and during
exercise in dogs. Pflugers Arch 1975; 357: 25-34.
(6) Philp RB, Bennett PB, Andersen JC, Fields GN, McIntyre BA, Francey
I, Briner W. Effects of aspirin and dipyridamole on platelet function,
hematology, and blood chemistry of saturation divers. Undersea Biomed
Res 1979 Jun;6(2):127-46
(7) Smith WL, et al. Prostaglandin and thromboxane biosynthesis.
Pharmacol Ther. 1991;49(3):153-79. Review.
(8) Adam O, et al. Platelet aggregation and prostaglandin turnover in
man during defined linoleic acid supply with formula diets. Res Exp Med
(Berl). 1980;177(3):227-35.
(9) Temme EH, et al. Individual saturated fatty acids and effects on
whole blood aggregation in vitro. Eur J Clin Nutr. 1998 Oct; 52
(10):697-702
(10) Turpeinen AM, et al. Replacement of dietary saturated by
unsaturated fatty acids: effects of platelet protein kinase C activity,
urinary content of 2,3-dinor-TXB2 and in vitro platelet aggregation in
healthy man. Thromb Haemost. 1998 Oct; 80(4):649-55.
(11) Aoki H, et al. In vivo and in vitro studies of the inhibitory
effect of propofol on human platelet aggregation. Anesthesiology. 1998
Feb; 88(2):362-70.
(12) Jha S, et al. Effect of variable doses of aspirin on platelet
functions. J Assoc Physicians India. 1989 Apr; 37(4):269-70.
(13) Heavey DJ, Barrow SE, Hickling NE, Ritter JM. Aspirin causes
short-lived inhibition of bradykinin-stimulated prostacyclin production
in man. Nature. 1985 Nov 14-20;318(6042):186-8.
(14) Bose S, et al. Effect of variable low doses of aspirin on platelet
functions. Indian J Physiol Pharmacol. 1994 Jan; 38(1):56-60.
(15) Harding R, Hooper SB, Han VK, "Abolition of fetal breathing
movements by spinal cord transection leads to reductions in fetal lung
liquid volume, lung growth, and IGF-II gene expression." Pediatr Res
(1993 Aug)34(2):148-53.
(16) Bove F. Diving medicine, Atrial Fibrillation. Skin diver. Mar
98: pg 110
--
Randy F. Milak
--
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